Broscience Busted

Top Exercise & Nutrition Scientists Address the HMB/ATP Supplement Controversy

This is not easy for me to post. I am actually on a paper with the lab in question and I was involved in discussions with this lab about their research from 2010-2012. However, I began to have questions about their results and at a certain point, it is no longer sufficient to rely on your degree or behind a scientific publication. Extraordinary claims require extraordinary evidence which is why I distanced myself from the lab in question and when I had the opportunity to be involved with a paper that criticized some of the results, I took that opportunity to try to make things right, because I feel my involvement with that lab was wrong (even though I was in no way involved with the studies in question). It is also why I stopped doing ‘Muscle College Radio’ a very successful podcast that I made a good amount of money from, because that podcast was co-hosted by the head of the lab in question. So with that said, here are my, along with a multitude of top experts in fitness academia’s, critiques of the HMB/ATP data by Wilson et al. as published in the Journal of Strength and Conditioning Research here:

Addressing the following study specifically: Changes in body composition and performance with supplemental HMB-FA+ATP

Stuart M. Phillips, Ph.D., McMaster University; Alan A. Aragon, M.S., California State University, Northridge; Paul J. Arciero, Ph.D., Skidmore College; Shawn M. Arent, Ph.D., Rutgers University; Graeme L. Close, Ph.D., Liverpool John Moores University; D. Lee Hamilton, Ph.D., University of Stirling; Eric R. Helms, M.S., M.Phil, Sports Performance Research Institute New Zealand; Menno Henselmans, M.Sc., Bayesian Bodybuilding Research and Development; Jeremy P. Loenneke, Ph.D., The University of Mississippi; Layne E. Norton, Ph.D., BioLayne LLC; Craig Sale, Ph.D., Nottingham-Trent University; Brad J. Schoenfeld, Ph.D., Lehman College; Abbie E. Smith-Ryan Ph.D., University of North Carolina; Kevin D. Tipton, Ph.D., University of Stirling; Matthew D. Vukovich, Ph.D., South Dakota State University; Colin Wilborn, Ph.D., University of Mary Hardin-Baylor; and Darryn S. Willoughby, Ph.D. Baylor University

A number of us just could not see how data reported here [6] were happening. The gains in muscle mass are better than what has been reported by steroid users: So perhaps HMB is as good as a steroid?

Lowery et al. [6] reported, in contrast to an often-observed heterogeneity in training-induced hypertrophy, remarkably consistent between-group changes in muscle mass to find statistical significance between an HMB-FA+AP supplemented (n=8) versus a placebo (n=9) groups. The difference divergence between the supplemented and placebo groups occurred despite optimal training and optimal nutritional support. We note that HMB has been shown to result in a trivial training-induced adaptive advantage [8] and that the gain in lean body mass was in previously resistance-trained subjects who would have had less propensity to gain lean body mass [7]. For absolute clarity, could the authors please present the absolute body weight and body composition (lean body mass and fat mass) as opposed to % change data? We believe this would be helpful for readers.

There are data for calcium HMB showing improved muscle protein turnover [9]. We are unaware of any similar data for FA-HMB despite greater bioavailability and uptake (into what tissue is unknown) [3]. Do the authors know of any data showing that HMB-FA affects human muscle protein turnover [9]? We note that leucine had the same anabolic effects as calcium-HMB [9] and that dietary protein can exert a positive effect on gains in muscle mass with resistance training [1]. The placebo group, recipients of optimal protein/leucine intake, did not appear to respond at all to the overreaching phase. Can the authors speculate why?

Lowery et al [6] supplemented with ATP, which has undetectable bioavailability [2]. Wilson et al. [10], reported that ATP (400mg/d) resulted in a positive effect on muscle mass, strength, and power gains. The authors state [4] that a previously reported increase in post-exercise blood flow induced by the ATP [5] in the supplemented group could be responsible. The magnitude of that flow increase was only about 100-150 ml/min, was not consistently observed across weeks of supplementation, and lasted no more than 3-6min post-exercise [5]. How do the authors think a small, inconsistent, and short-lasting increase in blood flow could affect performance?

