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13 Whats the ideal 6-set routine?

By Alan Aragon

Copyright Augist 1st, 2013 by Alan Aragon


Clearing up common misunderstandings that

plague the calorie debate, part 2: letters from the
By Alan Aragon

Effects of fructose-containing caloric sweeteners

on resting energy expenditure and energy
efficiency: a review of human trials.
Tappy L, Egli L, Lecoultre V, Schneider P. Nutr Metab
(Lond). 2013 Aug 13;10(1):54. [PubMed]

Preventing eating disorders among young elite

athletes: a randomized controlled trial.
Martinsen M, Bahr, R, Brresen R, Holme I, Pensgaard
AM, Sundgot-Borgen J. Med Sci Sports Exerc 2013. DOI:
10.1249/MSS.0b013e3182a702fc [Epub ahead of print]

The effects of pre versus post workout

supplementation of creatine monohydrate on body
composition and strength.
Antonio J, Ciccone V. J Int Soc Sports Nutr. 2013 Aug
6;10(1):36. [Epub ahead of print] [PubMed]

Significant effect of a pre-exercise high-fat meal

after a 3-day high-carbohydrate diet on endurance
Murakami I, Sakuragi T, Uemura H, Menda H, Shindo M,
Tanaka H. Nutrients. 2012 Jul;4(7):625-37. [PubMed]

10 Challenging the protein intake guideline of 1 g/lb.

By Alan Aragon
Alan Aragons Research Review August 2013

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Page 1

John S. Garrow, former University of London professor

Clearing up common misunderstandings that plague
the calorie debate, part 2: letters from the edge.
By Alan Aragon

A very short letter by Garrow flatly counters that energy

imbalance in obesity is not just a hypothesis.2 Ill quote nearly
the entirety of his letter since its actually more like a little blurb
of advice (my bolding for emphasis):
Council at Harrow published data from what was at that time
the worlds best equipped unit for research on human obesity
and related diseases. Taubes and Peter Attia are planning to
fund high quality research about obesity. Perhaps they should
energy imbalance.2 If Taubes and Attia were also convinced
that it is not just a hypothesis, but hard evidence, it might


Revolution, or empty speculation?

I was tempted to title this installment Part Taubes instead of
Part 2 since Im going to focus primarily on his recent highprofile publication in the British Medical Journal (BMJ).1 At the
heart of his essay, Taubes is challenging the idea that obesity is
caused by overeating. Instead, he postulates the converse that
overeating is caused by obesity. Furthermore, he asserts that
obesity is a hormonal, regulatory disorder rather than a
condition that can be manipulated by caloric balance. He even
goes as far as calling the mainstream scientific view of obesity
the energy balance hypothesis, implying that the modulation
of bodyweight through thermodynamic principles is merely
speculative. As you can imagine, this set off a wildfire of dissent
from academics who are more familiar with the current data than
Taubes is. Perhaps this controversy was intentional on some
level who knows. Whats clear is that Taubes is amazingly
good at being a journalistic provocateur. The problem I see is
that he plays this role by omitting or ignoring large segments of
the body of scientific evidence.
Jimmies a-rustlin in the mail

Garrow references a book he wrote,3 wherein he discusses

obesity research done in the 1970s & 1980s by the Medical
Research Council. Garrows underlying message to Taubes is
that his Nutrition Science Initiative or NuSi ( project is
essentially a waste of time and resources. I would have to
concur. It seems that the underlying agenda is to confirm preexistent beliefs that carbs are the bad guy in the war against
obesity. This is not an implausible hunch, since the founders of
NuSi (Gary Taubes and Peter Attia) are well-established lowcarbohydrate diet extremists. Attia has stated explicitly that he
eats no more than five grams of sugar per day.4
Further evidence of NuSis biased agenda comes from
something I witnessed myself. Jamie Hale, a friend and
colleague of mine who specializes in behavioral nutrition and
cognitive science, approached Gary Taubes and offered to help
NuSi by conducting studies on the cognitive & behavioral
aspects of overeating. This would have been great since a halfcentury of controlled research has consistently demonstrated that
a caloric deficit is the single most important factor influencing
weight loss, and more recently, that sufficient vs. insufficient
protein influences the nature of that weight loss.5 What we need
a better grip on are the factors that influence eating behavior.
Taubes would have none of that. Hes apparently bent on
seeking confirmation of his flawed and oversimplified
carbsinsulinobesity model.
Richard C. Cottrell, Director of the World Sugar Research

Getting your jimmies rustled is internet-speak for getting

anywhere from upset to infuriated. Im certain that many
researchers read Taubes essay in awe-stricken incredulity, with
steam coming out of their ears. Im also certain that many of
them wondered how Taubes essay made it past peer-review. I
would chalk this up to Taubes political genius, and also the
tendency for all publications even academic journals to strive
for greater exposure, even if its from controversy that lacks a
rigorous evidence basis. If its framed as an opinion, or in
Taubes case, an essay, then it has earned a pass of sorts. To
our benefit, BMJ published a handful of letters of disagreement,
so lets dig into each of them.

Cotrell lays out several contentions with Taubes article.6 First,

Taubes falls into a circular argument based on incorrect premises
and unproven assumptions. His claim that increased sugar
consumption is responsible for the worldwide increase in obesity
is false since the food and agricultural organization research
shows that human sugar consumption has been steady for the
past 40 years. I agree with this point. Its not just some cheap
ploy from the sugar industry. This claim aligns with data from
the USDA/ERS data showing that caloric sweetener
consumption since 1970 comprises less than 1% of total caloric
increase.8 Specifically, only 42 kcal out of a total of 445 kcal

Alan Aragons Research Review August 2013

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increase from 1970 to 2010 has come from added sugars to the
diet. To quote the actual WSRO report, the three key findings
are as follows:7
1) Worldwide trend data do not support the widely held view
that refined sugar as available for consumption has increased

refined sugar have remained relatively stable during a period

availability are dwarfed by the large increases in total food

Secondly, Taubes claim of carbohydrates being uniquely

obesogenic in healthy/normal individuals via insulin-mediated
means is simply incorrect. For anyone who has not yet done so,
I highly recommend reading James Kriegers article series
titled, Insulin: an undeserved bad reputation.9 James goes into
great detail, using abundant research and sound logic to
dismantle the insulin-to-obesity model.
Furthermore, the claim that obesity results from the efficient
conversion of carbohydrate to fat is false. Indeed, the hepatic
conversion of carbohydrate to fat (de novo lipogenesis, or DNL)
is a minor and highly inefficient pathway to the accumulation of
body fat. To illustrate this, Ill quote a review by Saris:10
Recently, a combination of wholebody indirect calorimetry
and isotope measurement of de novo hepatic lipogenesis
showed that de novo hepatic lipogenesis of 38 g/d was
stimulated by 4 d of excess 50% carbohydrate energy intake
(24). This total de novo lipogenesis represents a small fraction

