The last 6 months I have stopped making sad excuses for myself regarding my training and started (training) more seriously again, and I’ve found that the 8-10 hours a week that goes into lifting shit and putting it back on the ground comes from the time I used to have to sit down and pound the keyboard as is evident from the blog post frequency as of late. However, I’m back with a genuine rant on a pet peeve of mine. I have discussed this before in a danish language post, but since then, everyone’s favorite brofessor, Brad Schoenfeld, has published a scientific article relating to this topic that has relit the fire (no relation to the Take That song).
What is sarcoplasmic hypertrophy (supposedly)?
Well, it’s no secret that when you lift heavy stuff and eat enough food, your muscles will get bigger. In fitness circles it is commonly said that gross muscle hypertrophy can occur in one of two ways: Either through increases in the volume of myofibrils inside the muscles, termed myofibrillar hypertrophy, or through expansion of the “other stuff” (usually the fluid) in the muscle, termed sarcoplasmic hypertrophy. In normal cells, the fluid inside the cells is called cytoplasm, and in muscle fibers, the corresponding volume is called sarcoplasm (“sarco” meaning flesh). Supposedly, heavy, strength-oriented training (big weights, few reps, long breaks) will grow “denser”, myofibrillar hypertrophy, whereas lighter, pump oriented training will induce “puffy” (often claimed “nonfunctional”) sarcoplasmic hypertrophy. “Non-functional”, because this latter type should not be associated with increases in strength, as the capacity to produce force is derived from the contractile, myofibrillar protein. The really funky part about this idea is that it is the purest broscience and it lacks both solid evidence as well as a sound biological rationale and somehow it has managed to creep into the scientific literature anyway.
From where does this idea originate?
the origin of the concept “sarcoplasmic hypertrophy” is somewhat murky. It is described in several of Pavel’s books (power to the People) and some of Mel Siff’s books as well, naturally with reference to your run of the mill obscure Russian research naturally obtained from Vladimir Zatsiorsky (yes, the former Russian sports scientist that wrote “Science and Practice of Strength Training”). I have been in contact with him, and he stated that the concept arose from research from the 50’es and 60’es where differential myofibrillar density was apparently reported. He (Zatsiorsky) then posited this hypothesis in his first book.
This theory was picked up by Russian researchers and the rest is, as they say, history. I have not been able to find these original studies, but merely note that they must have been in the very, very early stages of muscle biology and that these findings are not present in the more modern literature and inconsistent with a lot of other observations (as described below).
When characters as prominent as Pavel, Poliquin or Mel Siff repeatedly states something like this, it very easily becomes pseudofact. This is a problem. Nowadays you can even find mention of sarcoplasmic hypertrophy in the “real” science literature (e.g. Schoenfeld et al, 2010). Hell, you can even find some (albeit speculative) notice of it as far back as 1967 in the JAMA journal (Gorden et al, 1967). Chronic sarcoplasmic hypertrophy does occur under certain pathological circumstances in cardiac muscle, but for a number of reasons, this cannot be compared with exercise-induced skeletal muscle hypertrophy.
And mind you, it is not because that I know that sarcoplasmic does not exist. I don’t know if it exists or not, but I don’t think it does. What I do know, however, is that there is no real evidence supporting that it exists and no one, particularly not scientists, should describe something as being a “thing” without any evidence.
Why has “sarcoplasmic hypertrophy” as a concept gained such traction?
Well, because it does initially appear to make some sense. Bodybuilders are not as strong as powerlifters or weightlifters or strongmen, despite having very large muscles with a cross-sectional area that appears to be bigger than the mentioned categories of strength athletes. The rationale seems to be that if these bodybuilding muscles are not as strong, then they cannot be filled with myofibrils, the contractile units of the muscle and therefore it must mean that “bodybuilder muscles” are filled with “something else”. But the thing is, this contrasts with the direct observational evidence. Histology of skeletal muscle cross-sections has never shown muscles to have empty spaces. And secondly, we really do not need such an physiologically obscure explanation to the observed strength/size discrepancy in bodybuilders. We actually have a lot of other explanations to this:
- Strength is a skill and not just dependent on passive tissue properties. Lifting stuff in the 1-5RM range requires specific motor skill adaptations that bodybuilding style training does not cause. Hence strength athletes will tend to have higher 1-5RM strength relative to their 10-15RM compared to bodybuilders.
- If you do resistance training with high volume and extreme fatigue, you will most likely develop hypertrophy in both Type I myofibers and type II fibers, whereas strength oriented training will almost exclusively affect type II fibers. Although type I fibers have an isometric force production capability is almost as good as that of Type II fibers, their capacity to produce power (force X velocity) is much lower. As power is critical to manifestable strength, this means that type I fibers are less strong, volume for volume than fast, Type II fibers.
