Sarcoplasmic hypertrophy: the bros were probably right Part 1

Here is a brief summary

1. Sarcoplasmic hypertrophy - growth of the sarcoplasm that outpaces the growth of myofibrils - appears to occur to a significant degree.
2. Simple increases in glycogen stores do not appear to be the primary driving factor of sarcoplasmic hypertrophy. Rather, it appears to be driven by an increase in sarcoplasmic protein content.
3. The degree to which sarcoplasmic hypertrophy occurs could be influenced by training, but whether one can specifically train for sarcoplasmic vs. myofibrillar hypertrophy is unclear. Rather, sarcoplasmic hypertrophy appears to be a consequence of muscle growth itself.
4. Looking at the strength differences between bodybuilders and powerlifters or weightlifters is not a valid way to estimate the degree of sarcoplasmic hypertrophy. To dismiss sarcoplasmic hypertrophy simply because there are better explanations for the observed differences in relative strength is foolish.
5. It is unclear whether banned performance enhancing substances such as steroids increase the amount of sarcoplasmic hypertrophy that occurs.

You may have heard the old bodybuilding "wisdom": bodybuilders are bulkier than powerlifters/weightlifters, but still move less weight because they have more sarcoplasmic hypertrophy.

You may also have seen pictures like the following from credible sources

If you're not sure what we're talking about at this point, here's a quick summary: It has been suggested that there are two pathways by which muscle fibers can grow:

1. Myofibrillar hypertrophy, which occurs through the growth and proliferation of myofibrils within each muscle fiber. The myofibrils are the actual "motors" of the muscle fiber, which consist of contractile protein and cause the muscle fibers to contract. This form of hypertrophy is illustrated by the image at the top right, in which the number of myofibrils has increased compared to the starting point (left).
2. Sarcoplasmic hypertrophy, which in theory is caused by an expansion of the sarcoplasm (the cytoplasm of the cells) within the muscle fiber. This is illustrated by the image above in the middle, where the volume of the muscle fiber has increased without an increase in myofibrils.

Now that we have defined these two terms as accurately as possible, it should be noted that neither mechanism implies that the sarcoplasm cannot expand at all. Rather, myofibrillar hypertrophy simply implies that the sarcoplasm increases at approximately the same rate that the myofibrils grow or increase in number. So if the myofibrils previously occupied 80% of the space within the muscle fiber, this ratio of myofibrils to sacoplasm would remain the same even after doubling the size/number of myofibrils.

Sarcoplasmic hypertrophy implies that the sarcoplasm increases at a significantly higher rate than the myofibrils grow and divide. So if the ratio of myofibrils to sarcoplasm was 80:20, it would be perhaps 70:30 or 60:40 after sarcoplasmic hypertrophy.

So does sarcoplasmic hypertrophy occur and does it contribute significantly to muscle growth? That's the million dollar question.

I was skeptical about sarcoplasmic hypertrophy for a long time, mainly because it was not an adequate explanation for the problems it was supposed to address.

The situation in which sarcoplasmic hypertrophy is most often invoked is when bodybuilders are compared to powerlifters or weightlifters. How can a 130 kilo bodybuilder be beaten on squats by an 80 kilo powerlifter?

The line of thought is that sarcoplasmic hypertrophy explains this difference. The bodybuilder must therefore have non-functional sarcoplasmic hypertrophy, which makes his muscles bigger without making them stronger, as it is the myofibrils that contain the contractile proteins.

In this context, however, one should be aware that strength also includes a massive component of technique. The strength athletes who regularly perform heavy squats in their training will generally have better technical squat skills. If the bodybuilder were to change his training style for a few months, his squat weights would skyrocket too.

You can observe both in the real world (for example, it didn't take long for Stan Efferding to handle well over 400 kilos on squats after he switched from bodybuilding to powerlifting) and in the scientific literature (it's such a consistent finding that strength is schema and load specific that it's not even worth the time to cite relevant studies).

On reflection, however, I realized that I may have been wrong in dismissing sarcoplasmic hypertrophy as irrelevant simply because it is a poor explanation for the phenomenon it is supposed to explain.

Formally speaking, if someone claims that "A is responsible for C", but B is a more likely cause than A for C, it cannot be concluded that A does not exist. The conclusion is merely that B is a better explanation for C than A is.

Here's a slightly more ridiculous example to make this clearer: If someone claims that cats caused a building to explode, but it is later discovered that there was a leak in a gas line and the gas led to the explosion, then one will merely conclude that ignited gas is a better explanation for the explosion. One cannot conclude from this that cats do not exist.

So the main argument for sarcoplasmic hypertrophy falls flat (because there is a better explanation for the force differences) and the main argument against sarcoplasmic hypertrophy is based on a logical fallacy.

Having gotten all this out of the way, we can now start to make a new beginning.

When people talk about sarcoplasmic hypertrophy, they are talking about something long-lasting that is directly affected by training and that makes a significant difference to muscle size.

In other words, you can cause an increase in sarcoplasmic volume by ingesting creatine, carbohydrate loading, performing BFR training or occlusion training (1) or by inducing muscle damage, but none of this will cause the kind of sarcoplasmic hypertrophy that people are interested in.

None of this can cause a very large increase in muscle volume and all of this will only have a fleeting, temporary effect. Stop taking creatine or loading with carbohydrates and the water will disappear. The fluid retention in the muscles after a BFR training session or a training session that causes a lot of muscle damage will disappear within 72 hours and the effects will progressively diminish over time.

So we have to ask ourselves: where could this sarcoplasmic hypertrophy be coming from?

There are 2 primary causes:

1. An increase in osmotic, dissolved non-protein components in the muscle fibers, which bind more water.
2. An increase in sarcoplasmic proteins (including all organelles except nuclei and myofibrils) relative to contractile proteins.

