Carb Back-Loading ™

Manual For Total Body Fat Control

John Kiefer, MS

DHPress

Carb Back-Loading™

Copyright © 2011-2012 by John Kiefer

All rights reserved. No part of this work may be reproduced or

transmitted in any form or by any means, electronic or mechanical,

including photocopying, recording, or by any information storage or

retrieval system, without the prior written permission of the

copyright owner and the publisher.

ISBN-13 (paperback): XXXXXXXXXXXXX

ISBN-10 (paperback): XXXXXXXXXX

ISBN-13 (electronic): XXXXXXXXXXXXX

ISBN-10 (electronic): XXXXXXXXXX

Series: F E D C B A 9 8 7 6 5 4 3 2 1

Trademarked names may appear in this book. Rather than use a

trademark symbol with every occurrence of a trademarked name,

we use the names only in an editorial fashion and to the benefit of

the trademark owner, with no intention of infringement of the

trademark.

Editorial Board: Bob Ihlenfeldt

Project Manager: Naomi Most

Cover Design: John Kiefer

This book is not medical or any other form of professional advice

that requires licensing in any jurisdiction. It is for scientific and

educational purposes only. Please consult a qualified health care

professional for medical advice. The author, any contributors,

publisher and copyright holder(s) (and their successors) are not

responsible for any adverse affects associated with any use of this

work.

Disclaimer

The Content presented herein is for informational purposes only

and intended for use by adults capable of understanding the Content

and capable of seeking medical advice from appropriately licensed

professionals when necessary or appropriate. Although I have

researched various topics extensively and attempted to organize

numerous issues associated with diet and exercise in a clarifying

manner, the Content is not intended as a substitute for professional

medical input or action. Always seek the advice of a qualified health

provider regarding a medical condition or your ability to apply the

Content in a safe manner. Please never disregard professional

medical advice or fail to seek it in a timely manner because of

something you have read anywhere, including here.

Contents

Get Started Now!

xii

About the Author

xiv

Acknowledgements

xvi

Section I

Introduction

Chapter 1

The Ultimate Drug

4

Chapter 2

Catalyst

8

Chapter 3

Cliff Notes:

Carb Back-Loading

14

Chapter 4

Modulated Tissue Response 16

Chapter 5

Always Improving

20

Section I

Essential Points

22

Section II

Bricks

Chapter 6

Controversy

26

Chapter 7

Insulin: The eXtreme

Growth Agent

28

Chapter 8

Carbs to Burn

30

vi

Chapter 9

Glucose Transport

32

Chapter 10 Why So Sensitive?

36

Chapter 11 Sensitivity, It Varies

38

Chapter 12 Exercise a Little Control

40

Section II

Essential Points

44

Section III

Mortar

Chapter 13 Some Assembly Required

48

Chapter 14 Best Breakfast Ever—None

50

Chapter 15 Eat At Night

52

Chapter 16 No Carbs, No Problems

56

Chapter 17 The Sweet Spot

58

Chapter 18 16 oz Carb Curls,

Post-Training

64

Chapter 19 Slam the Carbs

66

Chapter 20 Highly Inefficient Design

70

Section III Essential Points

76

Section IV

Aftermarket Add-Ons

Chapter 21 High Performance Tuning

80

Chapter 22 Omega-3s

82

Chapter 23 Medium Chain Triglycerides 86

Chapter 24 High-Insulinotropic Carbs

88

C a r b B a c k - L o a d i n g

Chapter 25 Whey Isolate

90

Chapter 26 Hydrolysates

94

Chapter 27 Leucine

96

Chapter 28 Caffeine

100

Chapter 29 Creatine

104

Section IV Essential Points

108

Section V

What To Do

Chapter 30 Tell Me How,

Hold the Details

112

Chapter 31 Strength Accumulation

& Density Bulking

114

Chapter 32 Preparation Phase

116

Chapter 33 Upon Waking

120

Chapter 34 Low-Carb Mealtimes

122

Chapter 35 Pre-Training

130

Chapter 36 Intra-Training

132

Chapter 37 Post-Training

136

Chapter 38 Carb Loading Mealtimes

140

Chapter 39 Before Bed

144

Chapter 40 Off-Days

146

Chapter 41 All Day Supplementation

150

Section V

Essential Points

152

viii

Section VI

Nobody’s Perfect

Chapter 42 Customize

156

Chapter 43 Training Fasted

158

Chapter 44 Middle Training

162

Chapter 45 Late Night Sessions

164

Section VI Essential Points

166

Section VII

Dos and Don’ts

Chapter 46 Everybody Needs Advice

170

Chapter 47 Don’t Be a Fat Kid

172

Chapter 48 Gluten Allergies

174

Chapter 49 Don’t Let Training

Derail You

176

Chapter 50 Cardio

180

Chapter 51 Gender Differences

184

Section VII Essential Points

186

Section VIII

Experiences

Chapter 52 Case Study:

Jay DeMayo

190

Chapter 53 Professionals

196

C a r b B a c k - L o a d i n g

Chapter 54 Everyday Success

Stories

206

Section IX

Appendix

Appendix A FAQs

216

Appendix B Ultra-Low Carb Vegetables

222

Appendix C Carb-Needs Calculators

224

Appendix D Pre Carb-Mealtimes Macro

Calculator

230

Appendix E Sample Days

238

Section X

References

x

C a r b B a c k - L o a d i n g

Get Started Now!

Read Essentials: p22, 44, 76, 108, 152, 166 & 186.

Read the FAQs, p216.

Determine carb needs, p224.

Determine protein and fat needs, p230.

Read attached sample diet plans (see Appendix E)

Get Jacked!

xii

C a r b B a c k - L o a d i n g

About the Author

KIEFER

WARNING: He goes only by Kiefer

John Kiefer is a highly sought after training and

nutrition consultant. To guide his work, he has

read over 40,000 medical research papers covering various facets of

human biology. His extensive knowledge of human nutrition and

performance is tempered by 15 years of experience applying,

observing and refining his methodology.

Kiefer holds two B.A.s (Mathematics and Physics) from Otterbein

College and a Master’s of Science in Physics from the University of

Florida. He published his first diet book for radical fat loss, The

Carb Nite® Solution, in 2005, which can be found at

http://www.CarbNite.com.

He is currently an advisor to Muscle&Fitness and Men’s Fitness

magazines and his clientele includes world-record powerlifters,

internationally ranked fitness competitors, CEOs and recreational

athletes who want super-human results without the super-human

torture.

Find more of Kiefer’s work at http://DangerouslyHardcore.com.

xiv

C a r b B a c k - L o a d i n g

Acknowledgements

I want to thank:

Brian Carroll for trying out a crazy new diet from a crazy physicist

and spreading the word once he realized I’m not a hack;

Bob Ihlenfeldt for his honest impression of the first version of this

book, which was that he hated it, he hated me and hated Carb Back-

Loading—luckily, that meant he thought it was pretty good;

Naomi Most for helping keep me and DH.com organized so I could

finish this book;

Caroline Gick for helping out in a pinch;

And everyone else who made this project possible.

xvi

C a r b B a c k - L o a d i n g

Section I

INTRODUCTION

S e c t i o n I : I n t r o d u c t i o n

C a r b B a c k - L o a d i n g

Chapter 1

The Ultimate Drug

Carbs are a drug. As with any drug, knowledge of

effects—and side effects—is the only way to guarantee the right

outcome. Drugs often hit the market before all the effects show,

leaving consumers scrambling for answers, alternatives and

adjuncts. Carbs share this trait, having become a part of the human

diet millennia ahead of our capacity to understand their full

influence. Years of ignorance left a trail of recommendations

prepackaged with folk-lore, hearsay and guesswork as to what type

to eat, when to eat and what, exactly, their role in the body is.

This common-sense approach to carb inclusion ranges from eating

carbs first thing in the morning, to cycling them; some people go

anabolic—eating carbs just on the weekend—and still others have

just one Carb Nite® a week. But only recently have people started

eating their carbs at night.

Oh that’s right, Oprah’s trainer says don’t eat them at night. As a

matter of fact, don’t eat anything at night. That’d just be dumb

according to the supposed experts. There’s nothing to gain but fat.

Wouldn’t it be nice, though, if a pepperoni pizza before bed—the

whole pizza—could cause fat loss and make muscles grow? Stop

right there, they say; that’s crazy talk.

4

S e c t i o n I : I n t r o d u c t i o n

Admittedly, not everyone’s concerned about their carbs, as some

people eat them at-will without affecting strength, muscle mass or

waistline. The rest of us, unfortunately, need to control the starchy

dinners and sugary sweets. Pancakes for breakfast; sure and how

about a serving of moobs—man boobs for the un-indoctrinated—in

a few weeks to go with it.

For those who don’t need to worry, the pancakes won’t matter, nor

will ice cream or pasta or even post-workout nutrition. They’re

freaks. Most of us seethe over the inequity of it because despite how

carbs cause body fat stores to bulge, carbs spark muscular growth

too. Forget the sweet savory taste, forget how they turn a boring

slab of breast meat into chicken and dumplings—growing huge

rounded shoulders, sculpted pecs and massive quads requires carbs.

They’re a means to an end.

Most people need the carbs to approach the realm of freakiness, but

on the way, fat accumulates and hides the hard work. That’s what

carbs do, they make things grow. They make lots of things grow like

fat cells and muscle cells. Carbs don’t discriminate. The solution:

limit the carbs, cut them out or cycle them in some way. It’s not fun

going sans carbs and even less fun going months without, only to

lose some of the muscle and strength gained along the way.

We can do better.

That’s what this book is about. Forget about the constant cycle of

bulking up, leaning down, bulking again, leaning down again and so

on, taking one step backward for every two steps forward. It’s time

to gain muscle and lose fat at the same time. An extra 100 pounds of

body fat is not a prerequisite, either. Starting at a typical low-20’s

C a r b B a c k - L o a d i n g

T h e U t i m a t e D r u g

body fat percentage, anyone can gain muscle, strength and maybe

even good looks while dropping into the sub-15% body fat range

and lower. No magical supplements or crazy food combinations

needed; it’s as easy as pie…literally.

I don’t live in a vacuum and know that these promises float around

the internet like fairy dust, and they’re about as real too. The empty

promises only empty the wallet. Yet gurus everywhere chant the

mythical formula: gain muscle and lose fat at the same time with

ease. Hell, the cover accompanying my article in the May 2011

Muscle&Fitness advertised Carb Back-Loading as The Holy Grail of

Dieting. Had I been a typical reader, I would have been skeptical, as

were the magazine editors when I first discussed it with them—

until they tried it. And loved it.

I'm not going to convince anyone to read further or to rush to the

checkout counter for those flipping these pages in the bookstore. I'm

not going to say, I’m awesome, trust me. I won’t even mention how

stupid-simple the program is and how anyone can get results with

only half-assed effort. But I will issue a warning: if you keep

reading, the excitement and impatience to achieve the physique of

your dreams—or your significant-other’s dreams—will overwhelm.

Knowledge is power; after reading this book, you’ll be omnipotent.

6

S e c t i o n I : I n t r o d u c t i o n

C a r b B a c k - L o a d i n g

Chapter 2

Catalyst

Every diet worth its salt has an origin story, some reason

the thing exists in the first place, the catalyst. Most of the time, it's

fabricated, a lot of marketing with a smidgen of personal history for

authenticity. Carb Back-Loading’s origin story is nothing of the

kind. I invented it twenty years ago when a group of military

scientists drafted me to become part of black-ops human

enhancement project with the ultimate goal of...

Wait a second. That's not what happened at all. I've been spending

too much time on the Internet again.

If no super-soldier origin story exists, then how did an average guy

from Podunk, Indiana come up with what everyone's chased for

years?

Simple: I was a fat kid. A very smart, very tenacious, very self-

conscious fat kid.

The details bore the paint off the walls, and there’s no reason to

share them, so here’s the short of it: my parents fed me breakfast

cereal, pop tarts and coca-cola, I grew moobs, students made fun of

me, my gym teacher made fun of me, I started working out and it

changed my life—sort of. Training brought strength, muscle and a

8

S e c t i o n I : I n t r o d u c t i o n

definite change in my physique, but I was still doughy. I wanted

jacked and I wanted ripped.

My diet needed help. Hell, my family taught me that washing down

a grilled cheese sandwich with ketchup packets constituted a

healthy lunch. Grains, dairy and vegetables: what more could a guy

need? The fact that I believed it is embarrassing enough, but the

physique it created was more so. The epiphany took time, but I did

realize that maybe my family—and their trouble with their own

weight—hindered me rather than helped. I did what any science-

minded youth would do, I hit the books.

This was before the Internet, so I literally hit the books. I quickly

learned that the books weren’t any better than my parents because

none of them could produce the results I wanted. Maintaining

muscle while leaning down seemed beyond the knowledge of the

most famous diet writers. And forget about getting shredded.

The first serious reduction in my body fat came with my near

religious dedication to—in my opinion—the first legitimate attempt

at harnessing the drug-like potential of carbs, Dr. Mauro

DiPasquale’s, The Anabolic Diet. This was back in 1995 when

science still didn’t know about things like ghrelin, leptin, nutrient-

activated protein synthesis channels and the function of glucose and

fatty acid transporters, but we were discovering new things every

day. The Renaissance had started and Dr. DiPasquale took advantage

of the emerging information, filling gaps with his experience.

The Anabolic Diet didn’t take me all the way, however, and I

definitely didn’t gain muscle, even when I tried the bulking phase.

C a r b B a c k - L o a d i n g

C a t a l y s t

But I didn’t gain body fat either, I lost it—exclusively. For the first

time in my life, I didn't have love handles.

That was a long time ago. Discoveries built upon discoveries,

growing faster than all but the most diligent—and geeky—could

keep up with, and now, even they can’t ingest the deluge quickly

enough. Everybody and their brother learned that to become

successful in the fitness world took no real knowledge at all: throw

out a few buzzwords, promise a quick-six-pack or eight minutes to a

sexy figure and spew random opinions about health on the Web and

success would follow. Who could have guessed that a Renaissance

would bring the Dieting Dark Ages that exist today?

I couldn’t take it anymore. The tallest boots I found still didn’t reach

high enough to avoid getting splattered with pseudo-knowledge

excrement. I devised The Carb Nite® Solution, an ultra-low carb

diet that includes a night of almost literal binging on carbs: pizza,

donuts, pasta, cupcakes, pretzels, popcorn, etc.

I spent a ridiculous amount of time researching the human body to

refine Carb Nite® to cause massive fat loss without a loss of muscle

tissue and without devastating metabolism in the process. No

excrement necessary. I’m not here to talk about Carb Nite, though,

because it has one fatal flaw: it doesn’t allow much muscle growth

unless starting off portly.

A few years ago, I found myself engineering software for a large

company, glued to my chair for some 80 hours per week. I didn’t

train, I didn’t eat well and it showed. My body reverted to its true

fat-kid nature, not only in function—because of all the shit I ate—

but also in form. I felt and looked disgusting.

1 0

S e c t i o n I : I n t r o d u c t i o n

Not a big deal. I quit my job, decided to build a business for myself,

trained my ass off and followed Carb Nite with the blind dedication

I once had for The Anabolic Diet. In no time, I dropped 20 lbs of fat,

was shredded, vascular, freaky and lifting big. But as short of a time

as it took to get back to normal, I became frustrated. I was stuck at

normal.

I didn’t want to be just shredded, I wanted to get huge again, back to

my 230 when I was cut and jacked, before diving full-time into the

software world. No matter how much I ate, even the addition of a

second Carb Nite per week, my muscle mass didn’t budge. What did

happen? I stayed shredded, felt exhausted most of the time and

started accumulating injuries.

Know the song Baby Got Back, by Sir Mix-a-Lot? One-hit wonder

without a doubt and I believe he still performs Baby Got Back at

some of the more progressive Bar Mitzvahs. Diet writers are like this

too: one-hit wonders who keep peddling an out-of-date product.

They don’t realize, or refuse to realize, that science learns more each

day and we’d be wise to take lessons, adapt and prosper.

That’s why I’m always poring over research. Maybe it’s a strength

routine to correct scoliosis, maybe it’s about cellular receptor sites

like the mammalian target of rapamycin, or maybe epigenetics and

why all those pop tarts as a kid screwed up how my genes express,

making it easier to stay and get fat. On the day of the epiphany that

sparked the creation of Carb Back-Loading, I was reading papers

about using resistance training to help type II diabetics control their

blood sugar.

C a r b B a c k - L o a d i n g

C a t a l y s t

This might seem like an odd topic to inspire the creation of the Holy

Grail of Dieting, but that’s where it started. I’ll explain with more

detail later, but basically, in type II diabetes the cells of the body no

longer react to insulin and, therefore, can’t absorb sugar. After

resistance training, however, the muscles of diabetic subjects can

absorb and burn sugar without increasing their sensitivity to insulin.

This set off a cascade of thoughts and a new research focus.

Before I explain why and how it works, maybe I should first tell you

how to do it.

1 2

S e c t i o n I : I n t r o d u c t i o n

C a r b B a c k - L o a d i n g

Chapter 3

Carb Back-Loading:

The Cliff Notes

Carb Back-Loading runs contrary to about everything out

there. It bucks many established norms. Many of these norms grew

from a time before a deep understanding of human metabolism and

performance existed, making some of the most common truths no

more than anecdote. Take breakfast’s place as the most important

meal of day in health folklore, or the idea to eat most calories before

evening or even ensuring that the first meal of the day needs to be

carby and fatless. Not a single one of these can be established as fact.

It’s not because scientists never researched the topics. They have.

That’s how I know they’re not fact; the research shows that none of

these ideas is true.

Carb Back-Loading snubs all three of these recommendations and

does so because of the existing research, not because I want to be a

contrarian. Back-Loading does, however, also complement many

lifestyles. Even with these seemingly thrown-in-for-convenience

rules, I base the prescription on science rather than marketability.

What results is an easy, ridiculously effective plan.

1 4

S e c t i o n I : I n t r o d u c t i o n

Carb Back-Loading Cliff Notes

1. Shift calories to later in the day, eating lighter in the

morning and early afternoon, and feast at night. This

may include skipping breakfast.

2. Keep carbs at an absolute minimum throughout the

day until training.

3. Train in the afternoon, at around 5pm or so.

4. Start ingesting carbs after your training session, up to

30 minutes later.

5. Continue eating carbs throughout the night.

That’s all there is to it. It may seem too good to be true, that I

designed this simply to sell, but it's how the body works. Eat bacon

and eggs, maybe a chicken salad, a few nuts, cottage cheese, a

hamburger patty with a tomato and some mustard—fat and protein

with some fiber—before training. Train in the evening, say from 5

to 6:30, then start slamming the carbs. When I say slam, I mean

slam. Pizza, French fries, donuts, sandwiches, ice cream, whatever,

as long as there’s carbs involved.

C a r b B a c k - L o a d i n g

Chapter 4

Modulated Tissue

Response (MTR™)

To the less astute, Carb Back-Loading may look like

normal nutrient timing: eat carbs post training, end of story. But this

misses the point—it misses the whole target. The mechanisms that

allow Carb Back-Loading to build muscle while simultaneously

losing fat with ease depend on daily biological rhythms, bio-

molecular manipulation and, unlike most diet protocols, a specific

window of time in which training should occur.

One of the guidelines is to train in the afternoon. Back-Loading

accommodates other training times while remaining simple but, as I

explain later in the book, the best results will come with an

optimum training schedule.

The reason is a principle I call Modulated Tissue Response™, or

MTR. It may sound complicated or esoteric, but the gist is not. MTR

describes the process by which we give each tissue of the body a

specific instruction, either through diet, activity or both.

Understanding the interaction of food, exercise, and daily rhythms

gives control over any aspect of the body, from health to

performance or simply aesthetics. MTR makes getting and staying

ripped stupid-simple, or it can make dropping even a few pounds of

fat impossible.

1 6

S e c t i o n I : I n t r o d u c t i o n

I am not going to tell a story involving post-WWII Bulgarian

research that defines the principles of MTR. Not until the last

decade has experimental methods existed to develop targeted

procedures of body-manipulation. Sure, we knew the basics: eat too

much and get fat, train enough and get muscular—but everything in

between was a crap shoot and created an industry of pet-programs

without basis in science and often without real-world results. Any

rationale—illogical or not—was enough to convince the desperate.

Hope fostered an unscrupulous industry of shit-slingers.

MTR utilizes the latest research to target and manipulate

biomolecular signals to achieve any goal with the least possible

effort. If I could choose a tagline, it would be work smarter, not

harder. This bleeding-edge research allowed the creation of the

soon-to-be-released Shockwave Protocols that integrate training

and diet for maximum results toward various goals. Carb Back-

Loading forms an integral component of the protocols.

Everyone, every day utilizes MTR. Look at the typical American,

the result of undirected MTR. The lack of activity tells the body to

lose muscle and bone, to waste and weaken; the standard desk-

posture tells the trapezius muscles to enervate and lengthen and

pecs and front delts to shorten and tighten; eating carbs while being

inactive signals fat cells to multiply and expand; and because they

give the body far more calories than it needs, it becomes diabetic,

the body’s last attempt to prevent the addition of more body fat.

Understanding MTR makes one thing clear: sole responsibility for

how the body looks and functions lies with the owner.

On the other hand, even a little direction creates huge change.

Training gives muscles the signal to grow, redirecting the growth

C a r b B a c k - L o a d i n g

M o d u l a t e d T i s s u e R e s p o n s e ( M T R )

signals produced by eating food. Lift heavy weights, eat carbs and

protein and muscles expand and strengthen, which in turn

strengthens bones and increases nervous system efficiency. But the

carbs give fat cells the instruction to grow as well. The side effect is

expanding fat mass along with muscle mass. Our signaling is still

100% anabolic.

Of course the signaling should be anabolic; growth requires anabolic

signals. That’s exactly what anabolic means, stimulating tissue to

grow. Catabolic, a word loathed in the health and fitness

community, means to destroy tissue. Testosterone is anabolic for

muscle tissue; estrogen is anabolic for fat tissue. Insulin is anabolic

for muscle and fat tissue; cortisol is anabolic for fat tissue and

catabolic for muscle tissue, but, depending on conditions, can be

catabolic for fat tissue instead. The list of actions goes on and on.

The short of it: hormones and other signals set the thermostat to

grow or shrink based on a large set of complicated interactions.

Manipulate these signals and transform the body. Even medication

plays a part. Think about it: 100 years ago the average person

needed to exert an incredible amount of effort to reach 300 lbs, but

now that food science and the drug industry have mastered the

correct signaling process for unlimited fat mass, we longer need to

pay a nickel to see the fat man or woman at the carnival. Sit in front

of Walmart and watch as 300-plus pounders stream by in herds.

MTR, however, does not and cannot define one perfect diet, as

many experts and authors like to assert about their plans. These

experts pick up a single fact or study—or worse, an unfounded

personal belief—and push it as the only option. There are no

alternatives, they say, but what they mean is that they know little

1 8

S e c t i o n I : I n t r o d u c t i o n

about the human body. They may know one diet and its effects, and

the rudimentary knowledge to defend it, but take them from their

sweet spot, and they're clueless.

No absolute best diet exists; no absolute best diet exists for anyone,

but there is an absolute best diet at a specific time for a specific goal.

This makes the principles of MTR invaluable by offering the

opportunity to fine-tune the body through diet and training to meet

any need at any moment. Acquiring the knowledge—not just a

collection of facts, but experience applying the information—to

competently invoke MTR takes a massive commitment, the time for

which few have.

But don’t worry, my job is to understand MTR and describe how to

use it. In this book, I teach a specific method of combining MTR

principles—Carb Back-Loading—to enhance performance and

aesthetics. You can use the content as a synergistic-whole or dissect

it, decompose it and reassemble it for other purposes. Each section

contains enough information to bend the MTR methods to your

needs if your needs are different than wanting to look and perform

like a super hero.

C a r b B a c k - L o a d i n g

Chapter 5

Always Improving

The Version 1.0 on the cover of a performance oriented

nutritional guide might seem odd. I designated this book Version

1.0, not because I engineer software—well, it obviously has

something to do with that—but because any nutritional protocol

claiming to be the bleeding edge needs to adapt quickly as new

research unfolds and as the author gathers more experience.

As such, the old publishing model of first edition, five years on the

shelf, second edition, five years on the shelf and so on is defunct and

for human performance manuals detrimental. As limiting as this

old-style procedure may be, it is mimicked by online eBook

publishers.

Adopting antiquated systems is not my style. I like to forge new

paths, so I decided to do the same here. In the software world

companies release the best product available at the time, then make

improvements as rapidly as possible. They designate each release

thereafter with versions, minor revisions or additions being labeled

by a 1.1 or 1.2 and major revisions—new editions in old-speak—

being labeled 2.0, 3.0, etc.

I made this mistake with my first published book, The Carb Nite

Solution, and now after five years, I feel I could have been adding

2 0

S e c t i o n I : I n t r o d u c t i o n

periodic refinements, producing an exceptional manual. The

information it contains is still cutting-edge and, most importantly, it

works better than its competitors. But it's no longer bleeding-edge.

As I incorporate newer information and add alterations based on

mounting experience, I will release new versions as warranted, and

for those of you jumping onto the ground floor with Version 1.0,

each minor upgrade will cost nothing; and each major upgrade will

be steeply discounted.

C a r b B a c k - L o a d i n g

••••••••••••••••••••••••••••••••••••••••••••••••

Section I

Essential Points

Carb Back-Loading Cliff Notes

1. Shift calories to later in the day, eating lighter in the

morning and early afternoon, and feast at night. This

may include skipping breakfast.

2. Keep carbs at an absolute minimum throughout the

day until training.

3. Train in the afternoon, at around 5pm or so.

4. Start ingesting carbs after your training session, up to

30 minutes later.

5. Continue eating carbs throughout the night.

Modulated Tissue Response (MTR)™

The ability to select which tissues grow and which shrink, e.g.

growing muscle while losing fat.

2 2

S e c t i o n I : I n t r o d u c t i o n

C a r b B a c k - L o a d i n g

Section II

BRICKS

2 4

S e c t i o n I I : B r i c k s

C a r b B a c k - L o a d i n g

Chapter 6

Controversy

Carbs cause controversy. While the health experts and

celebrity doctors battle over whether humans need carbs to

survive—we don't—the more performance minded nutrition

experts ponder an intelligent question: how best can we use carbs to

achieve various goals?

Science has yet to answer this question for all the various athletic

scenarios. Researchers drag trusted assumptions, like the

dependence of endurance training success on carbohydrates, into

the laboratory for verification and discover that the assumptions

were worthless. Deeper exploration of the carb conundrum reveals

that carbs impart little benefit except when used in precise, timed

fashion. For endurance, achieving maximum performance does not

require carbs during the training phase; but for peak performance at

the event, the body needs carbs. Precision is key.

To reach that level of precision, however, the simple ideas handed

down through the years about food, particularly carbs and insulin,

need to be modified and sometimes abandoned. With all the

discussion about sugar and insulin in the media, it might appear that

I'm wasting time talking about the two. Turn on the TV, fire up Dr.

Oz and listen to how simple it sounds: eat carbs, the carbs cause a

rise in insulin levels and then the insulin pushes the carbs into cells

2 6

S e c t i o n I I : B r i c k s

for energy. Throw in a little type II diabetes and the cells just don't

listen to insulin and then sugar floats around in the bloodstream

doing nothing.

For the average person who needs to lose 50 to 100 lbs of pure fat

and is probably only a week away from full-blown diabetes, this

explanation is good enough. But if you're 15% body fat, want to gain

30 lbs of pure muscle and maybe lose a few percentage points of

body fat along the way, you need to know more than 6th-grade

basics.

C a r b B a c k - L o a d i n g

Chapter 7

Insulin: The eXtreme

Growth Agent

Most people with whom I work don't fully understand the

function of insulin. From the information spewed all over the web

by the current cavalcade of health gurus, I know why: many of the

experts don't quite get it either.

In the health industry—to distinguish from the scientific

community—people see insulin like lighter fluid. Sugar is fuel. Hose

it down with a little insulin and a roaring inferno ensues. This is not

the case. Insulin’s main function in the body is anabolic: it wants to

build stuff. That’s why insulin rules amongst the anabolic elite: it

makes everything grow from muscle mass, fat mass and even

glycogen, which is essentially human starch.

Insulin, however, has no real plan about how to build anything, nor

does it participate directly. Its job—the most critical in any building

project—is to transport raw material. Insulin alerts cells to the

presence of material and gets them ready to absorb. This goes for

everything from blood sugar to cholesterol molecules1.

Most cells can absorb these raw materials to some extent without

insulin, but insulin turbo charges the process, which I’ll explain

later. A host of factors determines how cells use the raw material,

but if more material flows in than the cell needs, it’s going to store it

2 8

S e c t i o n I I : B r i c k s

as something: triaglycerol (fat), glycogen or even muscle tissue (of

which there is a type that’s made for storing protein and is

essentially non-functional).

Insulin does seem to know which material should be used first,

however. That’s why when insulin’s around, not only is it anabolic,

but it’s greatly anti-catabolic. It can stop muscle protein

breakdown2—which is good—but it also stops the body from

releasing and burning fat3. When insulin levels drop, however, fat

burning goes through the roof4. When insulin is high, it increases

the efficiency of fat storage—insulin makes storing fat easier for the

body5.

Eating carbs with all 6 to 8 of the traditional every-two-hour meals

tells the body that if there’s excess material, do something with it.

Protein, sure, is going to be used for tissue repair and growth,

enzyme and hormone production and so on. Fat, well, excess fat will

get stored as fat. For carbs, if glycogen levels are full—which they

normally are—fat cells convert the excess to fat before storing it

away.

The point: don’t think you need super-elevated levels of insulin

24/7. You don’t. It’s extremely useful to elevate insulin levels at

times, and detrimental at others. Carb Back-Loading is the easiest

way to optimize your eating and training schedule so that insulin is

always targeting the correct tissues while not interfering with fat

burning.

C a r b B a c k - L o a d i n g

Chapter 8

Carbs to Burn

Throughout this book I make reference to low-carb

portions of the day and yet meal plans located later in book contain

lots of vegetable suggestions like lettuce, asparagus, some tomatoes,

olives, cucumbers and so on.

Without clarification this may seem oxymoronic. It’s not. What

doesn’t make sense is using chemists' classifications for

carbohydrates instead of a modern system that recognizes effects on

the endocrine system. From the body’s point of view, only two types

of carb exist: usable carbs and fiber.

Carbs, in general, as is well known, cause a release of insulin, get

burned in lieu of fat, augment blood sugar levels and get stored as

fat. This last condition occurs when eating more than the body

needs at that moment, as I alluded in the previous chapter. These

burnable, fat-inducing carbs include sugar, starch, glycerine and

sugar alcohols—also called polyol—and make up what I term usable

carbs.

Fiber, however, doesn’t do any of these things and often does the

opposite. The only way for the body to get energy from fiber is

through fermentation in the colon1. The result of the fermentation

is not sugar or alcohol, but short chain fatty acids. Fiber—a

3 0

S e c t i o n I I : B r i c k s

carbohydrate—ultimately gets used as fat. This changes the calorie

count seen on standard U.S. nutritional labels significantly.

I didn't add fiber to the meal plans to make a performance oriented

diet look healthy. I am, however, using a bit of trickery that if the

health experts did know, they could probably get people to eat their

fiber. By including fiber, up to 20 percent of calories from a meal get

lost2. Beside other potential health benefits, fiber cuts calories while

creating a sense of fullness. If using Carb Back-Loading for fat loss,

including fiber enhances results.

So you can eat fiber during the low-carb portions of the plan but the

rest of the carb family fall within the usable carbs category because

the body uses them for fuel in lieu of fat—this includes glycerine3

and the polyols4. Avoid usable carbs during the low-carb part of the

day. Don't worry: you'll include them in mass quantities in the

evening.

Common Polyols:

Initial Calories5 and Calories After Regular

Consumption6

Calories After

Name

Initial Calories

7 Days

Erythritol

0.2

0.2

Isomalt

2

«4

Lactitol

2

[no data]

Maltitol

2.1

3.5

Mannitol

1.6

[no data]

Sorbitol

2.6

3.6

Xylitol

2.4

«3.5

C a r b B a c k - L o a d i n g

Chapter 9

Glucose Transport

In the chapter on insulin, I said that insulin helps provide

nutrients to cells, but it doesn't carry anything into cells. As a

matter of fact, if insulin were needed to carry sugar into all cells of

the body, then the sugar couldn't get into pancreatic beta-cells in

the first place to trigger the production of insulin. Insulin does not

shuttle sugar into cells. Specialized structures called GLUTs handle

that.

GLUT (pronounced 'gloot') stands for glucose transporter, which

comprises a family of proteins that belong to the Solute Carrier

family 2 (SLC2) group1. As the name implies, members of this family

of proteins carries things. We know of 14 GLUTs, named creative

things like GLUT1, GLUT2, … Despite their name, not all GLUTs

transport glucose into cells: some carry fructose (GLUT5); others,

polyols2.

GLUT reside in the jelly-like outer coating of cells. GLUT1-3 all

transport glucose and are always ready to do so. If a cell contains

enough of these GLUTs, it can absorb sugar whenever blood sugar

levels rise. The liver and cells of the central nervous system can

always use sugar whether there's insulin around or not1,2.

3 2

S e c t i o n I I : B r i c k s

The next GLUT, GLUT4 and its cohort GLUT12 are different. Both

transport glucose, just as GLUT 1-3, but are not normally exposed

on the cell’s surface. Rather, GLUT4 and 12 tuck below the surface

and within the cellular membrane, preventing them from

transporting sugar, even if blood levels rise to threatening levels.

Despite the withdrawn nature of GLUT4 and 12, they are the most

important of the GLUTs for this discussion.

Cells that contain GLUT4 and 12 react to the presence of insulin by

moving these GLUTs from the interior of the cellular membrane to

the surface3. This insulin-mediated translocation of the GLUT

enables the pathway through which high volumes of glucose enter

the cell. Once within the cell, glucose might be used to produce

energy or a cell might store it as glycogen or as triaglycerol. Since

GLUT4 and 12 act identically, I’ll use tGLUT to refer to both.

NOTE: Both GLUT4 and GLUT12 predominate

in muscle tissue and must translocate before trans-

porting glucose into cells. The two together are

referred to as tGLUT.

To illustrate the translocation process, I’ll use the example of eating

a banana. After the banana digests and sugar enters the bloodstream,

any cell that already contains GLUT1-3 will start sucking up the

sugar: the liver, nervous system cells and most importantly for our

discussion, the beta cells of the pancreas.

The beta cells produce insulin in response to the concentration of

glucose present in the bloodstream—the faster the sugar enters the

bloodstream, the greater the release of insulin. As the freshly

produced insulin traverses the body, it causes tGLUT to rise to the

C a r b B a c k - L o a d i n g

G l u c o s e T r a n s p o r t

surface of cells. Once this happens, the tGLUT-containing cells

absorb glucose and do whatever they feel like with it.

What tissues possess tGLUT? GLUT4 and GLUT12 represent the

predominant types of GLUT in skeletal muscle. Fat cells

unfortunately also contain abundant tGLUT. Because both muscle

and fat contain the same tGLUT, eating carbs sparks simultaneous

growth of both—biceps get jacked, but love handles start hanging

over the ever-tightening belt. It's this coupling or tying together of

growth signals for fat and muscle that makes people believe that

muscularity includes some level of fat-gain.

You don't need to resign yourself to such a fate. Properly structured

use of MTR makes growing muscle and losing fat simple by

decoupling the growth response of the two tissues. Carb Back-

Loading is the result.

3 4

S e c t i o n I I : B r i c k s

C a r b B a c k - L o a d i n g

Chapter 10

Why So Sensitive?

Being sensitive is often considered a bad thing for men.

Woman, would you want a guy who's crying all the time or who sits

on the steps after a physique contest choking back the tears shed

over a 4th place finish? I didn’t think so. Nothing repels the opposite

sex like the sound of sucking back one's mucus.

Doctors and pharmaceutical companies, personal trainers and

nutritionists think of a particular type of sensitivity as good for

everyone: insulin sensitivity. I would agree if discussing obese,

sedentary individuals. Such people need to increase their sensitivity

to insulin or risk becoming sick and suffering an amputation or two

before dying. Type II diabetes—characterized by a lack of insulin

sensitivity—kills people, but what does it mean to be insulin

sensitive or the opposite, insulin resistant?

In terms of the glucose transporters, insulin sensitivity only means

that when insulin hits muscle or fat, tGLUT rises to the surface and

begins clearing glucose from the blood stream by pulling it into

cells. For someone without much fat, muscle tissue absorbs most of

the sugar. Chubby folk, however—or formerly chubby —have a lot

of fat cells that will also soak up the carbs. Being insulin sensitive,

therefore, means fat and muscle can absorb glucose, and fat cells will

most likely store it…as fat.

3 6

S e c t i o n I I : B r i c k s

When tGLUT respond strongly to insulin, translocate to the cell

surface quickly and in abundance, cells are sensitive to insulin. If

this translocation is less than ideal, then it’s some degree of insulin

insensitivity and covers the spectrum from slightly insensitive—

some tGLUT response, but not total—to completely insulin resistant

where little to no tGLUT moves.

When resistant, no matter how much insulin the body produces, no

matter how much bathes muscle and fat cells, tGLUT never comes

to the surface and the two tissues that once cleared the majority of

sugar from the blood stream can't. Type II diabetics pretty much fall

into the completely-insensitive category.

That's the crux of it: insulin resistance makes it very difficult to

continue getting fat (although, normally, someone who has diet-

induced type II diabetes is pretty fat), but it's also difficult to grow

new muscle. Remember, insulin's main role is to make things grow.

Get too fat and the body tries to shut down the ability to get fatter,

i.e. prevents fat cells from absorbing more fat. Luckily, we live in

the modern age where doctors can prescribe drugs like metformin

and allow people to get even fatter.

On the other hand, insulin sensitivity helps trigger muscle growth

and recovery from exercise, but also increases fat accumulation. It's

the ultimate Catch-22 for anyone who cares about aesthetics. In a

perfect world, we could stop our fat cells from absorbing sugar, but

continue to allow our muscle cells to do so...or maybe it's possible in

a not-so-perfect world with the perfect diet.

C a r b B a c k - L o a d i n g

Chapter 11

Sensitivity, It Varies

Insulin sensitivity changes throughout our lives. As people

age, insulin sensitivity decreases and, of course, when an obese

person loses weight, or someone stops shoveling McDonald's into

their mouth, starts walking 30 minutes a day and eats a few

vegetables that weren't deep-fried, their insulin sensitivity

increases.

In addition to these long-term fluctuations in sensitivity, changes

also occur within the day. First thing in the morning, fat and muscle

cells react strongly to insulin and soak up sugar like a fat kid with a

gallon of melted ice cream and a straw, i.e. insulin sensitivity is high

in the morning. Insulin sensitivity then drops steadily until evening

when it hits a nadir1, making it hard for both fat and muscle to

absorb sugar.

NOTE: Both fat and muscle cells react

strongly to insulin in the morning and less so as the

day goes on, i.e. insulin sensitivity is high in the

morning.

See why every health expert and their sister recommends eating

carbs first thing in the morning as opposed to bed time? Wheaties it

is, or better yet, bring on the Coco Puffs, Lucky Charms, or some

3 8

S e c t i o n I I : B r i c k s

sugar-packed maple and brown sugar instant oatmeal...and that's

just for starters. We’re insulin sensitive, baby, and we might as well

take advantage of it. To be part of this complete breakfast we need

to throw in a banana, glass of OJ and some toast, but don't go crazy

on the protein, one egg will do. Bam, son, instant growth: all

because we were smart enough to eat carbs when we crawled out of

bed…but that's maximum growth of fat cells as well as muscle.

Compare this with what happens at night: muscle and fat tissue

don’t, under normal conditions, want to absorb excess sugar from

the bloodstream. This, of course, can cause a host of issues. If the

main avenues for glucose disposal take a break, then blood sugar

levels stay high longer than they should. Insulin levels will continue

to rise, attempting to clear the glucose. The brain and other tissue

that contain GLUTs 2 and 3—the always-on GLUTs—must do the

work. This process causes lethargy, affects logical thought and

makes it hard to focus on anything besides trash TV.

Eating carbs at night sounds like a horrible idea. With normal diet

and lifestyle—which includes overeating—I agree, eating carbs at

night is a bad idea. But if you're reading this book, you're not

normal. We may not be able to control the daily rhythm of insulin

sensitivity, but we can things that will allow us to use the nighttime

insulin resistance to our advantage.

C a r b B a c k - L o a d i n g

Chapter 12

Exercise a Little

Control

It probably sounds as though insulin sensitivity lies beyond

our control. Muscles will, however, use sugar efficiency and in high-

volume without manipulating insulin sensitivity. Bypassing the

whole sensitivity paradigm and moving tGLUT to the surface of

cells is possible and easy.

Any change in insulin sensitivity affects both fat cells and muscle

tissue in the same way. If muscles become more sensitive to insulin

and can store and use carbs, then so can fat cells. If, on the other

hand, fat cells become less sensitive and find it difficult to use and

store carbs, then so do muscles. It seems the choices are weak and

ripped or jacked and fat. Or, of course, get fat then spend 20 to 30

weeks leaning down as slowly as possible to see the hard-earned

gains without losing any.

Possessing the ability to translocate tGLUT at-will changes

everything. What is this magical power of which I speak? Resistance

training. I don’t expect this to be a massive revelation. Resistance

training triggers so many cellular reactions within muscle that it

seems reasonable that it can also replace part of insulin's

functionality. But how can we benefit from the translocation of

tGLUT without insulin playing a role?

4 0

S e c t i o n I I : B r i c k s

This is where the studies on diabetic patients paid off, and initiated

my autodidactic endeavor into the GLUT and other cellular

transport systems. I happened upon a paper that tested insulin

sensitivity and glucose clearance in type II diabetics after resistance

training1. Despite a lack of increase in insulin sensitivity

immediately post-exercise, glucose clearance from the bloodstream

increased. This seemed counterintuitive until I learned about the

insulin-independent translocation of tGLUT2.

Non-insulin mediated translocation of tGLUT occurs with resistance

training in all mammals, diabetic or otherwise3. Resistance training

prepares muscles to soak up sugar even before insulin is present. The

moment the sugar hits the bloodstream, skeletal muscle doesn’t need

to wait for a rise in insulin to absorb glucose. This pre-insulin

clearance of carbs can decrease the insulin response and robs fat

cells of both a large insulin spike and of all that precious sugar that

fat cells would love to convert into fat.

For diabetics, this process couldn’t be more extra-ordinary and

potentially life altering. It doesn’t matter that a type-II-diabetic’s

cells don't react to insulin any longer because resistance training

mimics a key function of insulin. With resistance training, a diabetic

can clear sugar from their bloodstream without medication while

their fat cells remain insulin resistant.

I want to be very clear: this process operates independently of

insulin. When talking about non-insulin mediated translocation

(note the ‘non’), we can ignore insulin, at least as far as its necessity

to increase glucose absorption and speed recovery from training.

Recovery and resynthesis of glycogen stores depends on

carbohydrate availability and not necessarily on insulin secretion

C a r b B a c k - L o a d i n g

E x e r c i s e a L i t t l e C o n t r o l

(although insulin may serve other purposes in the process of muscle

growth).

Don’t confuse the concepts. Translocation of tGLUT caused by

muscular contractions does not increase insulin sensitivity. It is

unrelated. Essentially, resistance training achieves results similar to

those initiated by insulin, but without it. It may sound redundant,

but there’s a lot of confusion about this topic and choosing proper

post-training nutrition to amplify and attenuate the right signals

depends on understanding this fact.

NOTE: The translocation of tGLUT that

occurs with exercise is not related to insulin

function or increased insulin sensitivity. tGLUT

move to the surface of muscle cells when

contracting under load. The process is called insulin

independent translocation.

This is an amazing process and exemplifies the concept of MTR:

targeting a response exclusively in one type of tissue that normally

affects multiple tissues. We choose which tissue absorbs carbs are

without increasing another tissue's absorption, despite the fact that

in other cases, the ability of both to use carbs rises and falls together.

Resistance training, however, decouples the two.

As an added advantage, resistance training triggers two more

desirable changes. Resistance training not only causes tGLUT to

move around without insulin, but also increase the amount and,

therefore, concentration of tGLUT in muscle cells4. So not only do

tGLUT activate with training, there’s more of them to active.

4 2

S e c t i o n I I : B r i c k s

Resistance training equips muscle cells to absorb sugar at a faster

rate, either for storage or energy production.

On top of that, muscle cells also become more sensitive to insulin

over time, so when things calm down from the training and

everything’s back to normal, the muscle cells react stronger and

faster to insulin than fat cells can, once again clearing glucose from

circulation before fat cells can get hold of it and turn it into fat.

This is just a small number of the biomolecular changes that occur

within muscle cells with resistance training. Covering all of the

changes and their implication on health, well being, strength, fat

loss, and so on, would fill its own volume, which is not my goal at

the moment—later, maybe, but not now. For now, focus is on the

changes dealing with GLUT and insulin.

For diabetics, the benefit is clear: instead of medication that makes

both muscle and fat cells sensitive to insulin again, allowing them to

get fatter and sicker, they can lift weights and get healthy. Wait,

what kind of nonsense am I talking? It'd be way easier to pop a pill

and get fatter. Maybe the real benefit is to you, who already trains

hard, battles with the iron on a day-to-day basis, who strives for

more than health—those of you who want to be exceptional.

C a r b B a c k - L o a d i n g

Section II

Essential Points

Insulin can make all tissue grow.

Usable carbs stop fat burning.

All carbs except fiber stop the body from burning fat

and are termed usable carbs.

GLUT carries glucose into cells.

Specialized proteins called glucose transporters (GLUT)

carry glucose into cells. The primary type in muscle and

fat is called tGLUT and needs insulin to work.

tGLUT responds best in the morning.

Specialized proteins called glucose transporters (GLUT)

carry glucose into cells. The primary type in muscle and

fat is called tGLUT and needs insulin to work.

Exercise makes tGLUT work without insulin.

Resistance training mimics the function of insulin in

muscle cells and puts tGLUT to work shuttling glucose

into skeletal muscle tissue.

4 4

S e c t i o n I I : B r i c k s

C a r b B a c k - L o a d i n g

Section III

MORTAR

4 6

S e c t i o n I I I : M o r t a r

C a r b B a c k - L o a d i n g

Chapter 13

Some Assembly

Required

I’ve written down all this heavy-handed science about

metabolism, insulin sensitivity and a whole section on cellular

glucose transporter proteins leading to some sort of explanation—or

so everyone hopes. Who knows, maybe I just wanted to sound

smart; then no one would question the protocol and jump right in

after seeing a few hundred citations.

I know the synopsis looked very basic and may not appear to

warrant such information for a plan that looks like the standard,

time-tested wisdom of eat, train, drink a post-workout shake with

carbs and go to bed. Admittedly, if someone introduced this to me

for the first time and I read only the synopsis, I would think the

same, Way to state the obvious, buddy.

Carb Back-Loading, however, requires more than a post workout

shake with a few carbs or a Gatorade during the training session. As

far as I know, it is the first dieting strategy diet integrating training

time and the timing and type of each meal. A method based on

hard-science and not anecdote. Carb Back-Loading works best when

training within an optimal window of time. And if someone can’t

work the ideal structure for Carb Back-Loading into their day,

unbelievable changes still result with few modifications. Even then,

this is the easiest, most maintainable dieting strategy ever devised.

4 8

S e c t i o n I I I : M o r t a r

The preceding section allows me to now explain how the pieces of

Carb Back-Loading fit together to create a plan in which fat loss and

muscle growth happen simultaneously, the Holy Grail of dieting.

Now it's time to drop all the pieces into place.

C a r b B a c k - L o a d i n g

Chapter 14

Best Breakfast

Ever—None

Inviting a bout of vitriol is as easy as standing in front of a

fitness guru or strength coach and mentioning that there might be

benefits to everyone if they skip breakfast. Why the anger? I have to

be honest, I really don't know because my reason for suggesting a

start to the day that does not include an immediate calorie load

stems from how the body works and the resulting research to prove

the effectiveness.

If you’re like me, you’ve skimmed ahead and noticed something

peculiar: I spend more time on breakfast than other topics—this

chapter is two to three times as long as other chapters. Eating (or

not eating) early in the day dictates the metabolic status of the body

for the rest of the day. Breakfast is simply that important.

By skipping breakfast, it’s easy to change several aspects of the

metabolism, like whether the body burns fat for energy or carbs. I

do realize that the gurus across all folds, from medical doctors to

bodybuilding coaches believe that breakfast is essential, preaching it

with zeal. Sometimes, it sounds as though death may occur from

skipping breakfast after some of the harangues I’ve heard, but the

facts don’t agree and don’t lie.

5 0

S e c t i o n I I I : M o r t a r

NOTE: Eating (or not eating) early in the day

dictates the metabolic status of the body for the

rest of the day. Breakfast is that important.

For the average individual, upon waking or thereabouts (say 7am),

levels of the potent hormone cortisol reach a high point for the day.

Cortisol elevates naturally through the night1,2 and peaks upon

waking1,3.

Cortisol is catabolic, a statement beyond dispute, but catabolic how?

Catabolic only means tearing down a more complex material in the

body for a different use. Destroying muscle tissue—as happens

during resistance training—is a normal and common catabolic

process associated with cortisol release. But releasing glucose from

glycogen stores is also catabolic; and so is releasing fat from fat cells.

Cortisol is like nega-insulin. Insulin's main purpose is to make tissue

grow; cortisol breaks things down. And like insulin that stimulates

both muscle and fat cells to grow, cortisol also stimulates the

breakdown of both fat and muscle. Also like insulin, diet and

exercise controls which tissue cortisol attacks.

When acting without elevated insulin levels and in a natural

manner—so without being constantly elevated like during chronic

stress—cortisol triggers the breakdown of triglycerides into free-

fatty acids (FFAs) for metabolization a process known as lipolysis1,4.

The morning before eating is the one consistent time when insulin

levels are very low and cortisol is high, i.e. cortisol accelerates fat

burning in the morning if nothing interferes.

More happens in the morning with hormones as well. The body

releases ghrelin—the main hunger-control hormone5—in a pulsatile

C a r b B a c k - L o a d i n g

B e s t B r e a k f a s t E v e r — N o n e

manner through the night with a peak occurring upon waking6. This

spike incites hunger and is why the stomach growls when getting

out of bed. Hunger’s not always something to avoid: ghrelin also

stimulates growth hormone release8. As growth hormone levels rise

the body releases more fat to be burned as fuel8 and decreases the

destruction of protein for use as fuel9. Growth hormone levels peaks

roughly two hours after waking if skipping breakfast10.

In other words, every day the body starts as a fat-burning furnace.

Even during exercise, without eating breakfast, the body burns far

higher levels of fat than normal11 and causes an increase in the

production of fat-burning enzymes, allowing the body to metabolize

fat faster12.

Wake

2 hours later

F i g u r e 1 : Levels of cortisol (ł), ghrelin (ł) and growth hormone (ł) after

waking that create the perfect fat burning environment if not disturbed by

breakfast.

Contrast this with what happens by eating a healthy, balanced

breakfast, one that contains as little as 30 grams of carbs. As is well

known, insulin levels rise with the rise in blood sugar, kick-starting

5 2

S e c t i o n I I I : M o r t a r

a downward spiral of fat burning: the early-morning release of

insulin hinders fat burning for the rest of the day13; while cortisol

levels remain high, the insulin release causes new empty fat cells to

be created14. The insulin also lowers levels of ghrelin and growth

hormone15. Maybe hunger drops, but so does fat burning.

