Eur J Appl Physiol DOI 10.

1007/s00421-011-2148-0

LETTER TO THE EDITOR

Strength and hypertrophy with resistance training: chasing a hormonal ghost

Stuart M. Phillips

Received: 22 March 2011 / Accepted: 24 August 2011 Springer-Verlag 2011

Dear Editor: I am writing with regards to the article recently published in the European Journal of Applied Physiology by Rnnestad et al. (2011). The authors report in their abstract that only L ? A [leg plus arm traininga high anabolic hormonal exposure condition] achieved increase in the CSA at the part of the arm exors with the largest crosssectional area (p \ 0.001), while no changes occurred in A [arm only traininga low anabolic hormonal exposure condition]. Oddly, examination of Fig. 6 in their paper reveals that signicant hypertrophy did occur at two sites (of 4 measured) in the A arm, which is misleading by comparison not only to the statement in their abstract but also to a redrawing of their same gure (see Fig. 1). Additionally, a nding for which incomplete statistical analysis was reported was the change in muscle volume which was not different between the A and the L ? A arms. Since the change in muscle volume would be the product of the change in muscle cross-sectional area (CSA) (see Fig. 1 below) and the length of the muscle, it is hard to reconcile that there were differences in CSA between conditions with no difference in muscle volume change. Do the authors believe that the A arm got longer? A more plausible explanation is that there was no greater change in muscle CSA in the L ? A versus the A arm overall, except for the one site of the largest CSA. It is notable that the statistical comparison of CSA changes or volume changes

Communicated by Susan A. Ward. S. M. Phillips (&) Department of Kinesiology, Exercise Metabolism Research Group, McMaster University, 1280 Main St. West, Hamilton, ON L8S 4K1, Canada e-mail: phillis@mcmaster.ca

between the conditions was not reported; however, it would be surprising if those changes in volume or CSA were different. Given the lack of a statistical comparison between arms in terms of hypertrophy, it seems impossible to conclude (from the authors abstract) that: L ? A had favorable muscle adaptations [no denition for favorable muscle adaptations is given anywhere in the authors paper] in elbow exors compared to A (p \ 0.05). In conclusion, performing leg exercises prior to arm exercises and thereby increasing the levels of serum testosterone and growth hormone induced superior strength training adaptations [also not dened] compared to arm training without acute elevation of hormones. In fact, graphing the changes at each slice for each condition side-by-side shows that the differential hypertrophy, if it existed at all, is trivial (see Fig. 1) and is due to an artifact of not correctly aligning the arm CSA slices in the magnetic resonance (MR) scanner. If all arguments put forward previously are correct, then we can rule out the possibility that differential changes in muscle CSA or volume (i.e., hypertrophy) occurred between the L ? A and A arms. Thus, we are left to conclude that what the arm that trained and was preceded by leg exercises experienced during training was a superior neuromuscular adaptation to account for the greater 1 RM gain in strength. Interestingly, the authors present the progression in training load and show that it was identical between the L ? A and the A arms (Fig. 1). Thus, the arms apparently gained strength during the training program at an equivalent rate and achieved the same nal load during training. Yet through some inexplicable mechanism during maximal 1 RM strength testing there was greater strength in the L ? A versus the A arm. This is a surprising observation and one that was not even alluded to in the paper. The rise in hormone levels were certainly not

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Fig. 1 A repositioned image from Rnnestad et al. (2011) allowing the reader to make between arm comparisons. The parallel lines are to allow extrapolation from the same pre- and post-training sites from the L ? A (left panel) and A (right panel) arms. Note that in the A

arm the cross-sectional area from Sect. 8 to Sect. 9 increases during the pre-training and decreases during post-training indicating either that muscle atrophy took place or, more likely, that the pre- and posttraining scans were not aligned at the same point along the arm

