Arms Don't Grow Faster With Leg Training: Stuart M. Phillips Busts Ronnestad's "Hormonal Ghosts"

Image 1: Although Tom Platz had massive
arms, as well, there is little conclusive scientific
evidence that this was a result of leg training.

Usually I am offering you my thoughts and comments on the results of the studies I am presenting here at the SuppVersity. In this case however, I am going to rely on the insightful analysis of Stuart M. Phillips, head of the Department of Kinesiology, Exercise Metabolism Research Group at the McMaster University, who spotted some interesting inconsistencies in a recently published paper by Ronnestad et al. who had reported that (contrary to conclusive findings from dozens of study by Phillips and others) endogenous hormone release from leg training had a major impact on the anabolic response in the arm flexors (cf. news from March, 2nd / I plead guilty of not having seen these inconsistencies, though I must say in mitigation that back in March I only reported, not commented on studies).

As Phillips points out, Ronnestad's conclusion that training legs+arms results in bigger guns or, rather, that without training legs, your arms won't grow at all is funded in

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 (Phillips. 2011)

In his analysis of the Ronnestad study, Phillips shows conclusively that, according to Ronnestad's own figures (Phillips refers to figure 6 of the paper, in particular), the authors' statement 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 cross-sectional area (p \ 0.001), while no changes occurred in A [arm only training—a low ‘anabolic’ hormonal exposure condition]. (Ronnestad. 2011)

is not sustainable, since "examination of Fig. 6 in their paper reveals that significant hypertrophy did occur at two sites (of 4 measured) in the A arm", i.e. the non-leg-trained arm. By means as simple as drawing a few vertical lines (cf. figure 1) Phillips is able to show that the hypertrophic response to the training stimulus was in fact identical in three out of the four measured cross sections.

Figure 1: Four horizontal lines are all it took Phillips to show that there must be something wrong with Ronnestad's data; after all, it is unlikely that section 8 of the biceps had atrophied in the course of the stud (illustration taken from Phillip's letter to the editor of the European Journal of Applied Physiology)

Phillips makes a point that, unless one assumes that - for whatever reasons - there has been a strictly localized atrophy in section 8 of the arm (cf. mismatch of pre-values in left and right graph of figure 1), the most likely explanation for the mismatch would be that "the pre- and post-training scans were not aligned at the same point along the arm". Smart-witted as Phillips is, he also observed that with the purportedly greater changes in muscle cross-sectional-area in the leg+arm condition it is strictly impossible for the muscle volume to be identical, unless "the authors believe that the A arm got longer". I would assume that you agree with me that even with eccentric muscle training this would be a rather surprising event. Consequently, this is another argument in favor of the obvious absence of measurable effects of an overall more anabolic milieu in the "arm + leg training"-condition on the hypertrophy response to strength training - or, in short, we still have no conclusive evidence that training legs before arms would make the latter grow faster.

Image 2: Make your biceps grow with the SuppVersity EMG series!

Now, if the hypertophy response was identical, it is even more surprising that the "leg+arm" group exhibited "through some inexplicable mechanism" (Phillips. 2011) an overall greater 1RM strength than the control group. Phillips, who does not refrain from pointing out that "this [was] a surprising observation that was not even alluded to in the paper", argues that this result stands in stark contrast to the "central fatigue" hypothesis Ronnestad et al. cite as an explanation for the "dampened" (Ronnestad. 2011) training loads in the "leg+arm" training group. Phillips, on the other hand, speculates that it could be a direct result of a "a superior neuromuscular adaptation" (Phillips. 2011, my emphasis), which would be the exact opposite of what Ronnestad et al. had in mind.

Even if one neglects the questionable measuring practice of Ronnestad et al., in the course of which the "scanned arm [was] stretched behind the head and centered in the middle of the machine" (Ronnestad. 2011), the absence of an "estimate of variability of the procedure they used in their lab" and the questionable reference to "similarities" to magneto resonance scans (note that Ronnestad et al. used CT scans ;-) carried out by Moss et al. (Moss. 1997), the Ronnestad study is a particularly good example for the way research hypotheses can interfere with the "objective results" of scientific studies by establishing a (often unconscious) bias towards "desired" results. Selective reporting, incomplete statistical analysis and ad-hoc explanations for differences to the findings of previous studies are the undesirable, yet completely human manifestations of this phenomenon, I want everyone of you to be aware of - even if this means that my own thoughts and conclusions, which are almost always produced under time-pressure, are about to get more critical comments in the future ;-)