From the facts above—this is fact, not guesswork—one would come

to the conclusion that maybe holding breakfast off for a few hours is

a good idea, or at least until cortisol levels return to normal and

growth hormone levels fall naturally, which takes a few hours.

Skipping breakfast looks like a way to lose body fat faster, or at least

to keep it off.

It might seem that skipping carbs would be enough, but truthfully,

it'd be best to skip everything but pure fat. In the supplement

chapter, I mention how most fats aren't available for energy for

several hours after eating, which works perfectly, but protein can

absorb quickly and even cause insulin spikes.

The morning is a time to avoid interfering with the natural

combination of hormones because if the body maintains the fat-

burning homeostasis, it casts a fat-burning shadow across the entire

day. When attempting to lose weight, moving the majority of daily

calories to the evening causes more fat loss and preserves muscle16.

Instead of fasting from 7 pm until bed time, eat a smaller amount of

calories before dinner time, then go-to-town from then on until bed

time, even if bed time is 10 pm. Sounds like Carb Back-Loading to

me.

Celebrity trainers will dismiss this out of hand, call it crazy,

disparage the research—that they’ll never read—and claim to be

C a r b B a c k - L o a d i n g

B e s t B r e a k f a s t E v e r — N o n e

right because they have become celebrities by proxy of working

with celebrities. But their clients—as seen on TV—struggle to hold

even an average waistline from year to year. It’s not solely the

breakfast rule plus the no-eating-after-7pm rule, but I would wager

a bet that their unfounded advice about these two points doesn’t

make it easy.

I know many people, even if convinced about the fat burning, fear a

mental-lethargy attack if they skip breakfast. There's no doubt that

after eating breakfast on a regular basis for years, skipping it for a

few days slows mental acuity a bit. This is transient.

My best IQ-driven work is done in the morning without breakfast,

without anything but coffee and this may go on until noon. And

when I say IQ-driven, I mean developing computer algorithms,

writing an excellent piece of prose or taking a four-hour test on

Quantum Mechanics—not that I feel like I'm better at reading the

newspaper. I’ve even outlined how to increase mental focus and

cerebral performance in an upcoming eBook, and one of the main

components is skipping breakfast.

NOTE: Eggs contain primarily fat and protein

and at most, one gram of carbohydrates. Despite

the overwhelming predominance of two non-insulin

stimulating macronutrients, eggs can spike insulin

levels17. Don't, therefore, eat eggs in great

abundance during the low-carb portion of the day.

One egg, not a problem; six or more all at once,

problem.

There's plenty of research to validate my personal experience and

the experience of others. Conditions in which breakfast does help

5 4

S e c t i o n I I I : M o r t a r

cognitive function involve malnourishment. I’m talking about true

malnourishment,

not

little-Timmy-didn’t-get-his-customary-

Twinkie-with-dinner-last-night malnourished, but someone who

hasn't eaten for days. In such a case, breakfast or any food

whatsoever, improves cognitive performance18. Who would have

guessed: give a starving kid a Pop Tart and suddenly they think

better.

For healthy kids, however, the story differs. Researchers took two

sets of academically matched students (they were all at about the

same performance level) and withheld breakfast from one group of

kids, letting them eat at lunch, and the other group had a balanced

breakfast.

When kids skip breakfast and have their first meal at lunch they pay

attention, behave, and perform better throughout the entire school

day18,19.

Whatever fears or concerns exist about skipping breakfast, abandon

them. I promise that the trepidation is based on anecdote, opinion

and, really, what amounts to an old wives’ tale. Having a goal means

taking the steps necessary to achieve it and that might mean

skipping breakfast, keeping calories light and pigging out at night.

And who knows, with one less thing to worry about, it might even

be more convenient for those rushing-around-the-house-to-get-

ready mornings.

C a r b B a c k - L o a d i n g

Chapter 15

Eat At Night

From the massive number of trainers and doctors teaching

to eat breakfast and not eat before bed, I’d expect them to base such

advice on scientific research. The research does exist to answer the

question, Should we eat more in the morning or in the afternoon?

There is, however one problem: the research says don’t eat the

majority of calories early in the day, eat them at night.

The current advice is a remnant of a reasonable assumption based on

reasonable logic that no one ever checked. The logic: when first

waking, the body is starving from the overnight fast; feed it and it’ll

start burning all those calories right away. But before bed, the

body’s going into torpor for hours and won’t burn any calories, so

don’t give it any food and it can’t store it.

Research shows something very different. As far as body weight is

concerned there’s no real difference between eating calories early in

the morning and few at night or vice versa. But checking the

difference in body composition tells a very different story. People

who eat a big breakfast and start fasting at 7pm lose mostly muscle

tissue. People who skip breakfast and eat after 7pm lose body fat

and may actually gain muscle. This, dear readers, is fact1.

5 6

S e c t i o n I I I : M o r t a r

To maximize the burning of fat and growth of muscle tissue during

Carb Back-Loading it seems obvious to eat in sync with how the

body also achieves that goal, by having fewer calories in the

morning and more at night.

C a r b B a c k - L o a d i n g

Chapter 16

No Carbs,

No Problem

For the vast majority of people, carbs sometimes seem like

the enemy and for good reason: once carbs enter the system, the

body no longer easily burns fat from fat cells, so it switches to carbs

for fuel. The available carbs, however, may or may not be enough to

sustain activity levels. If the body requires more than is available,

other processes initiate the production of glucose—carbs—from

various sources, one of which is lean tissue.

Not only will this happen immediately upon eating carbs—and

possibly anything that spikes insulin levels—but eating carbs for

breakfast inhibits fat burning for the entire day1. That’s a serious

problem.

One nearly universal goal these days is to burn a maximum amount

of body fat while still being able to grow. The earlier carbs slip into

the diet, the earlier the body stops burning fat. By cutting off the

supply of carbs, the body continues burning fat as it did through the

night. There’s no end of research to show that without carbs, the

body burns a lot of fat.

Limiting carbs, especially in the first half of the day, forces the

metabolism to rely on fat for energy needs. Coupled with the first

5 8

S e c t i o n I I I : M o r t a r

rule—limiting our intake of food—the body releases body fat to

keep up with energy needs.

Limiting carbs—and therefore limiting insulin release—is crucial for

another reason. This is when insulin affects fat cells and muscle cells

the strongest, allowing them to store carbohydrates. The body has

an almost unlimited capacity to convert and store carbs as fat, but

has limits on the amount of glycogen it can store.

Insulin also increases the efficiency of fat cells to store fat by making

the formation of triaglycerol—the main storage form of fat in fat

cells—easier. By avoiding carbs, it makes it difficult for fat cells to

store carbs as fat and to store fat as fat. At the same time, it makes it

hard for muscle cells to store carbs as glycogen.

F i g u r e 2 : Ingesting carbs pre-training, especially after an ultra-low carb day,

can cause blood sugar levels to dip during training, triggering hypoglycemia-

like symptoms. Some react strongly; others, hardly at all.

C a r b B a c k - L o a d i n g

N o C a r b s , N o P r o b l e m

Eating carbs immediately pre-training—has the potential to cause

rebound hypoglycemia2, which occurs when muscles, the liver and

other tissues clear glucose from the bloodstream too fast. This causes

shakiness, sweating, light-headedness and an inability to think

clearly, let alone focus on performing another set of a complex,

compound movement.

This risk comes with no advantages, nothing worth the possibility of

a bout of hypoglycemia. Because no advantage exists but there’s the

potential of looking like an intoxicated fool in the gym, skip the pre-

training carbs. This is not to say that pre-training nutrition should

be ignored, but it won’t include carbs.

Training in the low-carb state carries advantages: three distinct

strength-enhancing benefits, the collection of which I often refer to

as The Hulk Effect™.

Hulk Effect™

1. After adjusting to a low-carb diet the body releases

adrenaline faster and muscle cells react stronger than

when on a standard carb-based diet3.

2. Psychomotor performance increases, which is the

ability to perform coordinated movement, even under

load4.

3. The nervous system fires with greater amplitude than

normal, allowing maximum contraction strength5.

Maybe training without carbs isn’t so bad after all.

6 0

S e c t i o n I I I : M o r t a r

It also turns out that depleted glycogen levels do not affect strength

training, or at least not the outcome6. Ketones and fatty acids—with

the help of the enhanced sympathetic nervous system and

adrenaline release —pick up the slack of depleted glycogen levels.

And as I cover later, Carb Back-Loading helps maintain glycogen

levels for the next day’s training.

C a r b B a c k - L o a d i n g

Chapter 17

The Sweet Spot

The Carb Back-Loading day starts with a lighter caloric

load and no carbs, and as the evening approaches insulin sensitivity

wanes. Introducing too many carbs into the system at this time

could mean metabolic chaos. Ah…but wait: there’s a way to make

muscle cells soak up carbs even if insulin sensitivity tanks.

Resistance training.

Sure, someone can back-load calories and not eat carbs, but can’t

successfully reintroduce carbs without implementing resistance

training. By successfully reintroduce, I mean start eating carbs later

in the day, in massive abundance, without getting fat. Resistance

training, by causing the non-insulin mediated translocation of the

tGLUT discussed earlier, allows muscles to absorb all the carbs the

tissue can handle.

Remember, this movement and activation of tGLUT caused by

resistance training is independent of whether the muscle cells are

sensitive to insulin or not. A strong, powerful contraction and,

boom: muscles act as though they were bathed in insulin and start

absorbing sugar, assuming there’s sugar to absorb.

Strength, of course, is a concern for any athlete modifying their diet

or changing their schedule. As insulin sensitivity decreases through

6 2

S e c t i o n I I I : M o r t a r

the day, the rate of perceived exertion (RPE) goes down.

Translation: intensity is naturally higher when training at night

without realizing it1. That this correlates with the perfect time to

train for Carb Back-Loading only increases the number of reasons to

consider moving training into the sweet spot if possible.

There’s also a matter of the ideal hormonal environment for growth,

which—don’t be surprised—can depend on the time of day. It turns

out that training in the evening causes a lower cortisol response to

training than normal while leaving levels of other anabolic

hormones, like testosterone, the same or elevated2. This creates an

anabolic and anti-catabolic environment greater for evening

training than for morning training.

It’s nice that so many hormonal advantages for training line up with

other daily rhythms that make Carb Back-Loading effective. There

really is a perfect time to train.

C a r b B a c k - L o a d i n g

Chapter 18

16oz Carb Curls,

Post-Training

Insulin sensitivity decreases all day, and falls near its lowest

point in the afternoon hours. Resistance training during this

window of time—which will be time shifted by different amounts

for different people—doesn’t reestablish insulin sensitivity, but does

something better. It performs a little MTR magic by getting muscle

tissue to absorb carbs for energy production and glycogen repletion,

but leaves fat cells in their standard insulin-resistant state. Eating

carbs at this time does not enhance body fat storage, but rather, it

only supports the goal of our training efforts.

When engaged in resistance training, the body tries to deteriorate

muscle tissue, a process called proteolysis. Resistance training is

actually catabolic1.

During the training session, building muscle is impossible no matter

the nutritional or supplemental measures taken. The goal, therefore,

is to limit proteolysis to the greatest extent possible during our

training session. The less that’s torn down, the more new muscle we

can build.

Insulin attenuates and can possibly stop proteolysis after training

and maybe during, thus preserving our lean tissue and muscle mass1.

It might seem obvious then: eat carbs during training sessions. Some

6 4

S e c t i o n I I I : M o r t a r

situations warrant eating simple carbs during training sessions—like

strongman training—but certain dietary supplements increase

insulin levels without the carbs during training. In most cases, avoid

carbs for insulin spikes because better alternatives exist.

One thing I’ve noticed ever since I introduced the idea of tGLUT

manipulation for performance gains, is a shift in the

recommendation of post-workout carbs. The recommendation is to

focus on low-glycemic carbs post-training to stay lean. The

argument revolves around having carbs available for hours and

avoiding insulin spikes which can make people fat.

It couldn’t be further from the research, i.e. further from the truth.

After the completion of training, stopping the proteolysis that

occurs requires a large insulin spike: the larger, the better2.

Achieving a big spike takes high-glycemic, high-insulinemic carbs,

which we can enhance by adding the right proteins and amino

acids.

Don’t worry about getting fat either. After resistance training,

storing body fat is nearly impossible for up to an hour3. Another

good reason to get a huge, short-lived spike: get the carbs in and get

them out before the fat-resistant window closes.

C a r b B a c k - L o a d i n g

Chapter 19

Slam the Carbs

It’s time for the fun part of Carb Back-Loading: eating some

trash. After training, the one goal besides fueling muscle growth is

refilling glycogen levels. Rebuilding the depleted stores—depleted

assuming an ass-busting training session—isn’t necessarily for

muscle growth. Glycogen stores fuel performance, nervous system

recovery and help limit muscle breakdown during the next-day’s

training.

Skeletal muscle, even after the most grueling DOMS-creating

workouts, recovers within 48 hours1. The nervous system, in

contrast, can take 10 days2. I could accurately describe resistance

training as nervous system brutality.

As hard as muscles appear to work during training sessions, the

nervous system works at a far greater level for its capacity. Cells of

the nervous system will use ketones for fuel, but glucose is more

efficient. Having plenty of glycogen in reserve allows motor

neurons to fire at a higher level during training. If muscles don’t fire

with maximum force, they won’t experience maximum growth or

conditioning.

Glucose is also necessary for maximal contraction as a set

approaches failure. When hitting the anaerobic point during

6 6

S e c t i o n I I I : M o r t a r

training, glucose is needed to continue contracting as it enters the

glycolytic—glucose burning—cycle. Not ketone-burning cycle or

fatty-acid burning cycle, but glucose-burning.

As far as we know, muscles require glucose to squeeze out those last

few grueling reps. Topping off glycogen levels allows muscles to use

fatty acids during the training until the need for glucose arises, at

which point glycogen is broken down and used.

There’s some debate on whether glycogen levels help muscular

growth or not. Research shows that full glycogen reserves help limit

the protein breakdown caused by training sessions and increases

glycogen usage during the following days’ training session3. Once

again, replenishing glycogen levels is not to recover from today’s

training but to prepare for the next day’s.

These carbs should be trash, as I like to say, by which I mean

donuts, pizza, French fries, pecan pie and my personal favorite,

cherry turnovers with a healthy amount of icing. People think I’m

being facetious. I’m not. I have good reason to recommend such

stuff, as I always do.

We all know—or should know—that eating carbs before bed

disrupts nighttime release of growth hormone. I’m not going to

spend time talking about the benefits of growth hormone other than

to reiterate its role as a fat burner and a lean tissue builder:

something no one wants to screw up with poor food choice.

The poor choice here is low-glycemic carbs. The body will not

release growth hormone during sleep until roughly two hours after

blood sugar and insulin levels return to normal4. Low-glycemic

carbs keep insulin and blood sugar levels elevated for hours, while

C a r b B a c k - L o a d i n g

S l a m t h e C a r b s

high-glycemic create a spike that ends within an hour or so of

eating. Eating junk gives the benefit of replenishing glycogen stores

without interfering with the nocturnal hGH cycle.

When someone attempts to Carb Back-Load using brown rice and

whole-grain toast, they get crappy results. They want to do a

healthy version of the diet, only to realize healthy means impotent.

They too narrowly define healthy.

Eat like a fat kid to get jacked, end of story.

NOTE: Delayed Onset Muscle Soreness

(DOMS) is a condition that occurs with intense

training, most often associated with a person's first

excursion into resistance training or returning to

the gym after a long hiatus. The soreness occurs 24

to 48 hours post-training and is not related to lactic

acid buildup, but stems from muscle fiber damage5.

DOMS should not limit or affect training—although

one’s pain threshold will dictate training intensity

while experiencing the DOMS 6.

6 8

S e c t i o n I I I : M o r t a r

C a r b B a c k - L o a d i n g

Chapter 20

Highly Inefficient

Design

I’m recommending skipping breakfast and eating junk; I

expect skepticism. To be honest, I appreciate the skeptics: they keep

me on my toes, keep me digging, researching, refining and

rethinking. Without skeptics—including myself—I wouldn’t know

half of what I do.

What might be setting off some alarms is, how does this work? I

don’t talk about calories or restricting them in any way, only

shifting them around and splitting the macronutrient content of the

day between a low-carb morning and a high-carb night with a fuzzy

region between the two. I give reasons as to why, but those reasons

don’t necessarily explain how it’s possible. A calorie is a calorie,

after all.

The full explanation of why a calorie is not a calorie is beyond the

scope of this book. It covers topics like the second law of

thermodynamics and the expanded subject of statistical mechanics

to deal with kinetic flux and entropy1. What these subjects describe

and explain is efficiency.

The human body is no different than any machine that requires an

energy source to perform work. Whether it’s a car engine or a coal-

burning stove, fuel goes in, work gets done and heat gets produced.

7 0

S e c t i o n I I I : M o r t a r

Getting the maximum amount of work possible from the fuel while

wasting the least amount of heat is efficiency. While the 2nd law of

thermodynamics puts an upper limit on efficiency—it can never be

100% —there is no lower limit besides 0. It’s possible that all the

heat is lost and no useful work is done.

A car engine runs at various efficiencies and depends on several

factors like air temperature, rpm and even the type and temperature

of the fuel.

Pathways to Energy Production and

Efficiency1

Pathway

ATP/mole

Efficiency(%)

Glucose ĺ CO

38

38.5

2

Glucose ĺ glycogen

ĺ

36

35

glucose ĺ CO

2

“Average” AA ĺ CO

—

33

2

AA ĺ Protein ĺ AA

ĺ

-4

27

CO

2

Palmitate ĺ CO

129

40.9

2

Palmitate ĺ Ketone

ĺ

121

38.3

CO

2

A body’s efficiency depends on even more variables, variables that

depend on other variables, the duration a particular type of fuel has

been in use, the type of work done, levels of more than a dozen

different hormones, lean mass, time of day and so on. Each of these

alters the efficiency of the body and manipulated appropriately,

they can produce incredible, almost unbelievable effects—for fat

loss or even fat gain.

C a r b B a c k - L o a d i n g

H i g h l y I n e f f i c i e n t D e s i g n

Take the simple example of exercise. Researchers monitored four

groups of people—one group does nothing (group C), one diets

(group D), one exercises (group E), and a final group that diets and

exercises (group DE)—to assess weight loss, fat loss and muscle loss

over time. For periods of less than nine months, groups D and DE

lose identical amounts of weight, as do groups C and E.

In other words, over the length of the study, the extra calories

burned during exercise made no difference in weight loss2.

Sounds incredible, I’m sure—maybe impossible. How can exercise

not make a difference? Someone who sits on their ass all day loses

the same amount of weight as someone who exercises, which,

according to the study, is none. By all measures of sanity, the idea of

burning more calories with exercise and not losing additional

weight feels absurd. It’s not.

Adaptation is the hallmark of life and the human body excels at it.

When thrust into a new exhaustive activity, the body quickly

down-regulates thyroid hormone, which slows all aspects of

metabolism.

This is a conservation mechanism to save enough energy to make

sure that exercise does not jeopardize normal, day-to-day life

activities. Suddenly, the body is running at higher efficiency, which

means better gas mileage—i.e. it gets harder to lose fat.

But efficiency doesn’t have to go up. The process can go the other

direct. Several well-controlled studies record weight loss by

changing the macronutrient profile of a person’s diet while keeping

calories identical. The dietary switch: from high-carb to low-carb.

7 2

S e c t i o n I I I : M o r t a r

Weight Loss Differences By Switching From

Carb-based Diet to Fat-based3

%CHO

%CHO

Avg. Wt. Lost (lbs)

High

Reference

Low CHO

Low

High

CHO

group

group

Young et al (1971)

7

23

35.6

26.2

Rabast et al (1978)

10

68

30.8

21.6

Rabast et al (1981)

12

70

27.5

20.9

Golay, Allaz et al

15

45

19.6

16.5

(1996)

Golay, Eigenheer

25

45

22.4

18.9

et al (1996)

Lean et al (1997)

35

58

15.0

12.3

Baba et al (1999)

25

68

18.3

13.2

Greene et al (2003)

5

55

22.9

16.9

Layman et al

44

59

16.5

15.4

(2003)

Carb Back-Loading targets the same systems but in a complex way—

not simply stripping carbs from the diet—to modulate and utilize

these inefficiencies to burn body fat while maintaining the

efficiency of the processes necessary for muscle growth.

C a r b B a c k - L o a d i n g

H i g h l y I n e f f i c i e n t D e s i g n

This is MTR’s ultimate goal, control over metabolism, growth and

tissue repair. Although all of this may seem unbelievable at first,

there are multiple studies to vet the theory. There’s also an entire

branch of physics devoted to the subject and proves that the

underlying logic behind a calorie is a calorie violates the most basic

laws of the universe.

7 4

S e c t i o n I I I : M o r t a r

C a r b B a c k - L o a d i n g

Section III

Essential Points

Breakfast is extremely important—to skip.

When you first wake, the body is in a powerful fat-

burning mode. Eating could put you in fat-gaining mode.

Eating at night helps preserve muscle mass.

It’s safe to train without carbs.

Strength and hypertrophy training are unaffected by

day-time carbs as long as glycogen stays full.

Train at night.

Training at night lowers catabolic hormones, raises

anabolic and you’re stronger at night.

To recover from training use only high-GI

carbs.

High glycemic index carbs speed recovery, don’t

interfere with nighttime GH secretion and, post-

training, can’t store fat.

Not eating carbs makes you burn more fat.

7 6

S e c t i o n I I I : M o r t a r

C a r b B a c k - L o a d i n g

Section IV

AFTERMARKET

ADD-ONS

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

C a r b B a c k - L o a d i n g

Chapter 21

High Performance

Tuning

Carb Back-Loading, simple as it may be to do, is obviously

based on a substantial amount of research to nail the timing and

type of carbs that need to be eaten at the appropriate times. Some

people want the absolute basics and if you’re one of those people,

you can jump to the section on Implementation, which provides the

information necessary to implement the lowest level version of the

diet.

If you’re like me, though, you don’t want the basics. Sure, you can

have a stock Ferrari—which would be pretty bad-ass as-is—but if

you can strip a few hundred pounds from the car, add 400

horsepower and bump the top speed up to about 220 mph, why the

hell wouldn’t you? Especially if I told you it could be done for,

equivalently, pocket change.

And the first step of any successful human-performance

modifications is supplementation.

I can’t assess the value of the majority of the supplements out there,

mostly because absolutely no verifiable research exists that explores

the efficacy of most products. A couple of decades in this industry

taught me a valuable lesson. If the product makes any claim without

research, then the claim is false 99% of the time.

8 0

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

When I say research, I mean peer-reviewed, verified research, not

some clinical study performed at an undisclosed location with

undisclosed results. When researchers do get around to testing the

chemicals supposedly contained in the product, the results show,

without doubt, that it doesn’t work. That’s why companies try to get

patents on certain chemicals—this way, they can prevent

independent research of the substance.

This section of the book contains a list of supplements vetted by

research and experience. They are not exclusive to use with Carb

Back-Loading, but the guides later in the book explain how to

include these supplements for maximum effect while back-loading.

C a r b B a c k - L o a d i n g

Chapter 22

Omega-3s

Recommendations for supplementing diet with omega 3s

fall from the sky and for every recommendation there's a different

reason given. I'm not going to go into all the health aspects or what

the ideal ratio of omega-3s in your diet should be, but these

arguments, at best, are speculative. I'm going to discuss things we

actually know, like what omega-3s mean to cellular membranes and

how to use them for increased hypertrophy.

Fat is an essential nutrient. Of course, it’s used for fuel, but it also

forms the structure of every membrane of every cell in the body.

Stripping all fat from the diet—as recommended by a few

prominent doctors-turned-wellness-experts—would cause death,

but not before becoming an emaciated wreck of a human being—

look at the same doctors mentioned above.

Because fatty acids encase cells with a gooey membrane, the types of

fats in the membrane affect the properties of the coating, including

the viscosity, which dictates the ease with which things can move

through the membrane1. Things like tGLUTs. The higher the

viscosity, the harder it is for stuff to move through the membranes.

8 2

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

Slick, less viscous membranes, however, allow nutrients,

transporters and hormones to enter and exit cells efficiently. That’s

actually one indicator of biological age: the stiffness of cellular

membranes increases—becomes more viscous—as we age2. Diet,

however, plays a larger role. How much of what type of fats we

consume dictates cellular viscosity more than anything else.

Stiff fatty acids—like saturated fat—form the underlying structure

of the covering, but too much makes the membrane thick and rigid3.

Stiff membranes resist the flow of nutrients into and out of cells and

make the movement of transporters difficult. Cell function suffers.

Polyunsaturated omega-3s, on the other end of the spectrum, create

less-viscous coatings that allow nutrients and transporter proteins to

flow without effort4. This ease-of-flow allows cells to operate at

peak performance.

NOTE: Eating 5 grams or more of a

combination of the omega-3 fatty acids DHA and

EPA

can

enhance

the

hypertrophic

signals

associated with resistance training.

Since diet determines the raw materials available for cellular

membranes—you are what you eat—eating a lot of saturated fat

turns cells old before their time. Eat a lot of omega-3 fat and cells

contain much higher proportions. This goes for monounsaturated

fats in olive oil and the trans-fats in margarine.

Although nuts, seeds, soybeans, hemp and most grains contain

polyunsaturated fats in abundance, they don’t provide a full

C a r b B a c k - L o a d i n g

O m e g a - 3 s

spectrum of the polyunsaturated fat we need. They contain

predominantly omega-6s and we need both omega-6s and omega-3s.

Besides needing omega-3s to survive, the body is more anabolic as

dietary omega-3 increases. Supplementing with omega-3s in

quantities 3 to 4 times recommended can increase the anabolic

signaling of insulin and amino acids5. To build muscle efficiently

takes more than protein, the body needs omega-3s too.

One word probably comes to mind: Flax. Yes, flax oil does contain

omega-3s but it contains a form called alpha-linolenic acid. Not all

omega-3s are created equal, however and the right type is needed

for maximum efficacy and the right type is most readily available

from fish oils.

Although the plant-derived omega-3, alpha-linolenic acid (ALA), is

the essential omega-3 fatty acid, the body must use enzymes to

convert ALA to docosahexaenoic acid (DHA) and eicosapentaenoic

acid (EPA) and the amount of these enzymes is limited6.

Since we eat such large quantities of other fats that use the same

enzymes, we could ingest enough ALA to theoretically meet needs,

but still be deficient in DHA and EPA: the enzymatic system may be

maxed out. By ingesting these two directly, our bodies don’t rely on

enzymes to convert the omega-3s, thus allowing greater

incorporation into cells.

Also—and this is almost exclusively important to Carb Back-

Loading—omega-3 supplementation helps certain muscle fiber

structures to switch easily from burning fatty acids to glucose and

vice versa, depending on which substrate is most available7. Carb

Back-Loading causes this switch of nutrient availability on a daily

8 4

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

basis. Include liberal amounts of the omega-3s, 5 grams or more of

DHA and EPA, for maximum growth.

C a r b B a c k - L o a d i n g

Chapter 23

Medium Chain

Triglycerides (MCT)

People rarely talk about fat as functional. I think the most

I've heard relates to the release of cholecystokinin, CCK, as a hunger

satiating response from eating fat, any type of fat.

Maybe someone might get a little crazy with how eating fat changes

what eicosanoids get produced in what ratios, which is, I would

argue, functional, but that takes months. I'm interested how it

affects the system now...not next month, not next week, not even

two days from today, but now.

No one talks about fat as functional because digestion and

availability is slow. After eating fat, two to six hours pass before the

fat from the meal enters the blood stream and is available for use1.

As with everything, there's an exception to the rule. Medium chain

triglycerides—recently relabeled medium chain fatty acids since

triglyceride sounds scary—raise free fatty acid levels quickly after

ingestion2.

This rapid availability of fat can be advantageous when we're not

eating carbs, like during the first half of a Carb Back-Loading day.

The rapid rise in fatty acid and triglyceride levels can prolong the

morning ketogenesis that occurs when we wake, causing the body

8 6

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

to burn more fat and waste energy in the ongoing production of

ketones3.

MCT oil, because of the rapid influx of fat, increases the fat burning

and increases the rate of fat burning4; again activating another

pathway to enhanced fat burning by possibly increasing lipolytic

enzymes. When on a low-carb diet, or when eating low-carb during

a regular and consistent part of the day, MCT oil offers several ways

to accelerate fat loss.

I recommend coconut oil, but you can also find purified MCT oil

that's liquid at room temperature and tasteless. Good coconut milk is

also three-fifths MCT and is very low-carb.

NOTE: MCT oil is ingested rapidly into the

bloodstream and is available for energy faster than

other fats, causing the body to burn more fat.

Coconut oil is a rich source of medium chain

triglycerides.

C a r b B a c k - L o a d i n g

Chapter 24

High Insulinotropic

Carbs

Before ever supplementing with protein for post-workout

nutrition, I supplemented with carbs. I read weight gainer on the

bottle and downed copious amounts. I had no idea what I was doing,

all I knew was that it lacked fat and had only trace amounts of

protein and I wanted to be huge. Talk about bulking.

Times have changed and so has the extent of my ken. Now, I ignore

the carb count on the label and go straight to the ingredient list to

see what kind of carb the powder contains. With the advent of the

internet, I don’t even waste my time with that, to be honest. I open

my browser, click a few links and purchase the pure form of the

exact powder I want based on the function I need.

Today, I require one function and one only, to spike insulin and

blood sugar levels. Okay, that may seem like two functions, but, in

general, they go hand in hand when discussing carbs. If the carb

powder causes a rapid rise in glucose levels, there will be a

concomitant rise in insulin. It’s pretty much unavoidable.

The basics work best: dextrose, maltodextrin and waxy maize or

waxy rice. Functionally, there's not a big difference amongst them,

only their chemical structure distinguishes them. Dextrose (d-

glucose) powder is pure glucose and is a very simple sugar—as

8 8

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

simple as a saccharide gets. Maltodextrin, often labeled as a complex

carbohydrate, contains long chains of glucose and absorbs faster

than individual glucose molecules.

Finally, waxy maize and waxy rice are also complex branch-

structured starches called amylopectin. Amylopectin makes up a

part of most starches, the other part being amylose. Amylose, as

opposed to amylopectin, is not branched but is a long chain.

The ratio of amylose to amylopectin determines how fast the body

can absorb the starch and, consequently, how fast it can raise blood

sugar: the more amylopectin, the faster the absorption and the

better for insulin spikes1.

The ration of amylose to amylopectin helps determine the best carbs

for optimal results when Carb Back-Loading. For example, pick

waxy potatoes (purple) over russets, or sticky-rice over spaghetti. I

provide tables in the index.

C a r b B a c k - L o a d i n g

Chapter 25

Whey Isolate

Of all the supplement revolutions over the last few

decades to improve performance or help us get more from training, I

consider whey isolate the first legitimate one. Everyone who trains

knows that whey increases muscle growth better than most proteins

especially when taken post-workout. And its derivatives—like whey

hydrolysates—outperform almost all other proteins when it comes

to potentiating and supporting growth.

Other advantages to whey isolate besides hypertrophy exist that

modern nutrition experts ignore or are ignorant of. For one, whey

isolate is particularly effective at alleviating and preventing

oxidative damage.

It works by increasing levels of an amino acid called glutathione1,

which fuels the main anti-oxidant machinery of the cells in the

body2. Eating fruits and vegetables pales in comparison to the

glutathione mechanism. Glutathione also helps recycle other anti-

oxidants like vitamin C and vitamin E, decreasing the need for these

vitamins3.

The two systems differ wildly. Anti-oxidants of the fruit-and-veggie

type float around the blood stream and might bump into a free-

radical, neutralize it and prevent it from doing damage. Even with

9 0

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

massive amounts of blood-born anti-oxidants, it's still a crap-shoot

as to whether free radicals get nullified. The glutathione-driven

system, however, works within each cell, so cells neutralize the

free-radical, thus preventing an attack. It's no longer random chance

if the reactive-oxidative agent gets neutralized—it does.

CAVEAT EMPTOR: choose the form of whey

isolate wisely. Many pre-mixed drinks exist, but all

these drinks, no matter the label claims, no matter

what started off in the bottle, don't contain much

whey isolate. It's impossible. Isolate may have been

the original content, but all milk-derived products

in the United States must be pasteurized, and this

includes pre-mixed whey protein drinks. Whey,

however, is not heat stable and pasteurization

destroys it4. If you want your isolate, you need to

buy powder and mix it yourself.

The analogy I use involves burglars. The fruit-and-veggie anti-

oxidants represent the police and glutathione, three trained

Rottweilers. The police might stop a burglar from breaking-an-

entering if they drive by at the exact moment the burglars burgle, or

if they accidentally crash into the burglar's car en route. The

Rottweilers, however, will stop the burglars every time. Even if one

guard dog goes down, the others continue preventing damage.

Whey isolate feeds the pack of attack dogs in each cell.

Since resistance training—exercise in general—creates large

amounts of reactive-oxygen species, anti-oxidant protection keeps

the body healthy and growing without the burden of diverting

excess nutrients to the task of damage control and repair.

C a r b B a c k - L o a d i n g

W h e y I s o l a t e

Whey Isolate also enabled me to create peri-meal supplementation

for enhanced goals. I'm sure this sounds odd, as it means

supplementing around eating. Ingesting certain foods at certain

times around a meal changes how, when and to what extent the

body releases hormones.

Consuming 10 grams of whey isolate a few minutes before a meal,

for example, decreases the amount of insulin released and can

assuage hunger5. Depending on the meal and time of day, it can also

enhance ketone production, a wasteful metabolic process that burns

fat. Using whey isolate fine-tunes the power of Back-Loading.

9 2

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

C a r b B a c k - L o a d i n g

Chapter 26

Protein Hydrolysates

Hydrolyzed proteins—or protein hydrolysates—start as

intact proteins until heating, acids and enzymes break the longer

chains down into smaller pieces1. These smaller chunks—often

composed of just two or three amino acids—possess different

functional properties than the original. Sometimes, radically

different.

Before describing the functional properties of hydrolysates, I want

to avoid confusing them with their intact counterparts. Micellar

casein and calcium caseinate can taste pretty good. Casein

hydrolysate, on the other hand, is the most awful stuff I’ve ever put

in my mouth. The same is true of whey hydrolysates, all varieties.

They taste like flaming rubber with a hint of burnt cheese. There's

not many ways to mask the taste either—I have few effective

solutions which, arguably, aren’t solutions at all.

The enzymatic process creates the horrid taste accompanying

hydrolyzed milk proteins from casein and whey. An unfortunate

byproduct of the process produces large amounts of the amino acid

proline, which taste buds perceive as pure nasty bitterness2.

At least the benefits out-weigh the nasty taste. For example,

ingesting either whey or casein hydrolysate post training

9 4

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

substantially enhance post-training muscle protein synthesis and

decrease muscle protein breakdown3.

NOTE: Supplementing with hydrolysates

blocks the catabolic, protein-burning effects of

resistance training while potentially doubling the

growth over intact proteins4.

Ingesting hydrolysates, particularly casein and whey, rapidly

increases free amino acid and insulin levels5. Hydrolysates absorb

through the intestinal wall faster than individual amino acids while

not interfering with their absorption. An independent transport

mechanism for the di- and tripeptides contained in hydrolysates

moves these short peptides rapidly through the gut wall6.

The necessarily low carb and insulin segment of the day of Carb

Back-Loading limits use of hydrolysates because they spike insulin

levels independent of the presence of glucose as described above.

Back-Loading uses hydrolysates primarily around training and the

nighttime feedings because hydrolysates can also enhance muscular

usage of glucose7.

One last comment: Beware hydrolyzed collagen or collagen

hydrolysates. These are pretty much junk. Collagen lacks the

essential amino acid tryptophan—as does its hydrolysate—and isn't

used for skeletal muscle tissue growth or repair. Manufacturers

normally use it as a junk filler in concentrated liquid protein

supplements.

C a r b B a c k - L o a d i n g

Chapter 27

Leucine

I am a skeptic. Unless I can find peer reviewed research on

a supplement, I assume it's junk. That's why I warned against

branched-chain amino acids (BCAAs) for so many years, until

recently. All the accumulated studies, when qualitatively averaging

their results—this one showed benefits, this one didn't—failed to

answer a simple question: Can BCAAs enhance muscle growth?

It was a coin toss as to whether BCAAs carried any advantages for

strength athletes or not. Why spend the money when other, proven

supplements—like whey hydrolysates—show consistent increases in

muscle growth compared with a placebo? Just buy the good stuff

and let someone else gamble on BCAAs efficacy.

How training and nutrition triggers muscle growth is an interesting

process with many different components. The mammalian target of

rapamycin (mTOR) is one1.

For growth and differentiation to take place something must

activate the associated pathway of RNA transcription and

translation. Hypertrophy—like any growth process—depends on

the activation of such pathways. Think of the pathway as a chain of

steps and signaling proteins and hormones activate or deactivate

each step—they either strengthen chain links or break them.

9 6

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

The mTOR target is a link in the chain that allows dietary

components to activate the pathway of cellular hypertrophy. This is

the interesting quality of the mTOR receptor: it ties dietary

nutrients directly to the cellular signaling process2.

Normally, hormones need to mediate these signals. For example,

carbs cause a rise in insulin levels and insulin then potentiates the

growth pathway (it won’t cause growth without the necessary raw

materials). Certain dietary supplements, however, can bypass the

hormones and activate the pathway directly via mTOR. Just eating

the right food triggers muscular hypertrophy.

And the right food: the branched-chain amino acid, leucine. Hence

my renewed insterest in branched-chain amino acids. Leucine

directly binds to the mTOR receptor to trigger muscle growth and

limit muscle breakdown3. Anyone looking to change the

distribution of tissues in their body—say, going from less fat to more

muscle—should supplement with leucine.

All good things come with a price, and for leucine, it is the ability to

raise insulin levels independent of blood sugar. Other amino acids

only increase insulin secretion in the presence of ample amounts of

blood sugar, but not leucine4, making it difficult to include during

the low-carb portion of Carb Back-Loading. During the nighttime

carb-up, however, leucine gives us the advantage of enhancing

insulin release from a meal.

I'm not shy with the dosages as will become evident in the

supplement plans, sometimes recommending upwards of 40 grams

of additional dietary leucine in a day. If safety is a concern, a 150 lb

C a r b B a c k - L o a d i n g

L e u c i n e

male can eat upwards of 2.5 lbs without demonstrating any

problems, except, possibly, diarrhea5.

NOTE: Because of leucine’s anabolic and

anti-catabolic properties, everyone should supple-

ment with leucine regardless of weight loss or

weight gain goals.

9 8

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

C a r b B a c k - L o a d i n g

Chapter 28

Caffeine

Anyone, on any diet, can use caffeine as adjunct nutrition

with benefits. The basics of caffeine are impressive: accelerated fat

burning, increased adrenaline response, heightened awareness,

improved strength and possibly even greater nitrous oxide

accumulation in muscle tissue. But caffeine enhances certain aspects

of Carb Back-Loading making it indispensible.

The fat-burning properties complement the first half of the day

when Carb Back-Loading because of the lack of carbohydrates in the

diet, without which the body burns fat readily. Carbs and the

subsequent insulin release don't necessarily block the fat-burning

and mobilizing properties of caffeine but can interfere and limit it1.

By eliminating carbs during the first half of the day and including

caffeine, the body burns more fat.

Thus far, I've been referencing caffeine and I mean specifically

caffeine, which is found in coffee and guarana beans. Caffeine is the

strongest known natural member of a family of compounds called

methylxanthines2.

Other sources of caffeine actually don't have much true caffeine.

Chocolate contains a methylxanthine called theobromine and teas

contain theophylline. In terms of function, each of these acts

1 0 0

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

differently in the intensity of response. Theobromine and

theophylline do not stimulate the system with the strength of

caffeine, but their effects last longer3. Despite lasting longer,

caffeine’s stronger response and the infinite availability thereof

makes it a better choice for serious athletes. When I speak of

caffeine, thefore, I am referencing caffeine, not using it as a generic

catch-all phrase for methyxanthines.

Most of the time, I'm going to

recommend

coffee.

Not

because it's a cheap and

abundant source of caffeine,

but because roasted coffee

beans also contain chemicals

called cholinomimetics that

are minor stimulants, but can

also suppress hunger4. They

C a f fe i n e

can be found in decaffinated

coffee as well, which is why people still experience a stimulant

effect from decaf.

Those are the basics. What makes caffeine integral to Carb Back-

Loading is the ability to cause transient insulin insensitivity. Not

only does insulin interfere with the actions of caffeine, but caffeine

interferes with insulin's function as well, by decreasing insulin-

mediated tGLUT response5.

With caffeine, it's possible to both amplify Carb Back-Loading when

training at the perfect time, but also to modify insulin sensitivity to

accommodate training at non-ideal times, such as in first thing in

the morning. People are the most sensitive to insulin in the

C a r b B a c k - L o a d i n g

C a f f e i n e

morning, and most apt to store excess carbs as fat —caffeine changes

that.

Caffeine can also increase the speed at which we resynthesize and

replenish glycogen after training6. The reason for this, I suspect, is

the same reason Carb Back-Loading works: caffeine shuts down

insulin sensitivity instead of depending on circadian rhythms, while

training causes the all-important translocation of tGLUT. Since fat

cells no longer compete for blood sugar, there will be larger

amounts of sugar available for muscles to refill drained glycogen

stores.

As it seems to go with any extended talk about caffeine, people often

get confused about caffeine’s role with insulin, mistaken in the

belief that caffeine causes insulin release. This is absolutely not

true7, despite Barry Sears’ ranting in The Zone.

What is true, however, is that caffeine ingestion with carbohydrates

increases the amount of insulin released8. Caffeine’s ability to

desensitize cells to the action of insulin drives greater total insulin

production as the body tries to clear blood sugar.

Cells can no longer clear glucose as rapidly, so the extended

elevation in blood sugar causes the body to release higher amounts

of insulin, attempting to clear the sugar faster. It’s a positive-

feedback loop: caffeine inhibits insulin action and the body

interrupts this as a need to produce more insulin.

NOTE: Caffeine in capsule or powder form—

caffeine alkyloids—cause greater insulin insens-

itivity, i.e. greater resistance than does coffee9.

1 0 2

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

In general, I prescribe a lot of optional caffeine. When training

times are not ideal however—e.g. training in the morning as

opposed to training in the evening—caffeine becomes essential in

the plan. Recommended levels may be upwards of 800 mg in a

sitting, an amount tolerated well by most people10. The plans make

it obvious when you need a cup of joe, and when to skip it.

C a r b B a c k - L o a d i n g

Chapter 29

Creatine

Few supplements boast the amount of human-based

performance research as creatine. Scientists study everything from

endurance to greater power production and enhanced hypertrophy,

so science knows a lot about creatine and how it affects metabolism,

hormone levels and how many extra reps it might enable.

There’s nothing unnatural about creatine. The body manufactures it.

Muscles metabolize ATP into ADP and, if ATP is not produced fast

enough, ADP can be metabolized into AMP and after that, the

muscle’s producing lactic acid, at which point, it can’t fire

effectively or for much longer. Creatine is the active chemical

transporter that helps recycle AMP and ADP back into ATP1.

By supplementing correctly, and raising intramuscular levels to

supraphysiological levels—way above normal—creatine helps

extend a set of squats because the excess amount holds back lactic-

acid production. Without all those free positive-ion donors, we can

push rep counts higher2.

While it is true that creatine can improve strength and muscle

growth beyond normal3, I prefer to focus on a recent discovery

about creatine, which, instead of being an anabolic effect, is

anticatabolic. Creatine may block myostatin production, which can

1 0 4

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

allow significant growth because myostatin is a powerful anti-

growth factor4. Knock out an antigrowth factor and, consequently,

trigger new growth.

Many hormones signal growth as levels increase, myostatin,

however stops muscular growth and cell differentiation when levels

are high. Myostatin is one of the key factors that limit the size of

skeletal muscle and training lowers the production of myostatin

thus allowing muscular hypertrophy5.

Effects of Myostatin Deficiency Vs. Blockade6

Myostatin

Myostatin

Natural Mouse

Deficient

Blockers

Figure 3: By blocking myostatin, muscular hypertrophy is extreme compared

to the natural mouse.

Creatine’s got another mode of action, one only recently discovered,

that can enhance the efficacy of Carb Back-Loading. When dosed

properly, creatine increases the amount of glycogen muscles can

C a r b B a c k - L o a d i n g

C r e a t i n e

store and tGLUT action7. One of the main goals of Carb Back-

Loading is to refill glycogen stores to the maximum amount possible

given the limited time for refeeding. Creatine augments storage,

giving the capacity to store more, and hence endure longer, more

intense training sessions the next day.

1 0 6

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

C a r b B a c k - L o a d i n g

Section IV

Essential Points

Omega-3s increase hypertrophy.

Everyone should supplement with whey

isolate.

Not only is whey isolate anabolic for muscle tissue but it

fuels the most powerful antioxidant system in the body.

Premade whey drinks don’t contain whey.

Because of the pasteurization process required for all

milk-derived liquid products in the U.S., nearly all of

the whey protein is destroyed in these drinks.

Leucine is powerfully anabolic.

It doesn’t matter if your goal is more muscle mass or less

body fat, take leucine.

Caffeine can simulate daily insulin

resistance.

Because caffeine can cause transient insulin resistance,

taking it earlier in the day can allow you to use Carb

Back-Loading based on your schedule, not your body’s.

Creatine can cause hypertrophy.

If you’ve been avoiding creatine because you don’t care

1 0 8

S e c t i o n I V : A f t e r m a r k e t A d d - O n s

about that last extra rep or two, think again: creatine

may be a potent anti-catabolic supplement.

C a r b B a c k - L o a d i n g

Section V

WHAT TO DO

S e c t i o n V : W h a t T o D o

C a r b B a c k - L o a d i n g

Chapter 30

Tell Me How,

Hold the Details

People use Carb Back-Loading for multiple purposes

ranging from pure bulking to exposing their six-pack. By employing

MTR to create and enhance metabolic inefficiencies while

amplifying hypertrophy, Carb Back-Loading is the easiest way to eat

for most goals; and it fits most people’s lives.

Busy during the first half of the day, making it hard to get in the

number of calories suggested by another program? Back-Loading

requires only light eating during the first half of the day and

mountains of food before bed—no calorie counting necessary. No

time to train on the random schedule of other exercise plans—after

work is the only possibility? Back-Loading is perfect.

What I get from people, more than any other question, is, “So what

should I eat for .” Fill in the blank with any name ever given

for any meal on any diet. I wish a boilerplate answer existed,

something simple, something everyone wants to hear, like, “have a

glass of milk and six donuts.” Okay, well, I do say that from time to

time, but I can’t say that every time to everyone.

I understand the frustration when they have to start planning. As

straight forward as it may seem in the reading, it suddenly turns into

a convoluted mess. They attempt to put all the pieces together as the

1 1 2

S e c t i o n V : W h a t T o D o

program outlines, except more pieces exist than slots to fill. And

that’s almost always the way, the simpler a diet plan sounds the

harder it is to get right. The Zone, for example, sounds simple: 40-

30-30. Ever try it? When compared with other diets, more people

quit than with any other because it’s near impossible to actually do1.

Carb Back-Loading is different: it is that simple. Nothing’s hidden

from view. No carbs until you train; hit the gym in the afternoon;

slam the carbs.

But, be honest, questions are already forming. Not everyone has

time to dig through the research, experiment on several dozen

human-guinea pig, collect the results and answer all the unknowns.

This section, therefore, is dedicated to making implementation as

simple as possible by outlining each meal of the day, step-by-step,

from breakfast (or lack thereof) to pre-, intra- and post-training to

the best carbs to eat before hitting the sack.

C a r b B a c k - L o a d i n g

Chapter 31

Strength Accumulation

& Density Bulking

For every goal and training style, tweaks and alterations

exist to optimize Carb Back-Loading. Covering all possibilities in a

single tome is unrealistic and even if I tried, I’d still miss a couple

hundred variants. In this book, I focus on using back-loading for one

of two main purposes: Strength Accumulation™ and Density

Bulking™.

Strength Accumulation™

The Strength Accumulation protocol delivers significant increases in

strength, moderate to low mass gain, and massive fat loss. Besides

those already starting at a body fat percent below 10, lean body mass

gain is likely and even then is still possible. Very few people who

follow the lean strength plan don’t gain muscle. The result: ripped

and jacked.

Density Bulking™

Use the Density Bulking protocol if the ultimate goal is an increase

in body weight by 10 to 20% while keeping body fat percentage the

same. This could mean a small increase in body fat, but not much. In

1 1 4

S e c t i o n V : W h a t T o D o

most instances, depending on starting body-fat levels—over 15%—

body fat percentage decreases while adding rock-solid mass.

Throughout the implementation section, I specify how and where to

make alterations to optimize for one protocol or another.

Recognizing the differences is easy, although sometimes, even with

what seems like two distinct goals, the separation between the two

is fuzzy. Like I said, I can’t include an infinite number of variations,

but I try to provide enough information that it’s easy to make

changes for individual goals and lifestyles.

C a r b B a c k - L o a d i n g

Chapter 32

Preparation Phase

For those implementing the Density Bulk protocol or with

a body fat level already at or below the 10% level, the preparation

procedure in this chapter is optional. Otherwise, use this phase to

wipe out glycogen reserves and get the body primed for fat burning.

The prep phase is rather straight forward. Eliminate usable carbs—

all carbs except fiber—for 10 days. Basically, it’s Carb Back-Loading

without the back-loading: ultra-low carb for 10 days—all day every

day.

Stripping carbs from the diet to near non-existent levels carries a

few surprises for the uninitiated. Without understanding what

happens the first few days, many people quit because they don’t

recognize what their experience as normal. Here is what normally

happens during these 10 days1, broken into three segments.

Carb Depletion (days 1p4)

The body will burn through stored glycogen reserves within about

three days. The body stores 3 grams of water for every gram of

carbohydrates2 so as the glycogen stores dwindle, excess water is

flushed from the body. Significant weight loss occurs during this

period, of which roughly 60% is water and the rest is fat3, give or

1 1 6

S e c t i o n V : W h a t T o D o

take a few percentage points. Expect the water weight to come back

when carbs re-enter the diet.

Ketone Buildup (days 3p6)

As carb reserves drain, the body replaces its quick-fuel needs with

ketones4. Ketone production cover energy needs for short-duration

exertion and for brain activity. By the 6th day, the body’s capacity

for ketone production reaches a peak. This timeframe contains the

cross-over point, the moment at which the body no longer has carbs

to burn, but ketone production and utilization still lags. Prepare for

a bit of mental lethargy.

Fuel Reorientation (days 7p10)

The brain fails to use the ketones at first because, like glucose,

ketones require special transporters to cross what’s known as the

blood-brain barrier5. Without prior exposure to an ultra-low carb

plan, there’s a good chance the brain hasn’t used ketones since

infancy. The end of the mental lethargy from the last segment

marks the beginning of this stage. By the end of this phase, the body

has adapted to life without carbohydrates5,6.

It is possible to shorten the duration of the first segment and almost

avoid it altogether. This shortens the entire process by 3 or 4 days,

but makes for a potentially miserable experience. For most people,

regularly scheduled training should wipe out carb reserves to

shorten the entire process by a day or two—if it doesn’t, get a new

training program.