helping the muscle train harder or more as evidenced by equivalent training loads lifted (see the authors Fig. 1). In fact, the authors report in their discussion that central fatigue was an issue and that it may explain why training loads were dampened in L ? A; this is in striking, and I would argue inexplicable contrast to the superior pre-topost strength gains in the L ? A versus A condition. The authors attempt to ascribe the greater strength gain to the greater gain in the muscle CSA at the largest point citing Bamman et al. (2000) in which, however, measurements of the triceps surae were made rather than of the biceps muscle as was studied by Rnnestad et al. (2011). What is more troubling is that the measurements of the muscle CSA were made according to the authors with The scanned arm stretched behind head and centered in the middle of the machine. The authors did not attempt (or at least did not report that they did) to align the pre- and post-training scans in terms of performing a coronal view of the arm or using bony landmarks (see my comment in Fig. 1). The authors also gave no estimate of variability of the procedure they used in their lab instead citing a procedure that they indicate as being similar to the MR scans they carried out by Moss et al. (1997). However, this is perplexing since, in the study by Moss et al. (1997) there is no mention of the subjects placing their arm over their head for the bicep scan and also the procedure used in that study to measure muscle CSA was computed tomography and not MR. The authors argue that differences between their ndings and our study in which hormonal increments affected neither strength nor hypertrophy were simply attributed to differences in exercise order (i.e., ours was arm before legs and theirs was legs then arms). My question is on what basis do they make this assertion? No evidence (or even speculation) is given as to how providing hormones to the muscle at the time of exercise (i.e., legs before arms) could be benecial. The difference in timing would be one of minutes, which seems like scant time to explain the

phenomenon the authors claim exists. If circulating hormones are interacting in some unknown way with protein synthesis, for example, then one would expect the elevation of these hormones in the time period when protein synthesis is known to be elevated would enhance protein synthesis, strength and/or hypertrophy; but this does not occur (West et al. 2009; Spiering et al. 2008). A number of studies indicate that increases in supposedly anabolic hormones (testosterone, growth hormone, and insulin-like growth factor) are not necessary for hypertrophy (Wilkinson et al. 2006), are not mechanistically linked to changes in local signalling (West et al. 2009; Spiering et al. 2008), do not elevate or in any way perpetuate muscle protein synthesis (MPS) (West et al. 2009), and have not been shown to result in increased muscle or muscle ber CSA or strength when leg exercises followed arm exercises but were followed by appropriate nutrition to effectively stimulate MPS and hypertrophy (Burd et al. 2009; West and Phillips 2010; West et al. 2010). The ndings of Rnnestad et al. (2011) are no more proof that systemic hormones exert an inuence in the resistance exercise training-induced adaptations than any previous paper in this area. It appears that selective reporting (considering only the site of the largest CSA), incomplete statistical analysis (not comparing the changes in CSA between arms), and questionable MR practices are the main messages from this paper.

References
Bamman MM, Newcomer BR, Larson-Meyer DE, Weinsier RL, Hunter GR (2000) Evaluation of the strength-size relationship in vivo using various muscle size indices. Med Sci Sports Exerc 32:13071313 Burd NA, Tang JE, Moore DR, Phillips SM (2009) Exercise training and protein metabolism: inuences of contraction, protein

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Eur J Appl Physiol intake, and sex-based differences. J Appl Physiol 106:1692 1701 Moss BM, Refsnes PE, Abildgaard A, Nicolaysen K, Jensen J (1997) Effects of maximal effort strength training with different loads on dynamic strength, cross-sectional area, load-power and loadvelocity relationships. Eur J Appl Physiol Occup Physiol 75:193199 Ronnestad BR, Nygaard H, Raastad T (2011) Physiological elevation of endogenous hormones results in superior strength training adaptation. Eur J Appl Physiol 111:22492259 Spiering BA, Kraemer WJ, Anderson JM, Armstrong LE, Nindl BC, Volek JS, Judelson DA, Joseph M, Vingren JL, Hateld DL, Fragala MS, Ho JY, Maresh CM (2008) Effects of elevated circulating hormones on resistance exercise-induced Akt signaling. Med Sci Sports Exerc 40:10391048 West DW, Phillips SM (2010) Anabolic processes in human skeletal muscle: restoring the identities of growth hormone and testosterone. Phys Sportsmed 38:97104 West DW, Kujbida GW, Moore DR, Atherton P, Burd NA, Padzik JP, De LM, Tang JE, Parise G, Rennie MJ, Baker SK, Phillips SM (2009) Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men. J Physiol 587:52395247 West DW, Burd NA, Staples AW, Phillips SM (2010) Human exercise-mediated skeletal muscle hypertrophy is an intrinsic process. Int J Biochem Cell Biol 42:13711375 Wilkinson SB, Tarnopolsky MA, Grant EJ, Correia CE, Phillips SM (2006) Hypertrophy with unilateral resistance exercise occurs without increases in endogenous anabolic hormone concentration. Eur J Appl Physiol 98:546555

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