number fibers

Despite the fact that a person receives proteins from food, the proteins of other living organisms consumed by man are not directly used for the construction of his body tissues. The entire protein entering the human body is first broken down in the digestive system into its constituent parts of the protein – amino acids. In the intestine, amino acids seep into the blood and are carried to all cells of the body. And only then in each cell of the amino acids entering it, the proteins characteristic of the given cell of the given organism are collected (some proteins differ from others in the sequence of amino acids in the protein molecule). The proteins synthesized by the cells are not included in the cell structure “for the ages”, in the body tissues the reverse decomposition of proteins to their amino acids constantly occurs. Some of the amino acids that are products of protein breakdown are further broken down to simpler compounds, but most of these amino acids, along with new amino acids, coming from food or synthesized by the body, are immediately included in new protein molecules that are embedded in tissues instead of decayed.

It has been established that in 10 days half of all proteins of human liver and blood are renewed, muscle proteins also live a little longer, so it is known that myofibrillary proteins in rabbit muscles are completely updated within a month. Thus, the existence of muscle tissue is a continuous process of updating the proteins of its components. Accordingly, the ratio of decay rates and protein synthesis determines whether a person gains muscle mass or loses it. Moreover, an increase in muscle strength or endurance without a significant change in their mass or volume is also associated with the accumulation in the muscles of certain types of protein that perform the functions of providing muscle contraction. For example, the accumulation in the muscles of oxidative enzymes and myoglobin, a protein that carries out intracellular oxygen transport, leads to an increase in the rate of energy reproduction due to oxidative processes, which generally increases muscle endurance. Consequently, training any orientation, training “on the ground”, strength training, or training endurance muscles, if it reaches its goal, leads to an increase in the content in the muscles of certain types of protein. It would be more accurate to say: an increase in the content of certain types of protein in the muscles is the cause of changes in the functional properties of the muscles during their training.

Therefore, in order to understand how exercise affects the size and strength characteristics of muscles, it is important to know what kind of training and how it helps the accumulation of certain types of protein in the muscles.

The effect of training on the accumulation in the muscles of certain types of protein

Theoretically, an increase in the protein content in the muscles is possible both due to the activation of protein synthesis, and due to a decrease in its decomposition rate. However, it has been reliably established that intensive muscle work activates protein catabolism in muscle tissue, while an increased level of protein breakdown can be observed up to several days after exercise. And this, in turn, means that an increase in the protein content in the muscles under the influence of training can in no way be a consequence of a decrease in the intensity of catabolic processes, therefore, training should activate protein synthesis to a greater extent than its breakdown.

The last statement at the moment is a truth that is not questioned; nevertheless, the mechanisms themselves of the effect of training on the processes of protein synthesis in muscles have not been fully studied yet and are the subject of discussion.

In a very rough approximation, the process of protein synthesis can be described by the following scheme.

In every cell of the human body, including the muscular, there is a nucleus, inside which is enclosed the DNA molecule. The DNA molecule contains information about the structure of all proteins in the body. Since one type of protein differs from another only the sequence of amino acids in the amino acid chain of a protein, it is the sequence of amino acids in a molecule of one protein or another that is encoded in DNA. The DNA segment containing information about the structure of one type of protein is called the gene. If it is necessary to synthesize a certain protein in the cell, a special copy is taken from the gene of this protein, called matrix RNA, then RNA leaves the nucleus into the cell, and then the protein molecule is arranged on the RNA as a template. The construction of the protein is carried out by combining with each other the free amino acids present in the cell in the order that is “recorded” in the RNA. An RNA molecule is used in the construction of a protein not as an expendable material, but as a drawing, construction plan, therefore many molecules of protein can be collected on the basis of one RNA molecule, but it is clear that the more RNA in a cell, the greater the number of protein molecules can be collected at the same time . In addition, RNA tends to decay over time, and for the continuity of protein synthesis requires constant replenishment of RNA molecules in the cell.