C a r b B a c k - L o a d i n g

P r e p a r a t i o n P h a s e

To skip the first three days worth of depletion and head straight for

the mental-sloth stage, include a few high-intensity interval

training (HIIT) cycles7. I go into more detail about HIIT later in the

book and charts specify the appropriate HIIT cycle for differing

goals.

In lieu of a rapid depletion, or just to be on the safe side, take a full

10 days without usable carbs.

NOTE: Ketones are a high-efficiency fuel for

muscle and nervous tissue in times of glucose

depletion or situations when the body can't get

glucose where it's needed fast enough8. The body

produces ketones from fatty acids or amino-acids

and although ketones burn efficiently, production is

metabolically

inefficient9,

i.e.

making

ketones

wastes a lot of energy. Most health experts believe

that

ketone

production

is

dangerous,

but

production occurs during exercise and first thing in

the morning before eating.

1 1 8

S e c t i o n V : W h a t T o D o

C a r b B a c k - L o a d i n g

Chapter 33

Upon Waking

What you eat—carbs, fat, protein, some combination

thereof of nothing at all—determines your body’s reaction to food

and training for the rest of that day. Getting lean or staying lean,

and adding muscle, therefore, requires doing things right, and that

includes starting the day with a single goal: keep the body burning

fat for as long as possible.

Me and the majority of my clients delay eating breakfast by a few

hours for this goal—the easiest solution. I often get up at 5 a.m., but

if I eat breakfast, it won't be until 8 am or later—sometimes much,

much later—around 1pm.

That's a long gap to go without anything—most people need

something to curb their appetite, which may be pretty strong in the

morning due to the release of the hunger-stimulating hormone

ghrelin.

Earlier, I described the state of the body’s metabolism when first

getting moving in the morning: a fat-burning inferno. Maybe

delicate smolder describes the process better because eating the

wrong thing interrupts the fat burning process. Depending on the

food, knocking the body out of fat-burning mode might not take

much.

1 2 0

S e c t i o n V : W h a t T o D o

One thing I didn’t mention earlier in the book about the fat-burning

forces at play in the morning is ketone production. Ketone

production is wasteful but fragile. Ketogenesis—the production of

ketones—turns itself off by being too effective. Once enough

ketones accumulate in the blood stream, insulin levels rise and shut

down ketone production1. By adding the right supplements at the

right time, we can prolong ketogenesis well past the normal shut-off

time.

It looks like there are now four goals when first waking, listed in

order of importance for succeeding with Carb Back-Loading:

Four Early-Morning Goals

1. Control hunger;

2. Keep burning body fat;

3. Prevent muscle loss; and

4. Prolong ketogenesis.

Control Hunger

Morning hunger can become nauseating and hard to stave off with

sheer force of will. Your first option is coffee, no sugar—although

an intense sweetener is okay in limited quantity. Caffeine can

increase fat burning and doesn’t interrupt metabolism while the

cholinomimetics help control hunger. This is what many people

already do whether they understand or even know the effect.

C a r b B a c k - L o a d i n g

U p o n W a k i n g

Another option, if that’s not satiating enough, is to add heavy

whipping cream—a slow-absorbing source of pure fat.

Coffee is the key to controlling hunger, not the caffeine which is

not an appetite suppressant; the cholinomimetics from roasted

coffee beans are. Don't tolerate caffeine well? Not a problem—drink

decaf. Fat burning may not be enhanced, but the decaf still curbs

appetite because of the cholinomimetics, which also stimulate

nervous system activity, only not as much as caffeine.

NOTE: Using caffeinated energy drinks is not

an option, although I wish they were with the

variety and prevalence. The sugar-free versions

don’t work—not normally, anyway—because they

contain

the

artificial

sweetener

acesulfame

potassium also labeled as acesulfame-K. Of all the

sweeteners, wouldn’t it figure that the only one that

spikes insulin levels2 is the one that’s in nearly all

sugar-free drinks?

Keep Burning Body Fat

Goal number two—to enhance and prolong fat burning—requires

eating little to no food and including optional supplements for a

boost. Caffeine is the best and most readily available options, either

from coffee, tea or even caffeine pills. Remember, though, getting

caffeine through a source other than coffee will not help with

appetite— I'm going to keep repeating this.

1 2 2

S e c t i o n V : W h a t T o D o

Prevent Muscle Loss

Preventing muscle loss while not hindering fat burning or

interfering with the next goal (prolonging ketogenesis) requires a bit

of finesse. Increasing free amino acid (FAA) levels stops or

attenuates potential destruction of muscle by sparing lean tissue

from proteolysis, the technical term for the breakdown of intact

protein structures like muscle. A rapid rise in FAA levels in the

bloodstream however spikes insulin levels. That’s no good because

insulin can stop fat burning.

A slow and small rise in FAA levels helps prevent proteolysis and

prolong ketogenesis. Whey Isolate to the rescue. Ten grams or so—

about half a serving for most commercial formulations —raises FAA

levels without over-stimulating insulin release3. There may be a

small increase, but not enough to derail fat-burning and not enough

to throw off ketogenesis.

Prolong Ketogenesis

Prolonging ketogenesis, I would say, is the least important of the

goals, but why not squeeze every last bit of performance from the

body? Ketogenesis requires two things to work.

The first is a lack of carbs. The second is an ample supply of

triglycerides4. Keeping triglyceride levels elevated forces the body to

continue producing ketones.

MCT oil, because it absorbs quickly unlike other fats, raises

triglyceride levels. So now, instead of adding heavy whipping cream

to coffee, add coconut oil or unsweetened, full-fat coconut milk. Or

C a r b B a c k - L o a d i n g

U p o n W a k i n g

throw in a tablespoon or two of coconut milk into the whey isolate

protein shake.

Result: A.M. Accelerator Shake

Mixing the above components makes a tasty shake. I often combine

all the ingredients—coffee, vanilla-flavored whey isolate powder

and coconut milk—into a single latte-like concoction. Don’t worry

about adding whey isolate to hot coffee.

Although intact whey breaks down with heat, the amount that

breaks down depends on time and temperature. Coffee doesn’t stay

hot enough long enough to destroy much of the protein, nor should

the shake survive long before downing the whole thing.

This ideal fat-burning formula isn’t limited to a one-time shot. Have

it twice; maybe three times. Each time, it sparks the same metabolic

and hormonal reactions, assuming that the time between ingestions

is a couple of hours or more.

Skipping food until the afternoon can accelerate fat loss during a

Strength Accumulation protocol, but not for Density Bulking.

Gaining muscle requires creating a strong and persistent anabolic

state which in turn requires food.

For Density Bulking, it’s best to drink the magic concoction first

thing in the morning an hour before breakfast, which is the subject

of the next chapter.

1 2 4

S e c t i o n V : W h a t T o D o

A.M. Accelerator Shake

Component

Amount

Purpose

Coffee

1 to 2 cups

Hunger Control

(decaf or regular )

Caffeine

200-400 mg

Fat Burning

(coffee or other )

Catabolism

Whey Isolate

10 g

Prevention

MCT oil

1 tbsp of MCT

Ketogenesis

(coconut milk/oil )

C a r b B a c k - L o a d i n g

Chapter 34

Low-Carb Mealtimes

Some people may or may not consider the suggested

formulation from the last chapter as a meal, but even with the

addition of all components, it's a paltry amount of sustenance—

exactly right depending on goals, but still minuscule. To me, it's

targeted, functional nutrition and I hesitate to designate it breakfast.

Breakfast, like all meals before training, falls into the ultra-low-carb

part of the day and is composed of solid food.

The number of meals eaten before training depends on goals and

personal preference. Actually, it depends more on personal

preference than anything else. I don't prescribe a specific number of

meals or any specific schedule on which to ingest food. There's no

evidence to support doing anything other than what works with the

daily routine1: the breakdown and distribution of calories and macro

nutrients throughout the day matters far more than the number of

meals2.

The goal for all meals in this part of the day—the ultra-low part—is

to keep the total grams of carbs from all meals under 30 grams.

That's not much in the way of carbs, but it’s pretty easy to achieve.

Green vegetables, meats, cheeses, fats and limited amounts of nuts

comprise the diet during this portion of the day.

1 2 6

S e c t i o n V : W h a t T o D o

Example Low-Carb Meals

A ham steak with asparagus sautéed in butter

Hamburger patty with a slice of cheddar cheese

on a bed of spinach

Half a cup of nuts and a pound of low-fat

cottage cheese

Sliced turkey, avocado and tomato

Okay, tomatoes aren’t green and both avocado and tomatoes aren't

vegetables, but they're safe in limited quantities depending on

variety. There's a basic list of vegetable selections in the appendix. I

suggest referring to it.

Eggs may seem like an obvious choice, but I didn’t include them in

the examples for a reason. Not that they're not safe—they can be—

but I wanted to draw particular attention to them because eggs,

eaten alone can raise insulin levels, something I noted earlier. We

want to limit insulin release during the first half of the day.

The solution: eat eggs with something fatty. Fried in plenty of

butter, omelets, scrambles with cheese, hardboiled with a handful of

nuts, whatever…bacon and eggs works well too.

Later in the book I discuss how to determine calories for the first

half of the day. This section focuses on food selection and meal

choice. Remember to eat vegetables. People who fail to recognize

C a r b B a c k - L o a d i n g

L o w - C a r b M e a l t i m e s

the importance of the vegetables during this part of the day often do

poorly compared to their veggie-including counterparts. As

explained in the chapter about usable carbs, eating fiber combined

with fat helps reduce the number of usable calories from a meal by

up to 20%.

The take-away message from this chapter is simple: no bread—

whole-grain or otherwise—pasta, fruit, sugary treats, chips, donuts,

rice, potatoes, sugar-laden condiments, and so on. The easiest thing

to remember might be that if it's green or once had a face—or both I

suppose—it’s safe to eat.

NOTE: Usable carbs include all carbohydrates

except fiber. Sugar, starch, glycerine and sugar

alcohols all qualify as usable carbs.

1 2 8

S e c t i o n V : W h a t T o D o

C a r b B a c k - L o a d i n g

Chapter 35

Pre-Training

Often cited as a critical time for growth and performance

gains, pre-workout gets a lot of attention from the current cult of

gurus, but the dearth of evidence should convince us otherwise. The

best I can say is that it might make a difference; and if it does, the

effects of advanced post-workout nutrition will make any

advantages insignificant.

Although there’s not much evidence for pre-workout nutrition for

growth, formulations exist to increase ketone production and,

consequently, increased fat burning. And choosing a slow-absorbing

source of amino acids—like whey isolate—helps limit proteolysis

without interfering with fat burning1. Pre-workout nutrition may

not enhance growth, but it can increase fat burning and stop muscle

burning.

The formula mimics that of the A.M. Accelerator Shake: 10 to 20

grams of whey isolate, 600 to 800 mg of caffeine and 5 to 10 grams

of MCTs. This time, any source of caffeine produces the desired

effect since hunger control is not a concern: tea, powder, coffee,

even carb-free energy drinks (in moderation).

Adding the caffeine causes a certain level of resistance to insulin. In

the pre workout shake, it amplifies the effectiveness of Carb Back-

1 3 0

S e c t i o n V : W h a t T o D o

Loading. Research also shows that consuming caffeine before

training accelerates the rate at which the body replenishes glycogen,

another important component of Carb Back-Loading: filling carb

stores after our training session empties them.

Consume this formula 30 minutes before training. The whole thing

is optional and applies equally to Density Bulking and Strength

Accumulation, but I do highly recommend ingesting a healthy

amount of pre-training caffeine.

Before I discuss intra-workout nutrition, notice that I didn’t

recommend pre-training carbs. That’s not an oversight on my part.

Eating carbs before training offers no benefit, and only stymies fat

burning. So, stay clear of the pre-workout carbs—include them

when they matter most, after the training session.

Ignition Formula

Amount

Component

Strength

Density

Accumulation

Bulking

Caffeine

400-800 mg

200-400 mg

(coffee or other)

Whey Isolate

10 g

20-30 g

MCT oil

2-3 tbsp of

1 tbsp of MCT

(coconut milk/oil)

MCT

Creatine

5 g

5 g

C a r b B a c k - L o a d i n g

Chapter 36

Intra-Training

Consuming nutrients during the training session is

nothing new, whether it’s Gatorade or a part of a peri-workout

protocol. The problem is how to know exactly what to consume or

if consuming anything is even a good idea.

Resistance training is inherently catabolic, increasing muscle

protein breakdown. However, after resistance training ends,

providing adequate raw materials, like amino acids or di- and tri-

peptides, however, stimulates muscle protein synthesis after

resistance training ends. The combination of the two—muscle

protein breakdown (MPB) and muscle protein synthesis (MPS)—is

the skeletal muscle turnover rate.

If the rate leans too far toward MPB, we lose muscle. Shifting

toward MPS sparks hypertrophy and we get jacked. The combined

goals of increasing MPS and decreasing MPB should drive every

nutritional decision made around training time.

Recognizing that two goals exist and not just one—trying to grow

and trying to prevent destruction—allows supplement and food

choice to target either or both. Training doesn't need to tear muscle

down for growth to occur, as many high school gym teachers still

1 3 2

S e c t i o n V : W h a t T o D o

preach. We can build and forgo the destruction. Just as there are

two goals, two tools exist: insulin and amino acids.

Insulin supports growth of nearly all tissues in the body and often

triggers the growth process. During training, however, insulin

doesn’t trigger muscle growth, doesn’t increase potential growth or

activate any pathways to hypertrophy, but it does stop the

breakdown of muscle tissue. The last decade of research revealed

insulin as purely anti-catabolic during training rather than anabolic.

High insulin levels suppress MPB—protect muscle—up to some

critical point at which higher levels make no difference.

Spiking insulin during a workout is easy: drink a sugary drink. This

works, but Carb Back-Loading—for either Density Bulking or

Strength Accumulation—works to decrease fat mass while growing

new muscle. That makes ingesting carbs during a workout a bad

idea, since carbs, in the specific context of avoiding carbs all day

until after training, decrease performance, impede fat burning and

can cause rebound hypoglycemia, also called glycemic distress: a

condition in which the body cannot maintain normal blood sugar

levels. The body actually has an easier time maintaining blood sugar

levels without exogenous carbs.

Without carbs, we have a limited range of strong insulin

secretagogues from which to choose. Eggs, as I pointed out early,

can raise insulin levels—not spike, unfortunately—but I’m not a fan

of downing eggs during my training session and I don’t know many

people who are. I elucidated two possibilities earlier: leucine and

protein hydrolysate. Both work together to raise insulin levels more

than either alone. The two, mixed appropriately, spike intra-

C a r b B a c k - L o a d i n g

I n t r a - T r a i n i n g

training insulin levels and, if taken during the training session, can

limit MPB1.

Using hydrolysates and leucine to trigger an insulin release gives us

a few advantages beyond continued fat burning. We need an excess

of leucine to trigger the maximum anabolic response from resistance

training because it activates the mTOR receptor, one of the positive

regulators of muscle growth. Because insulin is needed to potentiate

the action of the mTOR receptor on growth, leucine delivers a one-

two punch: decrease MPB and set the stage for increased MPS.

Adding leucine alone, even with its ability to trigger insulin

secretion, does not initiate muscle growth. MPS requires a large

supply of amino acids. Casein hydrolysate absorbs quickly in the gut

and causes an immediate jump in free amino-acid levels. Almost any

protein hydrolysate works, but hydrolyzed casein seems to be the

best. I recommend pure PeptoPro® because a patented debittering

process prevents it from tasting horrid, but regular hydrolyzed

casein works fine if taste isn’t a concern.

These two in combination—a hydrolyzed protein and leucine—do

everything: spike insulin levels to decrease MPB and potentiate

maximum muscle growth; supply leucine to trigger maximum

muscle growth; provides free amino acids to fuel MPS. All of this

sans carbs.

There’s another effect of raising insulin. During training, cortisol

levels rise2. It’s a normal reaction. The magnitude of that rise

depends on time of day—which I touched upon earlier—and also

insulin levels. As insulin levels rise during a training session, cortisol

1 3 4

S e c t i o n V : W h a t T o D o

levels drop3. This fact influences if and how we want to implement

an intra-workout shake.

In the absence of carbs and insulin—like when first waking in the

morning—cortisol enhances fat burning, which is also true during

training. For Strength Accumulation, it’s best to skip the intra-

workout nutrition and let the body burn as much extra fat as

possible during training. So, option number one: skip the intra-

workout shake.

The next option is for those who decided to Density Bulk. Here, the

entire program tries to achieve the maximum amount of lean mass

without adding body fat. The intra-training shake, in this case,

enhances the effect of back-loading by increasing hypertrophy4, if at

the expense of burning fat.

Sustainer Formula

Component

Amount

Whey Isolate

10 g

Casein

20 g

Hydrolysate

Leucine

3 g

C a r b B a c k - L o a d i n g

••••••••••••••••••••••••••••••••••••••••••••••••

Chapter 37

Post-Training

If there’s anything in this book of value, it’s the

information in this chapter. It describes building the perfect post-

workout shake—according to the latest available research and a

decade of results. Although I’m specifying this formula in the

context of Carb Back-loading, its applicability is universal for all

resistance training athletes battling against iron, steel or stone for a

singular purpose: to transcend limitations.

As I described in the previous chapter, training is intrinsically

catabolic but activates several anabolic channels. Just like the intra-

workout nutritional supplementation, the goal is to limit muscle

protein breakdown (MPB) and stimulate muscle protein synthesis

(MPS). Unlike the nutrition during training when most of the effort

fights MPB, in the wake of training the majority of the nutritional

effort goes toward building.

The marked difference in formulation from all the potential

previous shakes of the day differs by the addition of carbs. When

deciding on the carbs added to the post-workout (PWO) shake,

quality matters over quantity. The carb must spike blood sugar

levels and insulin levels, i.e. must be high-glycemic and

insulinotropic. Any from the chapter on supplements meet these

criteria: dextrose, maltodextrin and waxy maize or rice. Real food

1 3 6

S e c t i o n V : W h a t T o D o

options exist and work, although they don't perform as well. Two

such options are white bread or overly-ripe, brown-spotted bananas

(being overly ripe is important).

We don’t need much: 20 to 40 grams (that's one or two large

bananas’ worth). We’re hunting for a spike in blood sugar and

insulin, not trying to replenish the glycogen reserves drained during

training. That comes later. Immediately after training, blood sugar

and insulin production need a jolt. In conjunction with the carbs,

the post workout shake includes protein hydrolysates, as did the

intra-workout formula, but this time, hydrolysates derived from

both whey and casein. Throw in some leucine and the formula is

almost complete.

It’s reasonable to question the addition of carbs when all we need to

drive muscle protein turnover positive is insulin and a large supply

of amino acids. The bigger the insulin spike, the better, and carbs—

of the type listed above—plus protein hydrolysates and leucine raise

insulin levels two times that achieved by any of the three alone or

any combination of two. All three together act synergistically to

produce a massive increase in MPS1.

Most low-carb gurus fear this post-training suggestion because they

take as fact that in all metabolic situations with elevated insulin and

glucose levels, the body stores fat. As I mentioned in the chapter on

insulin, this can be true and is one of insulin’s possible modes of

actions. For the average couch-sitting American that spends 90% of

their day sitting or lying down, I would agree this is probably the

case. But at the outset, I excluded that group from the ranks of

individuals who should be reading this book.

C a r b B a c k - L o a d i n g

P o s t - T r a i n i n g

As resistance-trained athletes, we can create situations that nullify

even insulin’s ability to spark lipogenesis. Raising insulin levels

through the roof and supplying a little sugar won’t make a

difference because it’s nearly impossible to add fat for an hour or

two after training2.

Right now the formula sounds pretty good, but we can get even

more from the post-workout shake by adding caffeine and creatine.

Both increase the rate at which glycogen stores refill3. Don’t forget,

creatine blocks myostatin, making it hypertrophic.

In the end, the constituents of the formula aren’t far off of a hybrid

of the pre-workout and intra-workout suggestion with the addition

of three c’s: carbs, caffeine, and creatine. The quantities differ and

there’s the inclusion of whey protein isolate and a small amount of

intact casein, both added to create a sustained release of amino acids

necessary to support skeletal muscle hypertrophy.

The rapid rise in amino acids from the hydrolysates and leucine

ignite MPS, but the rush recedes too quickly to sustain MPS4. When

ingested post-training, intact casein, for example, increases 24 hour

MPS5.

Aside from the requisite constituents of what might be the best

possible post-workout shake, timing is a key factor. Although the

gurus recommend immediate ingestion of any post-workout

nutrition, the window is much wider and there may be benefit to

waiting up to 30 minutes after training to ingest the post-workout

shake.

1 3 8

S e c t i o n V : W h a t T o D o

Hypertrophic Potentiator

Amount

Component

Strength

Density

Accumulation

Bulking

Caffeine

200-600 mg

200-400 mg

(powder is best)

Whey Isolate

15-20 g

30 g

High-GI Carb

20-40 g

40-100 g

Casein (intact)

10-15g

15-25 g

Hydrolysate

( W h e y , C a s e i n o r B o t h )

10-15 g

25-30 g

Leucine

3 g

5 g

Creatine

5 g

5 g

C a r b B a c k - L o a d i n g

Chapter 38

Carb-Loading

Mealtimes

About thirty minutes to an hour after a PWO shake, the

time comes that everyone reading this book has been salivating

over: the carb back-load.

This is where pizzas, pastries, donuts, French fries and milk shakes

come in handy. Food-wise, the goal is to supply the nutrients

necessary to support the anabolic signaling triggered with training

and to refill glycogen levels for the next-day’s training. Everything

wants to grow—everything but fat cells. As a matter of fact, each

bout of resistance training creates a fat-burning shadow extending

across the next 24 hours.

Even though aminos, di- and tripeptides and insulin flooded the

blood stream during the most anabolic window of time—post

workout—there’s still more anabolic signaling to trigger. Eating

large amounts of carbs in successive meals prolongs the insulin spike

and not only keeps the anabolic machinery humming, but also

makes the body more efficient at burning carbs during the next

training session1.

The few health and diet gurus who’ve jumped on the back-loading

bandwagon suggest evening options based on pop-diet culture, e.g.

low-glycemic carbs. Not only is this advice wrong, but fat-inducing.

1 4 0

S e c t i o n V : W h a t T o D o

Choose foods that they say to avoid. This rule of thumb works well

with the addition of a simple qualifier: choose the bad foods which

are the least processed, e.g. a fresh made donut instead of a Twinkie,

homemade cookies over Oreos—or even natural cookies at the local

grocer. Get a hand-tossed pizza from the pizzeria down the street

rather than a frozen piece of cardboard with some rubbery cheese

from the frozen-foods section.

The less processed foods or rather the one’s closest to whole foods,

act differently than their highly-processed siblings. Even for two

meals of identical macro nutrient content—one that contains

whole-food, or lightly processed ingredients and another that’s

highly processed—the less processed version causes different

hormonal reactions than the highly processed one2. And we want

the clean one.

NOTE: You need to eat very high-glycemic

carbs for Carb Back-Loading to work. Trying to eat

healthy

carbs—low-glycemic

or

fibrous

food

items—will sabotage your results.

So, make a burger at home and get Wendy’s Natural-Cut fries

instead of something from the super-fast-food chain whose burgers

and fries start as pastes, formed later into the right shape with the

appropriate flavoring added. The meat in these products is of such

low quality, the fast-food chains invented beef flavoring to add so at

least the taste buds think it’s a burger even if the endocrine system

knows better.

C a r b B a c k - L o a d i n g

C a r b - L o a d i n g M e a l t i m e s

Don’t worry about the fat: post-training, the insulin response does

not stop the after-burn effect of resistance training—the body

continues burning fat for up to 36 hours3.

Now, pizza and a burger and fries sounds great, but significantly less

complex meals work. Stir fry chicken with white rice—yes, white;

and sticky is even better. Sushi, brown-mottled, super-ripe bananas,

sweet potatoes, red potatoes, waxy purple potatoes, grapes, a

sandwich on white bread, and so on.

Stay away from the healthy foods: avoid whole-grain breads, high-

fiber, low-glycemic foods. This is the time go get high—high

glycemic and insulinotropic. Cherry turnovers, apple pie or rice

pudding work.

These junk items, as health experts call them, spike insulin and

supply huge glucose boluses to help refill glycogen stores4. I specify

these foods for another reason.

The body releases growth hormone at night, but it won’t begin

doing so until insulin levels return to normal and stay at that level

for about two hours5. Eating the high-glycemic goodies causes a big

rush of blood sugar and jolt of insulin, then a quick drop as things

settle back to normal, leaving the nocturnal hours free of insulin

and full of growth hormone.

Let me say this a bit more clearly: absolutely avoid low-glycemic

carbs. They cause sustained and low-grade blood sugar and insulin

levels that may last hours, sabotaging the nightly release of a

powerful fat burning hormone and sabotaging your results.

1 4 2

S e c t i o n V : W h a t T o D o

Maybe the couch-potato neighbor needs to listen to Dr. Oz and eat

only low-glycemic tree-bark, but high-performance athletes don’t:

that’s why we train in the first place, to rise above the norm.

How to distribute the carbs

For the first meal after training, don’t limit carbs, but remember,

keep it trashy. Don’t forget, however, that glycogen is not the only

tissue trying to resynthesize and recover from the training.

Anabolic signaling for muscle tissue is active, so feed the machinery

what it needs to grow, not what it wants to burn. Intact animal

proteins support growth and attenuate any catabolic processes that

could occur during the evening and even through the next day, i.e.

eat beef, chicken, pork, cottage cheese and, as a supplement, use a

casein additive6. It also does an excellent job of preventing muscle

protein breakdown over a 24 hour period.

Don’t forget the hydrolysates. When taken with a mixed meal,

hydrolysates increase the insulin response of intact food by up to

50% and can help replenish glycogen stores faster7. Added leucine

can drive insulin levels even higher. Add a shake containing about

10 grams of hydrolysate and 5 grams of leucine to each of the carb-

laden evening meals, in addition to a cut of meat or fish for

maximum effect.

C a r b B a c k - L o a d i n g

Chapter 39

Before-Bed

Depending on what time evening training sessions end

and when the carb feeding-frenzy begins, there might be time for

one more meal before bedding down.

It’s all about raw materials for growth. In the evening, as before, the

main goal is to supply raw material for growth through the

nighttime torpor. This amounts to making sure that the final meal of

the day meets the body’s protein needs for sustained growth without

interfering with growth hormone release. Eat plenty of meat or

casein at each carb meal and don’t worry too much about it. But

there’s always room for tinkering.

Don’t think I’m about to recommend a slow-absorbing protein that

elevates amino acids through the night. There was a time when I

would have made such a recommendation, and it remains a very

guru-esque thing to say. Time, experience and emerging scientific

research forced me to let go of my proclivities and say, it doesn’t

matter.

Right before bed and after only a handful of hours from finishing

training, almost any type of protein supplies the material needed to

grow at the appropriate rate regardless of how fast it absorbs. Intact

sources like meat, fish, cottage cheese, eggs, milk or powders like

1 4 4

S e c t i o n V : W h a t T o D o

casein (calcium caseinate or micellar) and whey (concentrate or

isolate) all appear equivalent for 24 hour whole-body protein

synthesis despite varying rates of absorption.

C a r b B a c k - L o a d i n g

Chapter 40

Off-Days

Training regimens should include recovery days, which

should be off-days—off from resistance training, at least. If not,

consider changing training splits to include at least one day away

from weight lifting. Now that everyone’s on the same page and has

at least one day of the week without resistance training, I can

describe how to Carb Back-Load on off-days in the simplest terms

possible: don’t.

Now that that’s out of the way, here are the exceptions.

Exception No 1: Density Bulking

Density Bulking, particularly for those at an already low body fat

percentage (below 15%) benefits from back-loading on off-days, so

enjoy.

For Strength Accumulation, however, follow the general guidelines

above for back loading carbs in the evening: i.e. don’t do it. In this

case, dinner should be a chicken ceasar salad; meat balls with green

beans; or salmon with asparagus. Make sure to include the fat either

with a dressing for the salad or by sautéing the vegetables in butter

or nut oil.

1 4 6

S e c t i o n V : W h a t T o D o

Exception No 2: High Training Volume

Sometimes, depending on training volume, the body fails to ever

catch up with the continuous depletion of glycogen reserves.

Glycogen debt becomes a state of being.

If training in this state, lethargy signifies the end of workouts

because each night, time — partial, not total — disappears before an

over-load of carbs makes it down the hatch. The cycle continues day

after day. This problem occurs often with strongman competitors.

With this scenario, I advise clients to continue back-loading even on

off days. I’ve found the high-volume athletes sustain adequate

glycogen levels this way up to a point. If volume goes too high,

other modifications are needed and back-loading may not be

appropriate.

Exception No 3: Back-to-Back Off Days

One final exception: taking off more than one day in a row might

invite the need for an off-day back-load. On the final day of rest of a

contiguous block of off-days, back-load the carbs.

It’s always hard to gauge how much food the body needs on a non-

training back-loading night, and the only guidance I can provide

without direct supervision is to go by feel. Flat and lethargic: eat a

lot on the last off-day before training resumes; Full muscles, holding

some water: eat, at most, a single light meal of carbs.

With any of these scenarios—Density Bulking, high training

volume or consecutive off days—the back-load is like any training

day unless otherwise mentioned. No carbs through the first half of

C a r b B a c k - L o a d i n g

O f f - D a y s

the day, then simply have one or two big carby meals, the first at

dinner time. Grazing is also an alternative: ingesting copious

amounts of food, but doing so with constant small quantities.

1 4 8

S e c t i o n V : W h a t T o D o

C a r b B a c k - L o a d i n g

Chapter 41

All-Day

Supplementation

At this level of performance—the Super Hero In Training

(S.H.I.T.™) level—maximum results derive from extra-ordinary

measures. Carb Back-Loading may be the easiest nutritional protocol

in existence for reaching elite status, but we can tweak here and

there, which adds a bit of complexity but takes us further. Even

with the added complexity of advanced tweaking, back-loading is

stupid simple.

The worst, in almost all protocols, is the supplementation

requirements. Just read the full details of the protocol laid out in this

section: one type of shake before, one type during and yet a third

type after training, and then there’s the addition of protein

hydrolysates and leucine to each of the evening meals. Think that’s

extreme already? We haven’t yet talked about all-day, every meal

supplementation. Don’t worry that I’m going to suggest a handful of

pills, a cabinet full of liquids and a laxative or two. In my opinion,

only two supplements warrant attention in this chapter: fish oil and

creatine.

As was mentioned in the supplement section, fish oil helps increase

anabolic signaling, likely because of increased cellular function

when incorporated into cellular membranes. This allows nutrients

and hormones to exert stronger effects on cells1 and enhances

1 5 0

S e c t i o n V : W h a t T o D o

muscle tissue’s ability to switch between carb burning and fat

burning2.

It requires about five grams of a combination of the omega-3s DHA

and EPA. That’s five grams of the omega-3s, not five grams of fish

oil. Check the label. Most liquid fish-oil products—liquid is the

form I recommend—have ratios of fish oil to omega-3s of about 3:1.

So for every three grams of fish oil, you are only ingesting one gram

of omega-3s. For that reason, I suggest spreading the doses

throughout the day, taking a serving with each meal, but not in any

of the peri-workout — before, during, after — nutrition shakes.

The other all-day supplement is creatine. Many dosing schedules

exist amongst various expert advisors, gym rats, gurus, but in the

most recent, well controlled published studies, sustaining supra-

physiological intramuscular concentrations of creatine requires

roughly 60 grams of ingested creatine per day divided into multiple

doses. This is not a loading phase—for daily supra-physiological

levels, this procedure needs to be done every day3.

Now, do I expect anyone to consume 60g of creatine per day? Not

many people. The effect may not warrant the cost, but I suspect

someone will do it. I also suspect that taking 5 grams with each

feeding could be highly beneficial. Remember, besides allowing us

to squeeze one or two more reps per set, creatine blocks (down

regulates) myostatin. This regular dosing of creatine may also help

maintain excess storage of intramuscular glycogen by about 15%.

C a r b B a c k - L o a d i n g

Section V

Essential Points

A.M. Accelerator Shake, p125

Low-carb meal examples, p127

Pre-workout formula, p131

Intra-workout formula, p135

Post-workout formula, p139

What to do on off-days, p145

Sample meal plans, Appendix E

1 5 2

S e c t i o n V : W h a t T o D o

C a r b B a c k - L o a d i n g

Section VI

NOBODY’S

PERFECT

S e c t i o n V I : N o b o d y ’ s P e r f e c t

C a r b B a c k - L o a d i n g

Chapter 42

Customize

I don’t live in some dream world with a job that lets me lift

at the perfect time every day. Meetings, phone calls, editors, clients

and personal matters all vie for my time. Running a business is no

picnic. In other words, I get it: it may not be possible to train in the

Carb Back-Loading sweet spot. I would say, not a big deal, but it is a

big deal. Carb Back-Loading is only stupid-simple when done super-

strict. Sounds oxymoronic, but the principles that make Carb Back-

Loading work with relative ease depend on integrating training

schedule and eating schedule with immutable circadian rhythms.

For example, maybe the only available training time is early

morning. After I emphatically detailed why training in the

afternoon is critical to the effectiveness of back-loading, it may seem

that early morning training eliminates the possibility of back-

loading. But Carb Back-Loading still works. It just requires tuning.

Earlier-than-ideal training complements Strength Accumulation

more so than Density Bulking. Research even shows that Carb Back-

Loading works for leaning down and preserving muscle mass even

without training. That doesn’t mean Density Bulking is impossible

with early morning training, only that it requires more care. And by

more care, I mean more food. In either case—Strength

1 5 6

S e c t i o n V I : N o b o d y ’ s P e r f e c t

Accumulation or Density Bulking—resistance training increases the

concentration of tGLUT in muscles and increases skeletal muscle’s

sensitivity to insulin. Fat cells can no longer compete effectively for

nutrients to store.

Morning training sessions require a slightly different eating

schedule, but otherwise, the basics remain unchanged. Use the

following guidelines to modify Carb Back-Loading for your

particular training schedule. Note: none of the following alterations

produce results with the ease of the ideal version, but they all

produce amazing results and remain simple.

C a r b B a c k - L o a d i n g

Chapter 43

Training Fasted

Modifying Carb Back-Loading for training first thing in

the morning entails straightforward changes and additions.

Before training, drink coffee and…that’s it. Consume nothing else

except possibly water. Avoid intra-training nutrition as well. From

waking until training completion, ingest only caffeine in whatever

form works best: pills, coffee, tea, powder.

Many people complain about or resist the idea of training on an

empty stomach, but doing so does two things. First, it increases fat

burning and the production of fat-burning enzymes1.

The second effect of training fasted in the morning results from

increased activation of muscular growth factors. By including a

small amount of carbs after early-morning-fasted training, we

double the anabolic response of a regular, pre-fed training session2.

Immediately after the morning training, therefore, things remain

exactly as if training at the ideal time including the carbs: the post

training-formula is identical to normal. Some people prefer solid

food in the early morning and my best suggestion for something

that goes with the morning shake and seems breakfast-like is a very

ripe, large banana with those characteristic brown polka dots.

1 5 8

S e c t i o n V I : N o b o d y ’ s P e r f e c t

To get the largest insulin spike possible from our early-A.M.

training, consume the highest glycemic carbs possible the night

before the training session—the higher the insulin spike from the

carbs the night before, the higher the insulin response the next

morning3. Everything we eat causes a reaction, sometimes extending

over several hours.

This changes how we define an off-day. We no longer define a day

off as a day without training. An off-day is a day when you don’t

train the next morning. Remember, carb ingestion is to replenish

glycogen for the next-day’s training session. Therefore, eat carbs on

each night preceding a fasted-A.M. training session.

The rest of the program is identical: just withhold carbs until dinner

time, say 6 p.m. or so, and have one carb-laden meal and possibly a

sugary meal an hour or so after that. To determine the extent of the

carbs to eat, following these guidelines based on goals.

NOTE: When training fasted first thing in the

morning, you will include carbs in your post-

training shake, but not again until dinner time. If

you don’t train the next morning, either don’t eat

carbs for dinner or eat light.

C a r b B a c k - L o a d i n g

T r a i n i n g F a s t e d

Strength Accumulation

Guidelines

How Do You Feel

What You Should Eat

Soft, holding water

One carb meal

Strength is good and every

Two carb meals and a

morning the skin is visibly

dessert

tight

Tired, flat, training that

As much as possible, starting

morning was excessively

an hour or two before normal

difficult

Density Bulking

Guidelines

How Do You Feel

What You Should Eat

Waking up softer each

One carb meal

morning

Waking up soft, but no

noticeable loss of definition

Exactly as you have been;

from day to day, body weight change nothing

increases weekly

Not so much; slow down.

Cut down to one carb meal

Waking up fat

per night, or go sans carbs

for a couple of days.

1 6 0

S e c t i o n V I : N o b o d y ’ s P e r f e c t

C a r b B a c k - L o a d i n g

Chapter 44

Middle Training

Middle Training includes training any time between the

first meal of the day to shortly after noon and is possibly the worst

time to train for Carb Back-Loading because, unfortunately, no

special hormonal scenarios or bio rhythms exist from which we

could gain advantage. Nothing changes much other than inclusion

of the pre- or intra-workout formulas, or both. Only do this if

breakfast or some other meal came first—something other than

coffee or the a.m. metabolic accelerator shake.

For post-workout recovery nutrition, include everything from the

standard protocol—leucine, hydrolysates and caffeine—but sans

carbs. Since the body is not quite in the ideal window of time,

glycogen replenishment will start later in the day.

From post-training on, follow the modifications as outlined in the

previous chapter and judge carb load based on the chart therein.

1 6 2

S e c t i o n V I : N o b o d y ’ s P e r f e c t

C a r b B a c k - L o a d i n g

Chapter 45

Late-Night Sessions

Having to train late at night deviates the least from the

ideal form of Carb Back-Loading and still imparts all the hormonal,

circadian and biomolecular advantages. The difference—rather, the

problem—is the lack of adequate time to refill glycogen stores1.

A few ways exist to solve this problem. If Density Bulking, start

carbs at the normal time, say 6 p.m., even if this is before training.

The meal should be heavy and carby, i.e. a hamburger with French

fries or a few pieces of pizza with half a roasted chicken. In these

situations, I almost always go for some variation of Denny’s Moons

Over My Hammy: a ham, egg and cheese sandwich with tomatoes

on sourdough bread with hash browns into which I mix two over-

medium egg yolks. Twenty to thirty minutes before eating this

meal, drink about 10 to 20 grams of whey isolate and a cup of coffee.

I don’t think I’ve seen too many recommendations for Moons Over

My Hammy as pre-workout nutrition which leads me to believe it’s

exceedingly rare. My best guess is because it doesn’t jive with what’s

considered healthy. That’s fine for a diet book, but this is a guide

about targeted nutrition and there’s good reason to recommend the

greasy-carby combo.

1 6 4

S e c t i o n V I : N o b o d y ’ s P e r f e c t

The carbs and fat help create a long and even release of carbs and

energy to utilize during training and to help avoid completely

depleting glycogen since enough time to replenish post-training

doesn't exist. Unlike post training when a rollercoaster of insulin

release works to our advantage, pre-training, we need an even,

steady flow of carbs with moderate insulin levels to avoid rebound

hypoglycemia.

Pre-training nutrition doesn’t need to change, nor does the intra-

workout formula, although, if Density Bulking, I suggest adding

roughly 40 to 50 grams of a carb powder to the intra-training shake,

not the pre-training. Increase the carb content of the post-workout

formula to 100 to 200 grams of carb powder, the higher end of the

scale being appropriate if this is the only meal before bed—i.e. train,

drink, sleep. Including caffeine to the PWO shake may be a bad idea

in this case, obviously. If this is not the last meal, follow the ideal

guidelines from here on out: lower-fat and higher glycaemic.

C a r b B a c k - L o a d i n g

Section VI

Essential Points

Early A.M. training requires the most changes

Changes for early A.M. training, p160

Changes for middle-morning/afternoon, p162

Changes for late night, p165

Sample meal plans, Appendix E

1 6 6

S e c t i o n V I : N o b o d y ’ s P e r f e c t

C a r b B a c k - L o a d i n g

Section VII

DOS AND

DON’TS

S e c t i o n V I I : D o s a n d D o n ’ t s

C a r b B a c k - L o a d i n g

Chapter 46

Everybody Needs

Advice

No matter how much detail provide, it's never enough. I

try to lay things out in a clear and concise manner, giving loads of

detail and explanation when I feel it's necessary and turning to

stupid-simple explanations when it's time for implementation or

sample diet templates. Detailed explanation I like; confusing, hard to

figure out instructions, I don't. I assume the same of my audience.

Attempting to keep things simple in the Implementation Section, I

didn't want to delve into those pieces of advice that might specialize

the diet for a particular group or might prevent someone from

baking thirty pounds of bacon-and-maple infused brownies, pouring

the batter into the bathtub, and eating their way to the bottom—

and yes, similar things have happened.

I find some FAQs so fundamental, that in addition to an FAQ

section later, I added this section with extended advice for the most

common experiences. I hope this makes the diet quicker to

implement, to get you on the way to becoming a S.H.I.T.™

1 7 0

S e c t i o n V I I : D o s a n d D o n ’ t s

C a r b B a c k - L o a d i n g

Chapter 47

Don’t Be a Fat Kid

Some things seem obvious and I shouldn’t have to point

out that two triple cheeseburgers from a fast-food restaurant do not

count as carbs for a Carb Back-Loading evening. Making food

choices such as this is nothing more than using Back-Loading as an

excuse to eat like shit—excuse the expletive, but that’s the most

precise way to describe it.

People do this all the time, often misled by the local self-proclaimed

Carb Back-Loading expert. I don’t care if someone knows me or if

they’ve talked with me once or even worked with me, they’re not

an expert on Carb Back-Loading, trust me. Advice like this—the

triple cheeseburgers—makes people fat, pure and simple. I’ve

watched it happen because people would listen to their trainer

rather than the guy who invented the diet.

Another problem is the notion that once training is over, no matter

what time of day it is, pounding carbs for the next several hour

counts as carb back-loading. I’ve seen people try this over-and-over

again, creating a new diet—as they tell people.

I’ve also heard people tell me they’re Carb Back-Loading who train

at 7 a.m. then eat a scone or two, drink a cup of coffee then wolf-

down a huge pasta lunch. Sure, for the next two hours after lunch

1 7 2

S e c t i o n V I I : D o s a n d D o n ’ t s

they’ll skip carbs, but as soon as the evening rolls around they start

slamming them again like a fat kid who’s been locked up for a week

without his sugary cream-filled snack cakes. Guess what happens:

they get strong but they get fat—really fat.

Unless it’s in this book or straight from my lips, remain skeptical of

any advice on or interpretation of Carb Back-Loading. I didn’t do all

this research to leave gaps. If I don’t recommend certain things it’s

because I know they don’t work, not because I overlooked

something, like pigging out and calling it a diet.

C a r b B a c k - L o a d i n g

Chapter 48

Gluten Allergies

While I’m on the subject of pasta from the last chapter, it’s

a horrible carb for Back-Loading even when training at the ideal

time. Devouring that big plate of penne an hour after training in the

evening, the typical carbohydrate sweet spot, does not cause the

ideal hormonal response.

Pasta is low glycemic, which disqualifies it right there, but it’s also

primarily wheat, which might present an even bigger problem.

About 50% of people have some sort of adverse intestinal reaction to

gluten, which wheat contains in abundance1. A couple of different

types of allergies exist, but regardless of type, the reaction is the

same: bloating, discomfort and decreased nutrient absorption.

It’s hard to determine if one of these milder-gluten allergies exists.

One way to check is to remove all carbs from the diet for a week or

more—such as during the preparation phase—then eat something

like pasta, whole grain breads or even a bagel. If bloating occurs

almost immediately, appetite wanes or disappears, and pressure from

an inflated gut is crippling, that’s a good indication of a gluten

allergy.

1 7 4

S e c t i o n V I I : D o s a n d D o n ’ t s

This is one reason people succeed with pastry products for carb

choices rather than bread or pasta. Not only do pastry-type products

absorb quickly, the wheat used in pastry flour is gluten depleted.

Like I said, I recommend junk for a reason.

C a r b B a c k - L o a d i n g

Chapter 49

Don’t Let Training

Derail You

Although this is a book about targeted performance

nutrition, the outlined plan relies heavily upon training for its

efficacy. I need, therefore, to discuss training and what qualifies as

acceptable. All training is not created equal when it comes to back-

loading.

People like to oversimplify—because they want an excuse to be lazy

and still eat everything they want— and start finding random

excuses to justify back loading.

Vacuumed the living room today? Well, that’s kind of like resistance

training, all of those reps, pushing and pulling the vacuum cleaner.

Obviously, this calls for a Back-Load. Walked up and down the

stairs in the house several times today? Back-load. Turned page-

after-page of this book or clicked mouse-button after mouse-button

to get through the electronic version? Back-load!

This may sound asinine, and I am going a bit far, but not far beyond

things I’ve heard in real life. I once had a stay-at-home mother tell

me that she loved back-loading, but she couldn’t figure out why she

was gaining weight. After a few questions, it became clear, she

never exercised, barely made it off the couch during the day, yet, at

dinner every night, began slamming cupcakes, brownies and ice

1 7 6

S e c t i o n V I I : D o s a n d D o n ’ t s

cream. Hmmm…I wonder what the problem could have been. But

she worked out—which, to her, meant putting groceries away,

doing chores and vacuuming every now and again, pushing the

stroller around in the store.

Hopefully I made it clear that this protocol is for people who train,

but as important as training is to the program, so is the type of

training. I talked throughout the book about resistance training. It

should, therefore, not surprise anyone that Carb Back-Loading is not

intended for endurance training individuals.

Endurance training includes, but is not limited to running, cycling,

rowing, cross-country skiing, aerobics classes and spin classes.

Endurance training a muscle decreases tGLUT concentration and

does not translocate tGLUT as does resistance training and may even

impair tGLUT function1, thereby forgoing skeletal muscle

preference to store glucose and giving fat cells an opportunity to

store it as fat. .

NOTE: Neither endurance type training—e.g.

marathon training, CrossFit—or purely eccentric

training—e.g.

Mike

Mentzer’s

Heavy

Duty—

translocate tGLUT; therefore, don’t use either

exclusively while Back-Loading.

Be aware that some types of endurance training use resistance-

assisted movements in attempt to increase endurance. Despite the

use of a few bumper-plates, this resistance-assisted endurance

training is biomechanically and molecularly identical to traditional

modes of endurance training.

C a r b B a c k - L o a d i n g

D o n ’ t L e t T r a i n i n g D e r a i l Y o u

Recent years have blessed us with several of these hybrid whole-

body training programs designed to devastate the energy systems of

the body without providing much benefit. Such programs include

P90X and its successor P90X2, Insanity Training and CrossFit. Carb

Back-Loading, as outlined in this book, is not suited to these training

modalities for the same reasons as endurance training. In an

upcoming book, I will address advanced nutrition for these types of

programs.

What’s left is traditional goal-oriented forms of resistance training,

like strength, power or hypertrophy regiments. Even here, when it

comes to back-loading, not all forms of legitimate resistance training

work.

Mike Mentzer’s Heavy Duty training or variant thereof like Dorian

Yate’s Blood-and-Guts style of training, Dog Crap or any eccentric-

based resistance program fails to translocate tGLUT. Muscular

contractions—concentric movement—causes tGLUT translocation2.

Heavy Duty training, therefore, can’t produce the critical effect

necessary to make Carb Back-Loading work as advertised3.

This is not to say that eccentric training can’t be used in a training

program while back-loading, as it has many benefits, but make it a

component of an integrated protocol like my upcoming Shockwave

Protocol and not an exclusive way to train.

Finally, don’t think a frou-frou workout on the selectorized speed

circuit at the big-box gym counts either. The non-insulin mediated

translocation of tGLUT depends on training intensity just as it does

type4. Heavy contractions cause the greatest response in tGLUT

1 7 8

S e c t i o n V I I : D o s a n d D o n ’ t s

movement and increase in concentration thereof within skeletal

muscle cells.

When done right, resistance training and the insulin surge created

by our post-training formula will work synergistically to redirect

glucose intake away from fat tissue and toward skeletal muscle5. So

remember the ageless idiom: go big or go home.

C a r b B a c k - L o a d i n g

Chapter 50

Cardio

For those familiar with my writing, it comes as no surprise

that I don’t recommend cardio, at least not long duration, steady-

state cardio. I don’t care about the goal: this type of cardio is

essentially useless, even for marathon training.

This is not, however, a place for a diatribe on cardio, nor is it the

place to elucidate the best training methodologies for endurance

events. It is the place to discuss what kind of cardio is best while

back loading: HIIT.

Unfamiliar with HIIT? Many people are, so don’t fret. HIIT stands

for High Intensity Interval Training and athletes have used it for a

long time, arguably as long as 1937 with the invention of Fartlek

training.

With HIIT, endurance training is broken down into sets of very

high intensity work, separated by a prescribed period of active rest.

Sounds a lot like resistance training and that’s a fair comparison in

many ways. HIIT comprises sets of anaerobic training interspersed

with rest.

HIIT is rather spectacular because c the time and literally T the

workload produces the same benefits as moderate intensity steady-

1 8 0

S e c t i o n V I I : D o s a n d D o n ’ t s

state endurance training1. Plus it causes an accelerated rate of fat

burning2.

What sounds preferable, running on the treadmill for 2 hours or

doing six sprints, each one 30 seconds long spaced by four minutes

of rest? Both produce identical benefits. That would be 27 minutes

out of the day compared to the 2 hours—and of those 27 minutes, 3

minutes require intense effort.

The prescription for HIIT cycles is written somewhat like odds on a

horse race. As an example, one prescription would be 4:1, where the

4 specifies the amount of active rest—say walking—and the 1

specifies the time of maximum exertion—like all-out sprinting.

Using the walking-sprinting examples with the 4:1 prescription

would give: walk slowly for 4 minutes, sprint for 1 minute followed

by another 4 minutes of walking, then another minute of sprinting

and so on until reaching the desired time or number of sets.

The rest period between sprints should not exceed four minutes and

shouldn’t go below two minutes. For the full-throttle portions, the

minimum and maximum, respectively, are 30 seconds and 4

minutes.

Vary the amount of rest—a little longer between some sprints and

shorter between others—and adjust the duration of the sprint

portion. This makes HIIT more akin to the Fartlek training

mentioned above in which there is no defined rest period or full-

throttle period: go full-throttle as soon as breathing is back under

control, and sprint until loss of breath control or 30 seconds,

whichever comes first.

C a r b B a c k - L o a d i n g

C a r d i o

No matter the split—1:2, 2:4, 4:Z, 4:1, 3:1, etc. or Fartlek-style—I

suggest limiting the volume to 30 minutes total or 8 cycles,

whichever is shorter, per day.

High Intensity Interval Training (HIIT)

Prescriptions

Sprint

Rest

Cycles

Suggested For

Duration

Period

у

Strength Accumulation/

2min

4 min

5

Fat Loss

Density Bulking/

30 sec

2 to 4 min

6

General

1 8 2

S e c t i o n V I I : D o s a n d D o n ’ t s

C a r b B a c k - L o a d i n g

Chapter 51

Gender Differences

I wrote this book with men as my target audience, both in

the program and style of writing because—and this is unfortunate in

my opinion—not many women resistance train with the intensity

necessary to benefit from back loading.

Maybe it’s a fear of looking like a female bodybuilder from the late

nineties, or maybe they don’t want to lift heavy because they’re too

kind, trying to spare the typical big-box-gym male clientele the

embarrassment of being out-lifted by a woman. I don’t know for

sure (although my hunch is the latter). But I do know it’s a travesty.