Therefore, Taubes is boldly dishing out factual errors upon

which his case rests tenuously. Cottrell makes the valid point
that Taubes dismisses positive energy imbalance as merely a
hypothesis of obesity since attempts to alleviate the obesity
problem have been unsuccessful overall. This is a hasty
assumption based on the idea that the treatment is false rather
than dieters failing to carry out the treatment. Another good
point Cotrell makes is that Taubes alternative explanation for
the pathogenesis of obesity is based on anecdote rather than
objective evidence.
Ben Bradley, general practitioner at the Meuchedet Health
Care Organisation
Bradley challenges Taubes idea that there are two competing
hypotheses excess energy intake versus a hormonal disorder.10
Calling it a disorder would imply a pathological derangement of
normal function. The accumulation of excess body fat is simply
a rather normal, and expected biological consequence of
continued storage of (wait for it) excess total calories. I
would additionally question why Taubes believes that a
derangement of a healthy hormonal millieu is exclusive to the
overconsumption of carbohydrate, but not fat. Estadella recently
wrote a review discussing the potential adverse effects of
excessive intakes of saturated fatty acids (SFA) and trans fatty
acids (TFA) on insulin action and other biological processes.11
Alan Aragons Research Review August 2013

Note that I would read the latter review with caution since plenty
of the supporting literature is animal research; long-term
controlled/comparative human research is lacking in this area.
This makes Estadella et als paper more of a discussion of
hypothetical mechanisms involved in dietary lipid-mediated
pathologies, rather than a solid case against high intakes of
dietary fat. Nevertheless, unlike Taubes heavy reliance on
anecdote and observation, Estadella et al base much of their
speculations on peer-reviewed research. On this note, Id like to
quote the conclusion of a review by Lara-Castro and Garvey
since it sums up the situation very well:12
Popular lowcarbohydrate, highfat diets are being widely
embraced as an alternative to challenging modifications in
lifestyleandintentionalcaloriereduction. Currentdatadonot
as a substitute for highfiber, highcarbohydrate diets
emphasizing intake of fresh vegetables and fruits. Longterm
studies to determine the efficacy and safety of both popular

Before I move on to the next letter, I have to quote Bradleys

skepticism of Taubes agenda behind NuSi, echoing my
previously mentioned concerns:10
obesity is due to an unidentified disordered environmental
stimulus causing excess carbohydrate intake, and in turn
causing a disordered hormonal response, is leading an
organisation with vast resources to go looking for these
mechanisms. And this is despite perfectly adequate

J Lennert Veerman, senior research fellow, School of

Population Health, University of Queensland
Veermans letter shoots several stiff challenges at Taubes, and to
me is the most potent of the bunch.13 First of all, the
dichotomization, or pitting of excess energy intake versus
hormonal dysregulation (via excess carb intake) is false since it
implies that the two are mutually exclusive, when they are not.
Veerman asks the rhetorical question of whether previous
generations of researchers saw energy imbalance as the cause of
obesity without thinking that several factors influence that
imbalance and the answer is, of course not. Secondly,
Veerman echoes Garrows main point that Taubes is simply
ignoring a substantial body of well-designed obesity research
that has given us more answers than Taubes is willing to
concede. Veerman feels that Taubes is throwing the baby out
with the bathwater in his approach to the problem. Veermans
third contention reiterates the concerns of other researchers
about Taubes bias and ulterior motives (that plus a combination
of a general state of wishful confusion). The way he put this is
Taubess views are paralysing. If we dont know anything, we
cant do anything. We are reduced to waiting for the results
from research funded by the Nutrition Science Initiative. (But
it will find out, once and for all, what we need to eat to be

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An important contention raised by Veerman is Taubes failure to

consider societal influences. This goes back to my previous
point that we need to gain a better understanding of the
environmental factors that drive eating behavior. We have a
good working grasp of the physiology of fat loss and fat gain,
but the elements of the world around us that drive weight gain
(or re-gain) are still poorly understood. Veerman ends off by
cautioning against Taubes insistence on evidence from
randomized controlled trials, since this is an overly restrictive
approach that ignores the value of population-based
interventions such as limiting the direct advertising of
commonly overconsumed foods to children.



Concluding thoughts
So, now that weve gone over many things that are either
misguided or utterly wrong with Taubes views, is there any
merit to them? Thats a tough question, since theyre plagued
with a killer combination of bias and ignorance. Taubes puts up
a facade of objectivity and balance by claiming there are two
competing hypotheses: 1) carbs cause obesity via insulinmediated means, and 2) overeating and/or under-moving causes
obesity through the accumulation of stored energy. The weight
of the evidence shows that #1 is hypothetical and lacking
scientific support, while #2 holds the vast majority of the
evidential weight. Is alleviating the obesity problem a matter of
eating less and/or moving more? For the most part, yes. Is the
proposed solution to eat less, move more good advice on its
own? No not without sufficient of qualification and discussion
of the details involved. Well dive into that in the next issue. In
the meantime, Ill leave you with a salient excerpt from LaraCastro and Garveys review:12
Enhanced insulin sensitivity after weight loss is partially
related to the loss of total fat and highly correlated with the
loss of visceral and intramyocellular fat (21,25,26). In these
studies, it is important to emphasize that negative energy
balance produces weight loss regardless of the macronutrient
composition of the diet (27). Although various diet plans can
emphasize factors that affect hunger and satiety (28,29),
caloric reduction is the essential component and asine qua



World Sugar Research Organisation. WSRO Report on

Trends in Per Capita Sugar Supply, 1961-2007. [PDF]
Economic Research Service, USDA. Food Availability (Per
Capita) DataSystem: Summary Findings. Last Updated
Mon. Aug 20, 2012.
Krieger JW. Insulin: an undeserved bad reputation (part 1).
July, 2010. []
Bradley B. Am I missing something in the essay on the
science of obesity? BMJ. 2013 May 22;346:f3010.
Estadella D, da Penha Oller do Nascimento CM, Oyama
LM, Ribeiro EB, Dmaso AR, de Piano A. Lipotoxicity:
effects of dietary saturated and transfatty acids. Mediators
Inflamm. 2013;2013:137579. [PubMed]
Lara-Castro C, Garvey WT. Diet, insulin resistance, and
obesity: zoning in on data for Atkins dieters living in South
Beach. J Clin Endocrinol Metab. 2004 Sep;89(9):4197-205.
Veerman JL. Let's act on the best available evidence on
obesity. BMJ. 2013 May 22;346:f3015. [PubMed]



Taubes G. The science of obesity: what do we really know

about what makes us fat? An essay by Gary Taubes. BMJ.
2013 Apr 15;346:f1050. [PubMed]
Garrow JS. Energy imbalance in obesity is not "just a
hypothesis". BMJ. 2013 May 22;346:f3079. [PubMed]
Garrow JS. Obesity and related diseases. Churchill
Livingstone, 1988.
Attia P. Is sugar toxic? May 28, 2013 [The Eating
Soenen S, Bonomi AG, Lemmens SG, Scholte J, Thijssen
MA, van Berkum F, Westerterp-Plantenga MS. Relatively
high-protein or low-carb energy-restricted diets for body
weight loss and body weight maintenance? Physiol Behav.
2012 Oct 10;107(3):374-80. [PubMed]
Cottrell RC. Essay was based on incorrect premises and an
unproved assumption. BMJ. 2013 May 22;346:f3120.