Dissolved substances in the muscle

An increase in solutes within muscle is the first pathway by which one could potentially induce sarcoplasmic hypertrophy. Many readers may remember biology or physics lessons and the concept of osmosis.

If one were to induce sarcoplasmic hypertrophy by increasing the amount of solutes in the muscle tissue within the muscle fibers, this would correspond to the scenario where water flows through a membrane that is only permeable to water molecules, but not to larger solutes, into the area with the larger amount of solutes in order to balance the so-called solute gradient. Since water "follows" the solutes, by bringing more solutes into the muscle fiber, you would also draw more volume in the form of fluid into the muscle fiber, which would be nothing more than sarcoplasmic hypertrophy.

Unfortunately, this is not possible for non-protein substances. Ion concentrations (sodium, potassium, bicarbonate, calcium, hydrogen ions, etc.) will not change in the long term as long as you have healthy kidneys.

You also have some fatty acids stored in the muscle fibers and these lipid droplets can grow and divide during exercise (especially during aerobic exercise), but these lipid droplets don't attract much water and make up such a small fraction of the space within a muscle fiber that it's completely impossible for them to make a big difference.

Last but not least, there is glycogen. And yes, glycogen storage capacity can be increased through training. However, maximal glycogen concentrations can increase with pretty much any type of exercise. And they may also increase slightly more with aerobic training or the type of training that some people believe induces sarcoplasmic hypertrophy (lighter, high volume, bodybuilding style training).

Ultimately, however, even glycogen concentrations may not make a huge difference. Even if you deliver insulin and glucose directly into a muscle as an infusion over 8 hours, glycogen concentrations will peak at about 4 grams per 100 grams of muscle mass (3). One gram of glycogen binds 3 grams of water, which means that glycogen and stored water can account for a maximum of 16% of a muscle's total mass.

Average muscle glycogen concentrations are closer to 1.5 to 2 grams of glycogen per 100 grams of muscle. In other words, this means that increasing the average glycogen concentration of a muscle to the maximum possible value could increase total muscle mass by about 6 to 8% and these increases would consist of sarcoplasmic hypertrophy.

However, a 6 to 8% increase does not represent a huge increase in muscle mass (certainly not what most people would understand by this) and furthermore, regular strength training already increases the glycogen storage capacity of muscles, meaning that the difference to a maximal glycogen concentration would be perhaps only 2 to 3 instead of 6%.

Ultimately, glycogen concentrations are influenced more by diet than by training and, again, any increase would be temporary. The term "transient nature" is crucial here. If you max out completely depleted muscle glycogen stores then this can make a big, clearly visible difference (compare pictures of bodybuilders during the last few weeks of their diet to their appearance on stage), but it is not a permanent change and training style does not influence the extent of this glycogen pump to any great extent.

Non-contractile proteins

Could increasing the amount of non-contractile proteins relative to the amount of contractile protein cause sarcoplasmic hypertrophy?

Perhaps...

Protein and glycogen draw similar amounts of water into muscle fibers (4) (one gram of each binds about 3 grams of water). So if the concentration of sarcoplasmic proteins is higher than the amount of glycogen (so that this could make a more significant difference to overall muscle size) and the amount of sarcoplasmic proteins can be altered by training, then perhaps this would be a reasonable pathway by which sarcoplasmic hypertrophy could occur.

It was surprisingly difficult to find a source that compared the total amount of sarcoplasmic and myofibrillar protein in skeletal muscle. I guess most of these studies are really old and buried really deep in pubmed and Google Scholar search results. An introductory textbook on the science of meat production states that concentrations of myofibrillar proteins in mammals turn out to be about three times higher than concentrations of sarcoplasmic proteins.

This is similar to a study conducted in guinea pigs and rabbits published in the 1960s (5).

Stromal proteins are primarily proteins of the connective tissue, which we can neglect for the purpose of this article.

Now we might be getting closer. If a 3:1 ratio is typical, then perhaps this distribution could change.

Most studies that measure the rate of myofibrillar and sarcoplasmic protein synthesis separately conclude that they do not always follow the exact same pattern in response to the same stimulus. However, most of these data do not support sarcoplasmic hypertrophy. Although training with weights increases the rate of both myofibrillar and sarcoplasmic protein synthesis, the increase is generally greater and longer lasting for myofibrillar proteins.

The only two primary cases in which sarcoplasmic protein synthesis is at an advantage are inactivity and aging (6,7). Sarcoplasmic protein degradation progresses more slowly than myofibrillar protein degradation during complete unloading (i.e. no exercise) and sarcoplasmic protein synthesis does not decline with age, whereas myofibrillar protein synthesis does.

Furthermore, we must keep in mind that measurements of rates of protein synthesis do not necessarily tell us much about long-term muscle hypertrophy (8).

However, these studies also show that sarcoplasmic protein concentrations in muscle are not directly linked to myofibrillar protein concentrations by any mechanism. In fact, in the aforementioned rat study, the scientists observed a fairly wide distribution of the ratio of myofibrillar and sarcoplasmic proteins

In young, active rabbits, the ratio was slightly below the standard of 1:3 - at about 2.4:1. In rabbits forced to be physically inactive, the ratio shifted to about 1.6:1 and middle-aged rabbits had slightly higher concentrations of sarcoplasmic proteins than myofibrillar proteins.

Groups 1 and 2 were young and active. Group 3 was young and inactive. Group 4 was middle-aged.

In the second part of this article we will look at a number of human studies that look at other aspects of hypertrophy.

Source: https://www.strongerbyscience.com/sarcoplasmic-vs-myofibrillar-hypertrophy/