- Also, bodybuilding-style training will most likely cause other adaptations, like more mitochondria, more muscle glycogen, and more membrane proteins that serve to provide fatigue resistance. While these factors may contribute to gross hypertrophy, any such contribution would be very small.
- Bodybuilders focus their exercise on other muscles than strength athletes. If you compare hypertrophy across muscle groups, bodybuilders would most likely display much more pronounced chest, shoulder and arm hypertrophy, relative to strength athletes, but lesser hypertrophy of the erectors, core muscles, glutes, hamstrings, and possibly quads relative to strength athletes. All of those would translate into less measurable strength, relative to a power athletes of comparable body weight.
The bottom line is that the strength discrepancy can be explained wholly by other factors. Also, what is frequently omitted, is that as bodybuilding-style training gives other adaptations it also means that bodybuilders become good at other stuff than strength athletes. If you asked a person used to bodybuilding-style training, with high fatigue to perform as many reps as possible in the squat in 30 minutes at 60% of their 1RM, he or she would most likely beat the strength athletes as strength endurance is the domain of bodybuilding-style training.
Why can’t sarcoplasmic hypertrophy contribute to gross hypertrophy?
One of the reasons that this is a pet peeve of mine, is that I have done my fair share of muscle histology and if the sarcoplasmic hypertrophy does exist, there should be observable fluid-filled spaces in the muscle fiber or observable differences in myofibrillar packing density with light or electron microscopy and this is quite simply not the case. All muscle fibers are totally occupied by myofibrillar proteins, as in being 85-90% filled (Macdougall et al, 1982). The remaining space in a muscle fiber is made up of extracellular connective tissue, blood vessels, mitochondria, glycogen and membrane invaginations that serve to propagate the electric signals necessary for muscle activation. The space that is unoccupied by cellular organelles (the sarcoplasm) is very small in healthy muscle, as in a few (0.5-2) percent. From this, it should be obvious that even if the sarcoplasm is expanded by several hundred percent (independently of the remaining stuff that fills up the muscle), the contribution to gross muscle hypertrophy would be minuscule. And just to put the orders of change into context, 3 months of serious strength training will on average provide 15-25% of hypertrophy for men. For very trained individuals, the total hypertrophy relative to their untrained state can be in excess of 100%.
Some of the other stuff can expand, however. In trained endurance athletes, there is increased mitochondrial density, increased glycogen storage and increased capillary density. Normally (in untrained muscle), glycogen and mitochondrial combined occupies, something like 5-10% of muscle volume and this can increase to 15-20% in very trained individuals, but these are individuals in which the total myofibrillar volume have not changed. Technically, this could be termed sarcoplasmic hypertrophy or at least (more correctly) non-myofibrillar hypertrophy, but what’s the point? To these guys, hypertrophy is not relevant. But granted, Bodybuilding-style workouts stress fatigue tolerance more and may provide some degree or response on the mitochondrial volume or glycogen storage, compared to powerlifting style training, but still, the contribution to gross muscle hypertrophy would be minuscule.
What is the evidence for sarcoplasmic hypertrophy then?
One of the lines of evidence that I think have contributed to this notion is that protein synthesis can be measured in distinct muscle protein fractions. Simplified, this technology works by infusing subjects with stable isotope labeled amino acids for a period and then subsequent tissue samples (yes, muscle biopsies ;o) are taken out. The amount of the labeled amino acids having been incorporated into the biopsy is a consequence of the protein synthesis going on. In a lot of these studies, the investigators report both measures of mixed-muscle protein synthesis and Fractional Protein Synthesis for different muscle compartments, e.g. myofibrillar, mitochondrial and sarcoplasmic, with the former being for the total protein in the sample and the latter supposedly being for the specific compartment. And indeed, at least one study have shown doing resistance exercise to failure, at both high and low loads caused greater increases in sarcoplasmic fractional protein synthesis than not exercising to failure, as does slow, controlled repetitions compared to normal-speed repetitions, both of which lean towards the bodybuilding end of the resistance training continuum (Burd et al, 2010 and 2012).
However, there are two major hurdles to making inferences towards sarcoplasmic hypertrophy from this. First, the process of fractioning proteins in muscle samples into nuclear, myofibrillar, collagenous, mitochondrial and sarcoplasmic protein fraction is quite poorly validated, e.g. there is actually quite little proof that the mitochondrial fraction only contains mitochondrial proteins. Validating such a fractionation on a global scale (for the entirety of the proteins in a sample) is actually a rather brutal task as it requires some hefty technology and has quite simply not been done yet. This is just one of those “no questions” asked technologies that have some serious questions pertaining to it. At my old lab, ISMC, they have tried to validate this on a protein by protein basis and found that there is indeed significant contamination of protein species across these fractions (I don’t know if these data are on the way to being published, but if they are, I’ll, of course, update this post). Second, as already covered, even if these data can be trusted method-wise, the sarcoplasmic proteins constitute a very, very small portion of the muscle proteome. Even if this increase in sarcoplasmic protein synthesis could be translated into hypertrophy, the contribution relative to the expansion of the myofibrillar portion would be infinitesimal.
