So I’ll close out my unofficial Sarcoplasmic Hypertrophy month with one more short post then call it a day before the traffic on the site drops off completely. If you search the net for sarcoplasmic hypertrophy articles, it won’t take you long to notice that a functional distinction is made between sarcoplasmic and myofibrillar hypertrophy. I cringe every time I see anyone in the fitness world use the word ‘functional’, it’s likely the most abused and misunderstood word in the personal training dictionary. Debates on what constitutes functional and non-functional training are best saved for another article, but I’d like to take a closer look at what constitutes functional and non-functional muscle.
Bodybuilders in all their non-functional glory
Under the main tenets of the theory of sarcoplasmic hypertrophy, high repetition sets with short rest intervals provide a metabolically taxing stimulus that results in muscle growth (1,2). This muscle growth differs from conventional hypertrophy in that non-force producing structures and metabolites contribute most to the growth, whereas myofibrils (force-producing structures inside muscle) do not increase. It has been shown that increased metabolite concentrations (creatine, glycogen) can attract water into the cell (3,4), leading to swelling that could acutely increase muscle fibre size, or at the very least modify protein metabolism (5). While I’ve discussed that these metabolites can lead to cellular swelling before (3,4), it’s not likely that bodybuilders are just weaklings full of glycogen and water (6).
On the other end of the spectrum we have myofibrillar hypertrophy, or so-called ‘functional’ hypertrophy (1,2). This type of muscle growth, where muscle increases proteins related to force production (actin and myosin) and ultimately the number of myofibrils, results in increased force production (strength). This mode of growth is often attributed to powerlifters, where training consists of very high load sets for few repetitions with long rest intervals.
While there are a few problems with this theory that I’ve pointed out previously (Glycogen, Weak Pt.1, Weak Pt.2), and existing data seems to suggest that sarcoplasmic growth may occur with conventional strength training anyway (7), the real problem here is that we’ve defined what constitutes functional adaptations with one parameter, namely peak force output (strength). Is it possible that in either hypertrophy-inducing case (high-rep, moderate load vs low rep, high load) what constitutes a functional adaptation could be completely different?
Sarcoplasmic hypertrophy IS functional
In the case above, sarcoplasmic hypertrophy is deemed non-functional as it doesn’t elevate peak force (strength) of the muscle, which in my mind doesn’t make much sense. If the muscle undergoes substantial metabolic stress (in the case of this argument high repetition sets with moderate load and little rest between sets), a functional adaptation would be one that enhances the ability of the muscle to sustain force production. This is a classic example of one of the basic principles of exercise physiology that states that muscle adapts specifically to the imposed demands of the exercise. Any increase in muscle metabolites, in this case glycogen and/or creatine, would act to sustain force output under intense anaerobic conditions, like an extended series of high rep sets with a short rest interval. Any cell growth or swelling (Sarcoplasmic Hypertrophy), would likely be a consequence of this useful adaptation. For sarcoplasmic hypertrophy and so-called bodybuilding-style training (high rep, moderate load, low rest) a non-functional adaptation would be one that fails to contribute to the ability of muscle to sustain force production over the course of a fatiguing exercise.
Friends don’t let friends use the word functional
At the risk of overstating this, there is nothing overtly wrong with the word functional, it’s simply our misuse of the word that’s the problem. The same thing that happens with our exercise prescription strategies seems to have carried over to the cellular and sub-cellular levels, despite the fact that functional adaptations are always ones that suit the demands placed on the tissue. So while I don’t think that sarcoplasmic hypertrophy is the primary means of muscle growth in bodybuilders and that they’re as weak as we’ve made them out to be (6), in a hypothetical world where these guys are simply swollen sacs of glycogen and water, this would be a functional adaptation. Maybe bodybuilders aren’t as non-functional as we’ve made them out to be.
- 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.
- Safdar, A et al. (2008). Physiol Genomics 32: 219–228.
- Ziegenfuss TN et al. (1998). J Exerc Physiol 1: 1–14.
- Parise G et al. (2001). J Appl Physiol 91(3): 1041-1047.
- Johnson, GO et al. (1990). J Sports Med Phys Fitness 30, 361–364.
- Macdougall JD et al. (1982). Eur J Appl Physiol 48:117-126.