I’ve made it no secret that I think we’ve put the cart way too far in front of the horse when it comes to training for sarcoplasmic hypertrophy. What started out as a theory to explain increased muscle hypertrophy in the absence of strength gains in some early training texts (1,2) has morphed into complete training programs to target specific sub-cellular fractions (myofibrillar vs sarcoplasmic). In my previous posts, I’ve looked at some literature to explain how changes in metabolites alone (glycogen specifically) can’t explain hypertrophy, that bodybuilders aren’t that weak after all, how the approach to a rep can explain strength differences between bodybuilders and powerlifters and that even IF sarcoplasmic hypertrophy occurs we can’t call it non-functional.
After revisiting two recent papers (3,4) on the effects of load (%RM) on protein synthesis and hypertrophy in a discussion on Bret Contreras’s site, I had a light bulb moment about how these papers could relate to the idea of sarcoplasmic hypertrophy as well. You can find what I’ve previously written about these papers in my article entitled ‘30%‘ but it’s worth taking a specific look at the protein synthetic response of the myofibrillar and sarcoplasmic fractions following a single training session in Burd et al (3) with this idea in mind.
Does low load training have a preferential sarcoplasmic protein synthetic response?
If lower-load training preferentially targets the sarcoplasmic fraction, we would expect one of two effects when looking at the acute response to exercise: 1) a disproportionate sarcoplasmic response following lower-load relative to higher intensity training (either increased peak or sustained response) and that 2) the increase in sarcoplasmic protein synthesis may be greater than the myofibrillar fraction. Fortunately, Burd et al (3) took a look at both these fractions in groups of males who trained at either 90%-1RM to failure, 30%-1RM to failure or 30%-1RM work-matched to the 90%-1RM to failure condition. Lucky for us the paper has free full-text access online, so head over there to read the original, although for this discussion you can simply focus on figure one in the paper.
Looking at the acute protein synthetic response, we can see that training with 90%-1RM to failure resulted in a substantial increase in both myofibrillar and sarcoplasmic protein synthesis at four hours post-exericse (3.3 and 1.7 fold rest respectively). By 24 hours, protein synthesis was no longer elevated compared to rest with this training load. When looking at the group that trained with 30%-1RM to failure, there was increased myofibrillar protein synthesis at four hours (3.6x rest) only the response was sustained such that increased synthesis was detected at 24 hours post-exericse as well (2.9x rest). Conversely, while the 90%-1RM had increased sarcoplasmic synthesis at 4 hours, the increase in the 30%-1RM to failure group occurred at 4 and 24 hours post-exericse (1.4 and 1.5 fold rest respectively).
This sustained sarcoplasmic protein synthetic response in the low-load condition may seem supportive of the theory of sarcoplasmic hypertrophy, but given that myofibrillar protein synthesis was also sustained I still think that disproportionate sarcoplasmic growth is unlikely. We’ve met our first criteria from above and found that lower load training supported a longer synthetic response in the sarcoplasmic fraction, but fail to meet condition #2 as the myofibrillar fraction was also sustained. In fact, the authors of the paper make the case that this low-load training could be superior for overall hypertrophy training, and this is what ignited the hypertrophy blogosphere in a unified rage. It should be noted that the subsequent paper (4) failed to find increased hypertrophy as compared to high-load training despite the sustained synthetic response in the 30%-1RM group, so don’t throw out your heavy dumbbells just yet.
This isn’t the final nail in the coffin
This certainly isn’t the final nail in the coffin for the low-load training, sarcoplasmic hypertrophy theory. There’s no question that we can argue many more potential factors that could contribute to it, however the existing scientific literature just can’t support it right now. Can it contribute to overall muscle hypertrophy and occur following strength training? Sure it can! Can we say that it occurs preferentially or that we can target it with specific training programs? Absolutely not.
To date, I’ve still only found one paper (5) with a disproportionate sarcoplasmic response to training and it suggests that it was a consequence of strength training in general and not specific to bodybuilders or high-repetition training. If you’ve found some other resources, be sure to send them on to me because I LOVE reading and discussing anything hypertrophy-related. But at the very least this research still doesn’t support the idea that we can create strength training programs to engineer specific adaptations in these particular sub-cellular compartments (myofibrillar vs sarcoplasmic proteins).
All in all, sarcoplasmic hypertrophy remains a nice theory that needs more evidence in my mind, but I’m still not convinced that there are all these disproportionately weak bodybuilders waddling around with myofibril-deficient muscle. Are you?
- Zatsiorsky VM. (1995). Science and practice of strength training. Human Kinetics, Chapaign, IL. pp 63.
- Siff MC. (2003). Supertraining. Supertraining Institute, Denver, CO, pp 660.
- Burd, NA et al. (2010). PLoS One, 5(8).
- Mitchell, CJ et al (2012, April 19). Journal of Applied Physiology. Retrieved April 20, 2012 online
- Macdougall JD et al. (1982). Eur J Appl Physiol 48:117-126.