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Sarcoplasmic hypertrophy: the bros were probably right Part 3

Sarkoplasmatische Hypertrophie: die Bros lagen wahrscheinlich richtig Teil 3

Having discussed the phenomenon of sarcoplasmic hypertrophy in more detail in the first two parts of this article series and looked at a number of studies and mechanisms that may be associated with sarcoplasmic hypertrophy, in this final part of this article series I will summarize the current state of research and, in the appendix, discuss more recent findings that have emerged since the original article was completed.

What about steroids?

One more thing before we get to the summary: I know I'm going to get some questions about steroids. Do they contribute to sarcoplasmic hypertrophy?

Bro wisdom says yes. A lot of people report gaining weight quickly when they start using steroids (more weight than could be explained by just myofibrillar hypertrophy) and that they also lose this weight very quickly when they stop using these substances, probably indicating shifts in the amounts of water their body is storing.

However, it is not always obvious that this water is stored in the muscles themselves (some users report that their muscles feel 'fuller', while others perceive this phenomenon more as a bloated feeling) and the two studies that have looked at this issue so far have reported no increase in intramuscular water (32, 33).

However, dosing may be an issue here: The dosages used by exercisers in the real world are rarely used in scientific studies for ethical reasons. In the MacDougall study, sarcoplasmic volume relative to muscle fiber volume was much higher in the elite strength athletes (most of whom used steroids) compared to the "normal" study participants.

On the other hand, in the single muscle fiber studies comparing bodybuilders with power athletes and untrained control group members, no significant differences were observed between the muscle fibers of bodybuilders who reported steroid use and the muscle fibers of bodybuilders who reported no steroid use.

However, in one study, steroid-free strength athletes were able to produce almost 50% more force per unit of quadriceps muscle mass than bodybuilders who used steroids (34) (although training differences are also likely to have played a role).

In other words, it's hard to say what role steroids play, if any.

Let's summarize everything:

  1. Sarcoplasmic hypertrophy has never been measured convincingly in humans - at least not by the standards that would convince me personally. One study showed an increase in intracellular water after exercise, but the overall hypertrophy observed in this study was very small, so I wouldn't put too much faith in these results. Another study was able to show a low degree of sarcoplasmic hypertrophy combined with very robust overall hypertrophy after six months of training, but due to the very low degree of sarcoplasmic hypertrophy measured, I would not place too much confidence in this study either. The elite strength athletes in this study had more sarcoplasmic volume relative to muscle volume, but since they were not involved in any intervention, it is impossible to know if these differences were due to training or pre-existing differences.
  2. Although undissolved non-protein components in muscle (such as glycogen) could potentially contribute slightly to sarcoplasmic hypertrophy, any effect would be small and temporary. An increase in the proportion of sarcoplasmic proteins relative to the amount of myofibrillar protein would be more likely to be the cause if sarcoplasmic hypertrophy were to occur.
  3. We know that sarcoplasmic protein synthesis and sarcoplasmic protein degradation are not directly related to myofibrillar protein synthesis and myofibrillar protein degradation and that in mammalian muscle, although a 3:1 ratio of myofibrillar to sarcoplasmic protein is typical, a 1:1 ratio has also been observed (albeit only in medium aged rabbits) with no apparent adverse effects.
  4. The maximum force of individual muscle fibers is more closely related to muscle fiber diameter than to muscle fiber cross-sectional area. In general, as the cross-sectional area increases, the force relative to the cross-sectional area decreases. Without alternative explanations (all of which are unlikely under most circumstances in healthy young men - things like accumulation of inorganic phosphates and post-translational modifications of contractile proteins), the most obvious reason for this decrease is a decrease in myofibrillar density - i.e. sarcoplasmic hypertrophy.
  5. Although the picture painted by the currently available scientific literature is blurred, it appears that strength training maintains the relationship between strength and cross-sectional area as muscle fibers grow. And it could be that this is not the case with bodybuilding style training. However, some of the studies that showed increased strength per muscle cross-sectional area used lighter weights (60% of 1RM) and one study even showed that bodybuilders' quadriceps torque relative to muscle cross-sectional area was higher than that of powerlifters.
  6. It could also be that the likelihood of sarcoplasmic hypertrophy increases as muscle fibers become significantly larger. As muscle fibers grow, capillary density decreases relative to muscle fiber cross-sectional area and mitochondrial density also decreases, causing the muscle to rely more on anaerobic metabolism, which is carried out by sarcoplasmic proteins. Even in elite powerlifters, it was more muscle thickness that correlated very closely with strength (although this study did not measure muscle fiber cross-sectional area, it may have shown an equally strong correlation).
  7. Based on the currently available data with highly trained subjects, there are too many potentially confounding factors to say whether different training styles increase the likelihood of sarcoplasmic hypertrophy. In vivo measurements are influenced by muscle insertion points, muscle activation, cocontractions of antagonistic muscles, motivation, muscle lever arm, muscle flexion angle, etc. So far, most of the direct comparisons we have are in vivo comparisons, which means that there are not many studies at the level of individual muscle fibers from which we could see what is going on at the cellular level (which is the level to look at if you want to study sarcoplasmic hypertrophy). The only study that has compared muscle fibers of bodybuilders and power athletes seems to indicate sarcoplasmic hypertrophy in the bodybuilders, but this could also be related to innate differences that are independent of training or how much larger the muscle fibers of bodybuilders are.