Alan Aragons Research Review August 2013

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Effects of fructose-containing caloric sweeteners on

resting energy expenditure and energy efficiency: a
review of human trials.
Tappy L, Egli L, Lecoultre V, Schneider P. Nutr Metab (Lond).
2013 Aug 13;10(1):54. [PubMed]
BACKGROUND/PURPOSE: Epidemiological studies indicate that
the consumption of fructose-containing caloric sweeteners (FCCS:
mainly sucrose and high-fructose corn syrup) is associated with obesity.
The hypothesis that FCCS plays a causal role in the development of
obesity however implies that they would impair energy balance to a
larger extent than other nutrients, either by increasing food intake, or by
decreasing energy expenditure. METHODS: We therefore reviewed
the literature comparing a) diet-induced thermogenesis (DIT) after
ingestion of isocaloric FCCS vs glucose meals, and b) basal metabolic
rate (BMR) or c) post-prandial energy expenditure after consuming a
high FCCS diet for > 3 days vs basal,weight-maintenance low FCCS
diet. Nine studies compared the effects of single isocaloric FCCS and
glucose meals on DIT; of them, six studies reported that DIT was
significantly higher with FCCS than with glucose, 2 reported a nonsignificant increase with FCCS, and one reported no difference. The
higher DIT with fructose than glucose can be explained by the low
energy efficiency associated with fructose metabolism. Five studies
compared BMR after consumption of a high FCCS vs a low FCCS diet
for > 3 days. RESULTS: Four studies reported no change after 4-7 day
on a high FCCS diet, and only one study reported a 7% decrease after
12 week on a high FCCS diet. Three studies compared post-prandial EE
after consumption of a high FCCS vs a low FCCS diet for > 3 days, and
did not report any significant difference. One study compared 24-EE in
subjects fed a weight-maintenance diet and hypercaloric diets with 50%
excess energy as fructose, sucrose and glucose during 4 days: 24-EE
was increased with all 3 hypercaloric diets, but there was no difference
between fructose, sucrose and glucose. CONCLUSIONS: We conclude
that fructose has lower energy efficiency than glucose. Based on
available studies, there is presently no hint that dietary FCCS may
decrease EE. Larger, well controlled studies are however needed to
assess the longer term effects of FCCS on EE. SPONSORSHIP: SNF
grants 320030135782 and 320030138428 to LT. PS is supported by
SNF grant 31003A-138065.

Study strengths

stoichiometric presumptions for the oxidation of glucose, fat and

protein this collectively is subject to the accuracy of the
methods, which the authors note can have a large degree of
error under some conditions. They also acknowledged the
possibility of an under-reporting of studies showing no
differences between FCCS and glucose. They cited the most
important limitation being the lack of studies comparing mixed
meals containing FCCS or glucose, in contrast to the greater
number of studies comparing the acute effects of pure FCCS vs
glucose loads. Another limitation was that no study was
specifically designed to examine the diet-induced thermogenesis
(DIT defined as the increase in resting EE following ingestion
of a meal) of low versus high-FCCS diets. However, this was
done by default in one study that compared 24-hour EE of
normal-weight and overweight subjects on a diet supplemented
with 50% caloric surplus as glucose, fructose, or sucrose, and
found no significant difference in the EE increase between
conditions. A final limitation I would add is that exercise was
not taken into account in the analysis, but in all fairness would
not likely have altered the conclusions.
This analysis generated several findings worth illuminating:
The 2 studies compared the DIT of sucrose and glucose
found a 43% and 53% larger DIT with sucrose than with
Collectively, the DIT with FCCS exceeded that of glucose
by 62%. The difference was statistically significant in 6 out
of 9 studies.
There is strong evidence that ingestion of fructose causes
greater DIT than an isocaloric amount of glucose in
healthy subjects across varying age and gender (as well as
diabetic status).
Compared to glucose, fructose is metabolized with less
efficiency (hence the greater energetic cist seen via DIT,
depicted here). Its noteworthy that roughly 40-50% of a
pure fructose load is converted into glucose and released
into circulation within 6 hours after ingestion.

The authors acknowledged several limitations (which is always

nice to see, since authors of reviews commonly downplay or
overlook them). First, all of the studies used indirect
calorimetry to measure energy expenditure (EE), relying on both
total oxygen uptake and respiratory exchange ratio, as well as

Collectively, these findings challenge the claim that fructose is

more obesogenic than glucose at least from a thermic
perspective. Bray and Popkin have implicitly blamed the
fructose content of sugar-sweetened beverages for the obesity
epidemic.3 According to the present analysis, this may not be
correct. The authors stated specifically that, The low energy
efficiency of fructose is certainly not a causal factor for weight
gain, and may even limit energy storage during fructose
overfeeding. They also raise the possibility that since fructose
does not lower EE (and in fact has done the opposite), it could
potentially impact bodyweight by increasing energy intake.
However, they also cite Morenga et als recent meta-analysis
of controlled and observational studies,4 which refutes this
possibility, since added sugars (free or within beverages) were
not found to independently impact bodyweight compared to
isoenergetic exchange with other carbohydrate sources.
Furthermore, another recent meta-analysis of controlled feeding
trials by Sievenpiper et al concluded the following:5 Fructose
does not seem to cause weight gain when it is substituted for
other carbohydrates in diets providing similar calories.

Alan Aragons Research Review August 2013

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With the fructose controversy still in full-swing, this is a timely

and relevant study particularly with worldwide obesity
prevalence continuing to raise public health concerns. This
review is the first to ever compare the human consumption of
higher versus lower fructose consumption on energy
expenditure. Consumption of fructose-containing caloric
sweeteners (FCCS), whose consumption has paralleled the
obesity increase, was compared with the consumption of glucose
or lower intakes of FCCS. The paper delves into several
interesting biochemical differences between glucose and
fructose metabolism, which serve to explain their difference in
energy efficiency.
Study limitations

Page 5

Preventing eating disorders among

athletes: a randomized controlled trial.



Martinsen M, Bahr, R, Brresen R, Holme I, Pensgaard AM,

Sundgot-Borgen J.
Med Sci Sports Exerc 2013. DOI:
10.1249/MSS.0b013e3182a702fc [Epub ahead of print]
PURPOSE: To examine the effect of a one-year school-based
intervention programto prevent the development of new cases of
eating disorders (ED) and symptoms associated with ED among
adolescent female and male elite athletes. METHODS: All 16
Norwegian Elite Sport High Schools were included (intervention
group (n=9) and control group (n=7)). In total, 465 (93.8%) firstyear student athletes were followed during high school (2008
2011, 3 school years). The athletes completed the Eating Disorder
Inventory 2 and questions related to ED at pre-test, post-test1 and 9months after the intervention (post-test 2). Clinical interviews
(Eating Disorder Examination) were conducted after the pre-test (all
with symptoms (n=115, 97%) and a random sample without
symptoms (n=116, 97%), and at post-test 2 all athletes were
interviewed (n=463, 99.6%). RESULTS: Among females, there
were no new cases of ED in the intervention schools, while 13% at
the control schools had developed and fulfilled the DSM-IV criteria
for ED not otherwise specified (n=7) or bulimia nervosa (n=1),
p=0.001. The risk of reporting symptoms was lower in intervention
than control schools at post-test 1 (OR: 0.45, 95% CI 0.23 to 0.89).
This effect was attenuated by post-test 2 (OR: 0.57, 0.29 to 1.09).
The intervention showed a relative risk reduction for current dieting
(OR: 0.10, 0.02 to 0.54) and 3 weight loss attempts (OR: 0.47,0.25
to 0.90). Among males, there was one new case of ED at post-test 2
(control school), and no difference in the risk of reporting
symptoms between groups at post-test 1 or 2. CONCLUSION: A
one-year intervention program can prevent new cases of ED and
symptoms associated with ED in adolescent female elite athletes.
SPONSORSHIP: Oslo Sports Trauma Research Center and
through a grant from the Norwegian Olympic Sports Center