As a result, the intensity of the synthesis of a particular protein in the cell depends on the intensity of synthesis of the corresponding RNA in the cell nucleus, that is, on the frequency of reading RNA from the gene of a given protein. The nuclei of any cell of the human body have the same set of genes, that is, they contain information about all the proteins of the body (about 100,000 genes), but most of the genes in the cells are inactive, and only a small part of the genes contain RNA synthesis. Thus, in muscle cells, RNA reading from genes of myosin and actin, genes of other proteins characteristic of muscle cells is activated, but genes of other types of protein, for example, blood proteins or connective tissue proteins, are silent in muscle cells. Yes, and the activity of “muscle” genes in muscle cells is also not constant and may vary depending on the conditions of muscle activity. The fact that the properties of the muscles under the influence of training can change, that is, the relative content of certain types of protein in the muscle can change, indicates that training affects the mechanisms of RNA synthesis, activating the reading of RNA from the desired genes. Indeed, in a multitude of experiments, a sharp increase in the synthesis of various types of RNA in muscle cells was observed during the first hours after exercise.

Apparently, based on the above facts and considerations, scientists for a long time came to the conclusion that exercise contributes to the development of certain substances in the muscles – the so-called factor-regulators that activate RNA synthesis in the nuclei of muscle cells, so that after training in muscles, the synthesis is activated protein, and during regular workouts, there is an accumulation of proteins in the muscles, that is, muscle hypertrophy. It is believed that steroid hormones that penetrate the muscle cell and connect to the steroid receptors act on nuclear DNA, activate the RNA synthesis of some muscle proteins, thereby enhancing protein synthesis in the muscles.

In the future, I will not constantly describe the entire true sequence of events leading to the synthesis of protein molecules in the cell. All this process, starting from the synthesis of RNA in the cell nucleus and ending with the assembly of the protein molecule in the sarcoplasm of the cell, for brevity, I will call “protein synthesis as the cell nucleus”, and it should be remembered that the nucleus itself does not synthesize the protein, but only controls its synthesis . This trick will allow me to formulate some important thoughts more concisely and clearly for the reader. Thus, in particular, the muscle hypertrophy scheme described above under the influence of training can be replaced by the following brief statement: during intense muscle contractions in muscles, a number of regulator factors are developed that affect the muscle cell nuclei, which leads to acceleration of “protein synthesis by these nuclei” and further to muscle hypertrophy.

Many scientists involved in the problems of sports (in any case, in Russia) are still convinced precisely in this mechanism of muscular hypertrophy, which is confirmed both by the articles of these scientists and by the content of modern textbooks on the biochemistry of sports. At the same time, the totality of the experimental facts accumulated to date suggests that the ideas that muscle hypertrophy is a consequence of the intensification of “protein synthesis by the nuclei” of muscle cells are extremely far from the true state of affairs.

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Since this article is popular in nature, I will not bother to enumerate, and readers will read references to numerous studies confirming the information presented by me. Those readers who remain unsatisfied with the superficial presentation of the material in this article can find on the Internet on the website “Weightlifting Problems” ( or on the website of the Powerlifting Federation of Russia (http: // www my article “Functional hypertrophy of skeletal muscles. Local mechanisms of adaptation of skeletal muscles to the load “, in which the issues raised in this article are examined in more detail with a sufficient degree of rigor, and the statements made are supported by the necessary analysis and references to relevant studies conducted by both Soviet-Russian and foreign researchers over the past 40 years .

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So, in order to understand that something is wrong in traditional ideas about the mechanisms of muscle growth, it is enough to think about the features of the structure of muscle cells and the peculiarities of their formation during the development of the embryo. The first “striking” difference in muscle cells from cells of other tissues is their size. If in order to see most of the cells of the human body, you need a microscope, the muscle cell can be seen with the naked eye. The muscle cell is a muscle fiber, a tubular formation with a diameter approximately equal to the thickness of a human hair, and a length from a few millimeters to 12 cm (depending on the type of muscles and their structure). This supercell is formed at the stage of embryonic development by merging a large number of small-sized precursor cells (myoblasts) of a small size into long tubular structures (Fig. 1). Thus, in the muscle cells, the fibers are not one nucleus, as in other cells, but many nuclei (as a rule, several thousand), according to the number of embryo cells fused into the fiber. While the myofibrils are collected in the fiber, the nuclei occupy a central position along the entire fiber length, and then, after the fiber core formation is completed, they move to the fiber surface, where they stay further and control protein synthesis from where. The question arises, why the muscle fiber does not grow out of a single cell, and for its formation requires the fusion of so many cells? The answer suggests itself. Apparently, a single cell, more precisely, a single nucleus is completely inadequate for the synthesis of such amount of protein that is required for the formation and further maintenance of such a large structure as muscle fiber. Moreover, if there was only one core in the muscle fiber, even if it could provide unlimited protein synthesis, the synthesized proteins would have to be transported from the nucleus to the periphery of the fiber to distances that are too large by molecular standards. Thanks to the merging of a large number of cells together, the nuclei are evenly distributed along the entire muscle fiber, and the volume of the fiber that is served by one nucleus is not fundamentally different from the volume of an ordinary single-core cell.