This doesn’t mean, however, that women can’t back load

successfully. Many have, getting exceptional results with a

minimum of effort (e.g. read about Julia Ladewski’s experience on

page 209). The biggest trouble I’ve witnessed is training intensity

coupled with a proclivity to over-consume carbs.

Meeting the carb needs of a 130 lb female athlete takes far smaller

volumes than that of a 240 lb bodybuilding male. The amount of

carbs anyone can eat while Back-Loading depends on their quantity

of muscle mass. The average female athlete doesn’t have the muscle

mass necessary to get away with eating an entire box of chocolates

every night.

1 8 4

S e c t i o n V I I : D o s a n d D o n ’ t s

To be successful with Carb Back-Loading as a woman, do three

things:

Suggestions for Females

1. Lift heavy in the gym.

Wondering about your intensity and if it qualifies as intense

enough is a good sign that it’s not. Kicking ass in the gym is

unmistakable.

2. Eat one carb meal post-training and don’t binge.

A couple pieces of pizza or a sushi roll or two is more than

plenty. Even consider skipping the carbs in the post-training

shake and saving them for a single meal (which may include

dessert).

3. Include 2 to 3 HIIT sessions per week of the 2:4 type.

This helps to keep glycogen levels from getting or staying

full. Be sure to ditch all steady state cardio.

I also suggest—and this is not as important as the above list—to go

through the preparatory phase of the Implementation Section.

You’ll gain enough information to fine tune the total amount of

carbs needed for back-loaded meals by using Appendix C.

C a r b B a c k - L o a d i n g

Section VII

Essential Points

Don’t be a fat kid: follow Back-Loading

principles, not fat-guy-at-the-gym advice.

Limit gluten intake: there’s a 50% chance

that you have some type of allergy, and even a

minor one can derail back-loading.

Endurance and eccentric training do not work

with Carb Back-Loading.

If you do cardio, do HIIT, p182.

Women do not, in general, have the muscle

mass necessary to gorge like men.

1 8 6

S e c t i o n V I I : D o s a n d D o n ’ t s

C a r b B a c k - L o a d i n g

Section VIII

EXPERIENCES

S e c t i o n V I I I : E x p e r i e n c e s

C a r b B a c k - L o a d i n g

Chapter 52

Case Study:

Jay DeMayo

No other subject seems to bring harsh critics from the

woodwork faster than alternative dieting strategies and when the

author claims performance enhancing, it generates more heat than

any other. Strength coaches, I’ve found, get fired up and defensive

worst of all.

They’ve got one diet they use with their clients and they refuse to

deviate. I don’t blame them: why change something if it works. So

when I got text message from Jason DeMayo, CSCS and head

strength coach for the University of Richmond, Virginia, asking

about a Carb Back-Loading program, he surprised me. But when he

told me it was for him, I felt the sweat form on my brow.

I’ve been tailoring diets for a few years for everyone from

bodybuilders, powerlifters, CrossFitters and cyclists, at all levels,

from amateurs to world-record holders, but I knew from our

conversation that DeMayo needed results and wanted them fast.

He needed to lean out, he wanted to get stronger, wanted to build

muscle and he needed it to be stupid-simple because his schedule is

insanely complex. After his list of requirements, I relaxed: this was

going to be easy.

1 9 0

S e c t i o n V I I I : E x p e r i e n c e s

I agreed to work with Jay if he would agree to record his stats

through the dieting process. He agreed and I put together a very

simple diet for him as follow:

Simple Carb Back-Loading Diet

(Training @ 9am)

Approx Mealtime

Meal

Coffee, 1-2 tbsp heavy

Upon Waking (6am)

whipping cream

Late Breakfast (noon)

6 eggs, Z lb bacon

1 hamburger patty, mustard,

Late Lunch (3pm)

slice of cheese

3 Spicy Chicken Filets,

Late Dinner (7-8pm)

Frosty and a large fry from

Wendy’s or a pizza

Simple Carb Back-Loading Diet

(Off-Day)

Approx Mealtime

Meal

Coffee, 1-2 tbsp heavy

Upon Waking (6am)

whipping cream

6 eggs, Z lb bacon

Late Breakfast (noon)

(optional)

1 hamburger patty, mustard,

Late Lunch (3pm)

slice of cheese

(optional)

2 chicken breasts and a

Late Dinner (8pm)

salad

C a r b B a c k - L o a d i n g

C a s e S t u d y : J a y D e M a y o

Looking at the tables, you can see that Jay couldn’t train at the ideal

time of day, but I still had to make the diet as simple and easy as

possible. Notice that on off-days, I marked two meals as optional.

Depending on how Jay felt—tired, hungry or energetic, sated—he

would skip one meal or the other. He never skipped both.

Of course, on training days he included only the Hypertrophic

Potentiator Formula (p139) minus the carbs. Again, depending on

how he felt, he might include a ripe banana or two after his

morning training session. Also note that Jay trained completely

fasted except for a small amount of heavy whipping cream, which

was probably just getting into his system at training time—normal

fats, as discussed earlier, take a few hours before the body can access

them for energy.

Jay went for 8 weeks on the program and recorded his weight and

skin fold measurements.

Jay DeMayo’s

Skin Fold Measurements

Mid

Sub

Date

Tricep

Pec

Ab

Supra

Quad

Ax

Scap

2011/06/01

15

22

14

23

35

18

21

2011/06/29

16

19

14

17

23

15

21

2011/07/27

9

15

11

15

20

15

20

From the skin fold data it’s clear that Jay lost a lot of abdominal fat

fast (see circled column above) and tightened up substantially at all

points except the quadriceps where he started lean. The following

1 9 2

S e c t i o n V I I I : E x p e r i e n c e s

table translates these numbers into body-fat percentages (%BF) and

lean-body weight (LBW).

Jay DeMayo’s

Body Fat and Lean Mass Measurements

Date

Weight

% BF

% LBW

LBW

2011/06/01

214.5

21.2

78.8

168.9

2011/06/29

209.5

18.3

81.7

171.1

2011/07/27

203.5

15.6

84.4

171.7

Jay lost about 6% body fat while simultaneously gaining 4 lbs of

muscle in just 8 weeks. Someone on a forum once commented that

gaining muscle mass while losing body fat is alchemy—i.e.

impossible. Well, Carb Back-Loading must be the Philosopher’s

Stone (I’d prefer a Physicist’s Stone, but, technically, every rock

would qualify as such).

What about Jay’s strength? Something had to give; there’s no way to

gain muscle and lose fat at the same time without sacrificing

something, like strength. Jay also recorded his numbers on four lifts;

the movements and his best lift in each before and after back

loading tell the story.

Jay DeMayo’s PRs, Pre and Post

Squat

Bench

Deadlift

Overhead

Week Before

385×6

260×6

425×8

175×6

Week After

400×10

270×8

440×10

190×8

C a r b B a c k - L o a d i n g

C a s e S t u d y : J a y D e M a y o

Keep in mind that Jay achieved these results without training at the

ideal time for Carb Back-Loading. Scheduling forced him to train in

the morning and only gave him enough time for one meal later in

the day. Essentially, life forced him into a non-ideal Strength

Accumulation phase. The results…impressive.

There’s really not much else to say. Carb Back-Loading works. End

of story. DeMayo seemed a bit skeptical and had it not been for the

prodding of friends who’d tried it with great success—success he

witnessed—he never would have contacted me in the first place.

Now that he finished his personal trial with Back-Loading, he’s

discussed creating a version that complies with NCAA standards

that he can use with his athletes. So his opinion now…well, his

most recent message after I thanked him for his stats: No, thank you.

This is awesome!

To learn more about Jay DeMayo, his training and experience, go to:

http://www.cvasps.com/jay-demayo/

1 9 4

S e c t i o n V I I I : E x p e r i e n c e s

C a r b B a c k - L o a d i n g

Chapter 53

Professionals

People at the top of their game, the elite, strive to find the

best supplements, best training protocols and the best nutrition

possible. They do whatever it takes to get to the next level, trading

convenience and free time for a chance at glory.

In the last couple of years, things changed. Carb Back-Loading

snuck onto the performance nutrition scene, a blip on the radar, a

it’s-too-good-to-be-true rumor. But as athletes across various

disciplines tried Back-Loading, they found they could devote more

energy to training and recovery and worry less about diet. Because

Carb Back-Loading is stupid-simple.

It wasn’t long before they hit new personal records (PRs), required

less time to prepare for contests and started breaking world records.

This garnered a lot of attention from fitness industry professionals at

magazines like Muscle&Fitness and Men’s Fitness. The editors were,

of course, skeptical and refused to publish such wild dietary advice.

Then the staff started trying it. Then more staff. Then, the editors.

Soon after, Carb Back-Loading made it into print.

Here are their experiences.

1 9 6

S e c t i o n V I I I : E x p e r i e n c e s

Brian Carroll, 30

From: Jacksonville, FL

Profession: LMT and Strength and Conditioning Coach

Website: http://briangcarroll.com/

Accomplishments: EliteFTS sponsored athlete, Ranked top 10

in 3 weight classes, #2 in the world in the SPF powerlifting

organization with a total (squat, bench, deadlift) of 2730 lbs and a

world record 1185 lb squat, both in the 275 lb weight class.

In the past, I didn’t care about diet much and it didn’t seem to

matter. I trained and lifted and my lifts went up. Within a few years

of competing, I was a top lifter. When I knew I was close to world

records, I decided to take everything seriously, even my eating.

I had a chance to talk with the creator of Carb Back-Loading before

he called it Carb Back-Loading and before I even knew who the hell

he really was. It sounded like something I work with and make fit

with work and training.

Since I first started using back-loading, I’ve hit new PRs and a world

record squat. I also have abs. For a 275 lb powerlifter, it’s kind of

unheard of. The first time I ever used it, I cut my body fat % down

an average of 1% a week for 7 weeks. Not bad for nothing but

changing when I ate carbs!

C a r b B a c k - L o a d i n g

P r o f e s s i o n a l s

Alex Navarro, 27

From: San Francisco, CA

Profession: Personal Trainer and Fitness Model

Website: http://www.alexnavarrofitness.com/

Accomplishments: Ms. Natural Fitness Olympia

As a bikini and fitness competitor it’s important to have an off-

season nutritional program that allows me to maintain the physique

that I worked so hard for and yet still be able to make aesthetic and

strength improvements where necessary. Carb Back-Loading has

made this possible.

In my past experiences off-season can be tricky. There are always

areas for improvement in my physique, yet at the same time I don’t

want to blow up like so many competitors do off-season. It’s been

one of the hardest parts about competing: watching all your hard

work get covered up by extra body fat and bloat. Yet, I’m happy to

say that this post-season has been the easiest to date because of Carb

Back-Loading. It has allowed me to build muscle while keeping my

body fat low and my body picture-ready.

I was pleasantly surprised at how easy it is to push back my carb

intake to the evenings, especially knowing that I’m able to then

consume foods that I previously thought would destroy all my hard

work in the gym. I never imagined being able to eat high glycemic

foods such as white bread or rice and even ice cream, especially in

the evening. Now they are helping me make the changes that I want

and I still look and feel great. In fact, I feel even better than on past

diets that were meant to help me build muscle. My energy has

improved, my cravings are minimal and my strength and recovery

are beyond what I thought they could be.

1 9 8

S e c t i o n V I I I : E x p e r i e n c e s

Scott Paltos, 34

From: East Hanover, NJ

Profession: Owner/Operator PUMP CrossFit & Performance

Website: http://www.pumpcrossfit.com/

Accomplishments: #7 in the Northeast Region for CrossFit

and #75 in the World Wide CrossFit Open

I have been an athlete all of my life, from a stint in the NFL, to

being a highly competitive strongman & powerlifter, to starting on a

25+ amateur national championship baseball team, and now being a

top competitor in CrossFit.

I have never had results from my nutrition like I have had this past

six months. Carb Back-Loading has played a major part in the

success I have had in my new adventures in CrossFit. For those who

follow Kiefer, you know that CrossFit is not his most adored form of

training methods…but being that I don’t fit the normal CrossFitter

mold (5’11” 235lbs) he took me on.

There is no doubt of what we have done through nutrition for my

work capacity, anaerobic threshold, aerobic endurance and

recovery, while still getting leaner and increasing my strength. It’s

been a huge positive. With my background and with Carb Back-

Loading I was able to finish #7 in the Northeast Region for CrossFit

and was ranked #75 in the World Wide CrossFit Open going into

the Regional Competition.

C a r b B a c k - L o a d i n g

P r o f e s s i o n a l s

Rob Fitzgerald Ihlenfeldt, 38

From: New York, NY

Profession: Group Features Editorial Director

Men's Fitness, Muscle & Fitness magazines

A number of world class powerlifters told me about Kiefer's Carb

Back-Loading ideas, but I was extremely skeptical at first because

none of it made any sense. We're always taught to eat several meals

throughout the day, and that eating carbs at night is an absolute

cardinal sin.

Two things about Kiefer stood out to me, however. First, he's a

brilliant guy, and it was obvious he'd dug deeper into the science of

nutrition than anyone else and done his research. Next, everyone

who tried Carb Back-Loading was getting very favorable results. I

had Kiefer give me a very simple plan, and I ended up eating way

MORE supposed 'junk' than ever before, but waking up the

following morning looking visibly leaner. Best of all, I've gained

muscle mass and I'm getting stronger at a phenomenal rate.

Carb Back-Loading is the absolute, no-bullshit truth. I've seen the

results with my own eyes on both myself and with athletes I

know—and it's one of maybe only two or three things in the fitness

industry I'd ever endorse.

2 0 0

S e c t i o n V I I I : E x p e r i e n c e s

Caroline Gick, 40

From: Concord, CA

Profession: Senior Branch Manager, Contra Costa Libraries

Website: http://carolinegick.com/

Accomplishments: National Fitness Competitor

I started Carb Back-loading as a way to avoid the trap I see so many

fellow figure competitors fall into—bulk up in the off-season to put

on muscle, invariably putting on just as much fat, and then starving

themselves down to prepare for the stage, getting rid of all the fat,

but also losing almost all the muscle they spent so long working for.

It seemed debilitating, not to mention pointless! By Back-loading,

I’ve been able to put on muscle, nearly 4 pounds of lean muscle mass

just in the last year, while staying tight, lean and close to show

weight. I really have no off-season/on-season, no bulk and cut.

Carb Back-loading keeps me looking AND feeling good year round,

which is important to me and getting ready for competition is

nowhere near the traumatic event I see so many competitors

endure.

C a r b B a c k - L o a d i n g

P r o f e s s i o n a l s

Vincent Dizenzo, 42

From: Stratford, CT

Profession: Special Education Teacher

Accomplishments: EliteFTS sponsored athlete, Raw bench

press of 600 lbs at a body weight of 305.

The last time I had my body fat tested was July 22, 2011. I weighed

288 lbs. and my body fat was 17.5%. Back on June 5, 2010 I was 267

lbs at 18%. So basically in just a little over a year I gained 21 lbs and

am .5% leaner. I'd also like to note that the same person tested me

using the same sites and calipers.

I can't remember when I started playing with Carb Back-Loading,

but it made sense to me and it seemed sustainable. I don't much care

what I eat during the day, I'm busy so I don't mind getting down

whatever I need to. Back-loading offers more flexibility in the

evening which is when I like to sit down and enjoy my food a bit

more. Plus, with training in the late afternoon, Kiefer's plan just

made more sense to me than traditional plans.

After working with Kiefer, a little correspondence and trial and

error we developed the plan I am on now. I am leaner than I have

been in around 20 years and am putting up PR's in the gym

regardless of bodyweight.

I am confident that Carb Back-Loading will help me maintain my

top level benching. I have already bested my equipped bench of 820

at 308 lbs. with 830 at 275. I also hit a raw bench of 600 at 305 lbs.

whereas the first time I hit a 600 in competition I had to push my

bodyweight up to 329.

2 0 2

S e c t i o n V I I I : E x p e r i e n c e s

Sean Hyson, 30

From: New York, NY

Profession: Fitness Editorial Director, Men's Fitness and Muscle

& Fitness magazines.

Website: http://www.seanhyson.com/

Accomplishments: Lost 35 lbs in 12 weeks while hitting a PR

of 405 lbs on the squat.

Carb Back-loading is easily my favorite nutrition strategy that I've

ever experimented with. Kiefer has made the dream a reality: eat

anything you want and lose fat while building muscle. I wouldn't

have believed it if I hadn't tried it myself.

There’s a reason we called it Nutrition’s Holy Grail when we wrote

about it at the magazine: It works as advertised!

C a r b B a c k - L o a d i n g

P r o f e s s i o n a l s

Rob Luyando, 41

From: Rock Falls, IL

Profession: Detective

Accomplishments: All-time Single Ply World record, 848 lbs,

and Multi Ply, 948 lbs, both at a body weight of 275 lbs.

When I first started Carb Back-Loading, I was a sloppy and strong

305 lb Power lifter. My goal was to get back down under 270 lbs and

maintain my strength levels. So I thought I may be up against the

wall trying to drop at least 35 lbs and not lose any strength. Kiefer

introduced his carb back loading plan to me and at first I thought

there is no way I’m going to be able to maintain strength with while

not consuming carbs throughout the day. I was wrong. My energy

levels and strength increased using the carb back loading plan that

Kiefer structured for me.

I went from 305 lbs to a solid 268. I also went on to set two new All-

time Single Ply World records in the bench press. Now that I have

reached my goals of getting under 270 lbs with Carb Back-Loading

and maintaining World-Record-breaking strength I decided my

next goal was to bench press over 1000 lbs. Kiefer again restructured

my plan and I have increased mass and strength while burning away

fat. Carb Back-Loading, together with Kiefer’s cardio plan allows me

to get the necessary foods to fuel my body and also help speed up

my body’s recovery so I can push it to the limit every day of the

week. I highly recommend Carb Back-Loading to anyone serious

about improving!

2 0 4

S e c t i o n V I I I : E x p e r i e n c e s

C a r b B a c k - L o a d i n g

Chapter 54

Everyday Success

Stories

Carb Back-Loading obviously works for those who

dedicate their lives to fitness and performance to achieve super-

human results, for professionals who sought my help directly. Sure

they got stupid-simple results. They had an unfair advantage—my

help.

But what about the people who train with the simple goal of getting

better every time they enter the gym who didn’t get my help, who

went it alone. Maybe there’re competitive athletes, maybe they only

care about seeing their abs or stripping fat from the thighs. What are

their results? Is Carb Back-Loading really that easy?

After reading through the countless testimonials I received, my

amazement at people’s results made me want to call this chapter

S.H.I.T. s (Super-Heroes In Training), but I’m not sure everyone

likes being called a S.H.I.T.™

What follows are the words of those who found out how stupid-

simple Carb Back-Loading is. They all share the same experience:

disbelief at how easily they achieved results they thought were

impossible (i.e. they’re S.H.I.T. s, like it or not).

2 0 6

S e c t i o n V I I I : E x p e r i e n c e s

Tanner Fox

From: North Dakota

In 12 weeks I successfully went from a body weight of 225lb to

240lb, took my squat from 400lb to 500lb, my deadlift from 500lb to

600lb, and not gained one ounce of body fat during the process. The

log book, measurements, and mirror don't lie and I thank Carb

Back-Loading for it.

My life is easier from not having to stare at the clock every 3 hours

to obsess about food. When the time comes to eat, I am MORE than

satisfied and never go to bed hungry. Convenience is just a side

effect of Carb Back-Loading. My mind is clear throughout the day

with a consistent energy, my workouts have never been more

intense, and I have never had this amount of convenience in my life

combined with using food to enhance my goals in the gym to a

degree I've never experienced. It really is a win-win.

Carb Back-Loading has essentially allowed me to hack my body to

find out its true potential and I will eat this way for the rest of my

life.

Gabe L

From: Indiana

I was interested in LeanGains, but don't like the idea of carb cycling.

I am more of a creature of habit. If I eat low carb one day, it’s easier

for me to eat low carb the next. If I eat carbs one day, it’s easier to

C a r b B a c k - L o a d i n g

E v e r y d a y S u c c e s s S t o r i e s

eat carbs the next. This is what led me to Carb Back-Loading. If I

don’t eat carbs all day, but have them peri-workout (or back

loaded), I can do that the next day.

My results: 188lbs at 18% body fat (calipers) down to 170lbs and

11% body fat (estimate)

Now, I'm a little small for my liking, but I intend on using the same

approach to try to gain, just with more calories. The idea of the low

carb intro would probably be beneficial, and anything else I could

get out of the upcoming book will definitely help.

Danny K

From: DH Forums (http://dangerouslyhardcore.com/forum/)

I am a 38 year old power lifter who trains 3 days a week and does

martial arts 2 days a week. I have been back loading for about 6

months and I love it. It is the easiest way to eat and see results. In

the past I walked around between 215 and 220. When I started

back loading I lost 10lbs fast. It must have been mostly fat because

the only difference in my clothing is I now need a belt. My

powerlifting gear still fits and all my clothes and suits still fit fine

except in the waist. I am still hitting PRs in the gym and have

plenty of energy for my grueling training. I don't like to eat

breakfast so CBL fits my life style perfect. CBL allows me to still sit

down with my family and enjoy good ole fashion American home

cooked meals. As a bonus, when I walk around with my shirt of my

wife takes notice (in a good way). In the past she hated when I

dropped weight, calling me twerpy. But, when the weight you drop

2 0 8

S e c t i o n V I I I : E x p e r i e n c e s

is fat and you hold on to and even add muscle you actually look

bigger at a lower body weight.

Julia Ladewski

From: Midwest (http://www.julialadewski.com/)

I thought my husband was crazy when he mentioned the thought of

carb back-loading. He claimed that many strength athletes were

getting pretty good results with losing body fat and maintaining (or

building) strength. Pfft. I thought this was another "low-carb"

plan... which I've tried before and wasn't too fond of. And I was not

about to partake in anything of the sort again.

My husband had been back-loading for about a week. I took the

time to read up on it and learn a little more. Then, I finally gave in

and said, "Fine... I'll give it a shot."

Three weeks had passed and I never looked back. And below are

my findings.

1. I love back-loading way more than any other nutritional protocol

I've tried in the past. I don't feel as restricted and can still have some

of the things I enjoy. At the same time, I feel that I'm making better

choices, even during my back-loading time frame when I could

technically eat what I want.

2. I don't let eating this way control my life. It guides me in the

direction I want to go by eating the foods I should be eating and

love. When I have a family function to go to, I adjust accordingly.

C a r b B a c k - L o a d i n g

E v e r y d a y S u c c e s s S t o r i e s

Also, 99% of the functions I attend are in the afternoon or evening

anyway.

3. I train in the morning and it still works for me. I've just started

experimenting with adding in a banana to my post-workout shake

and while I haven't noticed any differences either way, I do like the

idea of getting in some carbs post training.

4. Learning how my body responds to carbohydrates has been a real

eye-opener. I never associated the afternoon fatigue, hunger and

bloat to the carbs I was eating in the morning. Also learning how to

time my carbohydrates has played a huge role in keeping my

strength and energy levels up for the intense training sessions.

5. Here's the big one... a REALLY BIG TAKE AWAY... I. Feel.

Better. I feel better about the choices I make. I feel better about the

foods I'm eating (no more processed junk). I feel better energy-

wise. I'm not hungry. I don't crash at 2:00 in the afternoon because

I've carbed up all morning. I'm strong(er) and my training rocks. I

feel better about the foods I'm feeding my kids.

After eating this way for nearly 9 months, I can honestly say that I

can eat this way continually. It's not a "diet" to follow; therefore,

it's not a "diet" to sabotage either. After doing it for a month, my

body felt so much better. I was comfortable and happy with the way

I was eating.

And after all, when mom is happy, everyone is happy.

2 1 0

S e c t i o n V I I I : E x p e r i e n c e s

Tony F

From: Melbourne, Victoria, Australia

I first came across Carb Back-Loading while I was dieting for my 1st

bodybuilding comp...and I was dying to use it but of course I had to

wait...

After a week off from training after my comps I started carb back-

loading as I was purely after some mass gains and I must say I’m

very impressed with my results!

I know what some people are thinking "that’s just post-comp

rebound"...which yes does help but I have plenty of natural

bodybuilder mates who just put a lot of weight on after a comp and

mostly all fat and hardly any gains at all if any...whereas I’m gaining

every week and getting stronger...

Thanks Kiefer for giving another weapon for us natural guys to keep

packing some muscle on!

Casey D

From: Maine

I'm beyond impressed at this point. When I was eating for size prior

to back-loading, I was trying my best to keep it extremely clean and

I was very regimented, much to the dismay of my wife. She loves

me being on this new diet, mostly because I can "eat like a normal

person again". I feel like a kid again when I get to eat my favorite

C a r b B a c k - L o a d i n g

E v e r y d a y S u c c e s s S t o r i e s

cereals like Lucky Charms and Fruity Pebbles. To sum up, best diet

ever.

Mark G

From: DH Forums (http://dangerouslyhardcore.com/forum/)

I first heard of Kiefer and Carb Back-Loading from the EliteFTS

article. I read his articles and thought that he was saying not much

more than John Berardi at Precision Nutrition has espoused for

years. I have seen so many people repackage his ideas that I initially

wrote Kiefer off.

What eventually drew me to Carb-Back Loading was the amount of

research he had done (which, as a skeptic, I checked out). As a

physics teacher and Engineering major in college, I appreciate the

work and proof that he provides for his program.

I decided to read and listen to everything he has written/spoken

about on the internet (and the article in Men's Fitness) and have

been giving it a try. I have been one of those carb-phobic

individuals, so it has been a difficult adjustment, but I'm slowly

getting the hang of it.

I still have trouble judging my daily/weekly progress and am unsure

if I am doing it correctly, which is why I am so looking forward to

the book.

2 1 2

S e c t i o n V I I I : E x p e r i e n c e s

Matt Tuthill (@MCTuthill)

From: Muscle&Fitness and Men’s Fitness Magazine (associate editor)

I read about Carb Back Loading in Muscle&Fitness and immediately

dismissed it as something that could only work for those gifted

people who never seem to gain an ounce despite eating junk food

their whole lives. A diet in which eating muffins and ice cream at

night is not only allowed, but actually encouraged on tough training

days could never work for me. A friend of mine was hooked on the

idea, though, and gave it a try. In no time, he was raving about his

results, and insisted I try it. What finally pushed me over the edge

was that Kiefer's story sounded a lot like mine; he created this diet

after years of eating clean, training hard, and still being frustrated

by his physique. I plunged in head-first.

Flash forward 12 weeks into the diet: I gained 12 pounds total—a

steady pace of one pound a week—and my waistline not only didn't

expand, but my pants actually fit better. The 12 pounds all went

straight to my legs, chest, back, shoulders, and arms.

The diet has spread like wildfire around my office, and everyone's

extremely happy with their results. If you follow the instructions, IT

WORKS. Don't waste your time looking for something better. I've

tried a lot of different diets, and nothing works as well as this.

Gaining muscle and losing fat are no longer mutually exclusive

pursuits, something I absolutely never thought possible. Thank you,

Kiefer!

C a r b B a c k - L o a d i n g

Section IX

APPENDIX

S e c t i o n I X : A p p e n d i x

C a r b B a c k - L o a d i n g

Appendix A

FAQs

Q: How does clean food fit into Carb Back-Loading?

A: Clean food fits pretty easily into Carb Back-

Loading. The first half of the day, the ultra-low carb portion, is

the perfect time to slam some vegetables. Asparagus, broccoli,

lettuce, zucchini and an assortment of other vegetables work

perfectly and should be included. It’s not carbs total, it’s usable

carbs that matter. Other than tuberous vegetables and winter

squashes—pumpkin, butternut squash, potatoes, carrots—you

can eat most vegetables in mass quantity.

At night, however, we should avoid these healthy carbs, as they

sabotage the whole reason back-loading works in the first place.

That doesn’t mean, however, that you have to eat trash. You need

to trigger a strong insulin response. Use white rice, sweet

potatoes, the winter squashes, ripe bananas and grapes, all of

which produce strong insulin reactions.

Carb Back-Loading does not depend on junk; it’s just that it

allows you to eat it without consequence.

2 1 6

S e c t i o n I X : A p p e n d i x

Q: Do I have to drink coffee?

A: You don’t have to do anything. I do, however,

recommend coffee, but it’s not necessary if you train in the

evening. Most people use coffee to control their appetite, not to

enhance the back-load. For hunger control, there is no simple

alternative to coffee (regular or decaf) other than brushing your

teeth when you become ravenous in lieu of eating.

If you train earlier in the day, say first thing in the morning, then

I highly recommend some type of caffeine—something. To shift

the temporary insulin insensitivity to around training time (i.e.

A.M. training), then your best option actually isn’t coffee but a

caffeine supplement, either a powder or an over-the-counter

wakefulness aid that’s packed with caffeine, like Vivarin®.

Q: Is whipping cream an absolute must if I do drink

coffee in the morning?

A: What, you don’t like heavy whipping cream in

your coffee? Anyway, it is by no means necessary and neither is

coconut milk or oil.

C a r b B a c k - L o a d i n g

F A Q s

Q: How do I back-load on off-days?

A: This is actually a complex question. See Chapter 40,

p145.

Q: How would one tailor a Carb Back-Loading plan to

focus more on weight loss instead of weight maintenance?

A: What you’re looking for, rather than the Density

Bulking that strength and physique athletes desire, is the

Strength Accumulation tailoring, which you can find in Section

V. A brief description is in Chapter 30, p114.

Q: Is there an ideal macro nutrient breakdown?

A: There is, for both portions of the day, but it matters

most during the night. There are charts in Appendix C and D that

help you determine the baseline macro nutrients levels you

should get while back-loading. Eat at, above or below this level

to maintain, grow or lean-down, respectively.

2 1 8

S e c t i o n I X : A p p e n d i x

Q: Since I can eat up to 30g of carbs in the first half of

the day, can I eat all of those at breakfast?

A: Yes, if you want to destroy the hormonal processes

that make back-loading work thereby getting fat instead of

shredded.

If that is not your goal, then no, you can’t. No more important

time of day exists for controlling metabolism than when you first

wake. What you eat, or don’t eat, literally determines if you burn

primarily fat for the rest of the day or not. By eating all of your

carbs at once, you actually force the body to stop burning fat,

causing it to flounder during periods of heightened energy

utilization, like during training.

Of course, there is an exception: early A.M. fasted training. In

that case, yes, you can but only immediately after the training

session. See Chapter 43, p158 for more detail.

Q: Can this protocol be coupled with Intermittent

Fasting?

A: In truth, intermittent fasting (IF) is a subset of Carb

Back-Loading. Without a good understanding of how metabolism

works under multiple scenarios—like high-protein, high-fat,

high-carb, mixed-ratios and fasting—I can see how one might

C a r b B a c k - L o a d i n g

F A Q s

stumble upon IF, tweak it here and there and get excellent

results. The problem, however, is that fasting intermittently

makes it easy to lose fat, but difficult to grow new muscle or

maintain a heavily muscled frame.

This is a complex subject and is beyond the scope of this book,

but metabolically there is no difference between eating ultra-low

carb (high fat) and fasting. The body acts identically. Even levels

of metabolic hormones drop equally, slowing metabolism if the

body goes too long without carbs almost as if fasting (hence the

reliance of my first diet, The Carb Nite Solution®, on weekly

carb feedings). Therefore, Carb Back-Loading is IF, evolved.

Q: Your first diet book, The Carb Nite Solution,

describes bulk carbohydrate sweeteners like fructose as bad; does

the same hold true for back-loading? And what about fruit?

A: Yes and no. Ideally, you don’t want to use Coca-

Cola® and Twinkies for you back-loading meals because they

have high amounts of fructose (either bound as sucrose or in

high-fructose corn syrup). When the body is in an energy

surplus, fructose can bypass the rate-limiting steps that prevent

glucose from creating infinite levels of fat.

That means fructose can create unlimited amounts of fat.

2 2 0

S e c t i o n I X : A p p e n d i x

Therefore fruit juice, agave nectar and similar natural alternatives

with higher percentages of fructose are even more heinous and

should be avoided with diligence.

Intact fruit, on the other hand, is restricted because it just doesn’t

produce the insulin spikes we’re looking for, in general but can

be filling, thus preventing us from getting in enough

insulinotropic carbs.

Some fruits, under some conditions, though, are perfect. Like

brown-spotted bananas which can trigger significant insulin

release.

Q: So I fell off the wagon and ate carbs all day for a

week or so. Should I do the preparation phase again before

starting back?

A: Maybe not. It depends on your goal. For the best

results and the best bio-feedback (reactions from your body from

food) I suggest doing the prep phase again.

C a r b B a c k - L o a d i n g

Appendix B

Ultra-Low Carb

Vegetables

Serving Usable

Vegetable

Fiber Fat Prot

Size

Carbs

Alfalfa

1 cup

0

1

0

1

Sprouts

Arugula,

1/2 cup

0

1

0

0

fresh

Asparagus,

4 spears

0

1

0

2

raw

Baby

3 cups

0

2

0

2

Spinach

Celery

2 stalks

0

2

0

1

Green

1 oz

0

1

4

0

Olives

Kimchee

1/2 cup

0

4

0

2

Pimientos

1 tsp

0

0

0

0

Romaine

Lettuce,

1 cup

0

1

0

0

shredded

Watercress,

1 cup

0

0

0

1

raw

Boston

1 cup

1

1

0

1

Lettuce

Cauliflower,

1/2 cup

1

2

0

1

Cooked

2 2 2

S e c t i o n I X : A p p e n d i x

Serving Usable

Vegetable

Fiber Fat Prot

Size

Carbs

Chinese

1 cup

1

2

1

1

Broccoli

Garlic

1 clove

1

0

0

0

Green Onion

3 stalks

1

1

0

0

Jalapeno

1/2 cup

1

1

0

0

Pickle, Dill

1 spear

1

0

0

0

Radicchio,

1 cup

1

0

0

0

raw

Rhubarb,

1 stalk

1

1

0

0

raw

Sauerkraut

1/2 up

1

2

0

0

Bamboo

Shoots,

1 cup

2

2

0

2

canned

Cabbage

1 cup

2

2

0

0

Zucchini

1/2 cup

2

1

0

0

Bell Pepper,

1

3

2

0

0

Green

medium

Turnips,

1/2 cup

3

2

0

0

cooked

Yellow

1/2 cup

3

2

0

2

C a r b B a c k - L o a d i n g

Beans

Appendix C

Carb Needs

Calculators

One of the trickiest parts of Carb Back-Loading is

determining the level of carbs to start eating for a baseline—to

maintain, neither gaining nor losing. Once you determine this

amount, it’s easy to modify carb levels for Density Bulking or

Strength Accumulation. There are two ways to determine baseline

carb needs.

Determine Baseline Carbs

1. Perform the Preparation Phase and note weight loss.

Once you know the amount of weight lost from the

Preparation Phase, you can use the Weight-Delta chart that

follows.

2. Record your body weight before back-loading.

You can use this value to look up your carb needs in the BW

to Carbs calculator that follows. This method is not nearly as

reliable as the first method.

2 2 4

S e c t i o n I X : A p p e n d i x

Delta-Weight Chart

Weight

Baseline

Weight Lost

Baseline

Lost (lbs)

Carbs (g)

(lbs)

Carbs (g)

0.25

23

5.25

477

0.5

45

5.5

500

0.75

68

5.75

523

1

91

6

545

1.25

114

6.25

568

1.5

136

6.5

591

1.75

159

6.75

614

2

182

7

636

2.25

205

7.25

659

2.5

227

7.5

682

2.75

250

7.75

705

3

273

8

727

3.25

295

8.25

750

3.5

318

8.5

773

3.75

341

8.75

795

4

364

9

818

4.25

386

9.25

841

4.5

409

9.5

864

4.75

432

9.75

886

5

455

10

909

C a r b B a c k - L o a d i n g

C a r b N e e d s C a l c u l a t o r s

Delta-Weight Chart (con’t)

Weight

Baseline

Weight Lost

Baseline

Lost (lbs)

Carbs (g)

(lbs)

Carbs (g)

10.25

932

15.25

1386

10.5

955

15.5

1409

10.75

977

15.75

1432

11

1000

16

1455

11.25

1023

16.25

1477

11.5

1045

16.5

1500

11.75

1068

16.75

1523

12

1091

17

1545

12.25

1114

17.25

1568

12.5

1136

17.5

1591

12.75

1159

17.75

1614

13

1182

18

1636

13.25

1205

18.25

1659

13.5

1227

18.5

1682

13.75

1250

18.75

1705

14

1273

19

1727

14.25

1295

19.25

1750

14.5

1318

19.5

1773

14.75

1341

19.75

1795

15

1364

20

1818

2 2 6

S e c t i o n I X : A p p e n d i x

Delta-Weight Chart (con’t)

Weight

Baseline

Weight Lost

Baseline

Lost (lbs)

Carbs (g)

(lbs)

Carbs (g)

20.25

1841

25.25

2295

20.5

1864

25.5

2318

20.75

1886

25.75

2341

21

1909

26

2364

21.25

1932

26.25

2386

21.5

1955

26.5

2409

21.75

1977

26.75

2432

22

2000

27

2455

22.25

2023

27.25

2477

22.5

2045

27.5

2500

22.75

2068

27.75

2523

23

2091

28

2545

23.25

2114

28.25

2568

23.5

2136

28.5

2591

23.75

2159

28.75

2614

24

2182

29

2636

24.25

2205

29.25

2659

24.5

2227

29.5

2682

24.75

2250

29.75

2705

25

2273

30

2727

C a r b B a c k - L o a d i n g

C a r b N e e d s C a l c u l a t o r s

BW To Carbs Calculator

Carbs

Carbs

Carbs

Carbs

BW

BW

BW

BW

(g)

(g)

(g)

(g)

90 315

144

504

198

693

252

882

92 322

146

511

200

700

254

889

94 329

148

518

202

707

256

896

96 336

150

525

204

714

258

903

98 343

152

532

206

721

260

910

100 350

154

539

208

728

262

917

102 357

156

546

210

735

264

924

104 364

158

553

212

742

266

931

106 371

160

560

214

749

268

938

108 378

162

567

216

756

270

945

110 385

164

574

218

763

272

952

112 392

166

581

220

770

274

959

114 399

168

588

222

777

276

966

116 406

170

595

224

784

278

973

118 413

172

602

226

791

280

980

120 420

174

609

228

798

282

987

122 427

176

616

230

805

284

994

124 434

178

623

232

812

286

1001

126 441

180

630

234

819

288

1008

128 448

182

637

236

826

290

1015

130 455

184

644

238

833

292

1022

132 462

186

651

240

840

294

1029

134 469

188

658

242

847

296

1036

136 476

190

665

244

854

298

1043

138 483

192

672

246

861

300

1050

140 490

194

679

248

868

142 497

196

686

250

875

2 2 8

S e c t i o n I X : A p p e n d i x

C a r b B a c k - L o a d i n g

Appendix D

Pre Carb-Mealtimes

Macro Calculator

The following tables will help you assess baseline fat and

protein needs for the low-carb portion of the day when Carb Back-

Loading. The tables contain estimates based on averaged scientific

data—i.e. this is a rough guide. You will need to experiment.

How to Use

1. Find your desired weight in the chart.

This is the weight you want to be. The column gives low and

high protein estimates needed for that level, along with fat

needs and estimated pre-carb meal calories.

2. Start experimenting.

The numbers given are starting points. Calorie estimates in

the table run low. To gain mass or lean down, use the high

end of the protein scale. To maintain or change the

composition of your body, use middle protein values. To lean

down, use the fat levels in the table. To grow, increase fat

content.

3. Note the protein deficits.

This is how much protein you should consume with your

carbs in the evening including post-training shake.

2 3 0

S e c t i o n I X : A p p e n d i x

Low-

Prot

Prot

Target

Prot Lo

Prot Hi

Fat

Carb

Deficit

Deficit

BW

Calories

Lo

Hi

101

43.1

77.0

18.7

410

27.6

49.2

102

43.6

77.8

18.9

410

27.8

49.7

103

44.0

78.5

19.1

420

28.1

50.2

104

44.4

79.3

19.2

420

28.4

50.7

105

44.8

80.1

19.4

420

28.7

51.2

106

45.3

80.8

19.6

430

28.9

51.7

107

45.7

81.6

19.8

430

29.2

52.2

108

46.1

82.4

20.0

440

29.5

52.7

109

46.5

83.1

20.2

440

29.8

53.1

110

47.0

83.9

20.4

440

30.0

53.6

111

47.4

84.6

20.5

450

30.3

54.1

112

47.8

85.4

20.7

450

30.6

54.6

113

48.3

86.2

20.9

460

30.8

55.1

114

48.7

86.9

21.1

460

31.1

55.6

115

49.1

87.7

21.3

470

31.4

56.1

116

49.5

88.5

21.5

470

31.7

56.6

117

50.0

89.2

21.6

470

31.9

57.0

118

50.4

90.0

21.8

480

32.2

57.5

119

50.8

90.7

22.0

480

32.5

58.0

120

51.2

91.5

22.2

490

32.8

58.5

121

51.7

92.3

22.4

490

33.0

59.0

122

52.1

93.0

22.6

490

33.3

59.5

123

52.5

93.8

22.8

500

33.6

60.0

124

52.9

94.6

22.9

500

33.9

60.5

125

53.4

95.3

23.1

510

34.1

60.9

126

53.8

96.1

23.3

510

34.4

61.4

127

54.2

96.8

23.5

510

34.7

61.9

128

54.7

97.6

23.7

520

34.9

62.4

129

55.1

98.4

23.9

520

35.2

62.9

130

55.5

99.1

24.1

530

35.5

63.4

C a r b B a c k - L o a d i n g

P r e C a r b - M e a l t i m e s M a c r o C a l c u l a t o r

Low-

Prot

Prot

Target

Prot Lo

Prot Hi

Fat

Carb

Deficit

Deficit

BW

Calories

Lo

Hi

131

55.9

99.9

24.2

530

35.8

63.9

132

56.4

100.7

24.4

530

36.0

64.4

133

56.8

101.4

24.6

540

36.3

64.8

134

57.2

102.2

24.8

540

36.6

65.3

135

57.6

102.9

25.0

550

36.9

65.8

136

58.1

103.7

25.2

550

37.1

66.3

137

58.5

104.5

25.3

550

37.4

66.8

138

58.9

105.2

25.5

560

37.7

67.3

139

59.4

106.0

25.7

560

37.9

67.8

140

59.8

106.8

25.9

570

38.2

68.3

141

60.2

107.5

26.1

570

38.5

68.7

142

60.6

108.3

26.3

570

38.8

69.2

143

61.1

109.0

26.5

580

39.0

69.7

144

61.5

109.8

26.6

580

39.3

70.2

145

61.9

110.6

26.8

590

39.6

70.7

146

62.3

111.3

27.0

590

39.9

71.2

147

62.8

112.1

27.2

590

40.1

71.7

148

63.2

112.9

27.4

600

40.4

72.2

149

63.6

113.6

27.6

600

40.7

72.6

150

64.1

114.4

27.8

610

41.0

73.1

151

64.5

115.1

27.9

610

41.2

73.6

152

64.9

115.9

28.1

610

41.5

74.1

153

65.3

116.7

28.3

620

41.8

74.6

154

65.8

117.4

28.5

620

42.0

75.1

155

66.2

118.2

28.7

630

42.3

75.6

156

66.6

119.0

28.9

630

42.6

76.1

157

67.0

119.7

29.1

630

42.9

76.5

158

67.5

120.5

29.2

640

43.1

77.0

159

67.9

121.2

29.4

640

43.4

77.5

160

68.3

122.0

29.6

650

43.7

78.0

2 3 2

S e c t i o n I X : A p p e n d i x

Low-

Prot

Prot

Target

Prot Lo

Prot Hi

Fat

Carb

Deficit

Deficit

BW

Calories

Lo

Hi

161

68.7

122.8

29.8

650

44.0

78.5

162

69.2

123.5

30.0

660

44.2

79.0

163

69.6

124.3

30.2

660

44.5

79.5

164

70.0

125.1

30.3

660

44.8

80.0

165

70.5

125.8

30.5

670

45.0

80.4

166

70.9

126.6

30.7

670

45.3

80.9

167

71.3

127.3

30.9

680

45.6

81.4

168

71.7

128.1

31.1

680

45.9

81.9

169

72.2

128.9

31.3

680

46.1

82.4

170

72.6

129.6

31.5

690

46.4

82.9

171

73.0

130.4

31.6

690

46.7

83.4

172

73.4

131.2

31.8

700

47.0

83.9

173

73.9

131.9

32.0

700

47.2

84.3

174

74.3

132.7

32.2

700

47.5

84.8

175

74.7

133.4

32.4

710

47.8

85.3

176

75.2

134.2

32.6

710

48.0

85.8

177

75.6

135.0

32.8

720

48.3

86.3

178

76.0

135.7

32.9

720

48.6

86.8

179

76.4

136.5

33.1

720

48.9

87.3

180

76.9

137.3

33.3

730

49.1

87.8

181

77.3

138.0

33.5

730

49.4

88.2

182

77.7

138.8

33.7

740

49.7

88.7

183

78.1

139.5

33.9

740

50.0

89.2

184

78.6

140.3

34.0

740

50.2

89.7

185

79.0

141.1

34.2

750

50.5

90.2

186

79.4

141.8

34.4

750

50.8

90.7

187

79.8

142.6

34.6

760

51.1

91.2

188

80.3

143.4

34.8

760

51.3

91.7

189

80.7

144.1

35.0

760

51.6

92.1

190

81.1

144.9

35.2

770

51.9

92.6

C a r b B a c k - L o a d i n g

P r e C a r b - M e a l t i m e s M a c r o C a l c u l a t o r

Low-

Prot

Prot

Target

Prot Lo

Prot Hi

Fat

Carb

Deficit

Deficit

BW

Calories

Lo

Hi

191

81.6

145.6

35.3

770

52.1

93.1

192

82.0

146.4

35.5

780

52.4

93.6

193

82.4

147.2

35.7

780

52.7

94.1

194

82.8

147.9

35.9

780

53.0

94.6

195

83.3

148.7

36.1

790

53.2

95.1

196

83.7

149.5

36.3

790

53.5

95.6

197

84.1

150.2

36.5

800

53.8

96.0

198

84.5

151.0

36.6

800

54.1

96.5

199

85.0

151.7

36.8

800

54.3

97.0

200

85.4

152.5

37.0

810

54.6

97.5

201

85.8

153.3

37.2

810

54.9

98.0

202

86.3

154.0

37.4

820

55.1

98.5

203

86.7

154.8

37.6

820

55.4

99.0

204

87.1

155.6

37.7

830

55.7

99.5

205

87.5

156.3

37.9

830

56.0

99.9

206

88.0

157.1

38.1

830

56.2

100.4

207

88.4

157.8

38.3

840

56.5

100.9

208

88.8

158.6

38.5

840

56.8

101.4

209

89.2

159.4

38.7

850

57.1

101.9

210

89.7

160.1

38.9

850

57.3

102.4

211

90.1

160.9

39.0

850

57.6

102.9

212

90.5

161.7

39.2

860

57.9

103.4

213

91.0

162.4

39.4

860

58.1

103.8

214

91.4

163.2

39.6

870

58.4

104.3

215

91.8

163.9

39.8

870

58.7

104.8

216

92.2

164.7

40.0

870

59.0

105.3

217

92.7

165.5

40.2

880

59.2

105.8

218

93.1

166.2

40.3

880

59.5

106.3

219

93.5

167.0

40.5

890

59.8

106.8

220

93.9

167.8

40.7

890

60.1

107.3

2 3 4

S e c t i o n I X : A p p e n d i x

Low-

Prot

Prot

Target

Prot Lo

Prot Hi

Fat

Carb

Deficit

Deficit

BW

Calories

Lo

Hi

221

94.4

168.5

40.9

890

60.3

107.7

222

94.8

169.3

41.1

900

60.6

108.2

223

95.2

170.0

41.3

900

60.9

108.7

224

95.6

170.8

41.4

910

61.2

109.2

225

96.1

171.6

41.6

910

61.4

109.7

226

96.5

172.3

41.8

910

61.7

110.2

227

96.9

173.1

42.0

920

62.0

110.7

228

97.4

173.9

42.2

920

62.2

111.2

229

97.8

174.6

42.4

930

62.5

111.6

230

98.2

175.4

42.6

930

62.8

112.1

231

98.6

176.1

42.7

930

63.1

112.6

232

99.1

176.9

42.9

940

63.3

113.1

233

99.5

177.7

43.1

940

63.6

113.6

234

99.9

178.4

43.3

950

63.9

114.1

235

100.3

179.2

43.5

950

64.2

114.6

236

100.8

180.0

43.7

950

64.4

115.1

237

101.2

180.7

43.9

960

64.7

115.5

238

101.6

181.5

44.0

960

65.0

116.0

239

102.1

182.2

44.2

970

65.2

116.5

240

102.5

183.0

44.4

970

65.5

117.0

241

102.9

183.8

44.6

970

65.8

117.5

242

103.3

184.5

44.8

980

66.1

118.0

243

103.8

185.3

45.0

980

66.3

118.5

244

104.2

186.1

45.1

990

66.6

119.0

245

104.6

186.8

45.3

990

66.9

119.4

246

105.0

187.6

45.5

990

67.2

119.9

247

105.5

188.3

45.7

1,000

67.4

120.4

248

105.9

189.1

45.9

1,000

67.7

120.9

249

106.3

189.9

46.1

1,010

68.0

121.4

250

106.8

190.6

46.3

1,010

68.3

121.9

C a r b B a c k - L o a d i n g

P r e C a r b - M e a l t i m e s M a c r o C a l c u l a t o r

Low-

Prot

Prot

Target

Prot Lo

Prot Hi

Fat

Carb

Deficit

Deficit

BW

Calories

Lo

Hi

251

107.2

191.4

46.4

1,020

68.5

122.4

252

107.6

192.2

46.6

1,020

68.8

122.9

253

108.0

192.9

46.8

1,020

69.1

123.3

254

108.5

193.7

47.0

1,030

69.3

123.8

255

108.9

194.4

47.2

1,030

69.6

124.3

256

109.3

195.2

47.4

1,040

69.9

124.8

257

109.7

196.0

47.6

1,040

70.2

125.3

258

110.2

196.7

47.7

1,040

70.4

125.8

259

110.6

197.5

47.9

1,050

70.7

126.3

260

111.0

198.3

48.1

1,050

71.0

126.8

261

111.4

199.0

48.3

1,060

71.3

127.2

262

111.9

199.8

48.5

1,060

71.5

127.7

263

112.3

200.5

48.7

1,060

71.8

128.2

264

112.7

201.3

48.8

1,070

72.1

128.7

265

113.2

202.1

49.0

1,070

72.3

129.2

266

113.6

202.8

49.2

1,080

72.6

129.7

267

114.0

203.6

49.4

1,080

72.9

130.2

268

114.4

204.4

49.6

1,080

73.2

130.7

269

114.9

205.1

49.8

1,090

73.4

131.1

270

115.3

205.9

50.0

1,090

73.7

131.6

271

115.7

206.6

50.1

1,100

74.0

132.1

272

116.1

207.4

50.3

1,100

74.3

132.6

273

116.6

208.2

50.5

1,100

74.5

133.1

274

117.0

208.9

50.7

1,110

74.8

133.6

275

117.4

209.7

50.9

1,110

75.1

134.1

276

117.9

210.5

51.1

1,120

75.3

134.6

277

118.3

211.2

51.3

1,120

75.6

135.0

278

118.7

212.0

51.4

1,120

75.9

135.5

279

119.1

212.7

51.6

1,130

76.2

136.0

280

119.6

213.5

51.8

1,130

76.4

136.5

2 3 6

S e c t i o n I X : A p p e n d i x

Low-

Prot

Prot

Target

Prot Lo

Prot Hi

Fat

Carb

Deficit

Deficit

BW

Calories

Lo

Hi

281

120.0

214.3

52.0

1,140

76.7

137.0

282

120.4

215.0

52.2

1,140

77.0

137.5

283

120.8

215.8

52.4

1,140

77.3

138.0

284

121.3

216.6

52.5

1,150

77.5

138.5

285

121.7

217.3

52.7

1,150

77.8

138.9

286

122.1

218.1

52.9

1,160

78.1

139.4

287

122.5

218.8

53.1

1,160

78.4

139.9

288

123.0

219.6

53.3

1,160

78.6

140.4

289

123.4

220.4

53.5

1,170

78.9

140.9

290

123.8

221.1

53.7

1,170

79.2

141.4

291

124.3

221.9

53.8

1,180

79.4

141.9

292

124.7

222.7

54.0

1,180

79.7

142.4

293

125.1

223.4

54.2

1,180

80.0

142.8

294

125.5

224.2

54.4

1,190

80.3

143.3

295

126.0

224.9

54.6

1,190

80.5

143.8

296

126.4

225.7

54.8

1,200

80.8

144.3

297

126.8

226.5

55.0

1,200

81.1

144.8

298

127.2

227.2

55.1

1,210

81.4

145.3

299

127.7

228.0

55.3

1,210

81.6

145.8

300

128.1

228.8

55.5

1,210

81.9

146.3

301

128.5

229.5

55.7

1,220

82.2

146.7

302

129.0

230.3

55.9

1,220

82.4

147.2

303

129.4

231.0

56.1

1,230

82.7

147.7

304

129.8

231.8

56.3

1,230

83.0

148.2

305

130.2

232.6

56.4

1,230

83.3

148.7

306

130.7

233.3

56.6

1,240

83.5

149.2

307

131.1

234.1

56.8

1,240

83.8

149.7

308

131.5

234.9

57.0

1,250

84.1

150.2

309

131.9

235.6

57.2

1,250

84.4

150.6

310

132.4

236.4

57.4

1,250

84.6

151.1

C a r b B a c k - L o a d i n g

Appendix E

Sample Meal Plans

Sample meal plans are attached at the end of the

document and are formatted for printing on standard, letter-sized

(8.5”×11”) paper.

