6 - aug - 2013

Alan Aragons Research Review August 2013 [Back to Contents] Page 1

Copyright Augist 1st, 2013 by Alan Aragon Home: www.alanaragon.com/researchreview Correspondence: [email protected]

2 Clearing up common misunderstandings that

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

5 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]

6 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]

7 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]

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

after a 3-day high-carbohydrate diet on endurance performance. 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

13 Whats the ideal 6-set routine?

By Alan Aragon


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

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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 high-profile 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

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.

John S. Garrow, former University of London professor

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):

Itistruethatclinicaltrialspublishedin1907werepoorsciencebecausetheenergyintakewasnotmeasuredreliably.However,in197088agroupofclinicalscientistsattheMedicalResearchCouncilatHarrowpublisheddata fromwhatwasat that timetheworldsbestequippedunit forresearchonhumanobesityand related diseases. Taubes and Peter Attia are planning tofundhighquality researchaboutobesity.Perhaps theyshouldreadtheHarrowdatabeforetheystart.TheevidenceproducedbytheHarrowgroupconvincedmethatobesityiscausedbyanenergy imbalance.2 If Taubes and Attia were also convincedthat it is not just a hypothesis, but hard evidence, it mightsavethemalotofmoney.

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 (nusi.org) project is essentially a waste of time and resources. I would have to concur. It seems that the underlying agenda is to confirm pre-existent 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 low-carbohydrate 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 half-century 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 Organisation

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


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 trenddatadonotsupport thewidelyheldviewthat refined sugarasavailable for consumptionhas increaseddramaticallyoverthelast4050years.

2)Attheworldlevel,bothabsoluteandrelative(%energy)fromrefined sugar have remained relatively stable during a periodwheretotalfoodenergyavailableforconsumptionhassteadilyincreased.

3)Atregionallevel,anysmallincreasingtrendsinrefinedsugaravailability are dwarfed by the large increases in total foodenergyavailableforconsumption.

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 calorimetryand isotope measurement of de novo hepatic lipogenesisshowed that de novo hepatic lipogenesis of 38 g/d wasstimulated by 4 d of excess 50% carbohydrate energy intake(24).This totaldenovo lipogenesisrepresentsasmall fractionofboththesurpluscarbohydratesingested(360390g)

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

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 widelyembraced as an alternative to challenging modifications inlifestyleand intentionalcaloriereduction.Currentdatadonotsupportsuchunbridledenthusiasmforthesediets,particularlyas a substitute for highfiber, highcarbohydrate dietsemphasizing intake of fresh vegetables and fruits. Longtermstudies to determine the efficacy and safety of both popularandexperimentaldietsarewarrantedinthecurrentcontextoftheobesityepidemic.

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

Itseemsworryingthatsomeonewhoisalreadyconvincedthatobesity is due to an unidentified disordered environmentalstimulus causing excess carbohydrate intake, and in turncausing a disordered hormonal response, is leading anorganisation with vast resources to go looking for thesemechanisms. And this is despite perfectly adequateexplanationsbeingexplicitandimplicitinhisarticle.

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 quoteworthy:

Taubessviewsareparalysing. Ifwedontknowanything,wecant do anything.We are reduced towaiting for the resultsfrom research fundedby theNutrition Science Initiative. (Butthatwillberewarding:accordingtotheorganisationswebsite,itwill findout,once and for all,whatweneed toeat tobehealthysoundsmorelikemiraclethanscience.)


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. C

oncluding 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 insulin-mediated 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 Lara-Castro and Garveys review:12

Enhanced insulin sensitivity after weight loss is partiallyrelated to the lossof total fat andhighly correlatedwith theloss of visceral and intramyocellular fat (21,25,26). In thesestudies, it is important to emphasize that negative energybalanceproducesweight loss regardlessof themacronutrientcomposition of the diet (27).Although various diet plans canemphasize factors that affect hunger and satiety (28,29),caloric reduction is the essential component and asine quanonofweightloss.

References

1. 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]

2. Garrow JS. Energy imbalance in obesity is not "just a hypothesis". BMJ. 2013 May 22;346:f3079. [PubMed]

3. Garrow JS. Obesity and related diseases. Churchill Livingstone, 1988.

4. Attia P. Is sugar toxic? May 28, 2013 [The Eating Academy]

5. 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]

6. Cottrell RC. Essay was based on incorrect premises and an unproved assumption. BMJ. 2013 May 22;346:f3120. [PubMed]

7. World Sugar Research Organisation. WSRO Report on Trends in Per Capita Sugar Supply, 1961-2007. [PDF]

8. Economic Research Service, USDA. Food Availability (Per Capita) DataSystem: Summary Findings. Last Updated Mon. Aug 20, 2012. http://www.ers.usda.gov/data-products/food-availability-(per-capita)-data-system/summary-findings.aspx

9. Krieger JW. Insulin: an undeserved bad reputation (part 1). July, 2010. [Weightology.net]

10. Bradley B. Am I missing something in the essay on the science of obesity? BMJ. 2013 May 22;346:f3010. [PubMed]

11. 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]

12. 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. [PubMed]

13. Veerman JL. Let's act on the best available evidence on obesity. BMJ. 2013 May 22;346:f3015. [PubMed]


Effects of fructose-containing caloric sweeteners on resting energy expenditure and energy efficiency: a eview of human trials. r

Tappy L, Egli L, Lecoultre V, Schneider P. Nutr Metab (Lond).