So, the multi-core muscle fibers themselves indicate that the volume of the muscle fibers, which is capable of serving one cell nucleus, is limited.

It is known that the muscles of a child, in order to achieve a size characteristic of an adult, must increase by about 20 times. If we proceed from the fact that muscle growth is associated with the acceleration of “protein synthesis by the nuclei,” then it should be recognized that as a person grows older, the volume of muscle fibers serviced by one nucleus should increase about twenty times in his muscles, and in the same proportion should increase the rate of “single-core protein synthesis”. In fact, of course, nothing like this happens. Studies conducted back in the 70s of the last century showed that the volume of muscle fibers per core is about the same in the muscles of people aged 1 to 70 years. This means that there are approximately 20 times more nuclei in the muscle fibers of an adult than in the muscles of a child.

Where do new nuclei appear in human muscle fibers?

It turns out that during the formation of muscle fibers, not all cells of the embryo, from which muscle tissue develops, completely merge with muscle fiber, part of the embryonic cells, approximately 3-10%, appear to be “conserved” under the muscle fiber membrane (Fig. 3). These satellite cells of the muscle fiber are called satellite cells or myosatellites. When certain chemical signals are received, satellite cells are released from the shell of the fiber, intensively divide, then a part of the multiplied cells again become satellite cells, and a part merges with the muscle fiber, losing its shell, and the nucleus of the satellite cells become the nuclei of the muscle fiber. Thereby, the number of nuclei capable of “synthesizing protein” increases in the muscle fiber, and after that the amount of protein in the fiber increases and, accordingly, the size of the muscle fiber increases.

It is the division of satellite cells and an increase in the number of nuclei in the muscle fiber, and not at all the acceleration of “protein synthesis by existing nuclei,” that causes muscle hypertrophy as the young organism grows.

But, perhaps, muscle growth due to cell division of satellites occurs only with age-related muscle growth in length, and an increase in muscle diameter, resulting from exercise, is not connected with an increase in the number of cell nuclei, and is a consequence of the acceleration of “protein synthesis by existing nuclei” ? Studies of the muscles of elite powerlifters with extremely developed muscles showed that the volume of muscle fibers per core (that is, the volume of fiber served by one core) is no more in athletes than in untrained people. And this, in turn, indicates that muscle hypertrophy caused by training is closely connected with the increase in the number of nuclei in the fiber.

This conclusion is confirmed by many experiments conducted over the past 25 years in humans and animals, in which both the activation of satellite cells and the increase in the number of nuclei in muscle fibers after intense loading were directly recorded. In one way or another, satellite cells are activated both after strength training with a barbell and after training for endurance, for example, after running training or working on a stationary bike. It was noted that the activation of satellite cells is one of the first reactions of muscle tissue to the load. Activation of satellite cells is recorded already 12–24 hours after muscle overload, but significant muscle hypertrophy is observed much later, after days or even weeks. In defense of the outdated perceptions, one would assume that the muscle fiber under the influence of training first increases its size due to the intensification of “protein synthesis with existing nuclei”, and only then, following the increase in muscle fiber, do satellite cells divide and add new nuclei to the fiber to restore the normal density of nuclei. The fact of satellite cell activation before and not after muscle hypertrophy refutes this assumption. Thus, it is safe to say that the division of satellite cells is the cause of muscle hypertrophy, and not its consequence.