I have to admit that I'm ending this article with a different opinion than I started it with. About 5 days ago I was sure that sarcoplasmic hypertrophy was either a myth or at best played a trivial role in muscle hypertrophy. Now I'm pretty sure that sarcoplasmic hypertrophy is happening, and while I'm still not completely convinced, I'm now much more open to the idea that it has a significant effect on overall muscle growth.

I remain skeptical when it comes to whether training in a specific way can either minimize the "risk" of sarcoplasmic hypertrophy (from a powerlifter's perspective) or increase the chance of sarcoplasmic hypertrophy (from a bodybuilder's perspective), but I am open to the idea that this may be possible.

Ultimately, this is a question that can't be answered conclusively until we have more high-quality studies on individual muscle fibers (or until a few brave souls are willing to donate a cubic centimeter of their muscles to science).

People with a wealth of knowledge on the subject of muscle physiology can be found on both sides of the debate. Dr. Stuart Phillips (35) and Dr. Anders Nedergaard (36) believe that sarcoplasmic hypertrophy is nonsense, while Dr. Brad Schoenfeld (37) believes that it occurs but plays only a small role in overall muscle growth and Lyle McDonald (38) seems convinced that sarcoplasmic hypertrophy does occur and can play a significant role in muscle growth.

I hope that this article has at least given the reader a better understanding of this topic and raised some questions that not every reader would have thought of.

Addendum, June 2017

A study published in 2007 by Cribb et al (39) adds another aspect to this discussion. I had overlooked this study in my original search as it was more of a supplement study (looking at the effects of creatine and whey protein) than a muscle physiology study.

The study participants were recreational bodybuilders who had a reasonable amount of training experience - the average performance at the start of the study was 100 kilos. These subjects were divided into four groups:

  • One group supplemented with carbohydrates
  • One group supplemented with carbohydrates and creatine
  • One group supplemented with whey protein
  • One group supplemented with whey protein and creatine

All subjects trained for 11 weeks with a Max-OT program.

The study examined (among other things) the muscle content of contractile proteins: the amount of contractile protein per unit mass. If the contractile protein content increases, then this is an indication of relative myofibrillar hypertrophy, while a reduction would be an indication of relative sarcoplasmic hypertrophy.

The groups taking whey protein and/or creatine showed greater increases in contractile protein content than the group supplementing carbohydrate alone (p<0.05). In addition, the two groups using creatine tended to have greater increases in contractile protein than the group using only whey protein (p=0.07-0.08).

But there are two other interesting notes to this study:

Increases in contractile protein content were independent of increases in 1RM weight during squats, and increases in contractile protein content correlated strongly with hypertrophy of all three primary muscle fiber types. This means that myofibrillar hypertrophy was the primary cause of overall muscle fiber hypertrophy in this study.

It is also worth mentioning that the changes in contractile protein content were quite small: up to 40 mg/g. This means that the proportion of muscle fiber weight consisting of contractile proteins had increased by a maximum of 4%. However, although this is a relatively small increase, it contrasts with the MacDougall study, which observed a small reduction in contractile protein content during exercise.

This may give us an indication that training style may actually influence the ratio of sarcoplasmic to myofibrillar hypertrophy. The subjects in the Cribb study trained with sets of 4 to 6 repetitions, while the subjects in the MacDougall study trained with sets of 8 to 10 repetitions.

However, it is always uncertain to make comparisons between studies, so this certainly cannot be taken as evidence that training style affects the ratio of sarcoplasmic to myofibrillar hypertrophy.

In addition, a study by Moore et. Al. found that even though protein consumption affects both myofibrillar and sarcoplasmic protein synthesis, strength training (10 sets of 8 to 10 RM weights) only affects myofibrillar protein synthesis (40). However, the question of training style remains unanswered, as the sarcoplasmic protein synthesis response could have been different with a different training intervention.

Lastly, this is a good study to share with people who claim that creatine only causes muscle growth (i.e. sarcoplasmic hypertrophy) via an increase in water content in the muscles. The groups that used creatine in this study had the greatest increase in contractile protein content - and even when the water content of the muscles had increased, it was outweighed by the observed increase in contractile protein content.

Addendum, January 2018

A recent meta-analysis by Schoenfeld et al. that looked at the effects of training load on hypertrophy, dynamic strength and isometric strength helps to refute one of the main arguments used by people to prove that light training with high repetitions causes sarcoplasmic hypertrophy. These people claim that because strength gains are greater with heavier training, heavy training must build more contractile protein (myofibrillar hypertrophy), while lighter training must increase muscle mass without building as much contractile protein (sarcoplasmic hypertrophy). I have already described earlier in this article why this is not a completely logical argument, but this meta-analysis gives us more direct evidence to refute this.

Unsurprisingly, this meta-analysis also concluded that heavy training is better for dynamic strength. However, there is a technical component to dynamic strength and heavier training helps to train these technical skills. On the other hand, there was no significant difference between high load and low load training for gains in isometric strength (i.e. a strength release where virtually no technical component comes into play).

This suggests that low training load builds contractile proteins just as effectively as high load training - low training load training is simply not as good a training for how to effectively use these contractile proteins for maximal dynamic contractions (e.g. maximal attempts).

From Schoenfeld et al (2017) (41). Figure from Volume 1, Issue 7 of MASS (42).


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