Study strengths
This study is conceptually strong since methods to alleviate
eating disorders (EDs) among athletes is an understudied yet
important area of research. Perhaps not surprisingly, SundgotBorgen & Torstveit found that ED prevalence is higher in
athletes than the general population, higher in female than male
athletes, and more common among competitors in leannessdependent and weight-dependent sports.6 This is the first largescale randomized controlled trial to study the prevention of ED
among elite adolescent athletes. To-date, studies investigating
the effectiveness of ED prevention programs have involved nonathletes, so the present study addresses that gap. As
uncommonly seen in the literature, the authors offered their
opinion of the studys strengths, which they listed as the cluster
randomization of schools in order to avoid the mixing-up of
intervention and control group, and a lengthy follow-up period
(9 mo) involving both a questionnaire and a clinical interview.
Study limitations
As acknowledged by the authors, a larger sample could have
added further strength to the outcomes. This seems unlikely
since they included the entire population of male and female
first-year students attending all Elite Sports High Schools in
Alan Aragons Research Review August 2013

Norway (465 athletes representing 50 sports/disciplines

completed the study). Nevertheless, a post hoc calculation
revealed that the study was underpowered to demonstrate even
gross intervention effects in ED females.
This study generated several interesting findings:
Of the 34 athletes with a pre-existing ED, 26 of them (13
in the intervention and 13 in the control) completed the
study. At the final clinical interview, 16 of the 26 no longer
fulfilled the diagnostic criteria for an ED (12 in the
intervention and 4 in the control group).
Among the athletes who were healthy at the pretest and
completed the study (n=439), 8 of 61 female athletes in the
control schools were diagnosed with an ED at post-test 2
compared to none of 87 female athletes from the
intervention schools (p=0.001). Among males, one athlete
from a control school was diagnosed with an ED.
Thus, the total prevalence of female athletes with ED at
post-test 2 (including those with an ED at baseline) was
20.8% in the control schools (15 out of 72) compared to
1.0% (1 out of 97) in the intervention schools (p<0.001).
A significant reduction in dieting behavior was observed
for females in the intervention schools. Among male
athletes, no significant change in dieting behavior was
Compliance was relatively high. 89% of the athletes from
the intervention schools attended at least 3 of the 4 lectures
during the intervention, and 94.3% of the athletes joined
the Facebook page (and no, I did not troll this particular
Facebook page).
Overall, this study demonstrated that its possible to prevent new
cases of ED from occurring among adolescent female athletes in
a year-long, school-based program. The general lack of effect on
males was a default result of there not being a significant
prevalence of ED among them in the first place. Specifically, no
male athletes attending intervention schools were diagnosed with
an ED, while 2.3% (3 out of 133) from control schools met the
ED criteria. It bears repeating that among the study completers
who were healthy at the pretest, none of the female athletes from
the intervention schools were diagnosed with an ED at post-test
2. In contrast, 8 of 61 female athletes in the control schools were
diagnosed with an ED at post-test 2. Furthermore, of the athletes
with an ED, only 4 out of 13 in the control group at pretest
recovered at post-test 2, whereas 12 out of 13 athletes in the
intervention group recovered at post-test 2. To quote one of the
studys salient conclusions:
Thesignificantreductionin dietingbehavior observed for the
female elite athletes attending the intervention schools with
the most pronounced changes at the oneyear followup is
therefore especially encouraging. Particularly, since in most
societies the group most concerned with dieting and weight
previous studies most of the adult elite athletes who met the
criteria for an ED reported having started dieting and

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supplementation of creatine monohydrate on body
composition and strength.
Antonio J, Ciccone V. J Int Soc Sports Nutr. 2013 Aug
6;10(1):36. [Epub ahead of print] [PubMed]
BACKGROUND: Chronic supplementation with creatine monohydrate
has been shown to promote increases in total intramuscular creatine,
phosphocreatine, skeletal muscle mass, lean body mass and muscle
fiber size. Furthermore, there is robust evidence that muscular strength
and power will also increase after supplementing with creatine.
However, it is not known if the timing of creatine supplementation will
affect the adaptive response to exercise. PURPOSE: Thus, the purpose
of this investigation was to determine the difference between pre versus
post exercise supplementation of creatine on measures of body
composition and strength. METHODS: Nineteen healthy recreational
male bodybuilders (mean +/- SD; age: 23.1 +/- 2.9; height: 166.0 +/23.2 cm; weight: 80.18 +/- 10.43 kg) participated in this study. Subjects
were randomly assigned to one of the following groups: PRE-SUPP or
POST-SUPP workout supplementation of creatine (5 grams). The PRESUPP group consumed 5 grams of creatine immediately before
exercise. On the other hand, the POST-SUPP group consumed 5 grams
immediately after exercise. Subjects trained on average five days per
week for four weeks. Subjects consumed the supplement on the two
non-training days at their convenience. Subjects performed a
periodized, split-routine, bodybuilding workout five days per week
(Chest-shoulders-triceps; Back-biceps, Legs, etc.). Body composition
(Bod Pod(R)) and 1-RM bench press (BP) were determined. Diet logs
were collected and analyzed (one random day per week; four total days
analyzed). RESULTS: 2x2 ANOVA results - There was a significant
time effect for fat-free mass (FFM) (F = 19.9; p = 0.001) and BP (F =
18.9; p < 0.001), however, fat mass (FM) and body weight did not reach
significance. While there were trends, no significant interactions were
found. However, using magnitude-based inference, supplementation
with creatine post workout is possibly more beneficial in comparison to
pre workout supplementation with regards to FFM, FM and 1-RM BP.
The mean change in the PRE-SUPP and POST-SUPP groups for body
weight (BW kg), FFM (kg), FM (kg) and 1-RM bench press (kg) were
as follows, respectively: Mean +/- SD; BW: 0.4 +/- 2.2 vs 0.8 +/- 0.9;
FFM: 0.9 +/- 1.8 vs 2.0 +/- 1.2; FM: -0.1 +/- 2.0 vs -1.2 +/- 1.6; Bench
Press 1-RM: 6.6 +/- 8.2 vs 7.6 +/- 6.1.Qualitative inference represents
the likelihood that the true value will have the observed magnitude.
Furthermore, there were no differences in caloric or macronutrient
intake between the groups. (p > 0.05) for blood pressure or resting heart
rate. CONCLUSIONS: Creatine supplementation plus resistance
exercise increases fat-free mass and strength. Based on the magnitude
inferences it appears that consuming creatine immediately post-workout
is superior to pre-workout vis a vis body composition and strength.
SPONSORSHIP: None listed.

content was assessed as well, since pre-existent creatine intake

can impact the relative effectiveness of supplemental intake.
However, the lack of significant macronutritional differences
mitigates this potential confounder to a certain degree. The
authors acknowledge that this study had a small sample size and
short duration (Ill speak more about the latter in the following
section). I would add to this that highly trained/athletic subjects
also need to be examined in a similar design in future research,
since the present studys recreational trainees response might
not apply to advanced trainees.

