There’s more to science than a title

I never thought I’d find so many people who passionately believe that bodybuilders are all universally weak, over-inflated sacs of sarcoplasm. After writing a few articles discussing my thoughts on strength differentials between bodybuilders and powerlifters and that the scientific evidence for the theory of preferential sarcoplasmic hypertrophy is weak at best, I’ve had more than a few email exchanges calling me out.

Most of these emails are based on hypothetical examples and observations of ‘the weak bodybuilder at my gym’, however occasionally I get one that references a 1992 study from Digby Sale (heavily referenced in my previous posts on this). It’s worth taking a closer look at this study as it seems there is some confusion over the results and how it relates to our theories about sarcoplasmic hypertrophy in the gym.

Hypertrophy without increased isometric strength after weight training.

If you’re looking for justification that bodybuilders are disproportionately weak for their size, a paper with the title above would be a good start. Study finds size without strength, clearly must be sarcoplasmic hypertrophy, therefore all bodybuilders are weak. Unfortunately there’s just a few holes in that logic.

Scanning the results of the study, we see that after the 19 week training program (bilateral leg press only, from 7-10RM to 15-20RM during training), muscle size was increased (roughly 10.95%) and 1RM leg press strength increased (29.1%) in eight young men relative to the sedentary control participants (n=6). So far this isn’t the best paper to use to support the idea of hypertrophy independent of strength gains, seeing as both muscle size and strength on the training exercise increased.

It seems the isometric testing results are causing the confusion. While strength on the dynamic, leg press exercise increased, voluntary isometric knee extension strength was unchanged along with muscle activation and electrically evoked twitch torque. Sure enough, after reading that title really closely again, we see that it’s not hypertrophy without increased strength, it’s hypertrophy without increased isometric strength, an important distinction.

It’s certainly tempting to use this study as indirect proof of sarcoplasmic hypertrophy, but the findings of this study relate more to the specificity of strength than the overall ‘weakness’ of the bodybuilding population. You’ll certainly find studies when isometric and dynamic strength change in concert, but you’ll also find times when it doesn’t (like this one). With this specific study, it’s tempting to conclude that the increased CSA failed to contribute to the gains in strength (neural adaptations), but there are more than a few leaps of faith going from evoked isometric contractile properties to strength in a multi-joint, dynamic exercise.

Thinking about our standard gym arguments, the fact that muscle size increased alongside dynamic strength as measured with the actual training exercises, we see that this paper clearly is not consistent with the theory of preferential sarcoplasmic hypertrophy in bodybuilders.


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Dan Ogborn