Muscle growth potential due to satellite cell division is very high. Thus, in one of the experiments for three months of cat muscle overload, the number of nuclei in the slow muscle fibers doubled, and in fast fibers 4 times! It should be noted that the division of satellite cells is not just an important mechanism of muscle hypertrophy, but mandatory and, in fact, the only one.

It is known that the removal of certain muscles in animals leads to a sharp increase in the load on the remaining muscles that perform similar functions (synergistic muscles), which leads to a significant hypertrophy of these muscles. It turns out that if radiation is irradiated before removing part of the muscles of animal muscles (radiation violates the processes of cell division of satellite cells, but does not violate the mechanisms of protein synthesis), then compensatory hypertrophy of the remaining muscles is not observed! This means that even in the conditions of an extreme need to increase the size of muscles, and the presence of appropriate stimuli, muscle growth without dividing the cells of satellites and adding new nuclei is impossible!

Effect of testosterone on protein synthesis

Here the reader may have a question, but what about the situation with the use of anabolic steroids? After all, it is known that testosterone accelerates the synthesis of protein in the muscles, binding to the corresponding receptors and acting on the nucleus of muscle cells, thereby accelerating the “synthesis of protein by the nuclei”. In addition, it is known that after the end of “steroid therapy” and muscle strength, and their volume can significantly decrease. Perhaps equipoise cycle, in the case of the use of anabolic steroids, the volume of muscle fibers may change (increase when using steroids and fall after their cancellation) and without changing the number of nuclei?

Surprisingly, studies show that athletes who use testosterone-containing medications do not have more muscle fiber per core than athletes who refrain from using these drugs, despite the fact that the size of the muscles of doping athletes significantly exceeds the size of the muscles of “natural” athletes. From this fact inevitably follows the conclusion – containing testosterone drugs should contribute to an increase in the number of nuclei in the muscle fibers. Indeed, in a number of experiments it was found that satellite cells, the division of which is activated under the influence of this hormone, are the target of testosterone exposure. So, when injecting testosterone to humans, an increase in the number of nuclei in the muscle fibers, proportional to the hormone dose, was recorded, while an increase in the volume of muscle fibers served by one core was not only not observed, but on the contrary, the fiber volume per core decreased! The latter phenomenon can be explained only by the fact that at the time of measurement the volume of muscle fibers in the muscles of the subjects had not yet managed to increase sufficiently following the rapidly proliferating nuclei.

A number of researchers have concluded that an increase in testosterone secretion during adolescent puberty and, as a result, more active division of satellite cells in the muscles of young men is the main cause of such a significant difference in the development of the muscles of men and women.

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It is interesting that the activity of cell division of satellite cells depends on the dosage of testosterone, the higher the dose of the administered drug, the more actively the satellite cells divide. The last observation helps to resolve one long-standing controversy, known to athletes and specialists in the field of “chemistry”, about which I once again had the opportunity to read about an article found on the web by José Antonio. Let me quote from this article:

“The addition of testosterone to the cell receptor gives rise to a command impulse that“ triggers ”myriads of biochemical reactions. Again, in theory, there are not so many androgenic receptors in cells. In any case, the testosterone secreted by the sex glands is enough to take them all. Then where does the anabolic effect of the additional intake of androgenic steroids come from? Here it is just not clear. Moreover, in the medical world there is a persistent view that the use of artificial steroids reduces the number of androgen receptors in cells. Conversely, if the level of testosterone in the blood is low, the receptor becomes larger. Like, this is an adaptive response – so the cells increase the chance of capturing rare testosterone molecules. Meanwhile, there were heretics who undertook to challenge this point of view. And what do you think? There is evidence that in practice everything is exactly the opposite: in neutered animals, the number of receptors in muscle cells decreases, and during the injection of testosterone by injection, it increases, and even in proportion to the amount of hormones: more testosterone – more receptors! ”