013 Aug 13;10(1):54. [2 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 non-significant 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

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

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

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. Comment/application

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 glucose.1,2

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.

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.


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]

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%) first-year 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 9-months 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 (Olympiatoppen). 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, Sundgot-Borgen & 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 leanness-dependent and weight-dependent sports.6 This is the first large-scale 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 non-athletes, 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

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. Comment/application

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


The effects of pre versus post workout supplementation of creatine monohydrate on body

omposition and strength. c 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 PRE-SUPP 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. 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

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

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. Comment/application

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 protein-carbohydrate-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

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.


Significant effect of a pre-exercise high-fat meal after a 3-day high-carbohydrate diet on endurance performance.

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. Study limitations

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

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

Avalidprotocolisonethatresemblestheperformancethatisbeingsimulatedascloselyaspossible.Wheninvestigatingracetype events, the two most common protocols are time toexhaustionandtimetrials.Timetrialshavegreatervaliditythantime toexhaustionbecause theyprovideagoodphysiologicalsimulation of actual performance and correlate with actualperformance.

Comment/application

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 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.

\


1. Blaak EE, Saris WH. Postprandial thermogenesis and substrate utilization after ingestion of different dietary carbohydrates. Metabolism. 1996;10(10):12351242. doi: 10.1016/S0026-0495(96)90241-3. [PubMed]

2. 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]

3. Bray GA, Popkin BM. Calorie-sweetened beverages and fructose: what have we learned 10 years later. Pediatr Obes. 2013 Aug;8(4):242-8. [PubMed]

4. 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]

5. Sievenpiper JL, de Souza RJ, Mirrahimi A, Yu ME, Carleton AJ, Beyene J, Chiavaroli L, Di Buono M, Jenkins AL, Leiter LA, Wolever TM, Kendall CW, Jenkins DJ. Effect of fructose on body weight in controlled feeding trials: a systematic review and meta-analysis. Ann Intern Med. 2012 Feb 21;156(4):291-304. [PubMed]

6. Sundgot-Borgen J, Torstveit MK. Prevalence of eating disorders in elite athletes is higher than in the general population. Clin J Sport Med. 2004 Jan;14(1):25-32. [PubMed]

7. Batterham AM, Hopkins WG. Making meaningful inferences about magnitudes. Int J Sports Physiol Perform. 2006 Mar;1(1):50-7. [PubMed]

8. Cribb PJ, Hayes A. Effects of supplement timing and resistance exercise on skeletal muscle hypertrophy. Med Sci Sports Exerc. 2006 Nov;38(11):1918-25. [PubMed]

9. Hultman E, Sderlund K, Timmons JA, Cederblad G, Greenhaff PL. Muscle creatine loading in men. J Appl Physiol. 1996 Jul;81(1):232-7. [PubMed]

10. Jeukendrup A, Saris WH, Brouns F, Kester AD. A new validated endurance performance test. Med Sci Sports Exerc. 1996 Feb;28(2):266-70. [PubMed]

11. Hopkins WG, Schabort EJ, Hawley JA. Reliability of power in physical performance tests. Sports Med. 2001;31(3):211-34. [PubMed]

12. Hinckson EA, Hopkins WG. Reliability of time to exhaustion analyzed with critical-power and log-log modeling. Med Sci Sports Exerc. 2005 Apr;37(4):696-701. [PubMed]

13. 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. [PubMed]

14. Currell K, Jeukendrup AE. Validity, reliability and sensitivity of measures of sporting performance. Sports Med. 2008;38(4):297-316. [PubMed]

15. Okano G, Sato Y, Takumi Y, Sugawara M. Effect of 4h preexercise high carbohydrate and high fat meal ingestion on endurance performance and metabolism. Int J Sports Med. 1996 Oct;17(7):530-4. [PubMed]

16. Whitley HA, Humphreys SM, Campbell IT, Keegan MA, Jayanetti TD, Sperry DA, MacLaren DP, Reilly T, Frayn KN. Metabolic and performance responses during endurance exercise after high-fat and high-carbohydrate meals. J Appl Physiol. 1998 Aug;85(2):418-24. [PubMed]

17. Paul D, Jacobs KA, Geor RJ, Hinchcliff KW. o effect of pre-exercise meal on substrate metabolism and time trial performance during intense endurance exercise. Int J Sport Nutr Exerc Metab. 2003 Dec;13(4):489-503. [PubMed]


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 Bodybuilding.com 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 composition.

