Training

Having provided an overview of what sarcoplasmic hypertrophy is in the first part of this article, in this second part of this article we will look at a number of human studies that consider other aspects of muscle hypertrophy.

Why are there so few meaningful studies on the subject?

At this point, the more scientifically minded readers will probably be asking themselves: "If you could do this kind of biochemical analysis back in the 1960s, how is it that today in the 21st century we still don't have a clear answer as to how sarcoplasmic hypertrophy behaves in humans?"

This is a good question and there are two main reasons, which have already been mentioned in the paper:

1. the necessary size of the samples.

Due to the nature of biochemical analysis, quite large tissue samples are required, as the smaller the tissue samples, the greater the error rate. Improved laboratory techniques may have solved this problem over the last 50 years since this paper was published, when one gram of muscle tissue had to be taken for each analysis.

One gram of muscle tissue is roughly equivalent to one cubic centimeter and I do not believe that many volunteers would be found who would allow scientists to take such large amounts of muscle tissue.

2. microscopic analyses are not sufficient

Histological techniques - which is essentially nothing more than analysis under a microscope - will not be able to accurately show changes in the ratio of sarcoplasmic vs. myofibrillar protein density. The authors had this to say:

"It would be feasible to perform such studies using histologic methods, but this would have two major drawbacks:

• Fixation and staining of the samples is accompanied by shrinkage of sections of the sample, which would make it impossible to determine the proportions of sarcoplasm and myofilaments in the total cell volume with sufficient precision
• The myofilaments form myofibrils, which are not clearly separated from the sarcoplasm in the sections examined by histological methods.

Electron microscopic studies have shown that myofibrils have small sheaths. It is also known that different chemical components of the sarcoplasm such as creatine phosphate, adenosine triphosphate and mitochondrial products are able to pass freely into and out of the myofibrils. Even large molecules such as inulin with a molecular weight of 6,000 can enter the myofibrils.

It is therefore difficult to say whether the larger sarcoplasmic proteins can also enter the myofibrils, but at least from a theoretical point of view there is room for them between the myofilaments, in which the I-bands are separated by wide spaces, as can be judged by the pure lack of staining with osmium.

Thus, methods other than histologic methods seem preferable for studying the relationship between sarcoplasmic volume and myofilamental volume."

Keeping in mind that we are unlikely to get a useful answer based on direct evidence, we must turn to indirect evidence, which comes from two other sources: Measurements of intramuscular water concentrations and studies of functional characteristics of individual muscle fibers.

To my knowledge, there are only two studies that have investigated the changes in intramuscular water levels after strength training.

The first of these two studies, published in 2014, was able to observe an increase in intramuscular water concentrations, which could lead one to believe that sarcoplasmic hypertrophy occurred (9). However, I'm not sure you could bet your money on this.

The biggest problem with this study was quite simply that the study participants didn't gain much muscle mass in the first place. The men had built up 1.3 kilos of muscle and the women about 0.8 kilos. This was a 12-week study with untrained subjects.

In other words, the amount of muscle mass built by the study participants was so small - especially considering the circumstances - that I don't think we can really draw any useful information from this study. Any amount of sarcoplasmic hypertrophy would necessarily be trivial because the total amount of muscle mass built was trivial.

The second study is a classic study from 1982, where researchers trained subjects for six months and examined their muscles before and after training, comparing the subjects' muscles to those of elite bodybuilders and powerlifters (10). The powerlifters and bodybuilders were lumped together, so it's impossible to make a distinction between these two groups of athletes, but it still gives us a reference point for people who are highly trained.

After six months of training, the subjects had built up a ton of muscle. In fact, the size of their individual muscle fibers had almost reached the muscle fiber size of elite athletes, meaning that lack of muscle growth was not a problem in the study.

The subjects' myofibrillar density had decreased slightly and their sarcoplasmic volume had increased relative to muscle fiber size over the course of the study. The changes were small, but reached statistical significance. When the subjects were compared with the group of elite strength athletes, these trends were even stronger.

The myofibrillar density of the elite strength athletes group was significantly lower (almost 10% lower) and their sarcoplasmic volume relative to muscle fiber size was higher (about 10% higher). In other words, there was a small amount of sarcoplasmic hypertrophy in the subjects, and although a causal relationship cannot be inferred from the fact that the elite bodybuilders, unlike the subjects, did not undergo an intervention, there appears to be significantly more sarcoplasmic hypertrophy separating the study participants from the elite strength athletes.

It should also be noted that mitochondrial density decreased over the six months of training and was even lower in the elite strength athletes. 6 of the 7 elite bodybuilders were also using steroids or had used steroids in the past. More on these things a little later.