As seen above, the main findings using magnitude-based

inferences7 were that creatine taken immediately after (as
opposed to immediately before) training caused a greater
increase in fat-free mass and decrease of fat mass. In addition,
the post-exercise creatine group experienced a greater gain in
bench press strength. The authors offered no mechanistic
speculations over what could have caused the superior effects
seen with post-exercise supplementation. However, they made
mention of Cribb & Hayes observation that a proteincarbohydrate-creatine supplement taken near the immediately
pre & post-training outperformed its ingestion at temporally
distant points from the training bout. Still, the latter design
doesnt specifically investigate pre- versus post-exercise timing.8

Although nutritional software analysis can be seen as a design

strength (some supplementation studies neglect diet tracking &
assessment altogether), it would be ideal if dietary creatine

My main issue with the present study is that, due to its short
duration, it doesnt necessarily address whether or not creatine
timing affects subjects who are already creatine-loaded. Hultman
et al observed that 3 g/day for 28 days was able to raise muscle
creatine levels similarly to a loading protocol of 20 g/day for 6
days.9 The dosing scheme of the present study was 5 g per day,
without a loading phase. Its possible that the subjects in both
groups were only fully creatine-loaded late in the study, shortly
after which it was over (possibly too soon to make a meaningful
comparison). To reiterate, the authors also acknowledge the
confounding potential of the small number of subjects, which are
compounded by strange results in both groups. For example, one
subject in the POST-SUPP and three in the PRE-SUPP group
had a minor reduction in FFM. Two subjects in the PRE-SUPP
group showed either no change or a decline in strength.
Ultimately, although this study breaks some ground, the question
of creatine timing needs further investigation.

Alan Aragons Research Review August 2013

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Study strengths
This study is innovative since its the first to investigate the
answer to one of the most frequently asked questions about
creatine dosing. A periodized resistance training program was
implemented. Dietary intake was tracked via recall at 4 separate
points in the trial, and analyzed with nutritional software.
Study limitations

Page 7

Significant effect of a pre-exercise high-fat meal after a

Murakami I, Sakuragi T, Uemura H, Menda H, Shindo M,
Tanaka H. Nutrients. 2012 Jul;4(7):625-37. [PubMed]
PURPOSE: We investigated the effect of macronutrient
composition of pre-exercise meals on endurance performance.
DESIGN: Subjects consumed a high-carbohydrate diet at each meal
for 3 days, followed by a high-fat meal (HFM; 1007 21 kcal, 30%
CHO, 55% F and 15% P) or high-carbohydrate meal (HCM; 1007
21 kcal, 71% CHO, 20% F and 9% P) 4 h before exercise.
Furthermore, just prior to the test, subjects in the HFM group
ingested either maltodextrin jelly (M) or a placebo jelly (P), while
subjects in the HCM ingested a placebo jelly. Endurance
performance was measured as running time until exhaustion at a
speed between lactate threshold and the onset of blood lactate
accumulation. All subjects participated in each trial, randomly
assigned at weekly intervals. RESULTS: We observed that the time
until exhaustion was significantly longer in the HFM + M (p < 0.05)
than in HFM + P and HCM + P conditions. Furthermore, the total
amount of fat oxidation during exercise was significantly higher in
HFM + M and HFM + P than in HCM + P (p < 0.05).
CONCLUSIONS: These results suggest that ingestion of a HFM
prior to exercise is more favorable for endurance performance than
HCM. In addition, HFM and maltodextrin ingestion following 3
days of carbohydrate loading enhances endurance running
performance. SPONSORSHIP: This study was supported by a
Grant-in-Aid from the Japanese Ministry of Education, Culture,
Sports, Science and Technology (No. 19200049), the Fukuoka
University Global FU program, and the Fukuoka University
Institute for Physical Activity.

Study strengths
This is quite an interesting study that has hasnt gotten a ton of
media exposure. To my knowledge, its the first to ever examine
the performance effects of a high-fat pre-load versus a high-carb
preload at the end of a structured carb-loading regime. The
subjects were collegiate long-distance athletes engaged in
physical training almost every day as opposed to
sedentary/deconditioned subjects. The carb-loading regime was
standardized to consist of 2562 kcal/day in total calories (71%
carbohydrates, 19% fat, and 10% protein) at all three meals for 3
days before the main trials.

time trial (TT).10-13 the problem is that TTE might not mimic
real-world race performance conditions as closely as TT. To
quote Currell and Jeukendrup:14
type events, the two most common protocols are time to
time to exhaustion because they provide a good physiological
simulation of actual performance and correlate with actual


The main finding of this study were that the high-fat meal (1007
kcal, 30% CHO, 55% F and 15% P) + maltodextrin (410 kcal)
outperformed both the high-fat + placebo & high-carb + placebo
meals. There was no significant performance difference between
the latter two conditions. the fact that fat oxidation was greater
in the high-fat meal conditions is no surprise, and its doubtful
that its of any functional importance. Its easy to mistakenly
conflate greater dietary fat oxidation with greater oxidation of
stored body fat.
To our benefit, the authors listed the results of each subject in
the table above. Notice how the worst performance in terms of
TTE belonged to one of the Subject A in the high-fat meal +
placebo condition; this subject did markedly better with the
high-carb meal + placebo. This outcome illustrates the
importance of not taking study outcomes as indisputably
applicable to all (especially given the small sample size),
without considering the variability of individual response.

The sample was small (8 subjects total). However, to alleviate

the compromised statistical power of a small sample, a crossover
was done. that is, all subjects underwent all 3 conditions with at
least 1 week washout between each trial. Its possible that the
applicability of the outcomes is limited to the endurance testing
protocol employed. Subjects first underwent am 80-minute
fixed-intensity bout at 71.8 % of VO2max (which corresponded
to the lactate threshold - LT), followed by a time-to-exhaustion
(TTE) test at a higher intensity (80% of VO2max), which was
between the LT and the onset of blood lactate accumulation
(OBLA). As I mentioned in the previous months issue, theres
some disagreement about validity of using TTE as opposed to

The authors concluded (in the abstract) that, ...ingestion of a

HFM prior to exercise is more favorable for endurance
performance than HCM. This is misleading since no significant
performance difference was seen between the isocaloric high-fat &
high-carb conditions. The only significant performance difference
was the superior TTE seen in the high-fat meal condition that
included an extra 410 kcal of carbs. This is put more
accurately in the conclusion in the full text which does omit
mention of the high-fat condition having a performance advantage
over the high-carb condition, except when extra carbs are consumed
instead of placebo. It should also be noted that the authors
conclusions are not supported by the outcomes of several previous
studies.15-17 The present study was missing an isocaloric high-carb
condition for comparison with the high-fat + carbs condition which
unsurprisingly topped the field in this case.