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 &

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):

Interestingly,leanbodymasswasincreasedby1.12.2kginAL,0.81.5kg inRLandnochange (0.01.6kg)seen inBL.However,thesechangeswerenotsignificantlydifferent.[...]

Although strength comparisons showed that subjects in ALhadthelargestmagnitudeinstrengthimprovementsinboth1RMsquat (63%and22%greater thanBLandRL, respectively)and1RMbenchpressstrength (35%and42%greaterthanBLand RL, respectively), these differences were not statisticallydifferent.

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

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.


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

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


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 maskindividual responses.Anumberof theparticipants respondedmuchmorefavourablytoonedietcomparedtotheother.Oneparticipant had an 11% increase in their peak force afterfollowingtheMPMFdietanda1%increaseaftertheHPLFdiet.Another experienced an 11% reduction in their peak forcefollowing theMPMF diet and a 4% reduction after the HPLFdiet.Likewiseoneparticipanthadatwofoldgreaterdecreaseintheir sum of 8 skinfolds after theHPLF diet compared to theMPMF interventionwhileanotherparticipantexperienced theexact opposite. Additionally, individual body compositionappeared to affect response. Therewere striking differencesbetween theparticipants lowest inbody fat compared to therest. The two leanest participants began both interventionswithasumofeightskinfoldsbetween36to45mm.Thesetwoparticipantsreportedthefirst,secondorthirdhighestlevelsofstress,fatigueandmooddisturbanceamongallparticipants."

References

1. Henselmans H. The myth of 1g/lb: optimal protein intake for bodybuilders. Feb 24, 2012. [Bayesian Bodybuilding]

2. Henselmans H. Weight loss: fast or slow? Apr/May 2013.. [AARR]

3. 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]

4. 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]

5. 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]

6. 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]

7. 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]

8. Campbell B, Kreider RB, Ziegenfuss T, La Bounty P, Roberts M, Burke D, Landis J, Lopez H, Antonio J. International Society of Sports Nutrition position stand: protein and exercise. J Int Soc Sports Nutr. 2007 Sep 26;4:8. [PubMed]

9. Lemon PW. Protein and amino acid needs of the strength athlete. Int J Sport Nutr. 1991 Jun;1(2):127-45. [PubMed]

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 readers.


W hats 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.

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. 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

(or more), depending on the strength of the trainee or the effort put into the previous sets. 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.

You'llsurelybeabletofindstudiessupportingsinglesets, but it appears that athletes benefit more frommultiple sets compared to novices. So, as a platform fordiscussion, Id like to use 6 sets to strike a balance betweenhighandlowvolumeprotocols.

However, I'vealwaysbeencuriousaboutsomething.Let'ssaythatwe'reseekingmaximum strengthandhypertrophygains,andwe'reallotted6setsperbodypartormovementpattern.Whichwouldyield thebest results;performing6 setsofoneexercise,3setsof2exercises,2setsof3exercises,or1setof6exercises (oranyother combination)?Howwouldyou setupthe programming formaximizing 1) bench press strength, 2)pechypertrophy,3)squattingstrength,4)deadliftingstrength,and5)legandglutehypertrophy?

Keepinmindthefollowingconditions:

Trainingsessionswilloccurtwiceperweek. Reprangescanvaryaccordingtotheexercise,butmust

stayconsistentthroughouttheentiretyofthestudy. Subjects perform no additional exercise (no cardio or

additionalstrengthtraining). Intrasetresttime is2minutes,atotalof6submaximal

warmup sets canbeused thatdon't count toward thetotal sets, allwork sets are performed close to failure,andnoadvanced techniquesareused (negatives,dropsets,supersets,orforcedreps).

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. 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.

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 [email protected].


Table of ContentsEditor's Cut: Clearing up common misunderstandings that plague the calorie debate, part 2: letters from the edge.Nutrition & ExerciseEffects of fructose-containing caloric sweeteners on resting energy expenditure and energy efficiency: a review of human trials.Preventing eating disorders among young elite athletes: a randomized controlled trial.

Supplementation: The effects of pre versus post workout supplementation of creatine monohydrate on body composition and strength.Less Recent Gem: Significant effect of a pre-exercise high-fat meal after a 3-day high-carbohydrate diet on endurance performance.Study Comment ReferencesIn the Lay Press: Challenging the protein intake guideline of 1 g/lb.Whats the ideal 6-set routine?

6 - aug - 2013

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