From MacDougall (1982)

(You may be wondering how the scientists were able to determine sarcoplasmic and myofibrillar volume when such large tissue samples are required. To be honest, I'm not sure, as no information was given on this in the range of butchers used in the study. The authors of the study cited two other papers that describe this method in more detail, but I don't have access to those papers. Apparently, an electron microscope was used, which does not require large tissue samples. Thus, such an investigation seems to be easier to perform today).

Let us turn to the functional data.

The myofibrillar density can be determined by measuring the force that a single muscle fiber can develop and dividing the force by the cross-sectional area of the fiber. This is also known as the specific tension of that fiber. A higher specific tension means a higher myofibrillar density as a nominal value and a lower specific tension means in most cases a lower myofibrillar density (and therefore a higher proportion of sarcoplasm).

The only primary factor that can alter this relationship, typically in non-exhausted muscles, is post-translational modification of contractile proteins. In other words, if the actin and myosin that cause muscle contraction are modified in some way that results in them not functioning correctly, this can cause a drop in specific tension that is independent of myofibrillar density. However, since a post-translational modification is very rare, the specific tension is a fairly good estimate of the myofibrillar density.

Of course, one might balk at the idea of trying to draw conclusions from single muscle fiber studies, but it should be kept in mind that the use of single fibers is one of the few ways to reduce the effects of a variety of confounding factors, exemplified by one study on this topic as follows (11):

"...differences in intramuscular muscle fiber orientation or pinnation, the presence of intramuscular connective tissue, differences in terms of mechanical leverage effects relative to joint position, possible coactivation of antagonistic muscles during the strength test, and variations in motor unit recruitment schemes, central drive, and subject motivation."

A recent study compared individual muscle fibers of bodybuilders, power athletes (American football players, track and field athletes and weightlifters) and subjects in a control group (12).

The bodybuilders had by far the largest muscle fibers (88% larger than the members of the control group and 67% larger than the power athletes). The muscle fibers of the bodybuilders produced more force than those of the control group members, but they produced slightly less force than the muscle fibers of the power athletes (however, the difference in total force between the muscle fibers of the bodybuilders and the power athletes were not statistically significant).

And here's the really interesting part: per unit cross-sectional area, the muscle fibers of the bodybuilders produced significantly less force than the muscle fibers of the power athletes or the members of the control group (66% less than the power athletes and 41% less than the subjects in the control group).

After figuring this out, the scientists conducted another analysis to see if post-translational modifications could explain the difference, after which they concluded that any post-translational modification could only have played a minimal role.

In other words, the bros were right all along. Training like a bodybuilder causes non-functional sarcoplasmic hypertrophy.

Right?

Not so fast. There are three potential problems with jumping to conclusions from this study:

1. There was no real intervention. It could have simply been that people with a certain type of abnormal muscle fiber are more likely to become bodybuilders.
2. The subject group in this study was quite small.
3. This statement is telling: "A negative trend between muscle fiber cross-sectional area and specific tension has previously been observed in individual muscle fiber segments of untrained humans and frogs. In the present study, this negative trend is evident in all groups. It has been suggested that this is related to an accumulation of inorganic phosphates due to longer diffusion times from the inside of the fiber to the surrounding incubation medium."

The third point is probably the most interesting.

While total muscle cross-sectional area generally correlates quite strongly with force production capacity, studies that looked at individual muscle fibers tell a different story.

One of these studies illustrates the difference. In the largest study of individual muscle fibers that I'm aware of, scientists found that capacity for force production was more related to diameter than to cross-sectional area. The scientists compared maximum force to diameter and found that the values for type 1 and type 2 fibers were quite similar. They plotted maximum force against diameter on double algorythmic paper and found that the slopes for type 1 and type 2 muscle fibers were very close.

As I described in a previous article, the slope of a double algorythmic graph tells us something about the exponential relationship between two variables. If the slope is 1, it means that the relationship is linear and not exponential.

Most importantly, they concluded that the slope of the line that best fit the double algorythmic graph was certainly not 2 - even when variability and potential errors were taken into account. If the slope had been 2, this would have meant that the maximum force would have increased with the square of the diameter, which in turn would have meant that the maximum force would have been linear to the cross-sectional area.

In other words, the fact that it is almost impossible for the slope of the double algorythmic graph to be 2 (p<.0001 for both type 1 and type 2 fibers) means that the maximum force of a single muscle fiber can be expected to be more related to the muscle fiber diameter than to the cross-sectional area.

With this in mind, let's take another look at the data from the study comparing bodybuilders, power athletes and members of a control group.

Since absolute values were not provided for all measurements, I have reported both cross-sectional area and maximal force relative to the control group and used arbitrary units. I maintained the relationship (percentage differences) reported in the study.