Alan Aragons Research Review August 2013

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Study limitations

Page 8








Blaak EE, Saris WH. Postprandial thermogenesis and substrate

utilization after ingestion of different dietary carbohydrates.
Metabolism. 1996;10(10):12351242. doi: 10.1016/S00260495(96)90241-3. [PubMed]
Sharief N, Macdonald I. Different effects of various
carbohydrates on the metabolic rate in rats. Ann Nutr Metab.
1982;10(1):6672. doi: 10.1159/000176546. [PubMed]
Bray GA, Popkin BM. Calorie-sweetened beverages and
fructose: what have we learned 10 years later. Pediatr Obes.
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Te Morenga L, Mallard S, Mann J. Dietary sugars and body
weight: systematic review and meta-analyses of randomised
controlled trials and cohort studies. BMJ. 2012 Jan
15;346:e7492. [PubMed]
Sievenpiper JL, de Souza RJ, Mirrahimi A, Yu ME, Carleton
AJ, Beyene J, Chiavaroli L, Di Buono M, Jenkins AL, Leiter
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Sundgot-Borgen J, Torstveit MK. Prevalence of eating
disorders in elite athletes is higher than in the general
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Batterham AM, Hopkins WG. Making meaningful inferences
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exercise on skeletal muscle hypertrophy. Med Sci Sports Exerc.
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Hultman E, Sderlund K, Timmons JA, Cederblad G,
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validated endurance performance test. Med Sci Sports Exerc.
1996 Feb;28(2):266-70. [PubMed]
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physical performance tests. Sports Med. 2001;31(3):211-34.
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analyzed with critical-power and log-log modeling. Med Sci
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Laursen PB, Francis GT, Abbiss CR, Newton MJ, Nosaka K.
Reliability of time-to-exhaustion versus time-trial running tests
in runners. Med Sci Sports Exerc. 2007 Aug;39(8):1374-9.
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of measures of sporting performance. Sports Med.
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Nutr Exerc Metab. 2003 Dec;13(4):489-503. [PubMed]

Alan Aragons Research Review August 2013

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Page 9

Challenging the protein intake guideline of 1 g/lb.

By Alan Aragon

Intro & background

The inspiration for the following discussion is an excellent
article by Menno Henselmans,1 who happens to be a subscriber
and contributor to AARR.2 This article has had a lot of impact
on the online fitness & bodybuilding community, since it makes
several important, well-supported points. In addition to Mennos
article (and a debate with him that followed shortly after its
publication), Ive recently discussed/debated this topic on the forums. All of this has finally led me here to
lay out my thoughts in an organized manner. The crux of the
debate is whether or not the 1 g/lb (2.2 g/kg) protein intake
guideline commonly recommended to bodybuilders and strength
athletes has sufficient scientific support. Menno makes a strong
case that it does not, and that the upper limit of effectiveness for
body composition goals is 0.82 g/lb (1.8 g/kg). Lets take a look
at the basis upon which this position stands.
The meat of the argument
Menno (Ill address by his first name since I know him
personally) listed a several studies that included at least one
condition where protein intake was significantly above the RDA
of 0.8 g/kg.3-6 However, among these 4 studies, only 3 of them
compare at least 2 conditions that markedly above the RDA,3-5
while one of them compared the RDA with double the RDA.6
Lets examine the 3 studies that matter and take note that Im
purposely going to skip over the studies that did not assess body

body density) between the middle and upper protein intakes.

Indeed, this study supports the idea that 2.2 g/kg is more than
enough, and 1.4 g/kg sufficed for strength-trained subjects, at
least within this short study duration of just under 2 weeks. In a
similar investigation, Lemon et al compared the 3.5-week effects
of a daily protein intake of 1.35 g/kg versus 2.62 g/kg in novice
bodybuilders.4 No significant difference in muscle mass or
strength gains were seen between conditions, again lending
support to the idea that 2.2 g/kg is excessive. Lets fast-forward
from the latter two 1992 studies to 2006. In strength/power
athletes, Hoffman et al compared 3 levels of protein intake (1.19,
1.74, and 2.36 g/kg) over a 12-week period, and found no
significant changes in body composition in any of the groups.5
Furthermore, there were no significant between-group
differences in strength gains. However, the authors pointed out
the following trends in body composition change and strength
gain which favored the upper end of protein intake (note that AL
= 2.36 g/kg, RL = 1.74 g/kg, and BL = 1.19 g/kg):
AL,0.81.5kginRLandno change(0.0 1.6kg)seenin BL.

Although strength comparisons showed that subjects in AL

RM squat (63% and 22% greater than BL and RL, respectively)
and RL, respectively), these differences were not statistically

It should be noted that contrary to the manuscript stating that

there were no statistically significant differences in strength gain
between the groups, Table 3 shows that 2.36 g/kg yielded a
significantly greater increase in 1-RM bench press strength than
1.74 g/kg (p < 0.05). Nevertheless, these studies overall show a
lack of cohesive support for protein intakes as high as the
proverbial 2.2 g/kg guideline.
Current position stands of the major authoritative organizations
are in line with these findings that fail to indicate the necessity
or optimality of 2.2 g/lb. The joint position stand of the
American Dietetic Association, Dietitians of Canada, and
American college of Sports Medicine lists 1.2-1.7 g/kg as an
appropriate range for strength-trained athletes.7 The position
stand of the International Society of Sports Nutrition (ISSN) lists
a slightly higher range for exercising individuals, 1.4-2.0 g/kg.8
Digging through the references of the ISSN position stand, I
found that the 2.0g/kg upper end was derived from a 1991
review paper by Lemon.9
Unaddressed research for & against

Using trained strength athletes and sedentary controls,

Tarnopolsky et al compared the effect of 0.86, 1.4, and 2.4 g/kg
over a 13-day period.3 2.4 g/kg did not increase whole-body
protein synthesis (WBPS) beyond that of 1.4 g/kg, but leucine
oxidation significantly increased in this condition, indicating
what the authors called nutrient overload. The sedentary
controls WBPS plateaued at 0.86 g/kg, and leucine oxidation
was increased at the two higher protein intake levels, which were
apparent nutrient overloads. There were no significant
differences in indexes of lean body mass (creatinine excretion &

There are a few bits of research worth examining that are not
included in Mennos article. Wilson and Wilson reported the
recommendations for athletes of 8 review papers and book
chapters ranged from 1.2-2.2 g/kg (table here).10 In support of
the 1.8 g/kg upper limit of effectiveness, Menno cites a 2011
review paper by Phillips and Van Loon.11 However, while they
recommend 1.3-1.8 g/kg for maximizing muscle protein
synthesis, they also state that athletes training under hypocaloric
conditions might optimize the ratio of fat-to-lean tissue loss from
higher intakes ranging 1.8-2.7 g/kg.