The riddle described by José Antonio is very easily solved if we take into account the fact that testosterone acts not only on muscle fibers, but also on satellite cells. In my opinion, it is very likely that the normal level of testosterone, which is typical for an adult man (or a slight excess, caused by small doses of the administered drug), may indeed be enough to fill all (or almost all) testosterone receptors present in muscle fibers. , and increasing the dose of testosterone above a certain level can not accelerate the “synthesis of protein by the nuclei.” In any case, this is in good agreement with the fact that any significant increase in the volume of muscle fibers served by one core is not observed in practice even with the injection of testosterone. But since testosterone can act not only on muscle fiber receptors, but also on satellite cell receptors, this leads to activation of satellite cell division, and to an increase in the number of nuclei in muscle fiber under the influence of a hormone. New nuclei, in turn, generate new testosterone receptors, because receptors are also proteins, and each nucleus itself provides for itself with the necessary number of receptors. It is the synthesis of receptors by newly formed nuclei that can explain the “mysterious” appearance of new receptors in muscle fibers after testosterone injections. And the influence of testosterone on the activity of cell division of satellite cells can explain the dependence of the anabolic effect of testosterone on the dosage of the hormone observed by athletes using steroids, and stubbornly denied by a number of theorists.

Effects of growth hormone on muscle hypertrophy

Let us now consider ways to affect the muscle hypertrophy of another important anabolic hormone, somatotropin, or, in other words, growth hormone. It is known that the injection of growth hormone or its mediator – IGF-1 (insulin-like growth factor) [1] contributes to muscle hypertrophy, but it turned out that when using these drugs, as well as using anabolic steroids, increasing the volume of muscle fiber, per nucleus is not observed. That is, the main anabolic effect of growth hormone and IGF-1 is the activation of satellite cell division.

The fact that growth hormone activates the reproduction of almost all cells capable of division, was known for a long time. For example, in any textbook of endocrinology, one can find mention of activating the division of cartilage cells in the so-called zones of bone growth under the influence of growth hormone, due to which the bones of a child grow in length. It is also well known about the effect of this hormone on the growth of internal organs, such as the liver and intestines. The overgrown cartilage tissues on the faces of elite bodybuilders, especially women, are sharply striking, there is also talk about an increase in the internal organs of bodybuilders who use growth hormone, there is even such a term – “hormonal stomach”. However, the effect of growth hormone on muscle tissue and scientists, and ordinary athletes stubbornly refused to associate with cell division, for a long time arguing only about the general acceleration of protein synthesis under the influence of this hormone. Awareness of the fact that any substantial growth of muscle tissue is possible only by dividing satellite cells helps to understand in more detail the ways in which growth hormone leads to muscle hypertrophy.

The question arises, can muscle growth occur not only by increasing the volume of muscle fibers, but also by increasing their number? Can activated satellite cells merge into new fibers, as it happens with myoblasts during muscle formation in the embryonic period? That is, is hyperplasia of muscle fibers possible?

There is nothing fundamentally impossible in such a development of events. In the scientific literature, cases have been repeatedly described where the damaged muscle fibers died from the damage received, but the satellite cells released from under the shell of the damaged fibers actively shared and then, merging with each other, formed new muscle fibers instead of the lost ones. Such regeneration processes are observed, including in the muscles of people, and in experiments on animals not only the facts of the regeneration of individual fibers are noted, but there are examples of the regeneration of whole muscles. So, if you remove a muscle in rats under sterile conditions, chop it and then chop the crushed mass back into the muscle bed, then after a while this biomass is transformed into a new muscle, the fibers of which are formed by reproducing satellite cells released from chopping. Of course, such a muscle after regeneration is significantly inferior in size to the muscle to damage, the number of fibers in the restored muscle is smaller than stanozolol dosage before the operation, and a significant part of the muscle tissue is replaced by connective tissue. Meanwhile, such experiments themselves show that satellite cells are fundamentally capable of repeating the embryonic developmental path and forming new muscle fibers. This potential ability of satellite cells to form muscle fibers is also in demand in the practice of physical muscle training. After intense physical exertion, thin newly formed muscle fibers are found both in the muscles of animals and in human muscles, for example, young newly formed fibers were found in trapezoid muscles of highly trained powerlifters.