What are presented are examples for various training times. Use

Sections III and IV of the book to determine food quantities better

than the guides suggest, which are for a 160-175 lb individual doing

Density Bulking or 200 lb person doing Strength Accumulation.

For females, throw out all snacks, and as the book details, use

discretion for the night meals. Consult the Carb Needs Calculators

in Appendix C for starting levels.

Keep in mind, these are samples to show various ways of choosing

meals and timing nutrients based on training schedule.

2 3 8

S e c t i o n I X : A p p e n d i x

C a r b B a c k - L o a d i n g

Section X

REFERENCES

2 4 0

S e c t i o n X : R e f e r e n c e s

C a r b B a c k - L o a d i n g

C h a p t e r 7

Chapter 7

Reference 1

ɽ Newsholme EA, Dimitriadis G. Integration of biochemical and physiologic effects of

insulin on glucose metabolism. Exp Clin Endocrinol Diabetes. 2001;109 Suppl 2:S122-

34. Review.

ɽ Rivellese AA, De Natale C, Di Marino L, Patti L, Iovine C, Coppola S, Del Prato S, Riccardi

G, Annuzzi G. Exogenous and endogenous postprandial lipid abnormalities in type 2

diabetic patients with optimal blood glucose control and optimal fasting triglyceride

levels. J Clin Endocrinol Metab. 2004 May;89(5):2153-9.

ɽ Chen YD, Swami S, Skowronski R, Coulston A, Reaven GM. Differences in postprandial

lipemia between patients with normal glucose tolerance and noninsulin-dependent

diabetes mellitus. J Clin Endocrinol Metab. 1993 Jan;76(1):172-7.

ɽ Stinson JC, Owens D, McBrinn S, Collins P, Johnson A, Tomkin GH. The regulation of

post-prandial cellular cholesterol metabolism in type 2 diabetic and non-diabetic

subjects. Diabet Med. 1993 Jun;10(5):420-6.

ɽ Strandberg TE, Tilvis RS, Lindberg O, Valvanne J, Sairanen S, Ehnholm C, Tuomilehto J.

High plasma insulin is associated with lower LDL cholesterol in elderly individuals.

Atherosclerosis. 1996 Apr 5;121(2):267-73.

Reference 2

ɽ Brandi LS, Santoro D, Natali A, Altomonte F, Baldi S, Frascerra S, Ferrannini E. Insulin

resistance of stress: sites and mechanisms. Clin Sci (Lond). 1993 Nov;85(5):525-35.

ɽ Petrides AS, Luzi L, DeFronzo RA. Time-dependent regulation by insulin of leucine

metabolism in young healthy adults. Am J Physiol. 1994 Sep;267(3 Pt 1):E361-8.

ɽ Jensen MD, Miles JM, Gerich JE, Cryer PE, Haymond MW. Preservation of insulin effects

on glucose production and proteolysis during fasting. Am J Physiol. 1988 Jun;254(6 Pt

1):E700-7.

ɽ Fryburg DA, Barrett EJ, Louard RJ, Gelfand RA. Effect of starvation on human muscle

protein metabolism and its response to insulin. Am J Physiol. 1990 Oct;259(4 Pt 1):E477-

82. -1-199-

ɽ Gelfand RA, Barrett EJ. Effect of physiologic hyperinsulinemia on skeletal muscle protein

synthesis and breakdown in man. J Clin Invest. 1987 Jul;80(1):1-6.

ɽ Bonadonna RC, Saccomani MP, Seely L, Zych KS, Ferrannini E, Cobelli C, DeFronzo RA.

Glucose transport in human skeletal muscle. The in vivo response to insulin. Diabetes.

1993 Jan;42(1):191-8.

ɽ Tessari P, Inchiostro S, Biolo G, Vincenti E, Sabadin L. Effects of acute systemic

hyperinsulinemia on forearm muscle proteolysis in healthy man. J Clin Invest. 1991

Jul;88(1):27-33.

ɽ Brooks DC, Bessey PQ, Black PR, Aoki TT, Wilmore DW. Insulin stimulates branched

chain amino acid uptake and diminishes nitrogen flux from skeletal muscle of injured

patients. J Surg Res. 1986 Apr;40(4):395-405.

ɽ Fryburg DA, Jahn LA, Hill SA, Oliveras DM, Barrett EJ. Insulin and insulin-like growth

factor-I enhance human skeletal muscle protein anabolism during hyperaminoacidemia

by different mechanisms. J Clin Invest. 1995 Oct;96(4):1722-9.

ɽ Denne SC, Liechty EA, Liu YM, Brechtel G, Baron AD. Proteolysis in skeletal muscle and

whole body in response to euglycemic hyperinsulinemia in normal adults. Am J Physiol.

1991 Dec;261(6 Pt 1):E809-14.

ɽ Inculet RI, Finley RJ, Duff JH, Pace R, Rose C, Groves AC, Woolf LI. Insulin decreases

muscle protein loss after operative trauma in man. Surgery. 1986 Jun;99(6):752-8.

2 4 2

S e c t i o n X : R e f e r e n c e s

ɽ Luzi L, Giordano M, Caloni, Castellino P. Effects of insulin and amino acids on leucine

metabolism in young and middle-aged humans. Eur J Nutr. 2001 Jun;40(3):106-12.

ɽ Biolo G, Wolfe RR. Insulin action on protein metabolism. Baillieres Clin Endocrinol

Metab. 1993 Oct;7(4):989-1005. Review.

ɽ Pozefsky T, Felig P, Tobin JD, Soeldner JS, Cahill GF Jr. Amino acid balance across

tissues of the forearm in postabsorptive man. Effects of insulin at two dose levels. J Clin

Invest. 1969 Dec;48(12):2273-82.

Reference 3:

ɽ Boden G, Chen X, Desantis RA, Kendrick Z. Effects of insulin on fatty acid

reesterification in healthy subjects. Diabetes. 1993 Nov;42(11):1588-93.

ɽ Campbell PJ, Carlson MG, Hill JO, Nurjhan N. Regulation of free fatty acid metabolism

by insulin in humans: role of lipolysis and reesterification. Am J Physiol. 1992 Dec;263(6

Pt 1):E1063-9.

ɽ Groop LC, Bonadonna RC, Simonson DC, Petrides AS, Shank M, DeFronzo RA. Effect of

insulin on oxidative and nonoxidative pathways of free fatty acid metabolism in human

obesity. Am J Physiol. 1992 Jul;263(1 Pt 1):E79-84.

ɽ Sidossis LS, Wolfe RR. Glucose and insulin-induced inhibition of fatty acid oxidation: the

glucose-fatty acid cycle reversed. Am J Physiol. 1996 Apr;270(4 Pt 1):E733-8.

ɽ Meek SE, Nair KS, Jensen MD. Insulin regulation of regional free fatty acid metabolism.

Diabetes. 1999 Jan;48(1):10-4.

ɽ Jacob S, Hauer B, Becker R, Artzner S, Grauer P, Loblein K, Nielsen M, Renn W, Rett K,

Wahl HG, Stumvoll M, Haring HU. Lipolysis in skeletal muscle is rapidly regulated by low

physiological doses of insulin. Diabetologia. 1999 Oct;42(10):1171-4.

ɽ Stumvoll M, Jacob S, Wahl HG, Hauer B, Loblein K, Grauer P, Becker R, Nielsen M,

Renn W, Haring H. Suppression of systemic, intramuscular, and subcutaneous adipose

tissue lipolysis by insulin in humans. J Clin Endocrinol Metab. 2000 Oct;85(10):3740-5.

ɽ Dyck DJ, Steinberg G, Bonen A. Insulin increases FA uptake and esterification but

reduces lipid utilization in isolated contracting muscle. Am J Physiol Endocrinol Metab.

2001 Sep;281(3): E600-7.

ɽ Bonadonna RC, Groop LC, Zych K, Shank M, DeFronzo RA. Dose-dependent effect of

insulin on plasma free fatty acid turnover and oxidation in humans. Am J Physiol. 1990

Nov;259(5 Pt 1):E736-50.

ɽ characteristics for suppression of glycerol release and conversion to glucose in humans.

Diabetes. 1986 Dec;35(12):1326-31.

ɽ Coppack SW, Frayn KN, Humphreys SM, Dhar H, Hockaday TD. Effects of insulin on

human adipose tissue metabolism in vivo. Clin Sci (Lond). 1989 Dec;77(6):663-70.

ɽ Arner P, Bolinder J, Ostman J. Glucose stimulation of the antilipolytic effect of insulin in

humans. Science. 1983 Jun 3;220(4601):1057-9.

ɽ Capaldo B, Napoli R, Di Marino L, Guida R, Pardo F, Sacca L. Role of insulin and free

fatty acid (FFA) availability on regional FFA kinetics in the human forearm. J Clin

Endocrinol Metab. 1994 Sep;79(3):879-82.

ɽ Pimenta WP, Saad MJ, Paccola GM, Piccinato CE, Foss MC. Effect of oral glucose on

peripheral muscle fuel metabolism in fasted men. Braz J Med Biol Res. 1989;22(4):465-

76.

Reference 4:

ɽ Borer KT. Hormonal regulation of fuel use in exercise. In: Exercise endocrinology.

Champaign, IL: Human Kinetics, 2003:97–120.

ɽ Volek JS, Sharman MJ, Love DM, Avery NG, Gómez AL, Scheett TP, Kraemer WJ. Body

composition and hormonal responses to a carbohydrate-restricted diet. Metabolism

2002;51: 864–70.

C a r b B a c k - L o a d i n g

C h a p t e r 8

ɽ Jensen MD, Haymond MW, Gerich JE, Cryer PE, Miles JM. Lipolysis during fasting.

Decreased suppression by insulin and increased stimulation by epinephrine. J Clin

Invest. 1987 Jan;79(1): 207-13.

Reference 5:

ɽ Feinman RD, Fine EJ. Nonequilibrium thermodynamics and energy efficiency in weight

loss diets. Theor Biol Med Model. 2007 Jul 30;4:27. Review.

ɽ Asmar M, Simonsen L, Madsbad S, Stallknecht B, Holst JJ, Bülow J. Glucose-dependent

insulinotropic polypeptide may enhance fatty acid re-esterification in subcutaneous

abdominal adipose tissue in lean humans. Diabetes. 2010 Sep;59(9):2160-3.

Chapter 8

Reference 1:

ɽ Macfarlane GT, Gibson GR, Cummings JH. Comparison of fermentation reactions in

different regions of the human colon. J Appl Bacteriol. 1992 Jan;72(1):57-64.

ɽ Sunvold GD, Hussein HS, Fahey GC Jr, Merchen NR, Reinhart GA. In vitro fermentation

of cellulose, beet pulp, citrus pulp, and citrus pectin using fecal inoculum from cats,

dogs, horses, humans, and pigs and ruminal fluid from cattle. J Anim Sci. 1995

Dec;73(12):3639-48.

ɽ Titgemeyer EC, Bourquin LD, Fahey GC Jr, Garleb KA. Fermentability of various fiber

sources by human fecal bacteria in vitro. Am J Clin Nutr. 1991 Jun;53(6):1418-24.

ɽ Bourquin LD, Titgemeyer EC, Fahey GC Jr. Vegetable fiber fermentation by human fecal

bacteria: cell wall polysaccharide disappearance and short-chain fatty acid production

during in vitro fermentation and water-holding capacity of unfermented residues. J Nutr.

1993 May;123(5):860-9.

ɽ Bourquin LD, Titgemeyer EC, Fahey GC Jr, Garleb KA. Fermentation of dietary fibre by

human colonic bacteria: disappearance of, short-chain fatty acid production from, and

potential water-holding capacity of, various substrates. Scand J Gastroenterol. 1993

Mar;28(3):249-55.

ɽ Bourquin LD, Titgemeyer EC, Garleb KA, Fahey GC Jr. Short-chain fatty acid production

and fiber degradation by human colonic bacteria: effects of substrate and cell wall

fractionation procedures. J Nutr. 1992 Jul;122(7):1508-20.

ɽ Daniel M, Wisker E, Rave G, Feldheim W. Fermentation in human subjects of nonstarch

polysaccharides in mixed diets, but not in a barley fiber concentrate, could be predicted

by in vitro fermentation using human fecal inocula. J Nutr. 1997 Oct;127(10):1981-8.

ɽ Fernandes J, Rao AV, Wolever TM. Different substrates and methane producing status

affect short-chain fatty acid profiles produced by In vitro fermentation of human feces. J

Nutr. 2000 Aug;130(8):1932-6.

ɽ Dongowski G, Lorenz A, Anger H. Degradation of pectins with different degrees of

esterification by Bacteroides thetaiotaomicron isolated from human gut flora. Appl

Environ Microbiol. 2000 Apr;66(4):1321-7.

ɽ Topping DL, Clifton PM. Short-chain fatty acids and human colonic function: roles of

resistant starch and nonstarch polysaccharides. Physiol Rev. 2001 Jul;81(3):1031-64.

Review.

Reference 2:

ɽ Baer DJ, Rumpler WV, Miles CW, Fahey GC Jr. Dietary fiber decreases the metabolizable

energy content and nutrient digestibility of mixed diets fed to humans. J Nutr. 1997

Apr;127(4):579-86.

2 4 4

S e c t i o n X : R e f e r e n c e s

ɽ Miles CW. The metabolizable energy of diets differing in dietary fat and fiber measured in

humans. J Nutr. 1992 Feb;122(2):306-11.

ɽ Miles CW, Kelsay JL, Wong NP. Effect of dietary fiber on the metabolizable energy of

human diets. J Nutr. 1988 Sep;118(9):1075-81.

ɽ Wisker E, Feldheim W. Metabolizable energy of diets low or high in dietary fiber from

fruits and vegetables when consumed by humans. J Nutr. 1990 Nov;120(11):1331-7.

ɽ Wisker E, Maltz A, Feldheim W. Metabolizable energy of diets low or high in dietary fiber

from cereals when eaten by humans. J Nutr. 1988 Aug;118(8):945-52.

ɽ Slavin JL, Marlett JA. Effect of refined cellulose on apparent energy, fat and nitrogen

digestibilities. J Nutr. 1980 Oct;110(10):2020-6.

ɽ Miyoshi H, Okuda T, Oi Y, Koishi H. Effects of rice fiber on fecal weight, apparent

digestibility of energy, nitrogen and fat, and degradation of neutral detergent fiber in

young men. J Nutr Sci Vitaminol (Tokyo). 1986 Dec;32(6):581-9.

Reference 3:

ɽ Bortz WM, Paul P, Haff AC, Holmes WL. Glycerol Turnover and Oxidation in Man. J. Clin

Invst 1972;51: 1537-1546.

ɽ Chambers WH, Deuel HJ. The metabolism of glycerol in phlorizin diabetes. J Biol Chem

1925;65: 21.

ɽ Teng CT, Karnovsky ML, Landau BR, Hastings AB, Nesbett FB. 1953. Metabolism of

C[14]-labeled glycerol and pyruvate by liver in vitro. J Biol Chem, Jun 1953;202: 705-

716. –E5-

ɽ McCulloch AJ, Johnston DG, Baylis PH, Kendall-Taylor P, Clark F, Young ET, Alberti KG.

Evidence that thyroid hormones regulate gluconeogenesis from glycerol in man. Clin

Endocrinol (Oxf). 1983 Jul;19(1):67-76.

ɽ McCulloch AJ, Steele NR, Kendall-Taylor P, Baylis PH, Alberti KG. Enhanced

gluconeogenic capacity from glycerol in hyperthyroid man: evidence in favour of a beta-

adrenergic mechanism. Clin Endocrinol (Oxf). 1984 Oct;21(4):399-407.

ɽ Peroni O, Large V, Beylot M. Measuring gluconeogenesis with [2-13C]glycerol and mass

isotopomer distribution analysis of glucose. Am J Physiol. 1995 Sep;269(3 Pt 1):E516-23.

ɽ Baba H, Zhang XJ, Wolfe RR. Glycerol gluconeogenesis in fasting humans. Nutrition.

1995 Mar-Apr;11(2):149-53.

ɽ Tibbling G. Glycerol turnover in hyperthyroidism. Clin Chim Acta. 1969 Apr;24(1):121-30.

ɽ Ackermans MT, Pereira Arias AM, Bisschop PH, Endert E, Sauerwein HP, Romijn JA.

The quantification of gluconeogenesis in healthy men by (2)H2O and [2-(13)C]glycerol

yields different results: rates of gluconeogenesis in healthy men measured with (2)H2O

are higher than those measured with [2-(13)C]glycerol. J Clin Endocrinol Metab. 2001

May;86(5):2220-6.

ɽ Trimmer JK, Casazza GA, Horning MA, Brooks GA. Autoregulation of glucose production

in men with a glycerol load during rest and exercise. Am J Physiol Endocrinol Metab.

2001 Apr;280(4):E657-68.

ɽ Hetenyi G, Perez G, Vranic M. Turnover and Precursor-Product Relationships of Nonlipid

Metabolites. Physiol Revs, Apr 1983;63(2): 606-667.

Reference 4:

ɽ Salminen S, Salminen E, Marks V. The effects of xylitol on the secretion of insulin and

gastric inhibitory polypeptide in man and rats. Diabetologia. 1982 Jun;22(6):480-2.

ɽ Forster H, Boecker S, Zagel D. Comparison of side effects of infusion of glucose and

glucose substitutes at different doses. Z Ernahrungswiss. 1978 Dec;17(4):224-39.

ɽ Forster H. Fructose and sorbitol as energy-supplying substrates for parenteral nutrition.

Infusionsther Klin Ernahr. 1987 Jun;14(3):98-109.

C a r b B a c k - L o a d i n g

C h a p t e r 9

ɽ Pellaton M, Acheson K, Maeder E, Jequier E, Felber JP. The comparative oxidation of

glucose, fructose, sorbitol and xylitol in normal man. JPEN J Parenter Enteral Nutr. 1978

Nov;2(5):627-33.

ɽ Makinen KK. Effect of long-term, peroral administration of sugar alcohols on man. Swed

Dent J. 1984;8(3):113-24.

ɽ Wang YM, van Eys J. Nutritional significance of fructose and sugar alcohols. Annu Rev

Nutr. 1981;1:437-75. Review.

ɽ Nilsson U, Jagerstad M. Hydrolysis of lactitol, maltitol and Palatinit by human intestinal

biopsies. Br J Nutr. 1987 Sep;58(2):199-206.

ɽ de Kalbermatten N, Ravussin E, Maeder E, Geser C, Jequier E, Felber JP. Comparison of

glucose, fructose, sorbitol, and xylitol utilization in humans during insulin suppression.

Metabolism. 1980 Jan;29(1):62-7.

ɽ Mehnert H. Sugar substitutes in the diabetic diet. Int Z Vitam Ernahrungsforsch Beih.

1976;15:295-324. Review.

ɽ Forster H. The metabolism of monosaccharides and polyoles. Infusionsther Klin Ernahr.

1975 Jun;2(3):187-201.

ɽ Langkilde AM, Andersson H, Schweizer TF, Wursch P. Digestion and absorption of

sorbitol, maltitol and isomalt from the small bowel. A study in ileostomy subjects. Eur J

Clin Nutr. 1994 Nov;48(11):768-75.

ɽ Fritz M, Siebert G, Kasper H. Dose dependence of breath hydrogen and methane in

healthy volunteers after ingestion of a commercial disaccharide mixture, Palatinit. Br J

Nutr. 1985 Sep;54(2):389-400.

ɽ Zunft HJ, Schulze J, Gartner H, Grutte FK. Digestion of maltitol in man, rat, and rabbit.

Ann Nutr Metab. 1983;27(6):470-6. -8-17-

ɽ Siebert G, Grupp U. Metabolic behavior of disaccharide alcohols and related

substances. Dtsch Zahnarztl Z. 1977;32(5 Suppl 1):S36-42.

ɽ Hamberg O, Almdal TP. Effects of xylitol on urea synthesis in normal humans: relation to

glucagon. JPEN J Parenter Enteral Nutr. 1996 Mar-Apr;20(2):139-44.

Reference 5:

ɽ Billaux, MS, Flourie B, Jacquemin C, Messing B. 1991. Sugar alcohols, p. 72-103. In S.

Marie and J. R. Piggott (ed.), Handbook of sweeteners. Blackie and Son Ltd., New York,

N.Y.

Reference 6:

ɽ Kruger D, Grossklaus R, Herold M, Lorenz S, Klingebiel L. Gastrointestinal transit and

digestibility of maltitol, sucrose and sorbitol in rats: a multicompartmental model and

recovery study. Experientia. 1992 Aug 15;48(8):733-40.

ɽ D'Alessandro A, Seri S. Bowel function in runners after ingestion of sweeteners. Clin Ter.

1999 Jan-Feb;150(1):29-32.

ɽ Beaugerie L, Flourie B, Marteau P, Pellier P, Franchisseur C, Rambaud JC. Digestion and

absorption in the human intestine of three sugar alcohols. Gastroenterology. 1990

Sep;99(3):717-23.

Chapter 9

Reference 1:

ɽ Uldry M, Thorens B. The SLC2 family of facilitated hexose and polyol transporters.

Pflugers Arch. 2004 Feb;447(5):480-9. Review.

2 4 6

S e c t i o n X : R e f e r e n c e s

Reference 2:

ɽ Augustin R. The protein family of glucose transport facilitators: It's not only about glucose

after all. IUBMB Life. 2010 May;62(5):315-33. Review.

Reference 3:

ɽ Gumà A, Zierath JR, Wallberg-Henriksson H, Klip A. Insulin induces translocation of

GLUT-4 glucose transporters in human skeletal muscle. Am J Physiol. 1995 Apr;268(4 Pt

1):E613-22.

ɽ Khayat ZA, Patel N, Klip A. Exercise- and insulin-stimulated muscle glucose transport:

distinct mechanisms of regulation. Can J Appl Physiol. 2002 Apr;27(2):129-51. Review.

ɽ Ryder JW, Chibalin AV, Zierath JR. Intracellular mechanisms underlying increases in

glucose uptake in response to insulin or exercise in skeletal muscle. Acta Physiol Scand.

2001 Mar;171(3):249-57. Review.

ɽ Barnard RJ, Youngren JF. Regulation of glucose transport in skeletal muscle. FASEB J.

1992 Nov;6(14):3238-44. Review.

ɽ Thorens B, Mueckler M. Glucose transporters in the 21st Century. Am J Physiol

Endocrinol Metab. 2010 Feb;298(2):E141-5. Review.

ɽ Stuart CA, Howell ME, Zhang Y, Yin D. Insulin-stimulated translocation of glucose

transporter (GLUT) 12 parallels that of GLUT4 in normal muscle. J Clin Endocrinol Metab.

2009 Sep;94(9):3535-42.

ɽ Stuart CA, Yin D, Howell ME, Dykes RJ, Laffan JJ, Ferrando AA. Hexose transporter

mRNAs for GLUT4, GLUT5, and GLUT12 predominate in human muscle. Am J Physiol

Endocrinol Metab. 2006 Nov;291(5):E1067-73.

Chapter 11

Reference 1:

ɽ Gautier JF, Cathelineau G. Insulin sensitivity and hepatic glucose production:

nycthemeral variations. Diabetes Metab. 1997 Nov;23 Suppl 4:35-8.

ɽ Benedict C, Kern W, Schmid SM, Schultes B, Born J, Hallschmid M.

Psychoneuroendocrinology. Early morning rise in hypothalamic-pituitary-adrenal activity:

a role for maintaining the brain’s energy balance. 2009 Apr;34(3):455-62.

ɽ Waldhäusl W. Circadian rhythms of insulin needs and actions. Diabetes Res Clin Pract.

1989 May 15;6(4):S17-24.

ɽ Pardini L, Kaeffer B. Feeding and circadian clocks. Reprod Nutr Dev. 2006 Sep-

Oct;46(5):463-80.

Chapter 12

Reference 1:

ɽ Christ-Roberts CY, Pratipanawatr T, Pratipanawatr W, Berria R, Belfort R, Kashyap S,

Mandarino LJ. Exercise training increases glycogen synthase activity and GLUT4

expression but not insulin signaling in overweight nondiabetic and type 2 diabetic

subjects. Metabolism. 2004 Sep;53(9):1233-42.

Reference 2:

ɽ Ivy JL. Role of exercise training in the prevention and treatment of insulin resistance and

non-insulin-dependent diabetes mellitus. Sports Med. 1997 Nov;24(5):321-36. Review.

C a r b B a c k - L o a d i n g

C h a p t e r 1 4

Reference 3:

ɽ Hayashi T, Wojtaszewski JF, Goodyear LJ. Exercise regulation of glucose transport in

skeletal muscle. Am J Physiol. 1997 Dec;273(6 Pt 1):E1039-51. Review.

ɽ Barnard RJ, Youngren JF. Regulation of glucose transport in skeletal muscle. FASEB J.

1992 Nov;6(14):3238-44. Review.

ɽ Pereira LO, Lancha AH Jr. Effect of insulin and contraction up on glucose transport in

skeletal muscle. Prog Biophys Mol Biol. 2004 Jan;84(1):1-27. Review.

ɽ Khayat ZA, Patel N, Klip A. Exercise- and insulin-stimulated muscle glucose transport:

distinct mechanisms of regulation. Can J Appl Physiol. 2002 Apr;27(2):129-51. Review.

ɽ Ryder JW, Chibalin AV, Zierath JR. Intracellular mechanisms underlying increases in

glucose uptake in response to insulin or exercise in skeletal muscle. Acta Physiol Scand.

2001 Mar;171(3):249-57. Review.

ɽ Goodyear LJ, Kahn BB. Exercise, glucose transport, and insulin sensitivity. Annu Rev

Med. 1998;49:235-61. Review.

ɽ Jessen N, Goodyear LJ. Contraction signaling to glucose transport in skeletal muscle. J

Appl Physiol. 2005 Jul;99(1):330-7. Review.

ɽ Tremblay F, Dubois MJ, Marette A. Regulation of GLUT4 traffic and function by insulin

and contraction in skeletal muscle. Front Biosci. 2003 Sep 1;8:d1072-84. Review.

ɽ Ryder JW, Gilbert M, Zierath JR. Skeletal muscle and insulin sensitivity:

pathophysiological alterations. Front Biosci. 2001 Feb 1;6:D154-63. Review.

Reference 4:

ɽ Hawley JA, Lessard SJ. Exercise training-induced improvements in insulin action. Acta

Physiol (Oxf). 2008 Jan;192(1):127-35. Review.

Chapter 14

Reference 1:

ɽ Samra JS, Clark ML, Humphreys SM, Macdonald IA, Matthews DR, Frayn KN. Effects of

morning rise in cortisol concentration on regulation of lipolysis in subcutaneous adipose

tissue. Am J Physiol. 1996 Dec;271(6 Pt 1):E996-1002.

Reference 2:

ɽ Dinneen S, Alzaid A, Miles J, Rizza R. Effects of the normal nocturnal rise in cortisol on

carbohydrate and fat metabolism in IDDM. Am J Physiol. 1995 Apr;268(4 Pt 1):E595-603.

ɽ Papanicolaou DA, Mullen N, Kyrou I, Nieman LK. Nighttime salivary cortisol: a useful test

for the diagnosis of Cushing's syndrome. J Clin Endocrinol Metab. 2002

Oct;87(10):4515-21.

ɽ Anderson IM, Crook WS, Gartside SE, Fairburn CG, Cowen PJ. The effect of moderate

weight loss on overnight growth hormone and cortisol secretion in healthy female

volunteers. J Affect Disord. 1989 Mar-Jun;16(2-3):197-202.

ɽ Scott RS, Scandrett MS. Nocturnal cortisol release during hypoglycemia in diabetes.

Diabetes Care. 1981 Sep-Oct;4(5):514-8.

ɽ Doman J, Thompson S, Grochocinski V, Jarrett D, Kupfer DJ. A computer algorithm to

determine

the

nadir

and

rise

time

in

nocturnal

cortisol

secretion.

Psychoneuroendocrinology. 1986;11(3):359-66.

ɽ Born J, Kern W, Bieber K, Fehm-Wolfsdorf G, Schiebe M, Fehm HL. Night-time plasma

cortisol secretion is associated with specific sleep stages. Biol Psychiatry. 1986

Dec;21(14):1415-24.

2 4 8

S e c t i o n X : R e f e r e n c e s

ɽ Hindmarsh KW, Tan L, Sankaran K, Laxdal VA. Diurnal rhythms of cortisol, ACTH, and

beta-endorphin levels in neonates and adults. West J Med. 1989 Aug;151(2):153-6.

ɽ Edwards S, Evans P, Hucklebridge F, Clow A. Association between time of awakening

and diurnal cortisol secretory activity. Psychoneuroendocrinology. 2001 Aug;26(6):613-

22.

Reference 3:

ɽ Trumper BG, Reschke K, Molling J. Circadian variation of insulin requirement in insulin

dependent diabetes mellitus the relationship between circadian change in insulin demand

and diurnal patterns of growth hormone, cortisol and glucagon during euglycemia. Horm

Metab Res. 1995 Mar;27(3):141-7.

ɽ Fehm HL, Klein E, Holl R, Voigt KH. Evidence for extrapituitary mechanisms mediating

the morning peak of plasma cortisol in man. J Clin Endocrinol Metab. 1984

Mar;58(3):410-4.

ɽ Schmidt-Reinwald A, Pruessner JC, Hellhammer DH, Federenko I, Rohleder N,

Schurmeyer TH, Kirschbaum C. The cortisol response to awakening in relation to

different challenge tests and a 12-hour cortisol rhythm. Life Sci. 1999;64(18):1653-60.

ɽ Bornstein SR, Licinio J, Tauchnitz R, Engelmann L, Negrao AB, Gold P, Chrousos GP.

Plasma leptin levels are increased in survivors of acute sepsis: associated loss of diurnal

rhythm, in cortisol and leptin secretion. J Clin Endocrinol Metab. 1998 Jan;83(1):280-3.

ɽ Nishiyama M, Makino S, Suemaru S, Nanamiya W, Asaba K, Kaneda T, Mimoto T,

Nishioka T, Takao T, Hashimoto K. Glucocorticoid effects on the diurnal rhythm of

circulating leptin levels. Horm Res. 2000;54(2):69-73.

Reference 4:

ɽ Rebuffe-Scrive M, Lonnroth P, Andersson B, Smith U, Bjorntorp. Effects of short-term

administration on the metabolism of human subcutaneous adipose tissue. J Obes

Weight Regul. 1988;7:22-33.

ɽ Fain JN. Inhibition of glucose transport in fat cells and activation of lipolysis by

glucocorticoids. In: Baxter JD, Rousseau GG, eds. Glucocorticoid hormone action.

Berlin, Heidelberg, New York 1979:Springer-Verlag;547-560.

ɽ Felig P, Baxter JD, Frohman LA. Endocrinology and Metabolism. New York

1995:McGraw-Hill.

ɽ Dinneen S, Alzaid A, Miles J, Rizza R. Metabolic effects of the nocturnal rise in cortisol

on carbohydrate metabolism in normal humans. J Clin Invest. 1993 Nov;92(5):2283-90.

ɽ Gemmill ME, Eskay RL, Hall NL, Douglass LW, Castonguay TW. Leptin suppresses food

intake and body weight in corticosterone-replaced adrenalectomized rats. J Nutr. 2003

Feb;133(2):504-9.

ɽ Tan JT, Patel BK, Kaplan LM, Koenig JI, Hooi SC. Regulation of leptin expression and

secretion by corticosteroids and insulin. Implications for body weight. Endocrine. 1998

Feb;8(1):85-92.

ɽ Masuzaki H, Ogawa Y, Hosoda K, Miyawaki T, Hanaoka I, Hiraoka J, Yasuno A,

Nishimura H, Yoshimasa Y, Nishi S, Nakao K. Glucocorticoid regulation of leptin

synthesis and secretion in humans: elevated plasma leptin levels in Cushing's syndrome.

J Clin Endocrinol Metab. 1997 Aug;82(8):2542-7.

ɽ Newcomer JW, Selke G, Melson AK, Gross J, Vogler GP, Dagogo-Jack S. Dose-

dependent cortisol-induced increases in plasma leptin concentration in healthy humans.

Arch Gen Psychiatry. 1998 Nov;55(11):995-1000.

ɽ Divertie GD, Jensen MD, Miles JM. Stimulation of lipolysis in humans by physiological

hypercortisolemia. Diabetes. 1991 Oct;40(10):1228-32.

C a r b B a c k - L o a d i n g

C h a p t e r 1 4

ɽ Gravholt CH, Dall R, Christiansen JS, Moller N, Schmitz O. Preferential stimulation of

abdominal subcutaneous lipolysis after prednisolone exposure in humans. Obes Res.

2002 Aug;10(8):774-81.

ɽ Djurhuus CB, Gravholt CH, Nielsen S, Mengel A, Christiansen JS, Schmitz OE, Moller N.

Effects of cortisol on lipolysis and regional interstitial glycerol levels in humans. Am J

Physiol Endocrinol Metab. 2002 Jul;283(1):E172-7.

ɽ Djurhuus CB, Gravholt CH, Nielsen S, Pedersen SB, Moller N, Schmitz O. Additive

effects of cortisol and growth hormone on regional and systemic lipolysis in humans. Am

J Physiol Endocrinol Metab. 2004 Mar;286(3):E488-94.

ɽ Dagogo-Jack S, Umamaheswaran I, Askari H, Tykodi G. Leptin response to

glucocorticoid occurs at physiological doses and is abolished by fasting. Obes Res.

2003 Feb;11(2):232-7.

ɽ Askari H, Liu J, Dagogo-Jack S. Hormonal regulation of human leptin in vivo: effects of

hydrocortisone and insulin. Int J Obes Relat Metab Disord. 2000 Oct;24(10):1254-9.

Reference 5:

ɽ Wren AM, Seal LJ, Cohen MA, Brynes AE, Frost GS, Murphy KG, Dhillo WS, Ghatei MA,

Bloom SR. Ghrelin enhances appetite and increases food intake in humans. J Clin

Endocrinol Metab. 2001 Dec;86(12):5992.

Reference 6:

ɽ Natalucci G, Riedl S, Gleiss A, Zidek T, Frisch H. Spontaneous 24-h ghrelin secretion

pattern in fasting subjects: maintenance of a meal-related pattern. Eur J Endocrinol. 2005

Jun;152(6):845-50.

ɽ Koutkia P, Canavan B, Breu J, Johnson ML, Grinspoon SK. Nocturnal ghrelin pulsatility

and response to growth hormone secretagogues in healthy men. Am J Physiol Endocrinol

Metab. 2004 Sep;287(3):E506-12.

ɽ Shiiya T, Nakazato M, Mizuta M, Date Y, Mondal MS, Tanaka M, Nozoe S, Hosoda H,

Kangawa K, and Matsukura S. Plasma ghrelin levels in lean and obese humans and the

effect of glucose on ghrelin secretion. J Clin Endocrinol Metab 87: 240–244, 2002.

Reference 7:

ɽ Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-

hormone-releasing acylated peptide from stomach. Nature. 1999 Dec 9;402(6762):656-

60.

ɽ Takaya K, Ariyasu H, Kanamoto N, Iwakura H, Yoshimoto A, Harada M, Mori K, Komatsu

Y, Usui T, Shimatsu A, Ogawa Y, Hosoda K, Akamizu T, Kojima M, Kangawa K, Nakao K.

Ghrelin strongly stimulates growth hormone release in humans. J Clin Endocrinol Metab.

2000 Dec;85(12):4908-11.

ɽ Tassone F, Broglio F, Destefanis S, Rovere S, Benso A, Gottero C, Prodam F, Rossetto

R, Gauna C, van der Lely AJ, Ghigo E, Maccario M. Neuroendocrine and metabolic

effects of acute ghrelin administration in human obesity. J Clin Endocrinol Metab. 2003

Nov;88(11):5478-83.

ɽ Groschl M, Knerr I, Topf HG, Schmid P, Rascher W, Rauh M. Endocrine responses to the

oral ingestion of a physiological dose of essential amino acids in humans. J Endocrinol.

2003 Nov;179(2):237-44.

ɽ Enomoto M, Nagaya N, Uematsu M, Okumura H, Nakagawa E, Ono F, Hosoda H, Oya H,

Kojima M, Kanmatsuse K, Kangawa K. Cardiovascular and hormonal effects of

subcutaneous administration of ghrelin, a novel growth hormone-releasing peptide, in

healthy humans. Clin Sci (Lond). 2003 Oct;105(4):431-5.

2 5 0

S e c t i o n X : R e f e r e n c e s

ɽ Broglio F, Benso A, Gottero C, Prodam F, Grottoli S, Tassone F, Maccario M, Casanueva

FF, Dieguez C, Deghenghi R, Ghigo E, Arvat E. Effects of glucose, free fatty acids or

arginine load on the GH-releasing activity of ghrelin in humans. Clin Endocrinol (Oxf).

2002 Aug;57(2):265-71.

ɽ Muller AF, Lamberts SW, Janssen JA, Hofland LJ, Koetsveld PV, Bidlingmaier M,

Strasburger CJ, Ghigo E, Van der Lely AJ. Ghrelin drives GH secretion during fasting in

man. Eur J Endocrinol. 2002 Feb;146(2):203-7.

ɽ Nagaya N, Uematsu M, Kojima M, Date Y, Nakazato M, Okumura H, Hosoda H, Shimizu

W, Yamagishi M, Oya H, Koh H, Yutani C, Kangawa K. Elevated circulating level of

ghrelin in cachexia associated with chronic heart failure: relationships between ghrelin

and anabolic/catabolic factors. Circulation. 2001 Oct 23;104(17):2034-8.

ɽ Broglio F, Arvat E, Benso A, Gottero C, Muccioli G, Papotti M, van der Lely AJ,

Deghenghi R, Ghigo E. Ghrelin, a natural GH secretagogue produced by the stomach,

induces hyperglycemia and reduces insulin secretion in humans. J Clin Endocrinol

Metab. 2001 Oct;86(10):5083-6.

ɽ Hataya Y, Akamizu T, Takaya K, Kanamoto N, Ariyasu H, Saijo M, Moriyama K, Shimatsu

A, Kojima M, Kangawa K, Nakao K. A low dose of ghrelin stimulates growth hormone

(GH) release synergistically with GH-releasing hormone in humans. J Clin Endocrinol

Metab. 2001 Sep;86(9):4552.

ɽ Peino R, Baldelli R, Rodriguez-Garcia J, Rodriguez-Segade S, Kojima M, Kangawa K,

Arvat E, Ghigo E, Dieguez C, Casanueva FF. Ghrelin-induced growth hormone secretion

in humans. Eur J Endocrinol. 2000 Dec;143(6):R11-4.

ɽ Arvat E, Di Vito L, Broglio F, Papotti M, Muccioli G, Dieguez C, Casanueva FF, Deghenghi

R, Camanni F, Ghigo E. Preliminary evidence that Ghrelin, the natural GH secretagogue

(GHS)-receptor ligand, strongly stimulates GH secretion in humans. J Endocrinol Invest.

2000 Sep;23(8):493-5.

Reference 8:

ɽ Moller L, Norrelund H, Jessen N, Flyvbjerg A, Pedersen SB, Gaylinn BD, Liu J, Thorner

MO, Moller N, Lunde Jorgensen JO. Impact of growth hormone receptor blockade on

substrate metabolism during fasting in healthy subjects. J Clin Endocrinol Metab. 2009

Nov;94(11):4524-32.

ɽ Møller N, Møller J, Jørgensen JO, Ovesen P, Schmitz O, Alberti KG, Christiansen JS.

Impact of 2 weeks high dose growth hormone treatment on basal and insulin stimulated

substrate metabolism in humans. Clin Endocrinol (Oxf). 1993 Nov;39(5):577-81.

ɽ Bianda TL, Hussain MA, Keller A, Glatz Y, Schmitz O, Christiansen JS, Alberti KG,

Froesch ER. Insulin-like growth factor-I in man enhances lipid mobilization and oxidation

induced by a growth hormone pulse. Diabetologia. 1996 Aug;39(8):961-9.

ɽ Møller N, Schmitz O, Pørksen N, Møller J, Jørgensen JO. Dose-response studies on the

metabolic effects of a growth hormone pulse in humans. Metabolism. 1992

Feb;41(2):172-5.

ɽ Møller N, Jørgensen JO, Alberti KG, Flyvbjerg A, Schmitz O. Short-term effects of growth

hormone on fuel oxidation and regional substrate metabolism in normal man. J Clin

Endocrinol Metab. 1990 Apr;70(4):1179-86.

Reference 9:

ɽ Nørrelund H, Møller N, Nair KS, Christiansen JS, Jørgensen JO. Continuation of growth

hormone (GH) substitution during fasting in GH-deficient patients decreases urea

excretion and conserves protein synthesis. J Clin Endocrinol Metab. 2001

Jul;86(7):3120-9.

C a r b B a c k - L o a d i n g

C h a p t e r 1 4

Reference 10:

ɽ Salgin B, Marcovecchio ML, Humphreys SM, Hill N, Chassin LJ, Lunn DJ, Hovorka R,

Dunger DB. Effects of prolonged fasting and sustained lipolysis on insulin secretion and

insulin sensitivity in normal subjects. Am J Physiol Endocrinol Metab. 2009

Mar;296(3):E454-61.

Reference 11:

ɽ Van Proeyen K, Deldique L, Nielens H, Szlufcik K, Francaux M, Ramaekers M, Hespel P.

Effects Of Training In The Fasted State In Conjunction With Fat-rich diet On Muscle

Metabolism: 721: June 3 8:15 AM - 8:30 AM. Medicine & Science in Sports & Exercise.

42(5):42, May 2010.

ɽ van Loon LJ, Koopman R, Stegen JH, Wagenmakers AJ, Keizer HA, Saris WH.

Intramyocellular lipids form an important substrate source during moderate intensity

exercise in endurance-trained males in a fasted state. J Physiol. 2003 Dec 1;553(Pt

2):611-25.

Reference 12:

ɽ De Bock K, Richter EA, Russell AP, Eijnde BO, Derave W, Ramaekers M, Koninckx E,

Léger B, Verhaeghe J, Hespel P. Exercise in the fasted state facilitates fibre type-specific

intramyocellular lipid breakdown and stimulates glycogen resynthesis in humans. J

Physiol. 2005 Apr 15;564(Pt 2):649-60.

Reference 13:

ɽ Martin A, Normand S, Sothier M, Peyrat J, Louche-Pelissier C, Laville M. Is advice for

breakfast consumption justified? Results from a short-term dietary and metabolic

experiment in young healthy men. Br J Nutr. 2000 Sep;84(3):337-44.

Reference 14:

ɽ Gregoire F, Genart C, Hauser N, Remacle C. Glucocorticoids induce a drastic inhibition

of proliferation and stimulate differentiation of adult rat fat cell precursors. Exp Cell Res.

1991 Oct;196(2):270-8.

ɽ Xu XF, Bjorntorp P. Effects of dexamethasone on multiplication and differentiation of rat

adipose precursor cells. Exp Cell Res. 1990 Aug;189(2):247-52.

ɽ Hentges EJ, Hausman GJ. Primary cultures of stromal-vascular cells from pig adipose

tissue: the influence of glucocorticoids and insulin as inducers of adipocyte

differentiation. Domest Anim Endocrinol. 1989 Jul;6(3):275-85.

ɽ Hauner H, Entenmann G, Wabitsch M, Gaillard D, Ailhaud G, Negrel R, Pfeiffer EF.

Promoting effect of glucocorticoids on the differentiation of human adipocyte precursor

cells cultured in a chemically defined medium. J Clin Invest. 1989 Nov;84(5):1663-70.

ɽ Hauner H, Schmid P, Pfeiffer EF. Glucocorticoids and insulin promote the differentiation

of human adipocyte precursor cells into fat cells. J Clin Endocrinol Metab. 1987

Apr;64(4):832-5.

ɽ Ramsay TG, White ME, Wolverton CK. Glucocorticoids and the differentiation of porcine

preadipocytes. J Anim Sci. 1989 Sep;67(9):2222-9.

ɽ Bujalska IJ, Kumar S, Hewison M, Stewart PM. Differentiation of adipose stromal cells:

the roles of glucocorticoids and 11beta-hydroxysteroid dehydrogenase. Endocrinology.

1999 Jul;140(7):3188-96.

ɽ Nougues J, Reyne Y, Barenton B, Chery T, Garandel V, Soriano J. Differentiation of

adipocyte precursors in a serum-free medium is influenced by glucocorticoids and

2 5 2

S e c t i o n X : R e f e r e n c e s

endogenously produced insulin-like growth factor-I. Int J Obes Relat Metab Disord. 1993

Mar;17(3):159-67.

ɽ Suryawan A, Swanson LV, Hu CY. Insulin and hydrocortisone, but not triiodothyronine,

are required for the differentiation of pig preadipocytes in primary culture. J Anim Sci.

1997 Jan;75(1):105-11.

Reference 15:

ɽ Natalucci G, Riedl S, Gleiss A, Zidek T, Frisch H. Spontaneous 24-h ghrelin secretion

pattern in fasting subjects: maintenance of a meal-related pattern. Eur J Endocrinol. 2005

Jun;152(6):845-50.

ɽ Koutkia P, Canavan B, Breu J, Johnson ML, Grinspoon SK. Nocturnal ghrelin pulsatility

and response to growth hormone secretagogues in healthy men. Am J Physiol Endocrinol

Metab. 2004 Sep;287(3):E506-12.

ɽ Shiiya T, Nakazato M, Mizuta M, Date Y, Mondal MS, Tanaka M, Nozoe S, Hosoda H,

Kangawa K, and Matsukura S. Plasma ghrelin levels in lean and obese humans and the

effect of glucose on ghrelin secretion. J Clin Endocrinol Metab 87: 240–244, 2002.

ɽ Salgin B, Marcovecchio ML, Humphreys SM, Hill N, Chassin LJ, Lunn DJ, Hovorka R,

Dunger DB. Effects of prolonged fasting and sustained lipolysis on insulin secretion and

insulin sensitivity in normal subjects. Am J Physiol Endocrinol Metab. 2009

Mar;296(3):E454-61.

Reference 16:

ɽ Keim NL, Van Loan MD, Horn WF, Barbieri TF, Mayclin PL. Weight loss is greater with

consumption of large morning meals and fat-free mass is preserved with large evening

meals in women on a controlled weight reduction regimen. J Nutr. 1997 Jan;127(1):75-

82.

ɽ Hirsh E, Halberg F, Goetz FC, Cressey D, Wendt H, Sothern R, Haus E, Stoney P, Minors

D, Rosen G, Hill B, Hilleren M, Garet K. Body weight change during 1 week on a single

daily 2000-calorie meal consumed as breakfast (B) or dinner (D). Chronobiologia

1975;2(suppl 1): 31-32.

ɽ Jacobs H, Thompson M, Halberg E, Halberg F, Fraeber C, Levine H, Haus E. Relative

body weight loss on limited free-choice meal consumed as breakfast rather than as

dinner. Chronobiologia 1975;2(suppl 1): 33.

ɽ Halberg F. Some aspects of the chronobiology of nutrition: more work is needed on

“when to eat”. J Nutr. 1989 Mar;119(3):333-43. Review.

ɽ Sensi S, Capani F. Chronobiological aspects of weight loss in obesity: effects of different

meal timing regimens. Chronobiol Int. 1987;4(2):251-61.

Reference 17:

ɽ Holt SH, Miller JC, Petocz P. An insulin index of foods: the insulin demand generated by

1000-kJ portions of common foods. Am J Clin Nutr. 1997 Nov;66(5):1264-76.

Reference 18:

ɽ Chandler AM, Walker SP, Connolly K, Grantham-McGregor SM. School breakfast

improves verbal fluency in undernourished Jamaican children. J Nutr. 1995

Apr;125(4):894-900.

ɽ Pollitt E, Jacoby E, Cueto S. School breakfast and cognition among nutritionally at-risk

children in the Peruvian Andes. Nutr Rev. 1996 Apr;54(4 Pt 2):S22-6.

ɽ Lopez I, de Andraca I, Perales CG, Heresi E, Castillo M, Colombo M. Breakfast omission

and cognitive performance of normal, wasted and stunted schoolchildren. Eur J Clin

Nutr. 1993 Aug;47(8):533-42.

C a r b B a c k - L o a d i n g

C h a p t e r 1 5

ɽ Simeon DT, Grantham-McGregor S. Effects of missing breakfast on the cognitive

functions of school children of differing nutritional status. Am J Clin Nutr. 1989

Apr;49(4):646-53.

Reference 19:

ɽ Dickie NH, Bender AE. Breakfast and performance in school children. Br J Nutr. 1982

Nov;48(3):483-96.

ɽ Lopez-Sobaler AM, Ortega RM, Quintas ME, Navia B, Requejo AM. Relationship

between habitual breakfast and intellectual performance (logical reasoning) in well-

nourished schoolchildren of Madrid (Spain). Eur J Clin Nutr. 2003 Sep;57 Suppl 1:S49-

53.