Alan Aragons Research Review August 2013

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Page 10

To the credit of Menno and other skeptics Ive debated, protein

intakes as high as 2.7 g/kg have not been specifically compared
with the amount that he and the major position stands maintain is
the upper limit. While intakes higher than 1.8 g/kg have been
shown to significantly benefit body composition, their
superiority has largely been seen in comparisons with either
inadequate amounts of protein (at or near the RDA), or with
amounts that are substantially below 1.8 g/kg, thus rendering
them unable to show a true advantage over this threshold.
Willoughby et al12 examined the effect of a protein & amino acid
supplement and found that the experimental group with an intake
of ~2.7 g/kg (supplement included) had greater gains in muscle
mass and greater increases in molecular markers of muscle
protein synthesis compared to the control group, whose protein
intake was ~2.2 g/kg. Notably, this occurred under hypercaloric
conditions. While its possible that the timing of the protein
supplement closely around the training bout was the critical
factor, theres also the strong possibility that the greater total
daily protein intake was responsible for the superior outcomes in
the experimental group especially since protein timing effects
are likely to diminish alongside abundant total protein intake.
Mettler et als recent work warrants discussion since it
investigated the protein needs of lean, trained subjects in
hypocaloric conditions,13 which is a scarcely investigated
scenario. The higher-protein group showed better lean mass
retention, and had an intake of 2.3 g/kg. The lower-protein
condition was assigned to 1.0 g/kg, which isnt an ideal
comparator since its an inadequate amount. An intermediate
value (e.g., 1.6-1.8 g/kg) would have made this comparison
much more meaningful. Its notable that although 2.3 g/kg
outperformed 1.0 g/kg, it still was not enough to completely
prevent the loss of lean mass. This could have been due to the
aggressive deficit, which was estimated to be 40% below
maintenance requirements. Another possibility is that more
protein than 2.3 g/kg was necessary to prevent lean tissue losses.
In any case, Mettler et al left big questions hanging by
neglecting to include an intermediate protein condition, despite
their conclusion that lean, trained subjects in hypocaloric
conditions have inherently higher protein requirements.
A very recent study by Pasiakos et al14 in certain ways improves
upon Mettlers design by comparing the RDA with double and
triple the RDA under hypocaloric conditions for 31 days
(Mettler et als study was only 2 weeks). No further benefits for
lean mass retention were seen in the 2x RDA compared with the
3x RDA group. In fact, a non-significant trend toward greater
lean mass retention occurred with 1.6 g/kg of protein compared
to 2.4 g/kg of protein. However, the applicability of these results
could be limited by the subjects confinement to low-intensity
cycling exercise, whereas Mettler et als subjects who were
leaner at baseline than Pasiakos subjects did a combination of
cardio and weights. Notably, Mettler et al saw a lower
proportion of LBM loss compared to what was seen by Pasiakos
et al. More detailed speculation over the discrepant outcomes of
these two studies is in the June 2013 issue of AARR.
Overall, the weight of the research evidence does not support the
superiority or optimality of protein intakes as high as the
common recommendation of 2.2 g/kg. The upper threshold of
Alan Aragons Research Review August 2013

effectiveness appears to be in the neighborhood of 1.6-1.8 g/kg.

Therefore, Menno has the licence to smile smugly, since his
assertions about the available literature are correct. However, a
big point I want to make is that the current body of evidence is
far from complete, so its wise to remain tentative and open to
uncharted conditions with different requirements, which Ill
discuss in the next section.
Another point I want to make is that rounding up protein
recommendations to a gram per pound for athletes is not an
impractical or detrimental move, as long as its not framed in a
more-is-better way. An admittedly small body of emerging data
suggests that reaching or slightly exceeding 2.2 g/kg might be
appropriate for some athletic populations. However, Ive seen
some folks blanketly recommend at least a gram per pound.
This is the erroneous more-is-better mentality that should be
cautioned against. It opens up the potential for grossly overdoing
protein intake to the point where it either impinges upon the
space allotted for optimized intakes of the other macronutrients,
or needlessly drives up total energy intake.
Gaps & limitations in the research
Optimal protein intakes of folks on ergogenic supplements like
creatine or androgenic/anabolic steroids have simply not been
investigated, let alone investigated for the purpose of
establishing dose-response relationships in hypocaloric,
hypercaloric, and eucaloric conditions. Its possible that these
cases have not only a higher ceiling of protein dosing
effectiveness (as seen in field observations), but also a lower
threshold of protein dosing for muscle retention.
Protein requirements for off-season and pre-contest bodybuilders
under varying degrees of surplus & deficit are still open to
investigation, particularly in the context of rigorous, periodized
training programs, and of course under various ergogenic
supplement or drug protocols. In fact, theres a scarcity of
studies investigating the needs of lean, hard-training athletes in
an energy deficit not just bodybuilders, but athletes across the
range of sports which have regulated weight classes.
Another confounder is that protein needs in the literature are
expressed in terms of total body mass. This is sort of a necessary
evil when discussing the literature, which does not express
protein needs as g/kg LBM. So, when mentioning that protein
needs are lower for eucaloric & hypercalorc conditions as
opposed to hypocaloric conditions in lean/athletic subjects, this
is more accurately in reference to proportional differences.
Absolute needs can be quite similar among those with the same
amount of lean mass. In theory, basing the protein target on
LBM is ideal. A gram per pound of net bodyweight would tend
to overestimate needs in obese individuals. However, estimating
LBM almost inevitably boils down to an educated guess. In
practice, I've set protein based on target bodyweight as a
surrogate measure of lean mass plus a small safety buffer. In my
field observations, one gram per pound of target bodyweight is a
simple and relatively fail-safe baseline protein intake from
which to adjust according to individual response.
The importance & variability of individual response
The figures listed in study outcomes are expressed as mean
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Page 11

values (averages). This means that a mixed bag of responses

occurred, some substantially higher or lower than the reported
mean. Rigidly latching on to a value such as 1.8 g/kg and
refusing to breach it is erroneously inductive reasoning; its a
gross overgeneralization. Assuming that it unquestionably
applies to your personal circumstances would be a large leap of
faith. To illustrate this point, Ill close with an excerpt from the
Masters thesis of Eric Helms, who examined the effect of
various maconutrient compositions on athletic subjects in
hypocaloric conditions:15
"Finally, it should be noted that mean effects can mask
individual responses. A number of the participants responded
participant had an 11% increase in their peak force after
Another experienced an 11% reduction in their peak force
following the MPMF diet and a 4% reduction after the HPLF
their sum of 8 skinfolds after the HPLF diet compared to the
MPMF intervention while another participant experienced the
exact opposite. Additionally, individual body composition
appeared to affect response. There were striking differences
between the participants lowest in body fat compared to the
rest. The two leanest participants began both interventions

10. Wilson J, Wilson GJ. Contemporary issues in protein

requirements and consumption for resistance trained athletes. J
Int Soc Sports Nutr. 2006 Jun 5;3:7-27. [PubMed]
11. Phillips SM, Van Loon LJ. tary protein for athletes: from
requirements to optimum adaptation. J Sports Sci. 2011;29
Suppl 1:S29-38. [PubMed]
12. Willoughby DS, Stout JR, Wilborn CD. ects of resistance
training and protein plus amino acid supplementation on
muscle anabolism, mass, and strength. Amino Acids.
2007;32(4):467-77. [PubMed]
13. Mettler S, Mitchell N, Tipton KD. Increased protein intake
reduces lean body mass loss during weight loss in athletes.
Med Sci Sports Exerc. 2010 Feb;42(2):326-37. [PubMed]
14. Pasiakos SM, Cao JJ, Margolis LM, Sauter ER, Whigham LD,
McClung JP, Rood JC, Carbone JW, Combs GF Jr, Young AJ.
ffects of high-protein diets on fat-free mass and muscle protein
synthesis following weight loss: a randomized controlled trial.
FASEB J. 2013 Sep;27(9):3837-47. [PubMed]
15. This is unpublished data straight from Eric himself, which is en
route to land in one of the peer-reviewed. Im extremely
thrilled to have the privilege of sharing this with the AARR