At the same time, the detection in the muscles of people and animals of young developing fibers is not yet evidence that muscle growth is possible by increasing the number of fibers. It has been reliably established that intense physical activity can lead to microdamages of muscle fibers (not to be confused with injuries associated with tearing or tearing of ligaments or muscles), up to the complete destruction of part of the muscle fibers. In the case of such significant fiber damage, cell cleaners living in the blood and connective tissue (neutrophils, macrophages, etc.) cleanse the inside of the fiber from damaged tissue, and then satellite cells build a new muscle fiber within the old membrane. It is likely that young thin muscle fibers found in the muscles of athletes are formed only instead of heavily damaged and completely degraded fibers, and the total number of fibers does not increase as a result of such regeneration processes. At the same time, a number of researchers, who recorded the formation of young fibers in muscles after overloading muscles, are inclined to believe that they are dealing not just with regenerated fibers, but precisely with the formation of new fibers in the intercellular space, that is, fibers that are additional to the existing ones . At the same time, it is safe to speak about hyperplasia of muscle fibers only in cases where the increase in the number of fibers is recorded in experiments, and not just the presence of young regenerating fibers in the muscle. And such experiments, in any case with reference to animals, are available.

Thus, an increase in the number of fibers in the muscles of rats in the first few weeks after birth was found. In this case, it is assumed that new fibers are formed either by merging satellite cells out of the muscle fiber to the outside, or by morphologically similar cells, which are not initially located inside the muscle fibers, but in the intercellular space. Meanwhile, the formation of new fibers in the forming animal organism also cannot be sufficient evidence that muscle growth in adulthood is possible due to fiber hyperplasia. Many of the researchers could not detect an increase in the number of fibers during muscle hypertrophy caused by certain types of overload. At the same time, there is a sufficient amount of research with the opposite result. Thus, Olway and co-workers attached the load to one wing of flightless birds, after a month of carrying the load on the wing, the number of muscle fibers in the loaded muscles of the birds was 51.8% greater than in the muscles on the other – not loaded – side. Antonio and Gonea, applying progressive load in similar experiments (with time they increased the weight attached to the wing), achieved an increase in the number of fibers relative to the unloaded muscle by as much as 82%. But I draw your attention to the fact that in these experiments scientists dealt with the muscles of birds, in the muscles of mammals, the achieved rates of hyperplasia were not so impressive, but still very significant.

So, Goneya was one of the first in 1977 to publish the results of research, in which hyperplasia of muscle fibers in mammals was recorded. The scientist conducted his experiments on cats, forcing them to lift the load with one paw for food reward. After forty-six weeks of training, the muscles of the trained and untrained paws of animals were subjected to histochemical analysis. The total number of muscle fibers in the trained paws of animals was 19.3% more than in untrained ones. Japanese researcher Tamaki recorded an increase of 14% in the number of muscle fibers in the muscles of the hind limbs of rats, which regularly (4-5 times a week) for 12 weeks performed an exercise similar to squats with a specially designed device.

Despite the success in experiments with animals, direct evidence of an increase in the number of muscle fibers under the influence of training in the muscles of man has not yet been found.

The fact that direct evidence of fiber hyperplasia in human muscles has not been found may be due to the limitations of functional muscle overload methods applicable to humans and methods for estimating the number of fibers in muscles: after all, such functional overload methods, such as prolonged stretching of muscles for several days degree causing hyperplasia of the fibers in birds), it is quite difficult to apply to humans. Significant hypertrophy of the human muscles (as in the case of the extreme development of the muscles of professional bodybuilders, weightlifters and powerlifters) occurs over many years of training; the comparison of the number of fibers in the muscles of athletes before training and after years of training has never been done (in any case, I am not aware of such experiments).

If the manifestations of fiber hyperplasia in humans are limited, and it (hyperplasia) makes a significant contribution to increasing muscle size only in the cumulative mode during a long-term training period, then the manifestation of hyperplasia after a relatively short training period limited by the time frame of the experiment will be quite problematic – especially given the limited methods of counting fibers applicable to humans. Experiments in which animals showed an increase in the number of fibers were usually accompanied by the killing of experimental animals and the counting of the total number of fibers in their muscles. Thus, in the already mentioned experiments with birds and cats, hyperplasia of the fibers was discovered by comparing the total number of fibers in the muscles extracted from the trained and untrained limbs of the same animal, it is clear that such direct methods of detecting human hyperplasia are not applicable.