ɽ Benton D, Parker PY. Breakfast, blood glucose, and cognition. Am J Clin Nutr. 1998

Apr;67(4):772S-778S.

ɽ Cueto S. Breakfast and performance. Public Health Nutr. 2001 Dec;4(6A):1429-31.

Review.

ɽ Martin A, Normand S, Sothier M, Peyrat J, Louche-Pelissier C, Laville M. Is advice for

breakfast consumption justified? Results from a short-term dietary and metabolic

experiment in young healthy men. Br J Nutr. 2000 Sep;84(3):337-44.

ɽ Vaisman N, Voet H, Akivis A, Vakil E. Effect of breakfast timing on the cognitive functions

of elementary school students. Arch Pediatr Adolesc Med. 1996 Oct;150(10):1089-92.

ɽ Pollitt E, Mathews R. Breakfast and cognition: an integrative summary. Am J Clin Nutr.

1998 Apr;67(4):804S-813S. Review.

ɽ Wesnes KA, Pincock C, Richardson D, Helm G, Hails S. Breakfast reduces declines in

attention and memory over the morning in schoolchildren. Appetite. 2003 Dec;41(3):329-

31.

ɽ Benton D, Slater O, Donohoe RT. The influence of breakfast and a snack on

psychological functioning. Physiol Behav. 2001 Nov-Dec;74(4-5):559-71.

ɽ Michaud C, Musse N, Nicolas JP, Mejean L. Effects of breakfast-size on short-term

memory, concentration, mood and blood glucose. J Adolesc Health. 1991 Jan;12(1):53-

7.

ɽ Kennedy E, Davis C. US Department of Agriculture School Breakfast Program. Am J Clin

Nutr. 1998 Apr;67(4):798S-803S. Review.

Chapter 15

Reference 1:

ɽ Keim NL, Van Loan MD, Horn WF, Barbieri TF, Mayclin PL. Weight loss is greater with

consumption of large morning meals and fat-free mass is preserved with large evening

meals in women on a controlled weight reduction regimen. J Nutr. 1997 Jan;127(1):75-

82.

ɽ Hirsh E, Halberg F, Goetz FC, Cressey D, Wendt H, Sothern R, Haus E, Stoney P, Minors

D, Rosen G, Hill B, Hilleren M, Garet K. Body weight change during 1 week on a single

daily 2000-calorie meal consumed as breakfast (B) or dinner (D). Chronobiologia

1975;2(suppl 1): 31-32.

ɽ Jacobs H, Thompson M, Halberg E, Halberg F, Fraeber C, Levine H, Haus E. Relative

body weight loss on limited free-choice meal consumed as breakfast rather than as

dinner. Chronobiologia 1975;2(suppl 1): 33.

ɽ Halberg F. Some aspects of the chronobiology of nutrition: more work is needed on

“when to eat”. J Nutr. 1989 Mar;119(3):333-43. Review.

ɽ Sensi S, Capani F. Chronobiological aspects of weight loss in obesity: effects of different

meal timing regimens. Chronobiol Int. 1987;4(2):251-61.

2 5 4

S e c t i o n X : R e f e r e n c e s

Chapter 16

Reference 1:

ɽ Martin A, Normand S, Sothier M, Peyrat J, Louche-Pelissier C, Laville M. Is advice for

breakfast consumption justified? Results from a short-term dietary and metabolic

experiment in young healthy men. Br J Nutr. 2000 Sep;84(3):337-44.

Reference 2:

ɽ Kuipers H, Fransen EJ, Keizer HA: Pre-exercise ingestion of carbohydrate and transient

hypoglycemia during exercise. Int J Sports Med 20: 227– 231, 1999.

ɽ Jentjens RL, Cale C, Gutch C, Jeukendrup AE: Effects of pre-exercise ingestion of

differing amounts of carbohydrate on subsequent metabolism and cycling performance.

Eur J Appl Physiol 88: 444– 452, 2003.

ɽ Thomas DE, Brotherhood JR, Brand JC: Carbohydrate feeding before exercise: effect of

glycemic index. Int J Sports Med 12: 180– 186, 1991.

ɽ DeMarco HM, Sucher KP, Cisar CJ, Butterfield GE. Pre-exercise carbohydrate meals:

application of glycemic index. Med Sci Sports Exerc 31: 164– 170, 1999.

ɽ Trenell MI, Stevenson E, Stockmann K, Brand-Miller J: Effect of high and low glycemic

index recovery diets on intramuscular lipid oxidation during aerobic exercise. Br J Nutr

99: 326– 332, 2008.

ɽ Thomas DE, Brotherhood JR, Miller JB: Plasma glucose levels after prolonged strenuous

exercise correlate inversely with glycemic response to food consumed before exercise.

Int J Sport Nutr 4: 361– 373, 1994.

ɽ Stevenson E, Williams C, Nute M: The influence of glycemic index of breakfast and lunch

on substrate utilisation during the postprandial periods and subsequent exercise. Br J

Nutr 93: 885– 893, 2005.

ɽ Jeukendrup AE, Killer SC. The myths surrounding pre-exercise carbohydrate feeding.

Ann Nutr Metab. 2010;57 Suppl 2:18-25. Review.

Reference 3:

ɽ Langfort J, Zarzeczny R, Pilis W, Nazar K, Kaciuba-UĞcitko H. The effect of a low-

carbohydrate diet on performance, hormonal and metabolic responses to a 30-s bout of

supramaximal exercise. Eur J Appl Physiol Occup Physiol. 1997;76(2):128-33.

ɽ Jansson E, Hjemdahl P, Kaijser L. Diet induced changes in sympatho-adrenal activity

during submaximal exercise in relation to substrate utilization in man. Acta Physiol

Scand. 1982 Feb;114(2):171-8.

ɽ Langfort JL, Zarzeczny R, Nazar K, Kaciuba-Uscilko H. The effect of low-carbohydrate

diet on the pattern of hormonal changes during incremental, graded exercise in young

men. Int J Sport Nutr Exerc Metab. 2001 Jun;11(2):248-57.

ɽ Langfort J, Czarnowski D, Zendzian-Piotrowska M, Zarzeczny R, Górski J. Short-term

low-carbohydrate diet dissociates lactate and ammonia thresholds in men. J Strength

Cond Res. 2004 May;18(2):260-5.

ɽ Langfort J, Pilis W, Zarzeczny R, Nazar K, Kaciuba-UĞciéko H. Effect of low-carbohydrate-

ketogenic diet on metabolic and hormonal responses to graded exercise in men. J

Physiol Pharmacol. 1996 Jun;47(2):361-71.

ɽ Sasaki H, Hotta N, Ishiko T. Comparison of sympatho-adrenal activity during endurance

exercise performed under high- and low-carbohydrate diet conditions. J Sports Med

Phys Fitness. 1991 Sep;31(3):407-12.

C a r b B a c k - L o a d i n g

C h a p t e r 1 7

Reference 4:

ɽ Chmura J, Krysztofiak H, Ziemba AW, Nazar K, Kaciuba-UĞcilko H. Psychomotor

performance during prolonged exercise above and below the blood lactate threshold. Eur

J Appl Physiol Occup Physiol. 1998;77(1-2):77-80.

Reference 5:

ɽ Grisdale RK, Jacobs I, Cafarelli E. Relative effects of glycogen depletion and previous

exercise on muscle force and endurance capacity. J Appl Physiol. 1990 Oct;69(4):1276-

82.

Reference 6:

ɽ Langfort J, Pilis W, Zarzeczny R, Nazar K, Kaciuba-UĞciéko H. Effect of low-carbohydrate-

ketogenic diet on metabolic and hormonal responses to graded exercise in men. J

Physiol Pharmacol. 1996 Jun;47(2):361-71.

ɽ Weltan SM, Bosch AN, Dennis SC, Noakes TD. Influence of muscle glycogen content on

metabolic regulation. Am J Physiol. 1998 Jan;274(1 Pt 1):E72-82.

ɽ Zderic TW, Schenk S, Davidson CJ, Byerley LO, Coyle EF. Manipulation of dietary

carbohydrate and muscle glycogen affects glucose uptake during exercise when fat

oxidation is impaired by beta-adrenergic blockade. Am J Physiol Endocrinol Metab. 2004

Dec;287(6):E1195-201.

ɽ Symons JD, Jacobs I. High-intensity exercise performance is not impaired by low

intramuscular glycogen. Med Sci Sports Exerc. 1989 Oct;21(5):550-7.

Chapter 17

Reference 1:

ɽ Sedliak M, Finni T, Peltonen J, Häkkinen K. Effect of time-of-day-specific strength

training on maximum strength and EMG activity of the leg extensors in men. J Sports Sci.

2008 Aug;26(10):1005-14.

Reference 2:

ɽ Hayes LD, Bickerstaff GF, Baker JS. Interactions of cortisol, testosterone, and resistance

training: influence of circadian rhythms. Chronobiol Int. 2010 Jun;27(4):675-705. Review.

ɽ Sedliak M, Finni T, Cheng S, Lind M, Häkkinen K. Effect of time-of-day-specific strength

training on muscular hypertrophy in men. J Strength Cond Res. 2009 Dec;23(9):2451-7.

ɽ Sedliak M, Finni T, Cheng S, Kraemer WJ, Häkkinen K. Effect of time-of-day-specific

strength training on serum hormone concentrations and isometric strength in men.

Chronobiol Int. 2007;24(6):1159-77.

ɽ Bird SP, Tarpenning KM. Influence of circadian time structure on acute hormonal

responses to a single bout of heavy-resistance exercise in weight-trained men.

Chronobiol Int. 2004 Jan;21(1):131-46.

2 5 6

S e c t i o n X : R e f e r e n c e s

Chapter 18

Reference 1:

ɽ Wolfe RR. Volpi E. Insulin and protein metabolism. In: Jefferson LS, Cherrington AD, eds.

The endocrine pancreas and regulation of metabolism. New York, Oxford University

Press, 2001:735–57.

Reference 2:

ɽ Ivy JL. Regulation of muscle glycogen repletion, muscle protein synthesis and repair

following exercise. J Sports Sci Medicine 2004;3:131–8.

ɽ Llewellyn W. Anabolics 2002: anabolic steroids reference manual. Patchogue, NY:

Molecular Nutrition, 2002.

Reference 3:

ɽ Bird SP, Tarenning KM, Marino FE. Independent and combined effects of liquid

carbohydrate/essential amino acid ingestion on hormonal and muscular adaptations

following resistance training in untrained men. Eur J Appl Physiol 2006;97:225–38.

ɽ Krzentowski G, Pirnay F, Luyckx, AS, Pallikarakis N, Lacroix M, Mosora F, Lefèbvre P J.

Metabolic adaptations in postexercise recovery. Clin Physiol 1982;2:277–88.

ɽ Folch N, Péronnet F, Massicotte D, Duclos M, Lavoie C, Hillaire-Marcel C. Metabolic

response to small and large 13C-labelled pasta meals following rest or exercise in man.

Br J Nutr 2001;85:671–80.

Chapter 19

Reference 1:

ɽ MacDougall JD, Gibala MJ, Tarnopolsky MA, MacDonald JR, Interisano SA, Yarasheski

KE. The time course for elevated muscle protein synthesis following heavy resistance

exercise. Can J Appl Physiol. 1995 Dec;20(4):480-6.

ɽ Reeds PJ, Palmer RM, Hay SM, McMillan DN. Protein synthesis in skeletal muscle

measured at different times during a 24 hour period. Biosci Rep. 1986 Feb;6(2):209-13.

ɽ Paddon-Jones D, Muthalib M, Jenkins D. The effects of a repeated bout of eccentric

exercise on indices of muscle damage and delayed onset muscle soreness. J Sci Med

Sport. 2000 Mar;3(1):35-43.

ɽ Nosaka K, Newton M. Repeated eccentric exercise bouts do not exacerbate muscle

damage and repair. J Strength Cond Res. 2002 Feb;16(1):117-22.

ɽ Nosaka K, Clarkson PM. Muscle damage following repeated bouts of high force

eccentric exercise. Med Sci Sports Exerc. 1995 Sep;27(9):1263-9.

ɽ Chen TC, Hsieh SS. Effects of a 7-day eccentric training period on muscle damage and

inflammation. Med Sci Sports Exerc. 2001 Oct;33(10):1732-8.

ɽ Chen TC, Hsieh SS. The effects of repeated maximal voluntary isokinetic eccentric

exercise on recovery from muscle damage. Res Q Exerc Sport. 2000 Sep;71(3):260-6.

ɽ Nosaka K, Newton M. Is recovery from muscle damage retarded by a subsequent bout

of eccentric exercise inducing larger decreases in force? J Sci Med Sport. 2002

Sep;5(3):204-18.

ɽ Chen TC. Effects of a second bout of maximal eccentric exercise on muscle damage and

electromyographic activity. Eur J Appl Physiol. 2003 Apr;89(2):115-21.

C a r b B a c k - L o a d i n g

C h a p t e r 1 9

Reference 2:

ɽ Saxton JM, Clarkson PM, James R, Miles M, Westerfer M, Clark S, Donnelly AE.

Neuromuscular dysfunction following eccentric exercise. Med Sci Sports Exerc. 1995

Aug;27(8):1185-93.

ɽ Deschenes MR, Brewer RE, Bush JA, McCoy RW, Volek JS, Kraemer WJ.

Neuromuscular disturbance outlasts other symptoms of exercise-induced muscle

damage. J Neurol Sci. 2000 Mar 15;174(2):92-9.

ɽ Pearce AJ, Sacco P, Byrnes ML, Thickbroom GW, Mastaglia FL. The effects of eccentric

exercise on neuromuscular function of the biceps brachii. J Sci Med Sport. 1998

Dec;1(4):236-44.

Reference 3:

ɽ Churchley EG, Coffey VG, Pedersen DJ, Shield A, Carey KA, Cameron-Smith D, Hawley

JA. Influence of preexercise muscle glycogen content on transcriptional activity of

metabolic and myogenic genes in well-trained humans. J Appl Physiol. 2007

Apr;102(4):1604-11.

ɽ Pilegaard H, Osada T, Andersen LT, Helge JW, Saltin B, Neufer PD. Substrate availability

and transcriptional regulation of metabolic genes in human skeletal muscle during

recovery from exercise. Metabolism. 2005 Aug;54(8):1048-55.

ɽ Steensberg A, van Hall G, Keller C, Osada T, Schjerling P, Pedersen BK, Saltin B,

Febbraio MA. Muscle glycogen content and glucose uptake during exercise in humans:

influence of prior exercise and dietary manipulation. J Physiol. 2002 May 15;541(Pt

1):273-81.

ɽ Pilegaard H, Keller C, Steensberg A, Helge JW, Pedersen BK, Saltin B, Neufer PD.

Influence of pre-exercise muscle glycogen content on exercise-induced transcriptional

regulation of metabolic genes. J Physiol. 2002 May 15;541(Pt 1):261-71.

ɽ Blomstrand E, Saltin B. Effect of muscle glycogen on glucose, lactate and amino acid

metabolism during exercise and recovery in human subjects. J Physiol. 1999 Jan 1;514 (

Pt 1):293-302.

ɽ Bangsbo J, Graham TE, Kiens B, Saltin B. Elevated muscle glycogen and anaerobic

energy production during exhaustive exercise in man. J Physiol. 1992;451:205-27.

ɽ Kaastra B, Manders RJ, Van Breda E, Kies A, Jeukendrup AE, Keizer HA, Kuipers H, Van

Loon LJ. Effects of increasing insulin secretion on acute postexercise blood glucose

disposal. Med Sci Sports Exerc. 2006 Feb;38(2):268-75.

ɽ Wee SL, Williams C, Tsintzas K, Boobis L. Ingestion of a high-glycemic index meal

increases muscle glycogen storage at rest but augments its utilization during subsequent

exercise. J Appl Physiol. 2005 Aug;99(2):707-14.

ɽ Stevenson E, Williams C, Nute M, Swaile P, Tsui M. The effect of the glycemic index of an

evening meal on the metabolic responses to a standard high glycemic index breakfast

and subsequent exercise in men. Int J Sport Nutr Exerc Metab. 2005 Jun;15(3):308-22.

ɽ Stevenson E, Williams C, Biscoe H. The metabolic responses to high carbohydrate meals

with different glycemic indices consumed during recovery from prolonged strenuous

exercise. Int J Sport Nutr Exerc Metab. 2005 Jun;15(3):291-307.

ɽ van Loon LJ, Saris WH, Kruijshoop M, Wagenmakers AJ. Maximizing postexercise

muscle glycogen synthesis: carbohydrate supplementation and the application of amino

acid or protein hydrolysate mixtures. Am J Clin Nutr. 2000 Jul;72(1):106-11.

ɽ Piehl Aulin K, Söderlund K, Hultman E. Muscle glycogen resynthesis rate in humans after

supplementation of drinks containing carbohydrates with low and high molecular masses.

Eur J Appl Physiol. 2000 Mar;81(4):346-51.

ɽ Ivy JL, Katz AL, Cutler CL, Sherman WM, Coyle EF. Muscle glycogen synthesis after

exercise: effect of time of carbohydrate ingestion. J Appl Physiol. 1988 Apr;64(4):1480-5.

2 5 8

S e c t i o n X : R e f e r e n c e s

Reference 4:

ɽ Schnure JJ, Raskin P, Lipman RL. Growth hormone secretion during sleep: impairment in

glucose tolerance and nonsuppressibility by hyperglycemia. J Clin Endocrinol Metab.

1971 Aug;33(2):234-41.

ɽ VanderLaan WP. Changing concepts on the control of growth hormone secretion in man.

Calif Med. 1971 Aug;115(2):38-46. Review.

Reference 5:

ɽ Kulig K, Powers CM, Shellock FG, Terk M. The effects of eccentric velocity on activation

of elbow flexors: evaluation by magnetic resonance imaging. Med Sci Sports Exerc.

2001 Feb;33(2):196-200.

ɽ Coudreuse JM, Dupont P, Nicol C. Delayed post effort muscle soreness. Ann Readapt

Med Phys. 2004 Aug;47(6):290-8. Review.

ɽ Kauranen K, Siira P, Vanharanta H. Delayed-onset muscle soreness and motor

performance of the upper extremity. Eur J Appl Physiol. 2001 Apr;84(4):302-9.

ɽ MacIntyre DL, Reid WD, McKenzie DC. Delayed muscle soreness. The inflammatory

response to muscle injury and its clinical implications. Sports Med. 1995 Jul;20(1):24-40.

ɽ Cleak MJ, Eston RG. Muscle soreness, swelling, stiffness and strength loss after intense

eccentric exercise. Br J Sports Med. 1992 Dec;26(4):267-72.

ɽ Nosaka K, Sakamoto K, Newton M, Sacco P. How long does the protective effect on

eccentric exercise-induced muscle damage last? Med Sci Sports Exerc. 2001

Sep;33(9):1490-5.

Reference 6:

ɽ Hilbert JE, Sforzo GA, Swensen T. The effects of massage on delayed onset muscle

soreness. Br J Sports Med. 2003 Feb;37(1):72-5.

ɽ Yu JG, Malm C, Thornell LE. Eccentric contractions leading to DOMS do not cause loss

of desmin nor fibre necrosis in human muscle. Histochem Cell Biol. 2002 Jul;118(1):29-

34.

ɽ Hamlin MJ, Quigley BM. Quadriceps concentric and eccentric exercise 2: differences in

muscle strength, fatigue and EMG activity in eccentrically-exercised sore and non-sore

muscles. J Sci Med Sport. 2001 Mar;4(1):104-15.

ɽ MacIntyre DL, Sorichter S, Mair J, Berg A, McKenzie DC. Markers of inflammation and

myofibrillar proteins following eccentric exercise in humans. Eur J Appl Physiol. 2001

Mar;84(3):180-6.

Chapter 20

Reference 1:

ɽ Feinman RD, Fine EJ. Thermodynamics and metabolic advantage of weight loss diets.

Metab Syndr Relat Disord. 2003 Sep;1(3):209-19.

ɽ Feinman RD, Fine EJ. Nonequilibrium thermodynamics and energy efficiency in weight

loss diets. Theor Biol Med Model. 2007 Jul 30;4:27. Review

ɽ Fine EJ, Feinman RD. Thermodynamics of weight loss diets. Nutr Metab (Lond). 2004

Dec 8;1(1):15.

ɽ Feinman RD, Fine EJ. Whatever happened to the second law of thermodynamics? Am J

Clin Nutr. 2004 Nov;80(5):1445-6; author reply 1446.

ɽ Feinman RD, Fine EJ. "A calorie is a calorie" violates the second law of thermodynamics.

Nutr J. 2004 Jul 28;3:9.

C a r b B a c k - L o a d i n g

C h a p t e r 2 0

Reference 2:

ɽ Evans EM, Saunders MJ, Spano MA, Arngrimsson SA, Lewis RD, Cureton KJ. Effects of

diet and exercise on the density and composition of the fat-free mass in obese women.

Med Sci Sports Exerc. 1999 Dec;31(12):1778-87.

ɽ Kraemer WJ, Volek JS, Clark KL, Gordon SE, Incledon T, Puhl SM, Triplett-McBride NT,

McBride JM, Putukian M, Sebastianelli WJ. Physiological adaptations to a weight-loss

dietary regimen and exercise programs in women. J Appl Physiol. 1997 Jul;83(1):270-9.

ɽ Geliebter A, Maher MM, Gerace L, Gutin B, Heymsfield SB, Hashim SA. Effects of

strength or aerobic training on body composition, resting metabolic rate, and peak

oxygen consumption in obese dieting subjects. Am J Clin Nutr. 1997 Sep;66(3):557-63.

ɽ Ballor DL, Poehlman ET. Exercise-training enhances fat-free mass preservation during

diet-induced weight loss: a meta-analytical finding. Int J Obes Relat Metab Disord. 1994

Jan;18(1):35-40.

ɽ Schwingshandl J, Sudi K, Eibl B, Wallner S, Borkenstein M. Effect of an individualised

training programme during weight reduction on body composition: a randomised trial.

Arch Dis Child. 1999 Nov;81(5):426-8.

ɽ Donnelly JE, Sharp T, Houmard J, Carlson MG, Hill JO, Whatley JE, Israel RG. Muscle

hypertrophy with large-scale weight loss and resistance training. Am J Clin Nutr. 1993

Oct;58(4):561-5.

ɽ Utter AC, Nieman DC, Shannonhouse EM, Butterworth DE, Nieman CN. Influence of diet

and/or exercise on body composition and cardiorespiratory fitness in obese women. Int

J Sport Nutr. 1998 Sep;8(3):213-22.

ɽ Dengel DR, Hagberg JM, Coon PJ, Drinkwater DT, Goldberg AP. Comparable effects of

diet and exercise on body composition and lipoproteins in older men. Med Sci Sports

Exerc. 1994 Nov;26(11):1307-15.

ɽ Gornall J, Villani RG. Short-term changes in body composition and metabolism with

severe dieting and resistance exercise. Int J Sport Nutr. 1996 Sep;6(3):285-94.

ɽ Van Dale D, Saris WH, Schoffelen PF, Ten Hoor F. Does exercise give an additional

effect in weight reduction regimens? Int J Obes. 1987;11(4):367-75.

ɽ Cox KL, Burke V, Morton AR, Beilin LJ, Puddey IB. The independent and combined

effects of 16 weeks of vigorous exercise and energy restriction on body mass and

composition in free-living overweight men--a randomized controlled trial. Metabolism.

2003 Jan;52(1):107-15.

ɽ Sweeney ME, Hill JO, Heller PA, Baney R, DiGirolamo M. Severe vs moderate energy

restriction with and without exercise in the treatment of obesity: efficiency of weight loss.

Am J Clin Nutr. 1993 Feb;57(2):127-34.

ɽ Donnelly JE, Pronk NP, Jacobsen DJ, Pronk SJ, Jakicic JM. Effects of a very-low-calorie

diet and physical-training regimens on body composition and resting metabolic rate in

obese females. Am J Clin Nutr. 1991 Jul;54(1):56-61.

ɽ Nieman DC, Brock DW, Butterworth D, Utter AC, Nieman CC. Reducing diet and/or

exercise training decreases the lipid and lipoprotein risk factors of moderately obese

women. J Am Coll Nutr. 2002 Aug;21(4):344-50.

ɽ Powell JJ, Tucker L, Fisher AG, Wilcox K. The effects of different percentages of dietary

fat intake, exercise, and calorie restriction on body composition and body weight in

obese females. Am J Health Promot. 1994 Jul-Aug;8(6):442-8.

ɽ Bryner RW, Ullrich IH, Sauers J, Donley D, Hornsby G, Kolar M, Yeater R. Effects of

resistance vs. aerobic training combined with an 800 calorie liquid diet on lean body

mass and resting metabolic rate. J Am Coll Nutr. 1999 Apr;18(2):115-21.

ɽ Evans EM, Saunders MJ, Spano MA, Arngrimsson SA, Lewis RD, Cureton KJ. Body-

composition changes with diet and exercise in obese women: a comparison of estimates

from clinical methods and a 4-component model. Am J Clin Nutr. 1999 Jul;70(1):5-12.

2 6 0

S e c t i o n X : R e f e r e n c e s

ɽ Dengel DR, Hagberg JM, Coon PJ, Drinkwater DT, Goldberg AP. Effects of weight loss

by diet alone or combined with aerobic exercise on body composition in older obese

men. Metabolism. 1994 Jul;43(7):867-71.

ɽ Lemons AD, Kreitzman SN, Coxon A, Howard A. Selection of appropriate exercise

regimens for weight reduction during VLCD and maintenance. Int J Obes. 1989;13 Suppl

2:119-23.

ɽ Janssen I, Fortier A, Hudson R, Ross R. Effects of an energy-restrictive diet with or

without exercise on abdominal fat, intermuscular fat, and metabolic risk factors in obese

women. Diabetes Care. 2002 Mar;25(3):431-8.

ɽ Lamarche B, Despres JP, Moorjani S, Nadeau A, Lupien PJ, Tremblay A, Theriault G,

Bouchard C. Evidence for a role of insulin in the regulation of abdominal adipose tissue

lipoprotein lipase response to exercise training in obese women. Int J Obes Relat Metab

Disord. 1993 May;17(5):255-61.

ɽ Poehlman ET, Dvorak RV, DeNino WF, Brochu M, Ades PA. Effects of resistance training

and endurance training on insulin sensitivity in nonobese, young women: a controlled

randomized trial. J Clin Endocrinol Metab. 2000 Jul;85(7):2463-8.

ɽ Stensel DJ, Brooke-Wavell K, Hardman AE, Jones PR, Norgan NG. The influence of a 1-

year programme of brisk walking on endurance fitness and body composition in

previously sedentary men aged 42-59 years. Eur J Appl Physiol Occup Physiol.

1994;68(6):531-7.

Reference 3:

ɽ Rabast U, Kasper H, Schonborn J. Comparative studies in obese subjects fed

carbohydrate-restricted and high carbohydrate 1,000-calorie formula diets. Nutr Metab.

1978;22:269–77.

ɽ Rabast U, Hahn A, Reiners C, Ehl M. Thyroid hormone changes in obese subjects during

fasting and a very-low-calorie diet. Int J Obes. 1981;5:305–11.

ɽ Golay A, Eigenheer C, Morel Y, Kujawski P, Lehmann T, de Tonnac N. Weight-loss with

low or high carbohydrate diet? Int J Obes Relat Metab Disord. 1996;20:1067–72.

ɽ Golay A, Allaz AF, Morel Y, de Tonnac N, Tankova S, Reaven G. Similar weight loss with

low- or high-carbohydrate diets. Am J Clin Nutr. 1996;63:174–8.

ɽ Layman DK, Boileau RA, Erickson DJ, Painter JE, Shiue H, Sather C, Christou DD. A

reduced ratio of dietary carbohydrate to protein improves body composition and blood

lipid profiles during weight loss in adult women. J Nutr. 2003;133:411–7.

ɽ Lean ME, Han TS, Prvan T, Richmond PR, Avenell A. Weight loss with high and low

carbohydrate 1200 kcal diets in free living women. Eur J Clin Nutr. 1997;51:243–8.

ɽ Baba NH, Sawaya S, Torbay N, Habbal Z, Azar S, Hashim SA. High protein vs high

carbohydrate hypoenergetic diet for the treatment of obese hyperinsulinemic subjects. Int

J Obes Relat Metab Disord. 1999;23:1202–6.

ɽ Young CM, Scanlan SS, Im HS, Lutwak L. Effect of body composition and other

parameters in obese young men of carbohydrate level of reduction diet. Am J Clin Nutr.

1971;24:290–6.

ɽ Greene P, Willett W, Devecis J, Skaf A. Pilot 12-Week Feeding Weight-Loss Comparison:

Low-Fat vs Low-Carbohydrate (Ketogenic) Diets. Obesity Research. 2003;11:A23.

Chapter 22

Reference 1:

ɽ Sardesai VM. The essential fatty acids. Nutr Clin Pract. 1992 Aug;7(4):179-86. Review.

C a r b B a c k - L o a d i n g

C h a p t e r 2 2

ɽ Hulbert AJ, Turner N, Storlien LH, Else PL. Dietary fats and membrane function:

implications for metabolism and disease. Biol Rev Camb Philos Soc. 2005 Feb;80(1):155-

69. Review

Reference 2:

ɽ Jackson SH, Weale MR, Weale RA. Biological age--what is it and can it be measured?

Arch Gerontol Geriatr. 2003 Mar-Apr;36(2):103-15.

Reference 3:

ɽ Whitcomb RW, Linehan WM, Knazek RA. Effects of long-chain, saturated fatty acids on

membrane

microviscosity

and

adrenocorticotropin

responsiveness

of

human

adrenocortical cells in vitro. J Clin Invest. 1988 Jan;81(1):185-8. -2-1-

ɽ Calder PC, Yaqoob P, Harvey DJ, Watts A, Newsholme EA. Incorporation of fatty acids

by concanavalin A-stimulated lymphocytes and the effect on fatty acid composition and

membrane fluidity. Biochem J. 1994 Jun 1;300 ( Pt 2):509-18.

Reference 4:

ɽ Dunham WR, Klein SB, Rhodes LM, Marcelo CL. Oleic acid and linoleic acid are the

major determinants of changes in keratinocyte plasma membrane viscosity. J Invest

Dermatol. 1996 Sep;107(3):332-5.

ɽ Lund EK, Harvey LJ, Ladha S, Clark DC, Johnson IT. Effects of dietary fish oil

supplementation on the phospholipid composition and fluidity of cell membranes from

human volunteers. Ann Nutr Metab. 1999;43(5):290-300.

ɽ Fickova M, Hubert P, Cremel G, Leray C. Dietary (n-3) and (n-6) polyunsaturated fatty

acids rapidly modify fatty acid composition and insulin effects in rat adipocytes. J Nutr.

1998 Mar;128(3):512-9.

ɽ Stillwell W, Wassall SR. Docosahexaenoic acid: membrane properties of a unique fatty

acid. Chem Phys Lipids. 2003 Nov;126(1):1-27. Review.

ɽ Aas V, Rokling-Andersen MH, Kase ET, Thoresen GH, Rustan AC. Eicosapentaenoic acid

(20:5 n-3) increases fatty acid and glucose uptake in cultured human skeletal muscle

cells. J Lipid Res. 2006 Feb;47(2):366-74.

Reference 5:

ɽ Smith GI, Atherton P, Reeds DN, Mohammed BS, Rankin D, Rennie MJ, Mittendorfer B.

Omega-3 polyunsaturated fatty acids augment the muscle protein anabolic response to

hyperinsulinaemia-hyperaminoacidaemia in healthy young and middle-aged men and

women. Clin Sci (Lond). 2011 Sep;121(6):267-78.

Reference 6:

ɽ Burdge GC, Wootton SA. Conversion of alpha-linolenic acid to palmitic, palmitoleic,

stearic and oleic acids in men and women. Prostaglandins Leukot Essent Fatty Acids.

2003 Oct;69(4):283-90.

ɽ Melin T, Nilsson A. Delta-6-desaturase and delta-5-desaturase in human Hep G2 cells

are both fatty acid interconversion rate limiting and are upregulated under essential fatty

acid deficient conditions. Prostaglandins Leukot Essent Fatty Acids. 1997 Jun;56(6):437-

42.

ɽ Cho HP, Nakamura MT, Clarke SD. Cloning, expression, and nutritional regulation of the

mammalian Delta-6 desaturase. J Biol Chem. 1999 Jan 1;274(1):471-7.

ɽ Ide T, Kobayashi H, Ashakumary L, Rouyer IA, Takahashi Y, Aoyama T, Hashimoto T,

Mizugaki M. Comparative effects of perilla and fish oils on the activity and gene

2 6 2

S e c t i o n X : R e f e r e n c e s

expression of fatty acid oxidation enzymes in rat liver. Biochim Biophys Acta. 2000 May

6;1485(1):23-35.

ɽ Conquer JA, Holub BJ. Supplementation with an algae source of docosahexaenoic acid

increases (n-3) fatty acid status and alters selected risk factors for heart disease in

vegetarian subjects. J Nutr. 1996 Dec;126(12):3032-9.

ɽ Nelson GJ, Schmidt PC, Bartolini GL, Kelley DS, Kyle D. The effect of dietary

docosahexaenoic acid on plasma lipoproteins and tissue fatty acid composition in

humans. Lipids. 1997 Nov;32(11):1137-46.

ɽ Burdge GC, Wootton SA. Conversion of alpha-linolenic acid to eicosapentaenoic,

docosapentaenoic and docosahexaenoic acids in young women. Br J Nutr. 2002

Oct;88(4):411-20.

ɽ Burdge GC, Jones AE, Wootton SA. Eicosapentaenoic and docosapentaenoic acids are

the principal products of alpha-linolenic acid metabolism in young men*. Br J Nutr. 2002

Oct;88(4):355-63.

ɽ Salem N Jr, Pawlosky R, Wegher B, Hibbeln J. In vivo conversion of linoleic acid to

arachidonic acid in human adults. Prostaglandins Leukot Essent Fatty Acids. 1999 May-

Jun;60(5-6):407-10.

ɽ Isseroff RR, Ziboh VA, Chapkin RS, Martinez DT. Conversion of linoleic acid into

arachidonic acid by cultured murine and human keratinocytes. J Lipid Res. 1987

Nov;28(11):1342-9. -33-8-

ɽ Sprecher H. Biochemistry of essential fatty acids. Prog Lipid Res. 1981;20:13-22.

Reference 7:

ɽ Hessvik NP, Bakke SS, Fredriksson K, Boekschoten MV, Fjørkenstad A, Koster G,

Hesselink MK, Kersten S, Kase ET, Rustan AC, Thoresen GH. Metabolic switching of

human myotubes is improved by n-3 fatty acids. J Lipid Res. 2010 Aug;51(8):2090-104.

Chapter 23

Reference 1:

ɽ Heath RB, Karpe F, Milne RW, Burdge GC, Wootton SA, Frayn KN. Selective partitioning

of dietary fatty acids into the VLDL TG pool in the early postprandial period. J Lipid Res.

2003 Nov;44(11):2065-72.

ɽ Hansen JB, Grimsgaard S, Nilsen H, Nordoy A, Bonaa KH. Effects of highly purified

eicosapentaenoic acid and docosahexaenoic acid on fatty acid absorption, incorporation

into serum phospholipids and postprandial triglyceridemia. Lipids. 1998 Feb;33(2):131-8.

ɽ Binnert C, Pachiaudi C, Beylot M, Croset M, Cohen R, Riou, JP, Laville M. Metabolic fate

of an oral long-chain triglyceride load in humans. Am J Physiol. 1996 Mar;270(3 Pt

1):E445-50.

ɽ Yli-Jokipii K, Kallio H, Schwab U, Mykkanen H, Kurvinen JP, Savolainen MJ, Tahvonen R.

Effects of palm oil and transesterified palm oil on chylomicron and VLDL triacylglycerol

structures and postprandial lipid response. J Lipid Res. 2001 Oct;42(10):1618-25.

Reference 2:

ɽ Bach AC, Babayan VK. Medium-chain triglycerides: an update. Am J Clin Nutr. 1982

Nov;36(5):950-62. Review.

ɽ Bach AC, Ingenbleek Y, Frey A. The usefulness of dietary medium-chain triglycerides in

body weight control: fact or fancy? J Lipid Res. 1996 Apr;37(4):708-26. Review.

C a r b B a c k - L o a d i n g

C h a p t e r 2 3

ɽ Swift LL, Hill JO, Peters JC, Greene HL. Medium-chain fatty acids: evidence for

incorporation into chylomicron triglycerides in humans. Am J Clin Nutr. 1990

Nov;52(5):834-6.

ɽ Greenberger NJ, Skillman TG. Medium-chain triglycerides. N Engl J Med. 1969 May

8;280(19):1045-58. Review.

ɽ Asakura L, Lottenberg AM, Neves MQ, Nunes VS, Rocha JC, Passarelli M, Nakandakare

ER, Quintao EC. Dietary medium-chain triacylglycerol prevents the postprandial rise of

plasma triacylglycerols but induces hypercholesterolemia in primary hypertriglyceridemic

subjects. Am J Clin Nutr. 2000 Mar;71(3):701-5.

ɽ Flatt JP, Ravussin E, Acheson KJ, Jequier E. Effects of dietary fat on postprandial

substrate oxidation and on carbohydrate and fat balances. J Clin Invest. 1985

Sep;76(3):1019-24.

Reference 3:

ɽ Miles JM, Haymond MW, Gerich JE. Effects of free fatty acids, insulin, glucagon and

adrenaline on ketone body production in humans. Ciba Found Symp. 1982;87:192-213.

ɽ Miles JM, Haymond MW, Nissen SL, Gerich JE. Effects of free fatty acid availability,

glucagon excess, and insulin deficiency on ketone body production in postabsorptive

man. J Clin Invest. 1983 Jun;71(6):1554-61.

ɽ Keller U, Lustenberger M, Müller-Brand J, Gerber PP, Stauffacher W. Human ketone

body production and utilization studied using tracer techniques: regulation by free fatty

acids, insulin, catecholamines, and thyroid hormones. Diabetes Metab Rev. 1989

May;5(3):285-98. Review.

ɽ Beylot M. Regulation of in vivo ketogenesis: role of free fatty acids and control by

epinephrine, thyroid hormones, insulin and glucagon. Diabetes Metab. 1996

Oct;22(5):299-304. Review.

ɽ Fukao T, Lopaschuk GD, Mitchell GA. Pathways and control of ketone body metabolism:

on the fringe of lipid biochemistry. Prostaglandins Leukot Essent Fatty Acids. 2004

Mar;70(3):243-51. Review.

Reference 4:

ɽ St-Onge MP, Bosarge A. Weight-loss diet that includes consumption of medium-chain

triacylglycerol oil leads to a greater rate of weight and fat mass loss than does olive oil.

Am J Clin Nutr. 2008 Mar;87(3):621-6.

ɽ Turner N, Hariharan K, TidAng J, Frangioudakis G, Beale SM, Wright LE, Zeng XY, Leslie

SJ, Li JY, Kraegen EW, Cooney GJ, Ye JM. Enhancement of muscle mitochondrial

oxidative capacity and alterations in insulin action are lipid species dependent: potent

tissue-specific effects of medium-chain fatty acids. Diabetes. 2009 Nov;58(11):2547-54.

ɽ Alexandrou E, Herzberg GR, White MD. High-level medium-chain triglyceride feeding and

energy expenditure in normal-weight women. Can J Physiol Pharmacol. 2007

May;85(5):507-13.

ɽ St-Onge MP, Jones PJ. Greater rise in fat oxidation with medium-chain triglyceride

consumption relative to long-chain triglyceride is associated with lower initial body weight

and greater loss of subcutaneous adipose tissue. Int J Obes Relat Metab Disord. 2003

Dec;27(12):1565-71.

ɽ Kasai M, Nosaka N, Maki H, Negishi S, Aoyama T, Nakamura M, Suzuki Y, Tsuji H, Uto H,

Okazaki M, Kondo K. Effect of dietary medium- and long-chain triacylglycerols (MLCT) on

accumulation of body fat in healthy humans. Asia Pac J Clin Nutr. 2003;12(2):151-60.

ɽ St-Onge MP, Ross R, Parsons WD, Jones PJ. Medium-chain triglycerides increase

energy expenditure and decrease adiposity in overweight men. Obes Res. 2003

Mar;11(3):395-402.

2 6 4

S e c t i o n X : R e f e r e n c e s

ɽ St-Onge MP, Bourque C, Jones PJ, Ross R, Parsons WE. Medium- versus long-chain

triglycerides for 27 days increases fat oxidation and energy expenditure without resulting

in changes in body composition in overweight women. Int J Obes Relat Metab Disord.

2003 Jan;27(1):95-102.

ɽ Piers LS, Walker KZ, Stoney RM, Soares MJ, O'Dea K. The influence of the type of

dietary fat on postprandial fat oxidation rates: monounsaturated (olive oil) vs saturated fat

(cream). Int J Obes Relat Metab Disord. 2002 Jun;26(6):814-21.

ɽ Tsuji H, Kasai M, Takeuchi H, Nakamura M, Okazaki M, Kondo K. Dietary medium-chain

triacylglycerols suppress accumulation of body fat in a double-blind, controlled trial in

healthy men and women. J Nutr. 2001 Nov;131(11):2853-9.

Chapter 24

Reference 1:

ɽ Björck I, Granfeldt Y, Liljeberg H, Tovar J, Asp NG. Food properties affecting the

digestion and absorption of carbohydrates. Am J Clin Nutr. 1994 Mar;59(3 Suppl):699S-

705S. Review.

ɽ Granfeldt Y, Liljeberg H, Drews A, Newman R, Björck I. Glucose and insulin responses to

barley products: influence of food structure and amylose-amylopectin ratio. Am J Clin

Nutr. 1994 May;59(5):1075-82.

ɽ Heijnen ML, van Amelsvoort JM, Weststrate JA. Interaction between physical structure

and amylose:amylopectin ratio of foods on postprandial glucose and insulin responses in

healthy subjects. Eur J Clin Nutr. 1995 Jun;49(6):446-57.

ɽ van Amelsvoort JM, Weststrate JA. Amylose-amylopectin ratio in a meal affects

postprandial variables in male volunteers. Am J Clin Nutr. 1992 Mar;55(3):712-8.

ɽ Behall KM, Scholfield DJ, Yuhaniak I, Canary J. Diets containing high amylose vs

amylopectin starch: effects on metabolic variables in human subjects. Am J Clin Nutr.

1989 Feb;49(2):337-44.

ɽ Behall KM, Scholfield DJ, Canary J. Effect of starch structure on glucose and insulin

responses in adults. Am J Clin Nutr. 1988 Mar;47(3):428-32.

Chapter 25

Reference 1:

ɽ Bounous G, Gold P. The biological activity of undenatured dietary whey proteins: role of

glutathione. Clin Invest Med. 1991 Aug;14(4):296-309.

ɽ Baruchel S, Viau G. In vitro selective modulation of cellular glutathione by a humanized

native milk protein isolate in normal cells and rat mammary carcinoma model. Anticancer

Res. 1996 May-Jun;16(3A):1095-9.

ɽ Marshall K. Therapeutic applications of whey protein. Altern Med Rev. 2004

Jun;9(2):136-156.

ɽ Micke P, Beeh KM, Buhl R. Effects of long-term supplementation with whey proteins on

plasma glutathione levels of HIV-infected patients. Eur J Nutr. 2002 Feb;41(1):12-8.

ɽ Micke P, Beeh KM, Schlaak JF, Buhl R. Oral supplementation with whey proteins

increases plasma glutathione levels of HIV-infected patients. Eur J Clin Invest. 2001

Feb;31(2):171-8.

ɽ Bounous G, Batist G, Gold P. Immunoenhancing property of dietary whey protein in

mice: role of glutathione. Clin Invest Med. 1989 Jun;12(3):154-61.

ɽ Bounous G, Gervais F, Amer V, Batist G, Gold P. The influence of dietary whey protein

on tissue glutathione and the diseases of aging. Clin Invest Med. 1989 Dec;12(6):343-9.

C a r b B a c k - L o a d i n g

C h a p t e r 2 5

ɽ Bounous G, Baruchel S, Falutz J, Gold P. Whey proteins as a food supplement in HIV-

seropositive individuals. Clin Invest Med. 1993 Jun;16(3):204-9.

ɽ Middleton N, Jelen P, Bell G. Whole blood and mononuclear cell glutathione response to

dietary whey protein supplementation in sedentary and trained male human subjects. Int

J Food Sci Nutr. 2004 Mar;55(2):131-41.

ɽ Stella V, Postaire E. Evaluation of the antiradical protector effect of multifermented milk

serum with reiterated dosage in rats. C R Seances Soc Biol Fil. 1995;189(6):1191-7.

ɽ Bartfay WJ, Davis MT, Medves JM, Lugowski S. Milk whey protein decreases oxygen

free radical production in a murine model of chronic iron-overload cardiomyopathy. Can

J Cardiol. 2003 Sep;19(10):1163-8.

ɽ Bounous G. Whey protein concentrate (WPC) and glutathione modulation in cancer

treatment. Anticancer Res. 2000 Nov-Dec;20(6C):4785-92. Review.

ɽ Mariotti F, Simbelie KL, Makarios-Lahham L, Huneau JF, Laplaize B, Tome D, Even PC.

Acute ingestion of dietary proteins improves post-exercise liver glutathione in rats in a

dose-dependent relationship with their cysteine content. J Nutr. 2004 Jan;134(1):128-31.

ɽ Lyons J, Rauh-Pfeiffer A, Yu YM, Lu XM, Zurakowski D, Tompkins RG, Ajami AM, Young

VR, Castillo L. Blood glutathione synthesis rates in healthy adults receiving a sulfur

amino acid-free diet. Proc Natl Acad Sci U S A. 2000 May 9;97(10):5071-6.-

ɽ Kent KD, Harper WJ, Bomser JA. Effect of whey protein isolate on intracellular

glutathione and oxidant-induced cell death in human prostate epithelial cells. Toxicol In

Vitro. 2003 Feb;17(1):27-33.

Reference 2:

ɽ Bounous G, Molson JH. The antioxidant system. Anticancer Res. 2003 Mar-

Apr;23(2B):1411-5. Review.

Reference 3:

ɽ Chow CK. Nutritional influence on cellular antioxidant defense systems. Am J Clin Nutr.

1979 May;32(5):1066-81. Review.

ɽ Guo Q, Packer L. Ascorbate-dependent recycling of the vitamin E homologue Trolox by

dihydrolipoate and glutathione in murine skin homogenates. Free Radic Biol Med. 2000

Aug;29(3-4):368-74.

ɽ Mendiratta S, Qu ZC, May JM. Enzyme-dependent ascorbate recycling in human

erythrocytes: role of thioredoxin reductase. Free Radic Biol Med. 1998 Jul 15;25(2):221-

8.

ɽ Wilson JX. Antioxidant defense of the brain: a role for astrocytes. Can J Physiol

Pharmacol. 1997 Oct-Nov;75(10-11):1149-63. Review

Reference 4:

ɽ Hidalgo J, Gamper E. Solubility and heat stability of whey protein concentrates. J Dairy

Sci. 1977 Oct;60(10):1515-8.

ɽ Kilshaw PJ, Heppell LM, Ford JE. Effects of heat treatment of cow's milk and whey on

the nutritional quality and antigenic properties. Arch Dis Child. 1982 Nov;57(11):842-7.

ɽ Carbonaro M, Lucarini M, Di Lullo G. Composition and calcium status of acid whey from

pasteurized, UHT-treated and in-bottle sterilized milk. Nahrung. 2000 Dec;44(6):422-5.

ɽ Bos C, Gaudichon C, Tome D. Nutritional and physiological criteria in the assessment of

milk protein quality for humans. J Am Coll Nutr. 2000 Apr;19(2 Suppl):191S-205S.

Review.

ɽ Enomoto A, Konishi M, Hachimura S, Kaminogawa S. Milk whey protein fed as a

constituent of the diet induced both oral tolerance and a systemic humoral response,

2 6 6

S e c t i o n X : R e f e r e n c e s

while heat-denatured whey protein induced only oral tolerance. Clin Immunol

Immunopathol. 1993 Feb;66(2):136-42.

Reference 5:

ɽ Pal S, Ellis V. The acute effects of four protein meals on insulin, glucose, appetite and

energy intake in lean men. Br J Nutr. 2010 Oct;104(8):1241-8.

ɽ Akhavan T, Luhovyy BL, Brown PH, Cho CE, Anderson GH. Effect of premeal

consumption of whey protein and its hydrolysate on food intake and postmeal glycemia

and insulin responses in young adults. Am J Clin Nutr. 2010 Apr;91(4):966-75.

ɽ Bowen J, Noakes M, Clifton PM. Appetite hormones and energy intake in obese men

after consumption of fructose, glucose and whey protein beverages. Int J Obes (Lond).

2007 Nov;31(11):1696-703

ɽ Claessens M, Saris WH, van Baak MA. Glucagon and insulin responses after ingestion of

different amounts of intact and hydrolysed proteins. Br J Nutr. 2008 Jul;100(1):61-9.

Chapter 26

Reference 1:

ɽ Bucci LR, Unlu L. Protein and amino acid supplements in exercise and sport. In: Wolinsky

I, Driskell JA, eds. Energy-yielding macronutrients and energy metabolism in sports

nutrition. Boca Raton, FL: CRC Press, 2000:191–212.

Reference 2:

ɽ FitzGerald RJ, O’Cuinn G. Enzymatic debittering of food protein hydrolysates. Biotechnol

Adv 2006;24:234–7.

Reference 3:

ɽ Koopman R, Wagenmakers AJ, Manders RJ, Zorenc AH, Senden JM, Gorselink M, Keizer

HA, van Loon LJ. Combined ingestion of protein and free leucine with carbohydrate

increases postexercise muscle protein synthesis in vivo in male subjects. Am J Physiol

Endocrinol Metab 2005;288:E645–53.

ɽ Tang JE, Moore DR, Kujbida GW, Tarnopolsky MA, Phillips SM. Ingestion of whey

hydrolysate, casein, or soy protein isolate: effects on mixed muscle protein synthesis at

rest and following resistance exercise in young men. J Appl Physiol. 2009

Sep;107(3):987-92.

ɽ Koopman R, Crombach N, Gijsen AP, Walrand S, Fauquant J, Kies AK, Lemosquet S,

Saris WH, Boirie Y, van Loon LJ. Ingestion of a protein hydrolysate is accompanied by an

accelerated in vivo digestion and absorption rate when compared with its intact protein.

Am J Clin Nutr. 2009 Jul;90(1):106-15.

ɽ Beelen M, Tieland M, Gijsen AP, Vandereyt H, Kies AK, Kuipers H, Saris WH, Koopman

R, van Loon LJ. Coingestion of carbohydrate and protein hydrolysate stimulates muscle

protein synthesis during exercise in young men, with no further increase during

subsequent overnight recovery. J Nutr. 2008 Nov;138(11):2198-204.

ɽ Beelen M, Koopman R, Gijsen AP, Vandereyt H, Kies AK, Kuipers H, Saris WH, van Loon

LJ. Protein coingestion stimulates muscle protein synthesis during resistance-type

exercise. Am J Physiol Endocrinol Metab. 2008 Jul;295(1):E70-7.

ɽ van Loon LJ. Application of protein or protein hydrolysates to improve postexercise

recovery. Int J Sport Nutr Exerc Metab. 2007 Aug;17 Suppl:S104-17. Review.