Brad Schoenfeld have been doing some interesting stuff as of late and in one of his studies he have been measuring the changes in body composition with resistance training using a technology called bioelectrical impedance spectroscopy, a technology that can supposedly separate the amount of total water and intracellular water on a whole-body level (Ribeiro et al, 2014). In this study, they find that intracellular water seems to increase more so than extracellular water as well as muscle mass. While the wording chosen in the paper itself is fairly conservative, Brad has been stating in the social media and his blog that this supports the existence of sarcoplasmic hypertrophy.
|Total body water||Intra-cellular water||Lean body mass|
However, when you read the paper you’ll see the study participants actually only grow about 1 kg of muscle during the resistance training (below), whereas the changes in body water is on the order of 1-3 Litres (see the graphs below). This means that most of the water that has been accumulated is outside of the muscle organ entirely.
Approximately 75% of muscle is water, so naturally, about 7-800 mL of water has been accumulated in the muscle and only 2-300 grams of muscle protein. As previously stated, this is oddly low as I know these guys can do a training study.
So, for several reasons, I have a hard time understanding how Brad can claim that this supports that sarcoplasmic hypertrophy has occurred:
- The method used is very indirect. It is validated by comparison to another indirect method, which is whole-body Deuterium and Bromide dilution which is in itself an indirect measure of water distributions in the body.
- The numbers in the study doesn’t really add up. They report quite small increases in muscle mass (4% for a 12 week period), and most of the increase in body water must be outside of the muscle (as it’s numerically bigger. And if the myofibrillar density (amount of protein per volume muscle) had decreased (as Brad suggests on social media), this would mean that the participants had gained less than the mentioned 2-300 grams of muscle protein (muscle dry weight), which would be almost inconceivable for a 12 week resistance training period in untrained individuals.
- But above all, there is no actual measure of the density of protein or myofibrils in skeletal muscle which would ultimately be needed to claim that this supports sarcoplasmic hypertrophy
Where does that leave us?
First of all, maybe we should discuss if it even makes sense to have a terminology for compartmentalized hypertrophy. Yes, mitochondrial volume, glycogen storage, and capillary volume can change with exercise, but with resistance exercise, this doesn’t contribute much to gross hypertrophy. Temporary cellular swelling following exercise or glycerol ingestion can also contribute to muscle size, as may longer-term swelling from creatine ingestion. But which of these should be considered “real hypertrophy” and does it even matter? As of now, there is absolute no evidence that supports that one form of training may lead to sarcoplasmic hypertrophy, whereas another leads to “real” hypertrophy. When muscle grows it is invariably because the cells are becoming filled up by cellular organelles of some sort, most frequently myofibrils.
And while I personally suspect that metabolically active tissue, e.g. during rapid changes in muscle mass or large energy turnovers, may require slightly bigger cytoplasms, I for one am not sure this can really be called hypertrophy and also I really think we should stop talking about sarcoplasmic hypertrophy as being proven fact, considering the blistering absence of evidence for it.
Thank you guys. That was a relief ;o)
Schoenfeld, B. J. (2010). The mechanisms of muscle hypertrophy and their application to resistance training. Journal of Strength and Conditioning Research / National Strength & Conditioning Association, 24(10), 2857–2872. doi:10.1519/JSC.0b013e3181e840f3
MacDougall, J. D., Sale, D. G., Elder, G. C. B., & Sutton, J. R. (1982). Muscle ultrastructural characteristics of elite powerlifters and bodybuilders. European Journal of Applied Physiology, 48(1), 117–126. doi:10.1007/BF00421171
Burd, N. A., Andrews, R. J., West, D. W. D., Little, J. P., Cochran, A. J. R., Hector, A. J., et al. (2012). Muscle time under tension during resistance exercise stimulates differential muscle protein sub-fractional synthetic responses in men. The Journal of Physiology, 590(Pt 2), 351–362. doi:10.1113/jphysiol.2011.221200
Burd, N. A., West, D. W. D., Staples, A. W., Atherton, P. J., Baker, J. M., Moore, D. R., et al. (2010). Low-Load High Volume Resistance Exercise Stimulates Muscle Protein Synthesis More Than High-Load Low Volume Resistance Exercise in Young Men. PloS One, 5(8), e12033. doi:10.1371/journal.pone.0012033
Ribeiro, A. S., Avelar, A., Schoenfeld, B. J., Ritti Dias, R. M., Altimari, L. R., & Cyrino, E. S. (2014). Resistance training promotes an increase in intracellular hydration in men and women. European Journal of Sport Science. doi:10.1080/17461391.2014.880192
Gordon, E. E. (1967). Anatomical and Biochemical Adaptations of Muscle to Different Exercises. Jama, 201(10), 755–758. doi:10.1001/jama.1967.03130100053013