Using the correct relationship (force relative to fiber diameter, rather than cross-sectional area), we see a different picture than above. The muscle fibers of the bodybuilders produced almost the same amount of units of diameter as the muscle fibers of the control group (bottom line: the muscle fibers of the bodybuilders produced only 3% less force per unit of diameter than the muscle fibers of the members of the control group).

This is in contrast to the 41% difference when using specific tension (force relative to cross-sectional area) The power athletes continued to have a significantly higher maximum force relative to diameter than the other groups.

In other words, the problem was not that the bodybuilders were doing something "wrong" that reduced their force relative to cross-sectional area. Based on how much larger their muscle fibers were compared to the control group, their muscles produced about as much force as you would expect based on muscle fiber diameter.

It is more likely that either the power athletes were doing something "right" to increase their strength relative to muscle fiber diameter beyond what would have been expected, or that people whose muscle fibers are naturally capable of producing more force than they "should" tend to become more power athletes. A combination of both is most likely. However, it should be kept in mind that even in power athletes, specific strength decreased while muscle fiber size increased.

However, this leads us to another dilemma. Since myofibrillar density should still be linear to cross-sectional area, but muscle strength is linear to diameter, the question arises as to whether sarcoplasmic hypertrophy goes hand in hand with hypertrophy itself? Is perhaps an increase or maintenance of myofibrillar density the actual "weird" thing that happens?

Perhaps.

However, I doubt we will see many more single muscle fiber studies in the near future as they are very time consuming and costly and this type of study is likely to be a very low priority for serious athletes. However, such studies would be relevant to geriatrics (so if there are any exercise physiologists among the readers who work with older people, they should take this as a subtle hint). For now, looking at studies that look at the whole muscle is the best we can do.

The first study that comes to mind in this regard is one conducted with elite powerlifters that found a very strong correlation between muscle thickness (rather than cross-sectional area) and strength (14).

Muscle studies show that the muscles of people who perform strength training have a higher specific tension than the muscles of untrained people (15). However, this study (16) is, to my knowledge, the only study that compared muscle width specific tension (force by cross-sectional area) with the specific tension of individual muscle fibers before and after training.

The authors found that the specific tension of individual muscle fibers remained unchanged, while the specific tension for the whole muscle increased. They postulated that lateral force transmission (lateral connections between muscle fibers that link these fibers together and aid in force transmission) was the most likely cause of the increase in whole muscle specific tension and that myofibrillar density within the individual fibers themselves remained unchanged, as the specific tension of individual muscle fibers did not change.

Two other studies (17, 18) came to similar results for individual muscle fibers (unchanged specific tension) before and after training, but the researchers did not compare the results with changes in total muscle tension.

In contrast, other studies (19, 20) observed an increase in specific tension for both whole muscle and individual muscle fibers without overall muscle hypertrophy, although the second study was confounded by the fact that it was conducted with older people who normally experience a decrease in specific tension with age (so an increase in specific tension in these people simply means a return to normal).

There are also a variety of other factors such as increased muscle activation, reduced activation of antagonistic muscles and even changes within the muscle architecture that can alter the lever arm of the muscle, all of which can increase force production relative to the muscle cross-sectional area (21).

With these potentially confounding factors in mind, high-intensity training appears to produce greater increases in specific tension than lighter training (22) and bodybuilders regularly produce less force per unit muscle cross-sectional area than strength athletes (23) and sometimes even less force than untrained subjects in the control group (24).

A negative correlation between muscle cross-sectional area was also observed in this study (25), while in another study (26) bodybuilders actually produced more force per unit of muscle cross-sectional area than powerlifters during knee extension.

Overall, strength training appears to increase the ratio of force to muscle cross-sectional area for the whole muscle, while it probably does not increase the force to muscle cross-sectional area ratio (and myofibrillar density) at the individual fiber level unless muscle growth occurs.

On the other hand, in most studies in bodybuilders, the ratio of strength to muscle cross-sectional area is lower than in strength athletes and is often similar to that found in untrained subjects in the control group. This is consistent with the observation that the ratio of strength relative to muscle size is most strongly related to fiber diameter and that this ratio generally decreases as muscle fiber size increases.

Strength training does not follow this trend and maintains the relationship between strength and cross-sectional area, but bodybuilding-style training appears to follow the trend of decreasing specific tension with increasing muscle fiber size as observed in larger studies.

Now, does this mean that sarcoplasmic hypertrophy (an increase in the percentage of sarcoplasmic proteins relative to myofibrillar proteins) typically goes hand in hand with muscle hypertrophy?

Possibly.

However, it should be remembered that there are several other potentially confounding factors. Most notable of these is the fact that larger muscle fibers may accumulate larger amounts of inorganic phosphates. Inorganic phosphates directly reduce the force of muscle contraction as they hinder the binding of myosin to actin, which could be responsible for a reduction in the force to cross-sectional area ratio without a change in myofibrillar density.