C a r b B a c k - L o a d i n g

C h a p t e r 2 6

ɽ Koopman R, Pennings B, Zorenc AH, van Loon LJ. Protein ingestion further augments

S6K1 phosphorylation in skeletal muscle following resistance type exercise in males. J

Nutr. 2007 Aug;137(8):1880-6.

Reference 4:

ɽ Demling RH, DeSanti L. Effect of a hypocaloric diet, increased protein intake and

resistance training on lean mass gains and fat mass loss in overweight police officers.

Ann Nutr Metab. 2000;44(1):21-9.

Reference 5:

ɽ Kaastra B, Manders RJ, Van Breda E, Kies A, Jeukendrup AE, Keizer HA, Kuipers H, Van

Loon LJ. Effects of increasing insulin secretion on acute postexercise blood glucose

disposal. Med Sci Sports Exerc 2006;38:268–75.

ɽ Manders RJ, Koopman R, Sluijsmans WE, van den Berg R, Verbeek K, Saris WH,

Wagenmakers AJ, van Loon LJ. Co-ingestion of a protein hydrolysate with or without

additional leucine effectively reduces postprandial blood glucose excursions in Type 2

diabetic men. J Nutr 2006;136:1294–9.

ɽ Calbet JA, MacLean DA. Plasma glucagon and insulin responses depend on the rate of

appearance of amino acids after ingestion of different protein solutions in humans. J Nutr

2002;132:2174–82.

ɽ Calbet JA, Holst JJ. Gastric emptying, gastric secretion and enterogastrone response

after administration of milk proteins or their peptide hydrolysates in humans. Eur J Nutr

2004;43:127–39.

ɽ Ivy JL, Goforth HW Jr, Damon BM, McCauley TR, Parsons EC, Price TB. Early

postexercise muscle glycogen recovery is enhanced with a carbohydrate-protein

supplement. J Appl Physiol 2002;93:1337–44.

ɽ Zawadzki KM, Yaspelkis BB III, Ivy JL. Carbohydrate-protein complex increases the rate

of muscle glycogen storage after exercise. J Appl Physiol 1992;72:1854–1859.

ɽ Berardi JM, Price TB, Noreen EE, Lemon PW. Postexercise muscle glycogen recovery

enhanced with a carbohydrate-protein supplement. Med Sci Sports Exerc. 2006

Jun;38(6):1106-13.

Reference 6:

ɽ Bucci LR, Unlu L. Protein and amino acid supplements in exercise and sport. In: Wolinsky

I, Driskell JA, eds. Energy-yielding macronutrients and energy metabolism in sports

nutrition. Boca Raton, FL: CRC Press, 2000:191–212.

ɽ FitzGerald RJ, O’Cuinn G. Enzymatic debittering of food protein hydrolysates. Biotechnol

Adv 2006;24:234–7.

ɽ Pasquale MG. Protein foods vs. protein and amino acid supplements. In: Amino acids

and proteins for the athlete: the anabolic edge. Boca Raton, FL: CRC Press, 1997:89–98.

ɽ Manninen AH. Protein hydrolysates in sports and exercise: a brief review. J Sports Med

Sci 2004;3:60–63.

Reference 7:

ɽ Morifuji M, Koga J, Kawanaka K, Higuchi M. Branched-chain amino acid-containing

dipeptides, identified from whey protein hydrolysates, stimulate glucose uptake rate in L6

myotubes and isolated skeletal muscles. J Nutr Sci Vitaminol (Tokyo). 2009 Feb;55(1):81-

6.

2 6 8

S e c t i o n X : R e f e r e n c e s

Chapter 27

Reference 1:

ɽ Wackerhage H, Ratkevicius A. Signal transduction pathways that regulate muscle growth.

Essays Biochem. 2008;44:99-108. Review.

Reference 2:

ɽ Rivas DA, Lessard SJ, Coffey VG. mTOR function in skeletal muscle: a focal point for

overnutrition and exercise. Appl Physiol Nutr Metab. 2009 Oct;34(5):807-16. Review.

ɽ Matsakas A, Patel K. Intracellular signalling pathways regulating the adaptation of skeletal

muscle to exercise and nutritional changes. Histol Histopathol. 2009 Feb;24(2):209-22.

Review.

ɽ Rennie MJ. Exercise- and nutrient-controlled mechanisms involved in maintenance of the

musculoskeletal mass. Biochem Soc Trans. 2007 Nov;35(Pt 5):1302-5. Review.

ɽ Vary TC, Lynch CJ. Nutrient signaling components controlling protein synthesis in

striated muscle. J Nutr. 2007 Aug;137(8):1835-43. Review.

ɽ Fujita S, Dreyer HC, Drummond MJ, Glynn EL, Cadenas JG, Yoshizawa F, Volpi E,

Rasmussen BB. Nutrient signalling in the regulation of human muscle protein synthesis. J

Physiol. 2007 Jul 15;582(Pt 2):813-23.

ɽ Kimball SR, Jefferson LS. New functions for amino acids: effects on gene transcription

and translation. Am J Clin Nutr. 2006 Feb;83(2):500S-507S. Review.

ɽ Kimball SR, Jefferson LS. Signaling pathways and molecular mechanisms through which

branched-chain amino acids mediate translational control of protein synthesis. J Nutr.

2006 Jan;136(1 Suppl):227S-31S. Review.

ɽ Hay N, Sonenberg N. Upstream and downstream of mTOR. Genes Dev. 2004 Aug

15;18(16):1926-45. Review.

Reference 3:

ɽ Borgenvik M, Apro W, Blomstrand E. Intake of Branched-Chain Amino Acids Influences

the Levels of MAFbx mRNA and MuRF-1 Total Protein in Resting and Exercising Human

Muscle. Am J Physiol Endocrinol Metab. 2011 Nov 29.

ɽ Pasiakos SM, McClung HL, McClung JP, Margolis LM, Andersen NE, Cloutier GJ,

Pikosky MA, Rood JC, Fielding RA, Young AJ. Leucine-enriched essential amino acid

supplementation during moderate steady state exercise enhances postexercise muscle

protein synthesis. Am J Clin Nutr. 2011 Sep;94(3):809-18.

ɽ Nelson AR, Phillips SM, Stellingwerff T, Rezzi S, Bruce SJ, Breton I, Thorimbert A, Guy

PA, Clarke J, Broadbent S, Rowlands DS. A Protein-Leucine Supplement Increases

BCAA and Nitrogen Turnover but not Performance. Med Sci Sports Exerc. 2011 Jun 16.

ɽ Coffey VG, Moore DR, Burd NA, Rerecich T, Stellingwerff T, Garnham AP, Phillips SM,

Hawley JA. Nutrient provision increases signalling and protein synthesis in human

skeletal muscle after repeated sprints. Eur J Appl Physiol. 2011 Jul;111(7):1473-83.

ɽ Apró W, Blomstrand E. Influence of supplementation with branched-chain amino acids in

combination with resistance exercise on p70S6 kinase phosphorylation in resting and

exercising human skeletal muscle. Acta Physiol (Oxf). 2010 Nov;200(3):237-48.

ɽ Drummond MJ, Rasmussen BB. Leucine-enriched nutrients and the regulation of

mammalian target of rapamycin signalling and human skeletal muscle protein synthesis.

Curr Opin Clin Nutr Metab Care. 2008 May;11(3):222-6. Review.

ɽ Dreyer HC, Drummond MJ, Pennings B, Fujita S, Glynn EL, Chinkes DL, Dhanani S, Volpi

E, Rasmussen BB. Leucine-enriched essential amino acid and carbohydrate ingestion

following resistance exercise enhances mTOR signaling and protein synthesis in human

muscle. Am J Physiol Endocrinol Metab. 2008 Feb;294(2):E392-400.

C a r b B a c k - L o a d i n g

C h a p t e r 2 8

ɽ Norton LE, Layman DK. Leucine regulates translation initiation of protein synthesis in

skeletal muscle after exercise. J Nutr. 2006 Feb;136(2):533S-537S.

ɽ Blomstrand E, Eliasson J, Karlsson HK, Köhnke R. Branched-chain amino acids activate

key enzymes in protein synthesis after physical exercise. J Nutr. 2006 Jan;136(1

Suppl):269S-73S. Review.

ɽ Rennie MJ, Bohé J, Smith K, Wackerhage H, Greenhaff P. Branched-chain amino acids

as fuels and anabolic signals in human muscle. J Nutr. 2006 Jan;136(1 Suppl):264S-8S.

Review.

ɽ Garlick PJ. The role of leucine in the regulation of protein metabolism. J Nutr. 2005

Jun;135(6 Suppl):1553S-6S. Review.

ɽ Karlsson HK, Nilsson PA, Nilsson J, Chibalin AV, Zierath JR, Blomstrand E. Branched-

chain amino acids increase p70S6k phosphorylation in human skeletal muscle after

resistance exercise. Am J Physiol Endocrinol Metab. 2004 Jul;287(1):E1-7.

ɽ Nishitani S, Ijichi C, Takehana K, Fujitani S, Sonaka I. Pharmacological activities of

branched-chain amino acids: specificity of tissue and signal transduction. Biochem

Biophys Res Commun. 2004 Jan 9;313(2):387-9. Review.

ɽ Nair KS, Schwartz RG, Welle S. Leucine as a regulator of whole body and skeletal muscle

protein metabolism in humans. Am J Physiol. 1992 Nov;263(5 Pt 1):E928-34.

Reference 4:

ɽ Matschinsky FM, Ellerman J, Stillings S, et al. Hexones and insulin secretion. In:

Hasselblatt A, Bruchhausen FV, eds. Handbook of experimental pharmacology. Berlin:

Springer-Verlag, 1975:79–114.

Reference 5:

ɽ Pencharz PB, Elango R, Ball RO. An approach to defining the upper safe limits of amino

acid intake. J Nutr. 2008 Oct;138(10):1996S-2002S.

ɽ Cook NE, Carpenter KJ. Leucine excess and niacin status in rats. J Nutr. 1987

Mar;117(3):519-26.

ɽ Meguid MM, Matthews DE, Bier DM, Meredith CN, Soeldner JS, Young VR. Leucine

kinetics at graded leucine intakes in young men. Am J Clin Nutr. 1986 May;43(5):770-80.

Chapter 28

Reference 1:

ɽ Czok G. Metabolic effect of coffee and caffeine. Z Ernahrungswiss. 1976 Mar;15(1):109-

12.

ɽ Ratzmann KP, Riemer D, Mannchen E, Paul I. Lipid mobilization in obesity without

carbohydrate

intolerance.

2.

Caffeine-stimulated

lipolysis.

Endokrinologie.

1976;68(3):319-26.

ɽ Goldrick RB, McLoughlin GM. Lipolysis and lipogenesis from glucose in human fat cells

of different sizes. Effects of insulin, epinephrine, and theophylline. J Clin Invest. 1970

Jun;49(6):1213-23.

ɽ Burns TW, Terry BE, Langley PE, Robison GA. Insulin inhibition of lipolysis of human

adipocytes: the role of cyclic adenosine monophosphate. Diabetes. 1979

Nov;28(11):957-61.

ɽ Erickson MA, Schwarzkopf RJ, McKenzie RD. Effects of caffeine, fructose, and glucose

ingestion on muscle glycogen utilization during exercise. Med Sci Sports Exerc. 1987

Dec;19(6):579-83.

2 7 0

S e c t i o n X : R e f e r e n c e s

ɽ Ryu S, Choi SK, Joung SS, Suh H, Cha YS, Lee S, Lim K. Caffeine as a lipolytic food

component increases endurance performance in rats and athletes. J Nutr Sci Vitaminol

(Tokyo). 2001 Apr;47(2):139-46. 88.

ɽ Fredholm BB. Astra Award Lecture. Adenosine, adenosine receptors and the actions of

caffeine. Pharmacol Toxicol. 1995 Feb;76(2):93-101. Review.

Reference 2:

ɽ Mumford GK, Evans SM, Kaminski BJ, Preston KL, Sannerud CA, Silverman K, Griffiths

RR. Discriminative stimulus and subjective effects of theobromine and caffeine in

humans. Psychopharmacology (Berl). 1994 Jun;115(1-2):1-8.

ɽ Yu G, Maskray V, Jackson SH, Swift CG, Tiplady B. A comparison of the central nervous

system effects of caffeine and theophylline in elderly subjects. Br J Clin Pharmacol. 1991

Sep;32(3):341-5.

Reference 3:

ɽ Arnaud MJ. The pharmacology of caffeine. Prog Drug Res. 1987;31:273-313. Review.

ɽ Blanchard J, Sawers SJ. Comparative pharmacokinetics of caffeine in young and elderly

men. J Pharmacokinet Biopharm. 1983 Apr;11(2):109-26.

Reference 4:

ɽ Tse SY. Coffee contains cholinomimetic compound distinct from caffeine. I: Purification

and chromatographic analysis. J Pharm Sci. 1991 Jul;80(7):665-9.

ɽ Tse SY. Cholinomimetic compound distinct from caffeine contained in coffee. II:

Muscarinic actions. J Pharm Sci. 1992 May;81(5):449-52.

Reference 5:

ɽ Petrie HJ, Chown SE, Belfie LM, Duncan AM, McLaren DH, Conquer JA, Graham TE.

Caffeine ingestion increases the insulin response to an oral-glucose-tolerance test in

obese men before and after weight loss. Am J Clin Nutr. 2004 Jul;80(1):22-8.

ɽ Keijzers GB, De Galan BE, Tack CJ, Smits P. Caffeine can decrease insulin sensitivity in

humans. Diabetes Care. 2002 Feb;25(2):364-9.

ɽ Greer F, Hudson R, Ross R, Graham T. Caffeine ingestion decreases glucose disposal

during a hyperinsulinemic-euglycemic clamp in sedentary humans. Diabetes. 2001

Oct;50(10):2349-54.

ɽ Graham TE, Sathasivam P, Rowland M, Marko N, Greer F, Battram D. Caffeine ingestion

elevates plasma insulin response in humans during an oral glucose tolerance test. Can J

Physiol Pharmacol. 2001 Jul;79(7):559-65.

ɽ Thong FS, Graham TE. Caffeine-induced impairment of glucose tolerance is abolished by

beta-adrenergic receptor blockade in humans. J Appl Physiol. 2002 Jun;92(6):2347-52.

ɽ Thong FS, Derave W, Kiens B, Graham TE, Urso B, Wojtaszewski JF, Hansen BF, Richter

EA. Caffeine-induced impairment of insulin action but not insulin signaling in human

skeletal muscle is reduced by exercise. Diabetes. 2002 Mar;51(3):583-90.

ɽ Robinson LE, Savani S, Battram DS, McLaren DH, Sathasivam P, Graham TE. Caffeine

ingestion before an oral glucose tolerance test impairs blood glucose management in

men with type 2 diabetes. J Nutr. 2004 Oct;134(10):2528-33.

ɽ Johnston KL, Clifford MN, Morgan LM. Coffee acutely modifies gastrointestinal hormone

secretion and glucose tolerance in humans: glycemic effects of chlorogenic acid and

caffeine. Am J Clin Nutr. 2003 Oct;78(4):728-33.

ɽ Sachs M, Forster H. Effect of caffeine on various metabolic parameters in vivo. Z

Ernahrungswiss. 1984 Sep;23(3):181-205.

C a r b B a c k - L o a d i n g

C h a p t e r 2 8

Reference 6:

ɽ Pedersen DJ, Lessard SJ, Coffey VG, Churchley EG, Wootton AM, Ng T, Watt MJ,

Hawley JA. High rates of muscle glycogen resynthesis after exhaustive exercise when

carbohydrate is coingested with caffeine. J Appl Physiol. 2008 Jul;105(1):7-13.

ɽ Battram DS, Shearer J, Robinson D, Graham TE. Caffeine ingestion does not impede the

resynthesis of proglycogen and macroglycogen after prolonged exercise and

carbohydrate supplementation in humans. J Appl Physiol. 2004 Mar;96(3):943-50.

ɽ Beelen M, Kranenburg JV, Senden JM, Kuipers H, van Loon LJ. Impact of Caffeine and

Protein on Post-Exercise Muscle Glycogen Synthesis. Med Sci Sports Exerc. 2011 Oct 7.

[Epub ahead of print]

Reference 7:

ɽ Johnston KL, Clifford MN, Morgan LM. Coffee acutely modifies gastrointestinal hormone

secretion and glucose tolerance in humans: glycemic effects of chlorogenic acid and

caffeine. Am J Clin Nutr. 2003 Oct;78(4):728-33.

Reference 8:

ɽ Petrie HJ, Chown SE, Belfie LM, Duncan AM, McLaren DH, Conquer JA, Graham TE.

Caffeine ingestion increases the insulin response to an oral-glucose-tolerance test in

obese men before and after weight loss. Am J Clin Nutr. 2004 Jul;80(1):22-8.

ɽ Singh SP, Patel DG, Snyder AK, Pullen GL. Ethanol influence on insulin secretion from

isolated rat islets. Experientia. 1986 Jan 15;42(1):58-60.

ɽ Brand-Miller J, Holt SH, de Jong V, Petocz P. Cocoa powder increases postprandial

insulinemia in lean young adults. J Nutr. 2003 Oct;133(10):3149-52.

ɽ Squires PE, Hills CE, Rogers GJ, Garland P, Farley SR, Morgan NG. The putative

imidazoline receptor agonist, harmane, promotes intracellular calcium mobilisation in

pancreatic beta-cells. Eur J Pharmacol. 2004 Oct 6;501(1-3):31-39.

ɽ Dyachok O, Gylfe E. Ca2+-induced Ca2+ release via inositol 1,4,5-trisphosphate

receptors is amplified by protein kinase A and triggers exocytosis in pancreatic Beta-

cells. J Biol Chem. 2004 Aug 16 [Epub ahead of print]

ɽ Bruton JD, Lemmens R, Shi CL, Persson-Sjogren S, Westerblad H, Ahmed M, Pyne NJ,

Frame M, Furman BL, Islam MS. Ryanodine receptors of pancreatic beta-cells mediate a

distinct context-dependent signal for insulin secretion. FASEB J. 2003 Feb;17(2):301-3.

Varadi A, Rutter GA. Dynamic imaging of endoplasmic reticulum Ca2+ concentration in

insulin-secreting MIN6 Cells using recombinant targeted cameleons: roles of

sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)-2 and ryanodine receptors.

Diabetes. 2002 Feb;51 Suppl 1:S190-201.

ɽ Bosqueiro JR, Carneiro EM, Bordin S, Boschero AC. Tetracaine stimulates insulin

secretion through the mobilization of Ca2+ from thapsigargin- and IP3-insensitive Ca2+

reservoir in pancreatic beta-cells. Can J Physiol Pharmacol. 2000 Jun;78(6):462-8.

ɽ Holz GG, Leech CA, Heller RS, Castonguay M, Habener JF. cAMP-dependent

mobilization of intracellular Ca2+ stores by activation of ryanodine receptors in pancreatic

beta-cells. A Ca2+ signaling system stimulated by the insulinotropic hormone glucagon-

like peptide-1-(7-37). J Biol Chem. 1999 May 14;274(20):14147-56.

ɽ Islam MS, Leibiger I, Leibiger B, Rossi D, Sorrentino V, Ekstrom TJ, Westerblad H,

Andrade FH, Berggren PO. In situ activation of the type 2 ryanodine receptor in

pancreatic beta cells requires cAMP-dependent phosphorylation. Proc Natl Acad Sci U S

A. 1998 May 26;95(11):6145-50.

2 7 2

S e c t i o n X : R e f e r e n c e s

Reference 9:

ɽ Battram DS, Arthur R, Weekes A, Graham TE. The glucose intolerance induced by

caffeinated coffee ingestion is less pronounced than that due to alkaloid caffeine in men.

J Nutr. 2006 May;136(5):1276-80.

Reference 10:

ɽ Brice CF, Smith AP. Effects of caffeine on mood and performance: a study of realistic

consumption. Psychopharmacology (Berl). 2002 Nov;164(2):188-92.

ɽ Greden JF. Anxiety or caffeinism: a diagnostic dilemma. Am J Psychiatry. 1974

Oct;131(10):1089-92.

ɽ Stern KN, Chait LD, Johanson CE. Reinforcing and subjective effects of caffeine in

normal human volunteers. Psychopharmacology (Berl). 1989;98(1):81-8.

ɽ Eaton WW, McLeod J. Consumption of coffee or tea and symptoms of anxiety. Am J

Public Health. 1984 Jan;74(1):66-8.

ɽ Lee MA, Cameron OG, Greden JF. Anxiety and caffeine consumption in people with

anxiety disorders. Psychiatry Res. 1985 Jul;15(3):211-7.

ɽ Rihs M, Muller C, Baumann P. Caffeine consumption in hospitalized psychiatric patients.

Eur Arch Psychiatry Clin Neurosci. 1996;246(2):83-92.

Chapter 29

Reference 1:

ɽ Wilkie DR. Muscular fatigue: effects of hydrogen ions and inorganic phosphate. Fed Proc.

1986 Dec;45(13):2921-3. Review.

ɽ Parkhouse WS, McKenzie DC. Possible contribution of skeletal muscle buffers to

enhanced anaerobic performance: a brief review. Med Sci Sports Exerc. 1984

Aug;16(4):328-38. Review.

ɽ Howald H, Decombaz J. Nutrient intake and energy regulation in physical exercise.

Experientia Suppl. 1983;44:77-88. Review.

Reference 2:

ɽ Bangsbo J, Madsen K, Kiens B, Richter EA. Effect of muscle acidity on muscle

metabolism and fatigue during intense exercise in man. J Physiol. 1996 Sep 1;495 ( Pt

2):587-96.

Reference 3:

ɽ Hespel P, Derave W. Ergogenic effects of creatine in sports and rehabilitation. Subcell

Biochem. 2007;46:245-59. Review.

Reference 4:

ɽ Deldicque L, Atherton P, Patel R, Theisen D, Nielens H, Rennie MJ, Francaux M. Effects

of resistance exercise with and without creatine supplementation on gene expression and

cell signaling in human skeletal muscle. J Appl Physiol. 2008 Feb;104(2):371-8.

ɽ Johnston AP, Burke DG, MacNeil LG, Candow DG. Effect of creatine supplementation

during cast-induced immobilization on the preservation of muscle mass, strength, and

endurance. J Strength Cond Res. 2009 Jan;23(1):116-20.

C a r b B a c k - L o a d i n g

C h a p t e r 2 9

Reference 5:

ɽ Rebbapragada A, Benchabane H, Wrana JL, Celeste AJ, Attisano L. Myostatin signals

through a transforming growth factor beta-like signaling pathway to block adipogenesis.

Mol Cell Biol. 2003 Oct;23(20):7230-42.

ɽ McMahon CD, Popovic L, Jeanplong F, Oldham JM, Kirk SP, Osepchook CC, Wong KW,

Sharma M, Kambadur R, Bass JJ. Sexual dimorphism is associated with decreased

expression of processed myostatin in males. Am J Physiol Endocrinol Metab. 2003

Feb;284(2):E377-81.

ɽ Lin J, Della-Fera MA, Li C, Page K, Choi YH, Hartzell DL, Baile CA. P27 knockout mice:

reduced myostatin in muscle and altered adipogenesis. Biochem Biophys Res Commun.

2003 Jan 24;300(4):938-42.

ɽ Langley B, Thomas M, Bishop A, Sharma M, Gilmour S, Kambadur R. Myostatin inhibits

myoblast differentiation by down-regulating MyoD expression. J Biol Chem. 2002 Dec

20;277(51):49831-40.

ɽ Lin J, Arnold HB, Della-Fera MA, Azain MJ, Hartzell DL, Baile CA. Myostatin knockout in

mice increases myogenesis and decreases adipogenesis. Biochem Biophys Res

Commun. 2002 Mar 1;291(3):701-6.

ɽ Lee SJ, McPherron AC. Regulation of myostatin activity and muscle growth. Proc Natl

Acad Sci U S A. 2001 Jul 31;98(16):9306-11.

ɽ Zhu X, Hadhazy M, Wehling M, Tidball JG, McNally EM. Dominant negative myostatin

produces hypertrophy without hyperplasia in muscle. FEBS Lett. 2000 May 26;474(1):71-

5.

ɽ McPherron AC, Lee SJ. Double muscling in cattle due to mutations in the myostatin

gene. Proc Natl Acad Sci U S A. 1997 Nov 11;94(23):12457-61.

ɽ McPherron AC, Lee SJ. Suppression of body fat accumulation in myostatin-deficient

mice. J Clin Invest. 2002 Mar;109(5):595-601.

ɽ Reisz-Porszasz S, Bhasin S, Artaza JN, Shen R, Sinha-Hikim I, Hogue A, Fielder TJ,

Gonzalez-Cadavid NF. Lower skeletal muscle mass in male transgenic mice with

muscle-specific overexpression of myostatin. Am J Physiol Endocrinol Metab. 2003

Oct;285(4):E876-88.

ɽ McCroskery S, Thomas M, Maxwell L, Sharma M, Kambadur R. Myostatin negatively

regulates satellite cell activation and self-renewal. J Cell Biol. 2003 Sep 15;162(6):1135-

47.

ɽ Joulia D, Bernardi H, Garandel V, Rabenoelina F, Vernus B, Cabello G. Mechanisms

involved in the inhibition of myoblast proliferation and differentiation by myostatin. Exp

Cell Res. 2003 Jun 10;286(2):263-75.

ɽ Zimmers TA, Davies MV, Koniaris LG, Haynes P, Esquela AF, Tomkinson KN, McPherron

AC, Wolfman NM, Lee SJ. Induction of cachexia in mice by systemically administered

myostatin. Science. 2002 May 24;296(5572):1486-8.

ɽ Rios R, Carneiro I, Arce VM, Devesa J. Myostatin is an inhibitor of myogenic

differentiation. Am J Physiol Cell Physiol. 2002 May;282(5):C993-9.

ɽ Reardon KA, Davis J, Kapsa RM, Choong P, Byrne E. Myostatin, insulin-like growth

factor-1, and leukemia inhibitory factor mRNAs are upregulated in chronic human disuse

muscle atrophy. Muscle Nerve. 2001 Jul;24(7):893-9.

ɽ Taylor WE, Bhasin S, Artaza J, Byhower F, Azam M, Willard DH Jr, Kull FC Jr, Gonzalez-

Cadavid N. Myostatin inhibits cell proliferation and protein synthesis in C2C12 muscle

cells. Am J Physiol Endocrinol Metab. 2001 Feb;280(2):E221-8.

ɽ Thomas M, Langley B, Berry C, Sharma M, Kirk S, Bass J, Kambadur R. Myostatin, a

negative regulator of muscle growth, functions by inhibiting myoblast proliferation. J Biol

Chem. 2000 Dec 22;275(51):40235-43.

ɽ Kirk S, Oldham J, Kambadur R, Sharma M, Dobbie P, Bass J. Myostatin regulation

during skeletal muscle regeneration. J Cell Physiol. 2000 Sep;184(3):356-63.

2 7 4

S e c t i o n X : R e f e r e n c e s

Reference 6:

ɽ Lee SJ, McPherron AC. Regulation of myostatin activity and muscle growth. Proc Natl

Acad Sci U S A. 2001 Jul 31;98(16):9306-11

Reference 7:

ɽ van Loon LJ, Murphy R, Oosterlaar AM, Cameron-Smith D, Hargreaves M, Wagenmakers

AJ, Snow R. Creatine supplementation increases glycogen storage but not GLUT-4

expression in human skeletal muscle. Clin Sci (Lond). 2004 Jan;106(1):99-106.

ɽ Derave W, Eijnde BO, Verbessem P, Ramaekers M, Van Leemputte M, Richter EA, Hespel

P. Combined creatine and protein supplementation in conjunction with resistance training

promotes muscle GLUT-4 content and glucose tolerance in humans. J Appl Physiol. 2003

May;94(5):1910-6.

ɽ Op 't Eijnde B, Ursø B, Richter EA, Greenhaff PL, Hespel P. Effect of oral creatine

supplementation on human muscle GLUT4 protein content after immobilization. Diabetes.

2001 Jan;50(1):18-23.

Chapter 30

Reference 1:

ɽ Landers P, Wolfe MM, Glore S, Guild R, Phillips L. Effect of weight loss plans on body

composition and diet duration. J Okla State Med Assoc. 2002 May;95(5):329-31.

Chapter 32

Reference 1:

ɽ Schrauwen P, van Marken Lichtenbelt WD, Saris WH, Westerterp KR. Changes in fat

oxidation in response to a high-fat diet. Am J Clin Nutr. 1997 Aug;66(2):276-82.

ɽ Benoit FL, Martin RL, Watten RH. Changes in body composition during weight reduction

in obesity: balance studies comparing effects of fasting and a ketogenic diet. Ann Int

Med. 1965;63(4);604-612.

Reference 2:

ɽ Chan ST, Johnson AW, Moore MH, Kapadia CR, Dudley HA. Early weight gain and

glycogen-obligated water during nutritional rehabilitation. Hum Nutr Clin Nutr.

1982;36(3):223-32.

Reference 3:

ɽ Yang MU, Van Itallie TB. Composition of weight lost during short-term weight reduction.

Metabolic responses of obese subjects to starvation and low-calorie ketogenic and

nonketogenic diets. J Clin Invest. 1976 Sep;58(3):722-30.

Reference 4:

ɽ Wirrell EC, Darwish HZ, Williams-Dyjur C, Blackman M, Lange V. Is a fast necessary

when initiating the ketogenic diet? J Child Neurol. 2002 Mar;17(3):179-82.

ɽ Keckwick A, Pawan GL. Metabolic study in human obesity with isocaloric diets high in

fat, protein or carbohydrate. Metabolism. 1957 Sep;6(5):447-60.

C a r b B a c k - L o a d i n g

C h a p t e r 3 2

Reference 5:

ɽ Klepper J, Voit T. Facilitated glucose transporter protein type 1 (GLUT1) deficiency

syndrome: impaired glucose transport into brain-- a review. Eur J Pediatr. 2002

Jun;161(6):295-304. Review.

ɽ De Vivo DC, Leary L, Wang D. Glucose transporter 1 deficiency syndrome and other

glycolytic defects. J Child Neurol. 2002 Dec;17 Suppl 3:3S15-23; discussion 3S24-5.

Review.

ɽ Nehlig A. Brain uptake and metabolism of ketone bodies in animal models.

Prostaglandins Leukot Essent Fatty Acids. 2004 Mar;70(3):265-75.

ɽ Hasselbalch SG, Knudsen GM, Jakobsen J, Hageman LP, Holm S, Paulson OB. Blood-

brain barrier permeability of glucose and ketone bodies during short-term starvation in

humans. Am J Physiol. 1995 Jun;268(6 Pt 1):E1161-6.

ɽ Gjedde A, Crone C. Induction processes in blood-brain transfer of ketone bodies during

starvation. Am J Physiol. 1975 Nov;229(5):1165-9.

ɽ Pollay M, Stevens FA. Starvation-induced changes in transport of ketone bodies across

the blood-brain barrier. J Neurosci Res. 1980;5(2):163-72.

Reference 6:

ɽ Hasselbalch SG, Knudsen GM, Jakobsen J, Hageman LP, Holm S, Paulson OB. Brain

metabolism during short-term starvation in humans. J Cereb Blood Flow Metab. 1994

Jan;14(1):125-31.

Reference 7:

ɽ Schrauwen P, van Marken Lichtenbelt WD, Saris WH, Westerterp KR. Role of glycogen-

lowering exercise in the change of fat oxidation in response to a high-fat diet. Am J

Physiol. 1997 Sep;273(3 Pt 1):E623-9.

ɽ Thomas CD, Peters JC, Reed GW, Abumrad NN, Sun M, Hill JO. Nutrient balance and

energy expenditure during ad libitum feeding of high-fat and high-carbohydrate diets in

humans. Am J Clin Nutr. 1992 May;55(5):934-42.

ɽ Schrauwen P, Lichtenbelt WD, Saris WH, Westerterp KR. Fat balance in obese subjects:

role of glycogen stores. Am J Physiol. 1998 Jun;274(6 Pt 1):E1027-33.

ɽ Smith SR, de Jonge L, Zachwieja JJ, Roy H, Nguyen T, Rood J, Windhauser M,

Volaufova J, Bray GA. Concurrent physical activity increases fat oxidation during the shift

to a high-fat diet. Am J Clin Nutr. 2000 Jul;72(1):131-8.

Reference 8:

ɽ Fery F, Balasse EO. Ketone body production and disposal in diabetic ketosis. A

comparison with fasting ketosis. Diabetes. 1985 Apr;34(4):326-32.

ɽ Koeslag JH, Noakes TD, Sloan AW. The effects of alanine, glucose and starch ingestion

on the ketosis produced by exercise and by starvation. J Physiol. 1982 Apr;325:363-76.

ɽ Fery F, Balasse EO. Ketone body turnover during and after exercise in overnight-fasted

and starved humans. Am J Physiol. 1983 Oct;245(4):E318-25.

ɽ Bougneres PF, Ferre P. Study of ketone body kinetics in children by a combined

perfusion of 13C and 2H3 tracers. Am J Physiol. 1987 Nov;253(5 Pt 1):E496-502.

ɽ Reichard GA Jr, Owen OE, Haff AC, Paul P, Bortz WM. Ketone-body production and

oxidation in fasting obese humans. J Clin Invest. 1974 Feb;53(2):508-15.

ɽ Koeslag JH. Post-exercise ketosis and the hormone response to exercise: a review.

Med Sci Sports Exerc. 1982;14(5):327-34. Review.

ɽ Fery F, Balasse EO. Response of ketone body metabolism to exercise during transition

from postabsorptive to fasted state. Am J Physiol. 1986 May;250(5 Pt 1):E495-501.

2 7 6

S e c t i o n X : R e f e r e n c e s

ɽ Wahren J, Hagenfeldt L. Free fatty acid and ketone body metabolism during exercise in

diabetes. Acta Paediatr Scand Suppl. 1980;283:39-44.

ɽ Fery F, Bourdoux P, Christophe J, Balasse EO. Hormonal and metabolic changes

induced by an isocaloric isoproteinic ketogenic diet in healthy subjects. Diabete Metab.

1982 Dec;8(4):299-305.

Reference 9:

ɽ VanItallie TB, Nufert TH. Ketones: metabolism's ugly duckling. Nutr Rev. 2003

Oct;61(10):327-41. Review.

Chapter 33

Reference 1:

ɽ Miles JM, Haymond MW, Gerich JE. Suppression of glucose production and stimulation

of insulin secretion by physiological concentrations of ketone bodies in man. J Clin

Endocrinol Metab. 1981 Jan;52(1):34-7.

ɽ Murdock DJ, Clarke J, Flatt PR, Barnett YA, Barnett CR. Role of CYP2E1 in ketone-

stimulated insulin release in pancreatic B-cells. Biochem Pharmacol. 2004 Mar

1;67(5):875-84.

ɽ Miles JM, Haymond MW, Gerich JE. Effects of free fatty acids, insulin, glucagon and

adrenaline on ketone body production in humans. Ciba Found Symp. 1982;87:192-213.

-5-29-

ɽ Schade DS, Eaton RP. The regulation of plasma ketone body concentration by

counterregulatory hormones in man. Diabetes. 1977 Oct;26(10):989-96.

ɽ Soeters MR, Sauerwein HP, Faas L, Smeenge M, Duran M, Wanders RJ, Ruiter AF,

Ackermans MT, Fliers E, Houten SM, Serlie MJ. Effects of insulin on ketogenesis

following fasting in lean and obese men. Obesity (Silver Spring). 2009 Jul;17(7):1326-31.

ɽ Fukao T, Lopaschuk GD, Mitchell GA. Pathways and control of ketone body metabolism:

on the fringe of lipid biochemistry. Prostaglandins Leukot Essent Fatty Acids. 2004

Mar;70(3):243-51. Review.

ɽ Beylot M. Regulation of in vivo ketogenesis: role of free fatty acids and control by

epinephrine, thyroid hormones, insulin and glucagon. Diabetes Metab. 1996

Oct;22(5):299-304. Review.

Reference 2:

ɽ Malaisse WJ, Vanonderbergen A, Louchami K, Jijakli H, Malaisse-Lagae F. Effects of

artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets. Cell

Signal. 1998 Nov;10(10):727-33.

ɽ Liang Y, Maier V, Steinbach G, Lalic L, Pfeiffer EF. The effect of artificial sweetener on

insulin secretion. II. Stimulation of insulin release from isolated rat islets by Acesulfame K

(in vitro experiments). Horm Metab Res. 1987 Jul;19(7):285-9.

ɽ Liang Y, Steinbach G, Maier V, Pfeiffer EF. The effect of artificial sweetener on insulin

secretion. 1. The effect of acesulfame K on insulin secretion in the rat (studies in vivo).

Horm Metab Res. 1987 Jun;19(6):233-8.

Reference 3:

ɽ Pal S, Ellis V. The acute effects of four protein meals on insulin, glucose, appetite and

energy intake in lean men. Br J Nutr. 2010 Oct;104(8):1241-8.

C a r b B a c k - L o a d i n g

C h a p t e r 3 4

ɽ Akhavan T, Luhovyy BL, Brown PH, Cho CE, Anderson GH. Effect of premeal

consumption of whey protein and its hydrolysate on food intake and postmeal glycemia

and insulin responses in young adults. Am J Clin Nutr. 2010 Apr;91(4):966-75.

ɽ Bowen J, Noakes M, Clifton PM. Appetite hormones and energy intake in obese men

after consumption of fructose, glucose and whey protein beverages. Int J Obes (Lond).

2007 Nov;31(11):1696-703.

Reference 4:

ɽ Bahnsen M, Burrin JM, Johnston DG, Pernet A, Walker M, Alberti KG. Mechanisms of

catecholamine effects on ketogenesis. Am J Physiol. 1984 Aug;247(2 Pt 1):E173-80.

Review.

ɽ Williamson DH, Whitelaw E. Physiological aspects of the regulation of ketogenesis.

Biochem Soc Symp. 1978(43):137-61.

ɽ Keller U, Gerber PP, Stauffacher W. Stimulatory effect of norepinephrine on ketogenesis

in normal and insulin-deficient humans. Am J Physiol. 1984 Dec;247(6 Pt 1):E732-9.

ɽ Weiss M, Keller U, Stauffacher W. Effect of epinephrine and somatostatin-induced insulin

deficiency on ketone body kinetics and lipolysis in man. Diabetes. 1984 Aug;33(8):738-

44.12-

ɽ Keller U, Gerber PP, Stauffacher W. Fatty acid-independent inhibition of hepatic ketone

body production by insulin in humans. Am J Physiol. 1988 Jun;254(6 Pt 1):E694-9.

ɽ Gerich JE, Lorenzi M, Bier DM, Tsalikian E, Schneider V, Karam JH, Forsham PH. Effects

of physiologic levels of glucagon and growth hormone on human carbohydrate and lipid

metabolism. Studies involving administration of exogenous hormone during suppression

of endogenous hormone secretion with somatostatin. J Clin Invest. 1976 Apr;57(4):875-

84.

Chapter 34

Reference 1:

ɽ Kinabo JL, Durnin JV. Effect of meal frequency on the thermic effect of food in women.

Eur J Clin Nutr. 1990 May;44(5):389-95.

ɽ Taylor MA, Garrow JS. Compared with nibbling, neither gorging nor a morning fast affect

short-term energy balance in obese patients in a chamber calorimeter. Int J Obes Relat

Metab Disord. 2001 Apr;25(4):519-28.

ɽ Bellisle F, McDevitt R, Prentice AM. Meal frequency and energy balance. Br J Nutr. 1997

Apr;77 Suppl 1:S57-70. Review.

ɽ Holmback U, Lowden A, Akerfeldt T, Lennernas M, Hambraeus L, Forslund J, Akerstedt

T, Stridsberg M, Forslund A. The human body may buffer small differences in meal size

and timing during a 24-h wake period provided energy balance is maintained. J Nutr.

2003 Sep;133(9):2748-55.

ɽ Jones PJ, Namchuk GL, Pederson RA. Meal frequency influences circulating hormone

levels but not lipogenesis rates in humans. Metabolism. 1995 Feb;44(2):218-23.

ɽ Arnold L, Ball M, Mann J. Metabolic effects of alterations in meal frequency in

hypercholesterolaemic individuals. Atherosclerosis. 1994 Aug;108(2):167-74.

ɽ Murphy MC, Chapman C, Lovegrove JA, Isherwood SG, Morgan LM, Wright JW, Williams

CM. Meal frequency; does it determine postprandial lipaemia? Eur J Clin Nutr. 1996

Aug;50(8):491-7.

ɽ Wolfram G, Kirchgessner M, Muller HL, Hollomey S. Thermogenesis in humans after

varying meal time frequency Ann Nutr Metab. 1987;31(2):88-97.

ɽ Mann J. Meal frequency and plasma lipids and lipoproteins. Br J Nutr. 1997 Apr;77

Suppl 1:S83-90. Review.

2 7 8

S e c t i o n X : R e f e r e n c e s

ɽ Verboeket-van de Venne WP, Westerterp KR. Frequency of feeding, weight reduction

and energy metabolism. Int J Obes Relat Metab Disord. 1993 Jan;17(1):31-6.

ɽ Dallosso HM, Murgatroyd PR, James WP. Feeding frequency and energy balance in

adult males. Hum Nutr Clin Nutr. 1982;36C(1):25-39.

ɽ Hill JO, Anderson JC, Lin D, Yakubu F. Effects of meal frequency on energy utilization in

rats. Am J Physiol. 1988 Oct;255(4 Pt 2):R616-21.

ɽ Garrow JS, Durrant M, Blaza S, Wilkins D, Royston P, Sunkin S. The effect of meal

frequency and protein concentration on the composition of the weight lost by obese

subjects. Br J Nutr. 1981 Jan;45(1):5-15.

ɽ Arnold L, Mann JI, Ball MJ. Metabolic effects of alterations in meal frequency in type 2

diabetes. Diabetes Care. 1997 Nov;20(11):1651-4.

ɽ Rashidi MR, Mahboob S, Sattarivand R. Effects of nibbling and gorging on lipid profiles,

blood glucose and insulin levels in healthy subjects. Saudi Med J. 2003 Sep;24(9):945-8.

ɽ Baker N, Palmquist DL, Learn DB. Equally rapid activation of lipogenesis in nibbling and

gorging mice. J Lipid Res. 1976 Sep;17(5):527-35.

ɽ Baker N, Huebotter RJ. Lipogenic activation after nibbling and gorging in mice. J Lipid

Res. 1973 Jan;14(1):87-94.

ɽ Sensi S, Capani F. Chronobiological aspects of weight loss in obesity: effects of different

meal timing regimens. Chronobiol Int. 1987;4(2):251-61.

ɽ Verboeket-van de Venne WP, Westerterp KR. Influence of the feeding frequency on

nutrient utilization in man: consequences for energy metabolism. Eur J Clin Nutr. 1991

Mar;45(3):161-9.

ɽ Holmback U, Lowden A, Akerfeldt T, Lennernas M, Hambraeus L, Forslund J, Akerstedt

T, Stridsberg M, Forslund A. The human body may buffer small differences in meal size

and timing during a 24-h wake period provided energy balance is maintained. J Nutr.

2003 Sep;133(9):2748-55.

ɽ [No authors listed] Effects of meal frequency during weight reduction. Nutr Rev. 1972

Jul;30(7):158-62. Review.

ɽ Young CM, Hutter LF, Scanlan SS, Rand CE, Lutwak L, Simko V. Metabolic effects of

meal frequency on normal young men. J Am Diet Assoc. 1972 Oct;61(4):391-8.

ɽ Finkelstein B, Fryer BA. Meal frequency and weight reduction of young women. Am J

Clin Nutr. 1971 Apr;24(4):465-8.

ɽ Young CM, Scanlan SS, Topping CM, Simko V, Lutwak L. Frequency of feeding, weight

reduction, and body composition. J Am Diet Assoc. 1971 Nov;59(5):466-72.

ɽ Wadhwa PS, Young EA, Schmidt K, Elson CE, Pringle DJ. Metabolic consequences of

feeding frequency in man. Am J Clin Nutr. 1973 Aug;26(8):823-30.

ɽ Romsos DR, Miller ER, Leveille GA. Influence of feeding frequency on body weight and

glucose tolerance in the pig. Proc Soc Exp Biol Med. 1978 Apr;157(4):528-30.

ɽ Bortz W, Wroldsen A, Issekutz B, Rodahl K. Weight loss and frequency of feeding. N

Engl J Med. 1966;274:376-379.

ɽ Swindells YE, Holmes SA, Robinson MF. The metabolic response of young women to

changes in the frequency of meals. Br J Nutr. 1968;22(4):667-680.

ɽ Wu H, Wu DY. Influence of feeding schedule on nitrogen utilization and excretion. Proc

Soc Exp Biol Med. 1950;74:78-82.

Reference 2:

ɽ Sofer S, Eliraz A, Kaplan S, Voet H, Fink G, Kima T, Madar Z. Greater weight loss and

hormonal changes after 6 months diet with carbohydrates eaten mostly at dinner. Obesity

(Silver Spring). 2011 Oct;19(10):2006-14.

C a r b B a c k - L o a d i n g

C h a p t e r 3 5

Chapter 35

Reference 1:

ɽ Lancaster GI, Jentjens RL, Moseley L, Jeukendrup AE, Gleeson M. Effect of pre-exercise

carbohydrate ingestion on plasma cytokine, stress hormone, and neutrophil

degranulation responses to continuous, high-intensity exercise. Int J Sport Nutr Exerc

Metab. 2003 Dec;13(4):436-53.

ɽ Hulmi JJ, Volek JS, Selänne H, Mero AA. Protein ingestion prior to strength exercise

affects blood hormones and metabolism. Med Sci Sports Exerc. 2005 Nov;37(11):1990-7.

Chapter 36

Reference 1:

ɽ Pasiakos SM, McClung HL, McClung JP, Margolis LM, Andersen NE, Cloutier GJ,

Pikosky MA, Rood JC, Fielding RA, Young AJ. Leucine-enriched essential amino acid

supplementation during moderate steady state exercise enhances postexercise muscle

protein synthesis. Am J Clin Nutr. 2011 Sep;94(3):809-18.

ɽ Kaastra B, Manders RJ, Van Breda E, Kies A, Jeukendrup AE, Keizer HA, Kuipers H, Van

Loon LJ. Effects of increasing insulin secretion on acute postexercise blood glucose

disposal. Med Sci Sports Exerc. 2006 Feb;38(2):268-75.

ɽ Nelson AR, Phillips SM, Stellingwerff T, Rezzi S, Bruce SJ, Breton I, Thorimbert A, Guy

PA, Clarke J, Broadbent S, Rowlands DS. A Protein-Leucine Supplement Increases

BCAA and Nitrogen Turnover but not Performance. Med Sci Sports Exerc. 2011 Jun 16.

[Epub ahead of print]

ɽ Apró W, Blomstrand E. Influence of supplementation with branched-chain amino acids in

combination with resistance exercise on p70S6 kinase phosphorylation in resting and

exercising human skeletal muscle. Acta Physiol (Oxf). 2010 Nov;200(3):237-48.

ɽ Beelen M, Tieland M, Gijsen AP, Vandereyt H, Kies AK, Kuipers H, Saris WH, Koopman

R, van Loon LJ. Coingestion of carbohydrate and protein hydrolysate stimulates muscle

protein synthesis during exercise in young men, with no further increase during

subsequent overnight recovery. J Nutr. 2008 Nov;138(11):2198-204.

ɽ Beelen M, Koopman R, Gijsen AP, Vandereyt H, Kies AK, Kuipers H, Saris WH, van Loon

LJ. Protein coingestion stimulates muscle protein synthesis during resistance-type

exercise. Am J Physiol Endocrinol Metab. 2008 Jul;295(1):E70-7.

ɽ Mero A. Leucine supplementation and intensive training. Sports Med. 1999

Jun;27(6):347-58. Review.

Reference 2:

ɽ Volek JS. Influence of nutrition on responses to resistance training. Med Sci Sports Exerc

2004;36:689–96.

ɽ Kraemer WJ, Ratamess NA. Hormonal responses and adaptations to resistance exercise

and training. Sports Med 2005;35:339–61.

ɽ Crewther B, Keogh J, Cronin J, Cook C. Possible stimuli for strength and power

adaptation: acute hormonal responses. Sports Med 2006;36:215–38.

ɽ Beaven CM, Gill ND, Ingram JR, Hopkins WG. Acute salivary hormone responses to

complex exercise bouts. J Strength Cond Res. 2011 Apr;25(4):1072-8.

2 8 0

S e c t i o n X : R e f e r e n c e s

Reference 3:

ɽ Baty JJ, Hwang H, Ding Z, Bernard JR, Wang B, Kwon B, Ivy JL. The effect of a

carbohydrate and protein supplement on resistance exercise performance, hormonal

response, and muscle damage. J Strength Cond Res. 2007 May;21(2):321-9.

ɽ Bird SP, Tarpenning KM, Marino FE. Liquid carbohydrate/essential amino acid ingestion

during a short-term bout of resistance exercise suppresses myofibrillar protein

degradation. Metabolism. 2006 May;55(5):570-7.

ɽ Bird SP, Tarpenning KM, Marino FE. Effects of liquid carbohydrate/essential amino acid

ingestion on acute hormonal response during a single bout of resistance exercise in

untrained men. Nutrition. 2006 Apr;22(4):367-75

ɽ Bird SP, Tarpenning KM, Marino FE. Independent and combined effects of liquid

carbohydrate/essential amino acid ingestion on hormonal and muscular adaptations

following resistance training in untrained men. Eur J Appl Physiol. 2006 May;97(2):225-38.

Reference 4:

ɽ Andersen LL, Tufekovic G, Zebis MK, Crameri RM, Verlaan G, Kjaer M, Suetta C,

Magnusson P, Aagaard P. The effect of resistance training combined with timed ingestion

of protein on muscle fiber size and muscle strength. Metabolism. 2005 Feb;54(2):151-6.

Chapter 37

Reference 1:

ɽ van Loon LJ, Kruijshoop M, Verhagen H, Saris WH, Wagenmakers AJ. Ingestion of

protein hydrolysate and amino acid-carbohydrate mixtures increases postexercise

plasma insulin responses in men. J Nutr 2000;130:2508–13.

ɽ Koopman R, Wagenmakers AJ, Manders RJ, Zorenc AH, Senden JM, Gorselink M, Keizer

HA, van Loon LJ. Combined ingestion of protein and free leucine with carbohydrate

increases postexercise muscle

ɽ protein synthesis in vivo in male subjects. Am J Physiol Endocrinol Metab

2005;288:E645–53.

ɽ Kaastra B, Manders RJ, Van Breda E, Kies A, Jeukendrup AE, Keizer HA, Kuipers H, Van

Loon LJ. Effects of increasing insulin secretion on acute postexercise blood glucose

disposal. Med Sci Sports Exerc 2006;38:268–75.

ɽ Manders RJ, Koopman R, Sluijsmans WE, van den Berg R, Verbeek K, Saris WH,

Wagenmakers AJ, van Loon LJ. Co-ingestion of a protein hydrolysate with or without

additional leucine effectively reduces postprandial blood glucose excursions in Type 2

diabetic men. J Nutr 2006;136:1294–9.

ɽ Rasmussen BB, Tipton KD, Miller SL, Wolf SE, Wolfe RR. An oral essential amino

acidcarbohydrate supplement enhances muscle protein anabolism after resistance

exercise. J Appl Physiol 2000;88:386–92.