Henselmans H. The myth of 1g/lb: optimal protein intake for

bodybuilders. Feb 24, 2012. [Bayesian Bodybuilding]
Henselmans H. Weight loss: fast or slow? Apr/May 2013..
Tarnopolsky MA, Atkinson SA, MacDougall JD, Chesley A,
Phillips S, Schwarcz HP. Evaluation of protein requirements
for trained strength athletes. J Appl Physiol. 1992
Nov;73(5):1986-95. [PubMed]
Lemon PW, Tarnopolsky MA, MacDougall JD, Atkinson SA.
Protein requirements and muscle mass/strength changes during
intensive training in novice bodybuilders. J Appl Physiol. 1992
Aug;73(2):767-75. [PubMed]
Hoffman JR, Ratamess NA, Kang J, Falvo MJ, Faigenbaum
AD. Effect of protein intake on strength, body composition and
endocrine changes in strength/power athletes. J Int Soc Sports
Nutr. 2006 Dec 13;3:12-8. [PubMed]
Walberg JL, Leidy MK, Sturgill DJ, Hinkle DE, Ritchey SJ,
Sebolt DR: Macronutrient content of a hypoenergy diet affects
nitrogen retention and muscle function in weight lifters. Int J
Sports Med 1988, 09:261,266. [PubMed]
Rodriguez NR, DiMarco NM, Langley S; American Dietetic
Association; Dietitians of Canada; American College of Sports
Medicine: Nutrition and Athletic Performance. J Am Diet
Assoc. 2009 Mar;109(3):509-27. [PubMed]
Campbell B, Kreider RB, Ziegenfuss T, La Bounty P, Roberts
M, Burke D, Landis J, Lopez H, Antonio J. International
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athlete. Int J Sport Nutr. 1991 Jun;1(2):127-45. [PubMed]

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Page 12

(or more), depending on the strength of the trainee or the effort

put into the previous sets.
Whats the ideal 6-set routine?
By Alan Aragon
The following is an actual question posed to me by a colleague
of mine discussing programming & research ideas. I dont get
questions like this all the time, nor would I answer them in this
kind of depth unless I knew I was going to present them to a
worthy audience which in this case is the AARR readership.

sets, but it appears that athletes benefit more from
multiple sets compared to novices. So, as a platform for
discussion, Id like to use 6 sets to strike a balance between

However, I've always been curious about something. Let's say

that we're seeking maximum strength and hypertrophy gains,
and we're allotted 6 sets per bodypart or movement pattern.
Which would yield the best results; performing 6 sets of one
exercises (or any other combination)? How would you set up
the programming for maximizing 1) bench press strength, 2)

Subjects perform no additional exercise (no cardio or
warmup sets can be used that don't count toward the
total sets, all work sets are performed close to failure,
and no advanced techniques are used (negatives, drop

1) The ideal 6-set routine for maximizing bench press strength

would involve mainly the bench press, since developing max
strength at any given exercise largely involves building the skill
of properly executing the movement with progressive loading.
This is best accomplished by not diluting your focus with an
excessive array of different exercises. I would go with 4 sets of
bench press (at the width you plan on improving your max on),
and 2 sets of dips for the purpose of sneaking in some emphasis
on building strength in the triceps and lower pec to assist the
movement we're trying to maximally strengthen.

2) The ideal 6-set routine for maximizing pec hypertrophy would

be more multi-planar, and it would involve a broader rep range;
60-85% of 1RM, with the sweet spot being about 70-85% of 1
RM (roughly 6-12 reps). I would go with 2 sets of flat dumbell
press followed by 2 sets of incline dumbell press or incline
hammer strength presses, and finish off with 2 sets of either
decline dumbell presses or dips. Reps in the first 2 sets would be
5-7, 2nd 2 sets would be 8-10, and the final 2 sets would
terminate at around 12 reps. Ideally, pec-deck flyes or cable
crossovers would be thrown into rotation in place of the final
exercise done.
3) The ideal 6-set routine for maximizing squatting strength
would involve mainly the squat, since developing max strength
at any given exercise largely involves building the skill of
properly executing the movement under progressive loads.
Again, this isn't going to be accomplished by diluting your
efforts across a bunch of different exercises. I would go with 4
sets of squats, 2 sets of weighted hyperextensions (hip thrusts
could be subbed in here). This would be done for the purpose of
building strength at the top of the range of motion, since the
torque curve of the squat shows a decreased resistance as the
body becomes fully upright. Again, this would be done to assist
the movement we're focused on strengthening. For experienced
lifters, the mean intensity that maximizes strength gains is 85%
of 1RM. With this in mind, the same principles apply, but I like
to nudge the rep range a bit higher with lower-body work. This
is just a field observation; there really isnt any solid research
backing for it. After the warm-up, the first 3 work sets would be
in the 4-6 range, the 4th set would be 7-10 reps. The first work
set of hyperextensions would be about 4-6 reps. The final set of
hyperextensions would be in the 7-10 rep range.
4) The ideal 6-set routine for maximizing deadlifting strength
would involve mainly you guessed it the deadlift, for reasons
stated previously. I would go with 4 sets of whichever type of
deadlift variation you want to increase your max on. Id then
assist the movement with 2 sets of weighted hyperextensions
(barbell hip thrusts could be subbed in here) for the same reasons
it was done with the squat. The same principles (i.e., filling in
the gaps in the torque curve) I discussed with squatting apply to
the deadlift. After the warm-up, the first 3 work sets would be in
the 4-6 range, the 4th set would be 7-10 reps. The first set of
hyperextensions (or hip thrusts) would be about 4-6 reps. The
final set of hyperextensions would be in the 7-10 rep range.

For experienced lifters, research indicates that the mean intensity

that maximizes strength gains is about 85% of 1RM. We would
thus want the majority of sets to collectively average 5-6 RM.
With this in mind, lower rep ranges should be done at the start of
the training bout to take advantage of when we're most
neurologically fresh. So, after the warm-up, the first 2 work sets
on the bench press would be in the 3-5 range, the 3rd & 4th sets
would be 6-8 reps. The first work set of dips would be weighted,
limiting the rep range to about 6-8 reps. The final set of dips
would be unweighted, and would default to the 12-20 rep range

5) The ideal 6-set routine for maximizing leg & glute

hypertrophy would involve more exercises and a broader rep
range; 60-85% of 1RM. I would go 2 sets of squats followed by
2 sets of barbell hip thrusts (or weighted hypers), and then finish
things off with 2 sets of leg extensions. Once again, Ive
observed better size gains with higher reps for the legs, and
admittedly cannot provide substantive research support for this.
Reps in the first 2 work sets would be 6-8, second 2 sets would
be 9-11, and the final 2 sets would be 12-15 reps. Note: if glutes
werent part of what we were trying to put size on, then I would
replace the second exercise with leg curls.

Alan Aragons Research Review August 2013

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Page 13

In this clip, Joseph Grenny discusses his research on

empowering consumers by systematically influencing behavioral
change. Ive seen his full presentation at a recent conference, and
this shortened version captures many of the important and
interesting points. If youve never been exposed to Grennys
work, get ready for a treat.

If you have any questions, comments, suggestions, bones of

contention, cheers, jeers, guest articles youd like to submit, or
any feedback at all, send it over to

Alan Aragons Research Review August 2013

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Page 14