However, it should be kept in mind that this is only a proposed mechanism and not a proven mechanism in this context. Typically, inorganic phosphates only accumulate when muscles become exhausted (when phosphates are stripped from ATP faster than energy systems can restore ATP levels). However, it is known that accumulation of inorganic phosphates is one of the main reasons for a decrease in the force to cross-sectional area ratio during limb immobilization, so it is conceivable that such accumulation could also occur in non-exhausted muscle fibres under certain circumstances.

There is a possible rationale for an increase in the levels of inorganic phosphates in the muscles of bodybuilders - inorganic phosphates can act as a buffer when muscle pH drops during exercise. Perhaps the muscles of bodybuilders accumulate inorganic phosphates in response to high repetition training, which causes local muscle acidosis.

However, inorganic phosphates are among the less important cellular buffers, and even if this explained why inorganic phosphates accumulate in the muscles of bodybuilders, it still would not help explain the more general trend of reduced force to cross-sectional area ratio with increasing muscle fiber size - especially in type I muscle fibers (which rely more on aerobic metabolism and do not reach such a low pH).

Let's assume for the moment that accumulation of inorganic phosphates plays at most a minor role. Let's also assume that post-translational modifications don't play a major role (and they don't except in older populations and animals that don't produce myostatin). The only other option I am aware of that could explain a decrease in force to muscle cross-sectional area ratio with increasing muscle fiber size is then a decrease in myofibrillar density.

In other words, a sarcoplasmic hypertrophy.

So we have to ask ourselves: "Why would this happen at all? And why might it happen in bodybuilders to a greater extent than in strength or power athletes?"

The simplest explanation I can think of is: energy.

A large proportion of sarcoplasmic proteins are involved in the various steps of anaerobic metabolism. As a muscle fiber gets bigger, it relies less and less on anaerobic metabolism for two reasons:

1. Unless you're doing dedicated aerobic exercise, mitochondrial density (mitochondria are where aerobic metabolism occurs) generally decreases. This was observed in the MacDougall study - the mitochondrial density decreased over the course of six months while the muscles of the study participants grew and it was already lower in the elite strength athletes at the beginning
2. The ratio of capillaries per unit of muscle fiber cross-sectional area decreases as muscle fiber size increases unless you are doing dedicated aerobic exercise. This means that you can no longer get as much oxygen to the mitochondria, which are closest to the myofibrils further inside the muscle fiber, as the diffusion distance from the muscle cell membrane (the sarcolemma) to the mitochondria deep inside the cell has increased. In turn, this promotes a shift towards an anaerobic metabolism.

This idea makes sense in light of the study above with individual muscle fibers, in which bodybuilders, power athletes and untrained members of the control group were compared. Not only were the muscle fibers of the bodybuilders much larger, but the bodybuilders were the only group that did not engage in dedicated cardio training.

However, this does not fully explain why specific tension (and therefore myofibrillar density) should not drop during heavy strength training as it does during lighter, higher volume, bodybuilding-style training. Increased training volume in general, and especially increased training volume to near the point of muscle failure with lighter weights, places higher energetic demands on the muscle which should help fuel some of those aerobic adaptations (increased capillary density and increased mitochondrial density) that would reduce the need for increased levels of protein associated with anaerobic metabolism.

I think (although I realize this explanation is very tenuous) that due to the fact that bodybuilding style training is both more aerobically and anaerobically demanding, the vastly increased anaerobic demands lead to greater anaerobic adaptations that outpace the increased aerobic adaptations. On heavy sets of three reps, you won't use much stored ATP and phosphocreatine, which means you won't need a ton of energy via glycolytic metabolism. However, things will look completely different if you perform several demanding sets of 8 to 15 reps in a row.

Looking at changes in sarcoplasmic protein metabolism after different training sessions and specifically separating mitochondrial proteins from other sarcoplasmic proteins might shed some light on this idea, but some studies include mitochondrial proteins in the sarcoplasmic protein fraction (such as this study (28), which showed that sarcoplasmic protein synthesis was increased for 24 hours after a training session to muscle failure at 30% of 1RM weight, but not at weights in the 90% of 1RM weight range or this study (29), which showed that training at a slower cadence produced greater increases in sarcoplasmic protein synthesis than training at a faster cadence), while other studies ignore mitochondrial proteins and only look at the non-mitochondrial sarcoplasmic proteins (such as these two studies (30, 31), which showed that a slower training cadence caused greater increases in sarcoplasmic protein synthesis than a faster training cadence).

In the final part of this series of articles, I will summarize the current state of research and in the appendix I will discuss more recent findings that have emerged since the original article was completed.

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

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/