Strength and hypertrophy with resistance training: chasing a hormonal ghost

Abstract

I am writing with regards to the article recently published in the European Journal of Applied Physiology by Ronnestad et al. (2011). The authors report in their abstract that ‘‘only L ? A [leg plus arm training—a high ‘anabolic’ hormonal exposure condition] achieved increase in the CSA at the part of the arm flexors with the largest crosssectional area (p \ 0.001), while no changes occurred in A [arm only training—a low ‘anabolic’ hormonal exposure condition].’’ Oddly, examination of Fig. 6 in their paper reveals that significant 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 figure (see Fig. 1). Additionally, a finding 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 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 author’s abstract) that: ‘‘L ? A had favorable muscle adaptations [no definition for ‘favorable muscle adaptations’ is given anywhere in the author’s paper] in elbow flexors 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 defined] 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 final 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 Communicated by Susan A. Ward.