ɽ Manders RJ, Praet SF, Vikström MH, Saris WH, van Loon LJ. Protein hydrolysate co-

ingestion does not modulate 24 h glycemic control in long-standing type 2 diabetes

patients. Eur J Clin Nutr. 2009 Jan;63(1):121-6.

ɽ Manders RJ, Wagenmakers AJ, Koopman R, Zorenc AH, Menheere PP, Schaper NC,

Saris WH, van Loon LJ. Co-ingestion of a protein hydrolysate and amino acid mixture

with carbohydrate improves plasma glucose disposal in patients with type 2 diabetes. Am

J Clin Nutr. 2005 Jul;82(1):76-83.

ɽ Koopman R, Pennings B, Zorenc AH, van Loon LJ. Protein ingestion further augments

S6K1 phosphorylation in skeletal muscle following resistance type exercise in males. J

Nutr. 2007 Aug;137(8):1880-6.

C a r b B a c k - L o a d i n g

C h a p t e r 3 7

ɽ van Loon LJ. Application of protein or protein hydrolysates to improve postexercise

recovery. Int J Sport Nutr Exerc Metab. 2007 Aug;17 Suppl:S104-17. Review.

ɽ Beelen M, Tieland M, Gijsen AP, Vandereyt H, Kies AK, Kuipers H, Saris WH, Koopman

R, van Loon LJ. Coingestion of carbohydrate and protein hydrolysate stimulates muscle

protein synthesis during exercise in young men, with no further increase during

subsequent overnight recovery. J Nutr. 2008 Nov;138(11):2198-204.

ɽ Koopman R, Crombach N, Gijsen AP, Walrand S, Fauquant J, Kies AK, Lemosquet S,

Saris WH, Boirie Y, van Loon LJ. Ingestion of a protein hydrolysate is accompanied by an

accelerated in vivo digestion and absorption rate when compared with its intact protein.

Am J Clin Nutr. 2009 Jul;90(1):106-15.

ɽ Tang JE, Moore DR, Kujbida GW, Tarnopolsky MA, Phillips SM. Ingestion of whey

hydrolysate, casein, or soy protein isolate: effects on mixed muscle protein synthesis at

rest and following resistance exercise in young men. J Appl Physiol. 2009

Sep;107(3):987-92.

Reference 2:

ɽ Bird SP, Tarenning KM, Marino FE. Independent and combined effects of liquid

carbohydrate/essential amino acid ingestion on hormonal and muscular adaptations

following resistance training in untrained men. Eur J Appl Physiol 2006;97:225–38.

ɽ Krzentowski G, Pirnay F, Luyckx AS, Pallikarakis N, Lacroix M, Mosora F, Lefèbvre PJ.

Metabolic adaptations in postexercise recovery. Clin Physiol 1982;2:277–88.

ɽ Folch N, Péronnet F, Massicotte D, Duclos M, Lavoie C, Hillaire-Marcel C. Metabolic

response to small and large 13C-labelled pasta meals following rest or exercise in man.

Br J Nutr 2001;85:671–80.

Reference 3:

ɽ Battram DS, Shearer J, Robinson D, Graham TE. Caffeine ingestion does not impede the

resynthesis of proglycogen and macroglycogen after prolonged exercise and

carbohydrate supplementation in humans. J Appl Physiol. 2004 Mar;96(3):943-50.

ɽ Pedersen DJ, Lessard SJ, Coffey VG, Churchley EG, Wootton AM, Ng T, Watt MJ,

Hawley JA. High rates of muscle glycogen resynthesis after exhaustive exercise when

carbohydrate is coingested with caffeine. J Appl Physiol. 2008 Jul;105(1):7-13.

ɽ Beelen M, Kranenburg JV, Senden JM, Kuipers H, van Loon LJ. Impact of Caffeine and

Protein on Post-Exercise Muscle Glycogen Synthesis. Med Sci Sports Exerc. 2011 Oct 7.

[Epub ahead of print]

ɽ van Loon LJ, Murphy R, Oosterlaar AM, Cameron-Smith D, Hargreaves M, Wagenmakers

AJ, Snow R. Creatine supplementation increases glycogen storage but not GLUT-4

expression in human skeletal muscle. Clin Sci (Lond). 2004 Jan;106(1):99-106.

ɽ Derave W, Eijnde BO, Verbessem P, Ramaekers M, Van Leemputte M, Richter EA, Hespel

P. Combined creatine and protein supplementation in conjunction with resistance training

promotes muscle GLUT-4 content and glucose tolerance in humans. J Appl Physiol. 2003

May;94(5):1910-6.

Reference 4:

ɽ Deglaire A, Fromentin C, Fouillet H, Airinei G, Gaudichon C, Boutry C, Benamouzig R,

Moughan PJ, Tomé D, Bos C. Hydrolyzed dietary casein as compared with the intact

protein reduces postprandial peripheral, but not whole-body, uptake of nitrogen in

humans. Am J Clin Nutr. 2009 Oct;90(4):1011-22.

ɽ Fouillet H, Mariotti F, Gaudichon C, Bos C, Tomé D. Peripheral and splanchnic

metabolism of dietary nitrogen are differently affected by the protein source in humans as

assessed by compartmental modeling. J Nutr. 2002 Jan;132(1):125-33.

2 8 2

S e c t i o n X : R e f e r e n c e s

ɽ Lacroix M, Bos C, Léonil J, Airinei G, Luengo C, Daré S, Benamouzig R, Fouillet H,

Fauquant J, Tomé D, Gaudichon C. Compared with casein or total milk protein, digestion

of milk soluble proteins is too rapid to sustain the anabolic postprandial amino acid

requirement. Am J Clin Nutr. 2006 Nov;84(5):1070-9.

ɽ Fouillet H, Juillet B, Gaudichon C, Mariotti F, Tomé D, Bos C. Absorption kinetics are a

key factor regulating postprandial protein metabolism in response to qualitative and

quantitative variations in protein intake. Am J Physiol Regul Integr Comp Physiol. 2009

Dec;297(6):R1691-705.

ɽ Boirie Y, Dangin M, Gachon P, Vasson MP, Maubois JL, Beaufrère B. Slow and fast

dietary proteins differently modulate postprandial protein accretion. Proc Natl Acad Sci U

S A. 1997 Dec 23;94(26):14930-5.

ɽ Fouillet H, Gaudichon C, Bos C, Mariotti F, Tomé D. Contribution of plasma proteins to

splanchnic and total anabolic utilization of dietary nitrogen in humans. Am J Physiol

Endocrinol Metab. 2003 Jul;285(1):E88-97.

ɽ Koopman R, Crombach N, Gijsen AP, Walrand S, Fauquant J, Kies AK, Lemosquet S,

Saris WH, Boirie Y, van Loon LJ. Ingestion of a protein hydrolysate is accompanied by an

accelerated in vivo digestion and absorption rate when compared with its intact protein.

Am J Clin Nutr. 2009 Jul;90(1):106-15.

ɽ Koopman R, Walrand S, Beelen M, Gijsen AP, Kies AK, Boirie Y, Saris WH, van Loon LJ.

Dietary protein digestion and absorption rates and the subsequent postprandial muscle

protein synthetic response do not differ between young and elderly men. J Nutr. 2009

Sep;139(9):1707-13.

Reference 5:

ɽ Tang JE, Moore DR, Kujbida GW, Tarnopolsky MA, Phillips SM. Ingestion of whey

hydrolysate, casein, or soy protein isolate: effects on mixed muscle protein synthesis at

rest and following resistance exercise in young men. J Appl Physiol. 2009

Sep;107(3):987-92.

ɽ Reitelseder S, Agergaard J, Doessing S, Helmark IC, Lund P, Kristensen NB, Frystyk J,

Flyvbjerg A, Schjerling P, van Hall G, Kjaer M, Holm L. Whey and casein labeled with L-

[1-13C]leucine and muscle protein synthesis: effect of resistance exercise and protein

ingestion. Am J Physiol Endocrinol Metab. 2011 Jan;300(1):E231-42.

ɽ Burk A, Timpmann S, Medijainen L, Vähi M, Oöpik V. Time-divided ingestion pattern of

casein-based protein supplement stimulates an increase in fat-free body mass during

resistance training in young untrained men. Nutr Res. 2009 Jun;29(6):405-13.

ɽ Willoughby DS, Stout JR, Wilborn CD. Effects of resistance training and protein plus

amino acid supplementation on muscle anabolism, mass, and strength. Amino Acids.

2007;32(4):467-77.

ɽ Kerksick CM, Rasmussen CJ, Lancaster SL, Magu B, Smith P, Melton C, Greenwood M,

Almada AL, Earnest CP, Kreider RB. The effects of protein and amino acid

supplementation on performance and training adaptations during ten weeks of resistance

training. J Strength Cond Res. 2006 Aug;20(3):643-53.

ɽ Kukuljan S, Nowson CA, Sanders K, Daly RM. Effects of resistance exercise and fortified

milk on skeletal muscle mass, muscle size, and functional performance in middle-aged

and older men: an 18-mo randomized controlled trial. J Appl Physiol. 2009

Dec;107(6):1864-73.

ɽ Josse AR, Tang JE, Tarnopolsky MA, Phillips SM. Body composition and strength

changes in women with milk and resistance exercise. Med Sci Sports Exerc. 2010

Jun;42(6):1122-30.

ɽ Lunn WR, Pasiakos SM, Colletto MR, Karfonta KE, Carbone JW, Anderson JM,

Rodriguez NR. Chocolate Milk & Endurance Exercise Recovery: Protein Balance,

Glycogen & Performance. Med Sci Sports Exerc. 2011 Sep 7. [Epub ahead of print]

C a r b B a c k - L o a d i n g

C h a p t e r 3 8

ɽ Wilkinson SB, Tarnopolsky MA, Macdonald MJ, Macdonald JR, Armstrong D, Phillips

SM. Consumption of fluid skim milk promotes greater muscle protein accretion after

resistance exercise than does consumption of an isonitrogenous and isoenergetic soy-

protein beverage. Am J Clin Nutr. 2007 Apr;85(4):1031-40.

ɽ Hartman JW, Tang JE, Wilkinson SB, Tarnopolsky MA, Lawrence RL, Fullerton AV,

Phillips SM. Consumption of fat-free fluid milk after resistance exercise promotes greater

lean mass accretion than does consumption of soy or carbohydrate in young, novice,

male weightlifters. Am J Clin Nutr. 2007 Aug;86(2):373-81.

Chapter 38

Reference 1:

ɽ Kaastra B, Manders RJ, Van Breda E, Kies A, Jeukendrup AE, Keizer HA, Kuipers H, Van

Loon LJ. Effects of increasing insulin secretion on acute postexercise blood glucose

disposal. Med Sci Sports Exerc. 2006 Feb;38(2):268-75.

ɽ Wee SL, Williams C, Tsintzas K, Boobis L. Ingestion of a high-glycemic index meal

increases muscle glycogen storage at rest but augments its utilization during subsequent

exercise. J Appl Physiol. 2005 Aug;99(2):707-14.

ɽ Stevenson E, Williams C, Nute M, Swaile P, Tsui M. The effect of the glycemic index of an

evening meal on the metabolic responses to a standard high glycemic index breakfast

and subsequent exercise in men. Int J Sport Nutr Exerc Metab. 2005 Jun;15(3):308-22.

ɽ Stevenson E, Williams C, Biscoe H. The metabolic responses to high carbohydrate meals

with different glycemic indices consumed during recovery from prolonged strenuous

exercise. Int J Sport Nutr Exerc Metab. 2005 Jun;15(3):291-307.

ɽ van Loon LJ, Saris WH, Kruijshoop M, Wagenmakers AJ. Maximizing postexercise

muscle glycogen synthesis: carbohydrate supplementation and the application of amino

acid or protein hydrolysate mixtures. Am J Clin Nutr. 2000 Jul;72(1):106-11.

ɽ Piehl Aulin K, Söderlund K, Hultman E. Muscle glycogen resynthesis rate in humans after

supplementation of drinks containing carbohydrates with low and high molecular masses.

Eur J Appl Physiol. 2000 Mar;81(4):346-51.

ɽ Ivy JL, Katz AL, Cutler CL, Sherman WM, Coyle EF. Muscle glycogen synthesis after

exercise: effect of time of carbohydrate ingestion. J Appl Physiol. 1988 Apr;64(4):1480-5.

Reference 2:

ɽ Venn BJ, Green TJ. Glycemic index and glycemic load: measurement issues and their

effect on diet-disease relationships. Eur J Clin Nutr. 2007 Dec;61 Suppl 1:S122-31.

Review.

ɽ Bray GA, Most M, Rood J, Redmann S, Smith SR. Hormonal responses to a fast-food

meal compared with nutritionally comparable meals of different composition. Ann Nutr

Metab. 2007;51(2):163-71.

Reference 3:

ɽ Kimber NE, Heigenhauser GJ, Spriet LL, Dyck DJ. Skeletal muscle fat and carbohydrate

metabolism during recovery from glycogen-depleting exercise in humans. J Physiol. 2003

May 1;548(Pt 3):919-27.

ɽ Fox AK, Kaufman AE, Horowitz JF. Adding fat calories to meals after exercise does not

alter glucose tolerance. J Appl Physiol. 2004 Jul;97(1):11-6.

ɽ Burke LM, Hawley JA, Angus DJ, Cox GR, Clark SA, Cummings NK, Desbrow B,

Hargreaves M. Adaptations to short-term high-fat diet persist during exercise despite

high carbohydrate availability. Med Sci Sports Exerc. 2002 Jan;34(1):83-91.

2 8 4

S e c t i o n X : R e f e r e n c e s

ɽ Burke LM, Collier GR, Beasley SK, Davis PG, Fricker PA, Heeley P, Walder K, Hargreaves

M. Effect of coingestion of fat and protein with carbohydrate feedings on muscle

glycogen storage. J Appl Physiol. 1995 Jun;78(6):2187-92.

Reference 4:

ɽ Wee SL, Williams C, Tsintzas K, Boobis L. Ingestion of a high-glycemic index meal

increases muscle glycogen storage at rest but augments its utilization during subsequent

exercise. J Appl Physiol. 2005 Aug;99(2):707-14.

ɽ Stevenson E, Williams C, Biscoe H. The metabolic responses to high carbohydrate meals

with different glycemic indices consumed during recovery from prolonged strenuous

exercise. Int J Sport Nutr Exerc Metab. 2005 Jun;15(3):291-307.

ɽ Kaastra B, Manders RJ, Van Breda E, Kies A, Jeukendrup AE, Keizer HA, Kuipers H, Van

Loon LJ. Effects of increasing insulin secretion on acute postexercise blood glucose

disposal. Med Sci Sports Exerc. 2006 Feb;38(2):268-75.

ɽ McInerney P, Lessard SJ, Burke LM, Coffey VG, Lo Giudice SL, Southgate RJ, Hawley

JA. Failure to repeatedly supercompensate muscle glycogen stores in highly trained men.

Med Sci Sports Exerc. 2005 Mar;37(3):404-11.

ɽ Rotman S, Slotboom J, Kreis R, Boesch C, Jéquier E. Muscle glycogen recovery after

exercise measured by 13C-magnetic resonance spectroscopy in humans: effect of

nutritional solutions. MAGMA. 2000 Dec;11(3):114-21.

ɽ van Loon LJ, Saris WH, Kruijshoop M, Wagenmakers AJ. Maximizing postexercise

muscle glycogen synthesis: carbohydrate supplementation and the application of amino

acid or protein hydrolysate mixtures. Am J Clin Nutr. 2000 Jul;72(1):106-11.

ɽ Piehl Aulin K, Söderlund K, Hultman E. Muscle glycogen resynthesis rate in humans after

supplementation of drinks containing carbohydrates with low and high molecular masses.

Eur J Appl Physiol. 2000 Mar;81(4):346-51.

ɽ Parkin JA, Carey MF, Martin IK, Stojanovska L, Febbraio MA. Muscle glycogen storage

following prolonged exercise: effect of timing of ingestion of high glycemic index food.

Med Sci Sports Exerc. 1997 Feb;29(2):220-4.

ɽ Burke LM, Collier GR, Davis PG, Fricker PA, Sanigorski AJ, Hargreaves M. Muscle

glycogen storage after prolonged exercise: effect of the frequency of carbohydrate

feedings. Am J Clin Nutr. 1996 Jul;64(1):115-9.

ɽ Burke LM, Collier GR, Hargreaves M. Muscle glycogen storage after prolonged exercise:

effect of the glycemic index of carbohydrate feedings. J Appl Physiol. 1993

Aug;75(2):1019-23.

ɽ Guezennec CY, Satabin P, Duforez F, Koziet J, Antoine JM. The role of type and structure

of complex carbohydrates response to physical exercise. Int J Sports Med. 1993

May;14(4):224-31.

ɽ Sparti A, Décombaz J. Effect of diet on glucose tolerance 36 hours after glycogen-

depleting exercise. Eur J Clin Nutr. 1992 Jun;46(6):377-85.

ɽ Reed MJ, Brozinick JT Jr, Lee MC, Ivy JL. Muscle glycogen storage postexercise: effect

of mode of carbohydrate administration. J Appl Physiol. 1989 Feb;66(2):720-6.

ɽ Ivy JL, Lee MC, Brozinick JT Jr, Reed MJ. Muscle glycogen storage after different

amounts of carbohydrate ingestion. J Appl Physiol. 1988 Nov;65(5):2018-23.

ɽ Ivy JL, Katz AL, Cutler CL, Sherman WM, Coyle EF. Muscle glycogen synthesis after

exercise: effect of time of carbohydrate ingestion. J Appl Physiol. 1988 Apr;64(4):1480-5.

Reference 5

ɽ Schnure JJ, Raskin P, Lipman RL. Growth hormone secretion during sleep: impairment in

glucose tolerance and nonsuppressibility by hyperglycemia. J Clin Endocrinol Metab.

1971 Aug;33(2):234-41.

C a r b B a c k - L o a d i n g

C h a p t e r 4 1

ɽ VanderLaan WP. Changing concepts on the control of growth hormone secretion in man.

Calif Med. 1971 Aug;115(2):38-46. Review.

ɽ Parker DC, Rossman LG. Human growth hormone release in sleep: nonsuppression by

acute hyperglycemia. J Clin Endocrinol Metab. 1971 Jan;32(1):65-9.

ɽ VanderLaan WP, Parker DC, Rossman LG, VanderLaan EF. Implications of growth

hormone release in sleep. Metabolism. 1970 Oct;19(10):891-7.

ɽ Quabbe HJ, Schilling E, Helge H. Pattern of growth hormone secretion during a 24-hour

fast in normal adults. J Clin Endocrinol Metab. 1966 Oct;26(10):1173-7.

Reference 6:

ɽ Tan SY, Batterham M, Tapsell L. Energy expenditure does not differ, but protein oxidation

rates appear lower in meals containing predominantly meat versus soy sources of

protein. Obes Facts. 2010;3(2):101-4.

Reference 7:

ɽ Morifuji M, Koga J, Kawanaka K, Higuchi M. Branched-chain amino acid-containing

dipeptides, identified from whey protein hydrolysates, stimulate glucose uptake rate in L6

myotubes and isolated skeletal muscles. J Nutr Sci Vitaminol (Tokyo). 2009 Feb;55(1):81-

6.

Chapter 41

Reference 1:

ɽ Smith GI, Atherton P, Reeds DN, Mohammed BS, Rankin D, Rennie MJ, Mittendorfer B.

Omega-3 polyunsaturated fatty acids augment the muscle protein anabolic response to

hyperinsulinaemia-hyperaminoacidaemia in healthy young and middle-aged men and

women. Clin Sci (Lond). 2011 Sep;121(6):267-78.

Reference 2:

ɽ Hessvik NP, Bakke SS, Fredriksson K, Boekschoten MV, Fjørkenstad A, Koster G,

Hesselink MK, Kersten S, Kase ET, Rustan AC, Thoresen GH. Metabolic switching of

human myotubes is improved by n-3 fatty acids. J Lipid Res. 2010 Aug;51(8):2090-104.

Reference 3:

ɽ van Loon LJ, Murphy R, Oosterlaar AM, Cameron-Smith D, Hargreaves M, Wagenmakers

AJ, Snow R. Creatine supplementation increases glycogen storage but not GLUT-4

expression in human skeletal muscle. Clin Sci (Lond). 2004 Jan;106(1):99-106.

Chapter 43

Reference 1:

ɽ Van Proeyen K, Deldique L, Nielens H, Szlufcik K, Francaux M, Ramaekers M, Hespel P.

Effects Of Training In The Fasted State In Conjunction With Fat-rich diet On Muscle

Metabolism: 721: June 3 8:15 AM – 8:30 AM. Medicine & Science in Sports & Exercise.

42(5):42, May 2010.

ɽ van Loon LJ, Koopman R, Stegen JH, Wagenmakers AJ, Keizer HA, Saris WH.

Intramyocellular lipids form an important substrate source during moderate intensity

2 8 6

S e c t i o n X : R e f e r e n c e s

exercise in endurance-trained males in a fasted state. J Physiol. 2003 Dec 1;553(Pt

2):611-25.

ɽ De Bock K, Richter EA, Russell AP, Eijnde BO, Derave W, Ramaekers M, Koninckx E,

Léger B, Verhaeghe J, Hespel P. Exercise in the fasted state facilitates fibre type-specific

intramyocellular lipid breakdown and stimulates glycogen resynthesis in humans. J

Physiol. 2005 Apr 15;564(Pt 2):649-60.

Reference 2:

ɽ Deldicque L, De Bock K, Maris M, Ramaekers M, Nielens H, Francaux M, Hespel P.

Increased p70s6k phosphorylation during intake of a protein-carbohydrate drink following

resistance exercise in the fasted state. Eur J Appl Physiol. 2010 Mar;108(4):791-800.

Reference 3:

ɽ Stevenson E, Williams C, Nute M, Humphrey L, Witard O. Influence of the glycaemic

index of an evening meal on substrate oxidation following breakfast and during exercise

the next day in healthy women. Eur J Clin Nutr. 2008 May;62(5):608-16.

ɽ Stevenson E, Williams C, Nute M, Swaile P, Tsui M. The effect of the glycemic index of an

evening meal on the metabolic responses to a standard high glycemic index breakfast

and subsequent exercise in men. Int J Sport Nutr Exerc Metab. 2005 Jun;15(3):308-22.

Chapter 45

Reference 1:

ɽ McInerney P, Lessard SJ, Burke LM, Coffey VG, Lo Giudice SL, Southgate RJ, Hawley

JA. Failure to repeatedly supercompensate muscle glycogen stores in highly trained men.

Med Sci Sports Exerc. 2005 Mar;37(3):404-11.

Chapter 48

Reference 1:

ɽ Sapone A, Lammers KM, Casolaro V, Cammarota M, Giuliano MT, De Rosa M, Stefanile

R, Mazzarella G, Tolone C, Russo MI, Esposito P, Ferraraccio F, Cartenì M, Riegler G, de

Magistris L, Fasano A. Divergence of gut permeability and mucosal immune gene

expression in two gluten-associated conditions: celiac disease and gluten sensitivity.

BMC Med. 2011 Mar 9;9:23.

ɽ Bouchez-Mahiout I, Pecquet C, Kerre S, Snégaroff J, Raison-Peyron N, Laurière M. High

molecular weight entities in industrial wheat protein hydrolysates are immunoreactive with

IgE from allergic patients. J Agric Food Chem. 2010 Apr 14;58(7):4207-15.

ɽ Lidén M, Kristjánsson G, Valtysdottir S, Venge P, Hällgren R. Self-reported food

intolerance and mucosal reactivity after rectal food protein challenge in patients with

rheumatoid arthritis. Scand J Rheumatol. 2010 Aug;39(4):292-8.

ɽ Hischenhuber C, Crevel R, Jarry B, Mäki M, Moneret-Vautrin DA, Romano A, Troncone R,

Ward R. Review article: safe amounts of gluten for patients with wheat allergy or coeliac

disease. Aliment Pharmacol Ther. 2006 Mar 1;23(5):559-75. Review.

ɽ Ciacci C, Cavallaro R, Iovino P, Sabbatini F, Palumbo A, Amoruso D, Tortora R,

Mazzacca G. Allergy prevalence in adult celiac disease. J Allergy Clin Immunol. 2004

Jun;113(6):1199-203.

C a r b B a c k - L o a d i n g

C h a p t e r 4 9

ɽ Morris CR, Agin MC. Syndrome of allergy, apraxia, and malabsorption: characterization of

a neurodevelopmental phenotype that responds to omega 3 and vitamin E

supplementation. Altern Ther Health Med. 2009 Jul-Aug;15(4):34-43

Chapter 49

Reference 1:

ɽ Richter EA, Kristiansen S, Wojtaszewski J, Daugaard JR, Asp S, Hespel P, Kiens B.

Training effects on muscle glucose transport during exercise. Adv Exp Med Biol.

1998;441:107-16. Review.

ɽ Wojtaszewski JF, Richter EA. Glucose utilization during exercise: influence of endurance

training. Acta Physiol Scand. 1998 Mar;162(3):351-8. Review.

ɽ Host HH, Hansen PA, Nolte LA, Chen MM, Holloszy JO. Rapid reversal of adaptive

increases in muscle GLUT-4 and glucose transport capacity after training cessation. J

Appl Physiol. 1998 Mar;84(3):798-802.

ɽ Richter EA, Jensen P, Kiens B, Kristiansen S. Sarcolemmal glucose transport and GLUT-

4 translocation during exercise are diminished by endurance training. Am J Physiol. 1998

Jan;274(1 Pt 1):E89-95.

ɽ Hardin DS, Azzarelli B, Edwards J, Wigglesworth J, Maianu L, Brechtel G, Johnson A,

Baron A, Garvey WT. Mechanisms of enhanced insulin sensitivity in endurance-trained

athletes: effects on blood flow and differential expression of GLUT 4 in skeletal muscles.

J Clin Endocrinol Metab. 1995 Aug;80(8):2437-46.

ɽ Dela F, Handberg A, Mikines KJ, Vinten J, Galbo H. GLUT 4 and insulin receptor binding

and kinase activity in trained human muscle. J Physiol. 1993 Sep;469:615-24.

ɽ Seki Y, Berggren JR, Houmard JA, Charron MJ. Glucose transporter expression in

skeletal muscle of endurance-trained individuals. Med Sci Sports Exerc. 2006

Jun;38(6):1088-92.

Reference 2:

ɽ Holloszy JO. Exercise-induced increase in muscle insulin sensitivity. J Appl Physiol. 2005

Jul;99(1):338-43. Review.

ɽ Jessen N, Goodyear LJ. Contraction signaling to glucose transport in skeletal muscle. J

Appl Physiol. 2005 Jul;99(1):330-7. Review.

ɽ Richter EA, Nielsen JN, Jørgensen SB, Frøsig C, Birk JB, Wojtaszewski JF. Exercise

signalling to glucose transport in skeletal muscle. Proc Nutr Soc. 2004 May;63(2):211-6.

Review.

ɽ Holten MK, Zacho M, Gaster M, Juel C, Wojtaszewski JF, Dela F. Strength training

increases insulin-mediated glucose uptake, GLUT4 content, and insulin signaling in

skeletal muscle in patients with type 2 diabetes. Diabetes. 2004 Feb;53(2):294-305.

ɽ Pereira LO, Lancha AH Jr. Effect of insulin and contraction up on glucose transport in

skeletal muscle. Prog Biophys Mol Biol. 2004 Jan;84(1):1-27. Review.

ɽ Lemieux K, Konrad D, Klip A, Marette A. The AMP-activated protein kinase activator

AICAR does not induce GLUT4 translocation to transverse tubules but stimulates glucose

uptake and p38 mitogen-activated protein kinases alpha and beta in skeletal muscle.

FASEB J. 2003 Sep;17(12):1658-65.

ɽ Richter EA, Nielsen JN, Jørgensen SB, Frøsig C, Wojtaszewski JF. Signalling to glucose

transport in skeletal muscle during exercise. Acta Physiol Scand. 2003 Aug;178(4):329-

35. Review.

ɽ Khayat ZA, Patel N, Klip A. Exercise- and insulin-stimulated muscle glucose transport:

distinct mechanisms of regulation. Can J Appl Physiol. 2002 Apr;27(2):129-51. Review.

2 8 8

S e c t i o n X : R e f e r e n c e s

ɽ Ryder JW, Chibalin AV, Zierath JR. Intracellular mechanisms underlying increases in

glucose uptake in response to insulin or exercise in skeletal muscle. Acta Physiol Scand.

2001 Mar;171(3):249-57. Review.

ɽ Borghouts LB, Keizer HA. Exercise and insulin sensitivity: a review. Int J Sports Med.

2000 Jan;21(1):1-12. Review.

ɽ Tabata I, Suzuki Y, Fukunaga T, Yokozeki T, Akima H, Funato K. Resistance training

affects GLUT-4 content in skeletal muscle of humans after 19 days of head-down bed

rest. J Appl Physiol. 1999 Mar;86(3):909-14.

ɽ Ivy JL, Kuo CH. Regulation of GLUT4 protein and glycogen synthase during muscle

glycogen synthesis after exercise. Acta Physiol Scand. 1998 Mar;162(3):295-304. Review.

ɽ Roberts CK, Barnard RJ, Scheck SH, Balon TW. Exercise-stimulated glucose transport in

skeletal muscle is nitric oxide dependent. Am J Physiol. 1997 Jul;273(1 Pt 1):E220-5.

ɽ Kristiansen S, Hargreaves M, Richter EA. Exercise-induced increase in glucose transport,

GLUT-4, and VAMP-2 in plasma membrane from human muscle. Am J Physiol. 1996

Jan;270(1 Pt 1):E197-201.

ɽ Klip A, Marette A. Acute and chronic signals controlling glucose transport in skeletal

muscle. J Cell Biochem. 1992 Jan;48(1):51-60. Review.

Reference 3:

ɽ Asp S, Daugaard JR, Kristiansen S, Kiens B, Richter EA. Exercise metabolism in human

skeletal muscle exposed to prior eccentric exercise. J Physiol. 1998 May 15;509 ( Pt

1):305-13.

ɽ Kristiansen S, Jones J, Handberg A, Dohm GL, Richter EA. Eccentric contractions

decrease glucose transporter transcription rate, mRNA, and protein in skeletal muscle.

Am J Physiol. 1997 May;272(5 Pt 1):C1734-8.

ɽ Asp S, Richter EA. Decreased insulin action on muscle glucose transport after eccentric

contractions in rats. J Appl Physiol. 1996 Nov;81(5):1924-8.

ɽ Asp S, Daugaard JR, Kristiansen S, Kiens B, Richter EA. Eccentric exercise decreases

maximal insulin action in humans: muscle and systemic effects. J Physiol. 1996 Aug

1;494 ( Pt 3):891-8.

ɽ Kristiansen S, Asp S, Richter EA. Decreased muscle GLUT-4 and contraction-induced

glucose transport after eccentric contractions. Am J Physiol. 1996 Aug;271(2 Pt 2):R477-

82.

ɽ Asp S, Kristiansen S, Richter EA. Eccentric muscle damage transiently decreases rat

skeletal muscle GLUT-4 protein. J Appl Physiol. 1995 Oct;79(4):1338-45.

ɽ Asp S, Daugaard JR, Richter EA. Eccentric exercise decreases glucose transporter

GLUT4 protein in human skeletal muscle. J Physiol. 1995 Feb 1;482 ( Pt 3):705-12.

Reference 4:

ɽ Luebbers PE, Potteiger JA, Warren BJ, Clore JN, Jennings C, Bond DS. Glucose uptake

after resistance training of different intensities but of equal work volume. J Strength Cond

Res. 2008 Jul;22(4):1094-100.

ɽ Kraniou GN, Cameron-Smith D, Hargreaves M. Acute exercise and GLUT4 expression in

human skeletal muscle: influence of exercise intensity. J Appl Physiol. 2006

Sep;101(3):934-7.

ɽ Daugaard JR, Nielsen JN, Kristiansen S, Andersen JL, Hargreaves M, Richter EA. Fiber

type-specific expression of GLUT4 in human skeletal muscle: influence of exercise

training. Diabetes. 2000 Jul;49(7):1092-5.

ɽ Borghouts LB, Backx K, Mensink MF, Keizer HA. Effect of training intensity on insulin

sensitivity as evaluated by insulin tolerance test. Eur J Appl Physiol Occup Physiol. 1999

Oct;80(5):461-6.

C a r b B a c k - L o a d i n g

C h a p t e r 5 0

Reference 5:

ɽ Gao J, Ren J, Gulve EA, Holloszy JO. Additive effect of contractions and insulin on

GLUT-4 translocation into the sarcolemma. J Appl Physiol. 1994 Oct;77(4):1597-601.

Chapter 50

Reference 1:

ɽ Gibala MJ, McGee SL. Metabolic adaptations to short-term high-intensity interval

training: a little pain for a lot of gain? Exerc Sport Sci Rev. 2008 Apr;36(2):58-63. Review.

ɽ McKay BR, Paterson DH, Kowalchuk JM. Effect of short-term high-intensity interval

training vs. continuous training on O2 uptake kinetics, muscle deoxygenation, and

exercise performance. J Appl Physiol. 2009 Jul;107(1):128-38.

ɽ Gibala MJ, McGee SL, Garnham AP, Howlett KF, Snow RJ, Hargreaves M. Brief intense

interval exercise activates AMPK and p38 MAPK signaling and increases the expression

of PGC-1alpha in human skeletal muscle. J Appl Physiol. 2009 Mar;106(3):929-34.

ɽ Burgomaster KA, Howarth KR, Phillips SM, Rakobowchuk M, Macdonald MJ, McGee SL,

Gibala MJ. Similar metabolic adaptations during exercise after low volume sprint interval

and traditional endurance training in humans. J Physiol. 2008 Jan 1;586(1):151-60.

ɽ Gibala MJ, Little JP, van Essen M, Wilkin GP, Burgomaster KA, Safdar A, Raha S,

Tarnopolsky MA. Short-term sprint interval versus traditional endurance training: similar

initial adaptations in human skeletal muscle and exercise performance. J Physiol. 2006

Sep 15;575(Pt 3):901-11.

Reference 2:

ɽ Little JP, Safdar A, Bishop D, Tarnopolsky MA, Gibala MJ. An acute bout of high-intensity

interval training increases the nuclear abundance of PGC-1Į and activates mitochondrial

biogenesis in human skeletal muscle. Am J Physiol Regul Integr Comp Physiol. 2011

Jun;300(6):R1303-10.

ɽ Hulston CJ, Venables MC, Mann CH, Martin C, Philp A, Baar K, Jeukendrup AE. Training

with low muscle glycogen enhances fat metabolism in well-trained cyclists. Med Sci

Sports Exerc. 2010 Nov;42(11):2046-55.

ɽ Little JP, Safdar A, Wilkin GP, Tarnopolsky MA, Gibala MJ. A practical model of low-

volume high-intensity interval training induces mitochondrial biogenesis in human skeletal

muscle: potential mechanisms. J Physiol. 2010 Mar 15;588(Pt 6):1011-22.

ɽ Perry CG, Heigenhauser GJ, Bonen A, Spriet LL. High-intensity aerobic interval training

increases fat and carbohydrate metabolic capacities in human skeletal muscle. Appl

Physiol Nutr Metab. 2008 Dec;33(6):1112-23.

ɽ Burgomaster KA, Hughes SC, Heigenhauser GJ, Bradwell SN, Gibala MJ. Six sessions of

sprint interval training increases muscle oxidative potential and cycle endurance capacity

in humans. J Appl Physiol. 2005 Jun;98(6):1985-90.

2 9 0

Preparation Phase

Off Day

Upon Waking

Item

QTY

Coffee

ad libitum

(optional)

Heavy Whipping Cream

2 tbsp

(optional)

OR

A.M. Accelerator Formula

1 shake

p125 (optional)

Lunch

Item

QTY

Chicken Breast

8 oz

Or some other lean meat

Romaine Lettuce

2 cup

Olive oil

1 to 2 tbsp

Vinegar

to taste

Additional veggies

variable

Olives, tomatoes, cucumbers, onions,

celery

Snack

Item

QTY

Protein shake

~20 g protein

Ultra-low carb whey isolate

Eggs

2 large

hardboiled

Almonds

¼ cup

Dinner

Item

QTY

Steak

1 lb

Tri-tip or some roast is good

Asparagus

1 to 2 cups

Butter

2 tbsp

Before Bed

Item

QTY

Cottage Cheese

1 to 2 cups

Low-fat

Copyright © 2011-2012 by Kiefer

Preparation Phase

Train @ 9 or 10 am

Upon Waking

Item

QTY

Coffee

ad libitum

(optional)

Heavy Whipping Cream

2 tbsp

(optional)

OR

A.M. Accelerator Formula

1 shake

p125 (optional)

Pre-Training

Item

Ignition Formula

1 shake

p131 (optional)

Intra-Training

Item

Sustainer Formula

1 shake

p135 (optional)

Post-Training

Item

Hypertrophic Potentiator Formula 1 shake

p139 (no carbs)

Lunch

Item

QTY

Chicken Breast

8 oz

Or some other lean meat

Romaine Lettuce

2 cup

Olive oil

1 to 2 tbsp

Vinegar

to taste

Additional veggies

variable

Olives, tomatoes, cucumbers, onions,

celery

Snack (optional)

Item

QTY

Protein shake

~10 g protein

Ultra-low carb whey isolate

Eggs

2 large

hardboiled

Almonds

¼ cup

Copyright © 2011-2012 by Kiefer

Dinner

Item

QTY

Chicken

1/2 to a whole

Roasted

Marinated Artichoke hearts, olives,

Greek-style salad

2 cup

cucumbers, tomatoes

Feta Cheese

2 oz

Olive Oil

1 tbsp

Vinegar

to taste

Rice, White, Red (no balsamic)

Before Bed (Weight Maintenance)

Item

QTY

Cottage Cheese

1 to 2 cups

Low-fat

Almond Butter

2 to 3 tbsp

Copyright © 2011-2012 by Kiefer

Preparation Phase

Train @ noon or 1

Upon Waking

Item

QTY

Coffee

ad libitum

(optional)

Heavy Whipping Cream

2 tbsp

(optional)

OR

A.M. Accelerator Formula

1 shake

p125

Meal 1

Item

QTY

Coffee

ad libitum

Eggs

3 large, whole

Breakfast meat

8 oz

Ham, sausage

Cottage Cheese

½ cup

Tomatoes

1 medium, sliced

Snack (optional)

Item

QTY

Protein shake

~20 g protein

Ultra-low carb whey isolate

Almonds

½ cup

Pre-Training

Item

Ignition Formula

1 shake

p131 (optional)

Intra-Training

Item

Sustainer Formula

1 shake

p135 (optional)

Post-Training

Item

Hypertrophic Potentiator Formu1 shake

p139 (no carbs)

Copyright © 2011-2012 by Kiefer

Lunch

Item

QTY

Chicken Breast

8 oz

Or some other lean meat

Romaine Lettuce

2 cup

Olive oil

1 to 2 tbsp

Vinegar

to taste

Additional veggies

variable

Olives, tomatoes, cucumbers, onions,

celery

Snack

Item

QTY

Protein shake

~20 g protein

Ultra-low carb whey isolate

Eggs

2 large

hardboiled

Almonds

¼ cup

Dinner

Item

QTY

Hamburger meat, extra lean

¾ lb-pre cooked

Broccoli

2 cup

Melted American or ultra-low carb

Cheese

2 to 4 slices or tbsqueso sauce

Before Bed (Weight Maintenance)

Item

QTY

Cottage Cheese

1 to 2 cups

Low-fat

Almond Butter

2 to 3 tbsp

Copyright © 2011-2012 by Kiefer

Back Loading

Off Day

Upon Waking

Item

QTY

Coffee

ad libitum

(optional)

Heavy Whipping Cream

2 tbsp

(optional)

OR

A.M. Accelerator Formula

1 shake

p125 (optional)

Breakfast (optional)

Item

QTY

Eggs

3 large, whole

Cottage Cheese

½ cup

Snack (optional)

Item

QTY

Protein shake

~20 g protein

Ultra-low carb whey isolate

Almonds

½ cup

Lunch

Item

QTY

Chicken Breast

8 oz

Or some other lean meat

Romaine Lettuce

2 cup

Olive oil

1 to 2 tbsp

Vinegar

to taste

Additional veggies

variable

Olives, tomatoes, cucumbers, onions,

celery

Snack

Item

QTY

Protein shake

~20 g protein

Ultra-low carb whey isolate

Leucine

5 g

Eggs

2 large

hardboiled

Almonds

¼ cup

Copyright © 2011-2012 by Kiefer

Dinner

Item

QTY

Hypertrophic Potentiator Formu1 shake

p139

Pizza

½ to a whole

Before Bed (eating carbs)

Item

QTY

Hypertrophic Potentiator Formu1 shake

p139

Cereal

2 bowls

Before Bed (not eating carbs)

Item

QTY

Cottage Cheese

1 to 2 cups

Low-fat

Copyright © 2011-2012 by Kiefer

Back Loading

Train @ 6am

Upon Waking

Item

QTY

Coffee

ad libitum

or caffeine pills

No other Food

Preworkout

Item

QTY

No Food

Post-Training

Item

Hypertrophic Potentiator Formula1 shake

p139

Approx 30 minutes later

Item

QTY

Ignition Formula

1 to 2 shakes

p131

Late Breakfast/Lunch

Item

QTY

Hamburger patty

¼ to ¾ lb

Salad

2 cups

Additional veggies

variable

Olives, cucumbers, onions, celery

Snack

Item

QTY

Protein shake

~10 g protein

Ultra-low carb whey isolate

Eggs

2 large

hardboiled

Almonds

¼ cup

Dinner (around 6 ish)

Item

QTY

Tri-Tip

½ to ¾ lb

However

Broccoli

2 cups

steamed

Butter

1 or 2 tbsp

Copyright © 2011-2012 by Kiefer

Before Bed (Weight Maintenance)

Item

QTY

Post-Training Formula

1 shake

p139

Density Meal

1 to 3

something like PB&J sandwich, milk,

tater-tots, eggs

Protein shake

30g protein

Blend D

Leucine

5 g

Before Bed (Weight Maintenance-Alternate)

Item

QTY

Hypertrophic Potentiator Formula1 shake

p139

Eggs

4 to 6

Fried, sunny-side up, scrambled

Flavored Oatmeal

2 to 3 packets

Copyright © 2011-2012 by Kiefer

Back Loading

Train @ 9am

Upon Waking

Item

QTY

Coffee

ad libitum

Heavy Whipping Cream

2 tbsp

Preworkout

Item

QTY

Coffee

ad libitum

Post-Training

Item

Hypertrophic Potentiator Formu1 shake

p139 (no carbs)

Approx 30 minutes later

Item

QTY

Ignition Formula

1 to 2 shakes

p131

Lunch

Item

QTY

Chicken Breast

8 oz

Or some other lean meat

Romaine Lettuce

2 cup

Olive oil

1 to 2 tbsp

Vinegar

to taste

Additional veggies

variable

Olives, tomatoes, cucumbers, onions,

celery

Snack

Item

QTY

Protein shake

~20 g protein

Ultra-low carb whey isolate (drink shake

Eggs

2 large

hardboiled

Almonds

¼ cup

Copyright © 2011-2012 by Kiefer

Dinner (around 6 ish)

Item

QTY

Chicken

1/2 to a whole

Roasted

Mashed Potatoes

whatever

Biscuit

1 or 2

Corn

whatever

Before Bed (Weight Maintenance)

Item

QTY

Hypertrophic Potentiator Formu1 shake

p139

Ice cream

pint

Copyright © 2011-2012 by Kiefer

Back Loading

Train @ 10am

Upon Waking

Item

QTY

Coffee

ad libitum

(optional)

Heavy Whipping Cream

2 tbsp

(optional)

OR

A.M. Accelerator Formula

1 shake

p125

Pre-Training

Item

Ignition Formula

1 shake

p131 (optional)

Intra-Training

Item

Sustainer Formula

1 shake

p135 (optional)

Post-Training

Item

Hypertrophic Potentiator Formu1 shake

p139 (no carbs)

Lunch

Item

QTY

Chicken

½ to a whole

Roasted

Marinated Artichoke hearts, olives,

Greek-style salad

2 cup

cucumbers, tomatoes

Feta Cheese

2 oz

Olive Oil

1 tbsp

Vinegar

to taste

Rice, White, Red (no balsamic)

Snack

Item

QTY

Protein shake

~20 g protein

Ultra-low carb whey isolate

Eggs

2 large

hardboiled

Almonds

¼ cup

Copyright © 2011-2012 by Kiefer

Dinner (around 6 ish)

Item

QTY

Moons Over My Hammy

1 sandwich

Just an example

Hashbrowns

1 serving

Hypertrophic Potentiator Formu½ shake

p139

Before Bed (Weight Maintenance)

Item

QTY

Hypertrophic Potentiator Formu1 shake

p139

Left over pizza, muffins, cereal,

Carbs

turnovers

Copyright © 2011-2012 by Kiefer

Back Loading

Train @ noon or 1

Breakfast

Item

QTY

Coffee

ad libitum

Breakfast meat

6 oz

ham, sausages, bacon

Cottage Cheese

½ cup

Tomatoes

1 medium, sliced

Pre-Training

Item

Ignition Formula

1 shake

p131 (optional)

Intra-Training

Item

Sustainer Formula

1 shake

p135 (optional)

Post-Training

Item

Hypertrophic Potentiator Formu1 shake

p139 (no carbs)

Lunch

Item

QTY

Chicken Breasts

1 large

Cheese

4 oz

Olive Oil

2 tbsp

Vinegar

to taste

Snack

Item

QTY

Almonds

½ cup

Cottage Cheese

1 to 2 cups

Dinner

Item

QTY

Hamburger

2/3 lb

Bun, mustard, no mayo, whatever

Fries

Leucine

5g

Copyright © 2011-2012 by Kiefer

Before Bed (Weight Maintenance)

Item

QTY

Hypertrophic Potentiator Formu1 shake

p139 (no carbs)

Left over pizza, muffins, cereal,

Carbs

turnovers

Copyright © 2011-2012 by Kiefer

Back Loading

Train @ 2pm

Upon Waking

Item

QTY

Coffee

ad libitum

(optional)

Heavy Whipping Cream

2 tbsp

(optional)

OR

A.M. Accelerator Formula

1 shake

p125 (optional)

Snack (optional)

Item

QTY

Almonds

¼ cup

any nut, pretty much

Breakfast/Lunch (noon)

Item

QTY

Breakfast meat (or bacon)

6 oz (or 6 slices)

Cottage Cheese

½ cup

Tomatoes

1 medium, sliced (optional)

Pre-Training

Item

Ignition Formula

1 shake

p131 (optional)

Intra-Training

Item

Sustainer Formula

1 shake

p135 (optional)

Post-Training

Item

Hypertrophic Potentiator Formu1 shake

p139

Copyright © 2011-2012 by Kiefer

Snack (30 minutes later)

Item

QTY

Pineapple

½ cup

Cottage Cheese

1 to 2 cups

Post-postworkout (start 2hr later)

Item

QTY

Splurge

Hypertrophic Potentiator Formu½ shake

With each meal

Copyright © 2011-2012 by Kiefer

Back Loading

Train @ 4pm

Upon Waking

Item

QTY

Coffee

ad libitum

(optional)

Heavy Whipping Cream

2 tbsp

(optional)

OR

A.M. Accelerator Formula

1 shake

p125 (optional)

Snack (optional)

Item

QTY

Almonds

¼ cup

any nut, pretty much

Breakfast/Lunch (noon)

Item

QTY

Breakfast meat (or bacon)

6 oz (or 6 slices)

Cottage Cheese

½ cup

Tomatoes

1 medium, sliced (optional)

Pre-Training

Item

Ignition Formula

1 shake

p131 (optional)

Intra-Training

Item

Sustainer Formula

1 shake

p135 (optional)

Post-Training

Item

Hypertrophic Potentiator Formu1 shake

p139 (no carbs)

Bananas, Mango or Carb Powd 40 to 50 g of carbs

Post-postworkout (start 1hr later)

Item

QTY

Splurge

Hypertrophic Potentiator Formu½ shake

With each meal

Copyright © 2011-2012 by Kiefer

Back Loading

Train @ 6pm

Upon Waking

Item

QTY

Coffee

ad libitum

Whey Protein Isolate

1 scoop (~20g)

Drink before the rest of the meal

Breakfast meat

6 oz

Tomatoes

1 medium, sliced

Lunch

Item

QTY

Chicken Breasts

1 large

Salad

2 to 3 cups

Greek Salad or a simple lettuce salad

Olive Oil

2 tbsp

Vinegar

to taste

Snack

Item

QTY

Almonds

¼ cup

Cottage Cheese

1 cup

Pre-Training

Item

Ignition Formula

1 shake

p131 (optional)

Intra-Training

Item

Sustainer Formula

1 shake

p135 (optional)

Post-Training

Item

Hypertrophic Potentiator Formu1 shake

p139 (no carbs)

Dinner

Item

QTY

Protein powder, lean meat, cottage

Protein

~60 grams

cheese, whatever

Pizza

at least 2 slices

Copyright © 2011-2012 by Kiefer

Back Loading

Train @ 9pm

Upon Waking

Item

QTY

Coffee

ad libitum

(optional)

Heavy Whipping Cream

2 tbsp

(optional)

OR

A.M. Accelerator Formula

1 shake

p125 (optional)

Breakfast

Item

QTY

Eggs

3 large, whole

Breakfast meat

8 oz

Tomatoes

1 medium, sliced

Lunch

Item

QTY

Hamburger meat, extra lean

1 lb-pre cooked

Broccoli

2 cup

Cheese

1 slice

Melted American or ultra-low carb

Snack

Item

QTY

Eggs

2 large

hardboiled

Cottage Cheese

1 cup

Almonds

½ to 1 cup

Dinner

Item

QTY

Hypertrophic Potentiator Formula1 shake

p139

Something heavy and carby:

Steak or chicken

4 to 8 oz

Mashed Potatoes

ad libitum

(alternatives:)

Hamburger with fries; Reuben with hashbrowns…

Copyright © 2011-2012 by Kiefer

Post-Training

Item

Hypertrophic Potentiator Formula1 shake

p139

Bananas (Very Ripe)

1 to 3 large

Could use carb powder instead

Bedtime

Item

QTY

Hypertrophic Potentiator Formula1 shake

p139

Cereal or Flavored Instant OatmeA bowl

Alt: donut, muffin, crackers, pretzels,

mashed potatoes.

Copyright © 2011-2012 by Kiefer

Table of Contents

Chapter 1

Chapter 2

Chapter 3

Chapter 4

Chapter 5

Chapter 6

Chapter 7

Chapter 8

Chapter 9

Chapter 1

Chapter 2

Chapter 3

Chapter 4

Chapter 5

Chapter 6

Chapter 7

Chapter 8

Chapter 9

Chapter 10

Chapter 11

Chapter 12

Chapter 13

Chapter 14

Chapter 15

Chapter 16

Chapter 17

Chapter 18

Chapter 19

Chapter 20

Chapter 21

Chapter 22

Chapter 23

Chapter 24

Chapter 25

Chapter 26

Chapter 27

Chapter 28

Chapter 29

Chapter 30

Chapter 31

Chapter 32

Chapter 33

Chapter 34

Chapter 35

Chapter 36

Chapter 37

Chapter 38

Chapter 39

Chapter 40

Chapter 41

Chapter 42

Chapter 43

Chapter 44

Chapter 45

Chapter 46

Chapter 47

Chapter 48

Chapter 49

Chapter 50

Chapter 51

Chapter 52

Chapter 53

Chapter 54