In the response to Hyde et al [4], Lowery et al. [6] stated that they selected “…a responsive population who possess a quantity of lean mass indicative of previous responses to resistance training…” What was the screening process to pick the participants? The authors state their subjects had muscle “…an order of magnitude [an order of magnitude is defined as 10-times greater, so this cannot be the case] higher than average lean mass…” Could the authors please state the exact criteria for inclusion as a participant were? It would be useful for the authors to describe how many participants were recruited and screened, the final number entered into the study and the number of dropouts. Were participants randomized to treatment and placebo groups, pair matched based on body mass, lean body mass, strength or another variable?

These results are extraordinary and thus require extraordinary justification, which is not forthcoming from the authors.



  1. Cermak NM, Res PT, de Groot LC, Saris WH and van Loon LJ. Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis. Am J Clin Nutr 96: 1454-1464, 2012.
  2. Coolen EJ, Arts IC, Bekers O, Vervaet C, Bast A and Dagnelie PC. Oral bioavailability of ATP after prolonged administration. Br J Nutr 105: 357-366, 2011.
  3. Fuller JC, Jr., Sharp RL, Angus HF, Baier SM and Rathmacher JA. Free acid gel form of beta-hydroxy-beta-methylbutyrate (HMB) improves HMB clearance from plasma in human subjects compared with the calcium HMB salt. Br J Nutr 105: 367-372, 2011.
  4. Hyde PN, Kendall KL and LaFountain RA. Interaction of beta-hydroxy-beta-methylbutyrate free acid and adenosine triphosphate on muscle mass, strength, and power, in resistance trained individuals. J Strength Cond Res 30: e10-e14, 2016.
  5. Jager R, Roberts MD, Lowery RP, Joy JM, Cruthirds CL, Lockwood CM, Rathmacher JA, Purpura M and Wilson JM. Oral adenosine-5′-triphosphate (ATP) administration increases blood flow following exercise in animals and humans. J Int Soc Sports Nutr 11: 28, 2014.
  6. Lowery RP, Joy JM, Rathmacher JA, Baier SM, Fuller JC, Jr., Shelley MC, Jager R, Purpura M, Wilson SM and Wilson JM. Interaction of Beta-Hydroxy-Beta-Methylbutyrate Free Acid and Adenosine Triphosphate on Muscle Mass, Strength, and Power in Resistance Trained Individuals. J Strength Cond Res 30: 1843-1854, 2016.
  7. Morton RW, Oikawa SY, Wavell CG, Mazara N, McGlory C, Quadrilatero J, Baechler BL, Baker SK and Phillips SM. Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men. J Appl Physiol (1985) 121: 129-138, 2016.
  8. Rowlands DS and Thomson JS. Effects of beta-hydroxy-beta-methylbutyrate supplementation during resistance training on strength, body composition, and muscle damage in trained and untrained young men: a meta-analysis. J Strength Cond Res 23: 836-846, 2009.
  9. Wilkinson DJ, Hossain T, Hill DS, Phillips BE, Crossland H, Williams J, Loughna P, Churchward-Venne TA, Breen L, Phillips SM, Etheridge T, Rathmacher JA, Smith K, Szewczyk NJ and Atherton PJ. Effects of leucine and its metabolite beta-hydroxy-beta-methylbutyrate on human skeletal muscle protein metabolism. J Physiol 591: 2911-2923, 2013.
  10. Wilson JM, Joy JM, Lowery RP, Roberts MD, Lockwood CM, Manninen AH, Fuller JC, De Souza EO, Baier SM, Wilson SM and Rathmacher JA. Effects of oral adenosine-5′-triphosphate supplementation on athletic performance, skeletal muscle hypertrophy and recovery in resistance-trained men. Nutr Metab (Lond) 10: 57, 2013.
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