However, there is at least one study published by Seostrom in 1991, in which manifestations of hyperplasia in human muscles were investigated by a similar method. Conducted this study, of course, not a sadistic doctor, but a pathologist – a scientist who studies the corpses of people who died their own death. It is clear that when studying corpses we cannot talk about some comparison of the number of fibers “before” and “after” training – the idea was to compare the number of fibers in the muscles of a more developed (dominant) and less developed (non-dominant) limb the same individual. For this comparison, a small leg muscle was chosen – anterior tibialis. It turned out that the muscles of the dominant supporting limb (left-handed for right-handers) had a slightly larger size and a large number of fibers, despite the fact that the average cross-section of the fibers in the muscles of both limbs was the same. These observations of Seostrom most convincingly suggest that functional hypertrophy of human muscles may still be related to fiber hyperplasia, although the initial genetic differences in the muscles of the dominant and non-dominant limbs cannot be ruled out.

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In most cases, the change in the number of fibers in a person under the influence of training has to be judged only on the basis of indirect estimates made by comparing the muscle size and the average cross section of the fibers in tissue samples taken from the muscle. But even the results of such studies are very controversial.

For example, when comparing the muscles of elite male and female bodybuilders, a link was established between the size of the muscle and the number of fibers in it. The muscles of men are on average twice as large as the muscles of women, while the larger size of the muscles of men is partly due to the larger cross-section of the muscle fibers in their muscles, but at the same time, the muscles of men have more fibers than the muscles of women . The latter may be a consequence of hyperplasia of the fibers, as well as a consequence of genetic differences between the sexes.

In one of the studies I was aware of, samples taken from the triceps of elite bodybuilders and world-class powerlifters were compared to samples taken from the muscles of athletes who practiced weight training for only six months. It turned out that, despite the large differences in strength and girth of hands, between elite athletes and amateurs there was no significant difference in the cross-section of muscle fibers. These observations are supported by a number of other studies, for example, it was found that the cross section of fibers in muscle samples taken from the muscles of the thigh and biceps of bodybuilders does not differ from the cross section of fibers of ordinary physically active people. The results of such studies indicate that a larger volume of muscles of athletes with extremely developed muscles is associated with a large number of fibers in their muscles. The explanation for this phenomenon can be found either in the fact that the sportsmen under study naturally possessed a large number of fibers, or in fiber hyperplasia as a result of training.

The genetic explanation seems to be the least convincing in this case, since it should follow that the initially studied elite athletes had very thin fibers and long-term workouts could only lead to the fact that their fibers reached the size typical of an average person. The mentioned observations could be considered reliable evidence of hyperplasia of muscle fibers in humans, if not the existence of similar studies, but with the opposite result. So in one of the studies it was revealed that elite bodybuilders with the most developed muscles, indeed, have a greater number of muscle fibers than their less advanced colleagues. But it turned out that such a spread in the number of fibers was observed in untrained people and a number of untrained people had the same number of fibers as elite bodybuilders. Moreover, it was found that the average number of fibers in the muscles of athletes is no more than in the muscles of untrained individuals, that is, there is no connection between training and the number of fibers. Based on these facts, the researchers came to the conclusion that such a parameter as the number of fibers in the muscle is most likely determined genetically.

Summing up, it should be recognized that hyperplasia of muscle fibers in animals is possible, and is a consequence of damage to the fibers as a result of functional muscle overload and subsequent regeneration processes associated with the activation of satellite cells, their active division and subsequent merging into new muscle fibers. The possibility of fiber hyperplasia in a person’s muscles is still questionable.

It is possible that the regenerative potential of human muscles is not so great that the restoration of muscle fibers after their microtrauma under the influence of exercise can cause their hyperplasia, but the use of cell division stimulants such as growth hormone and testosterone can significantly increase the regenerative potential of human muscles. The question of whether such pharmacological intensification of satellite cell activity may contribute to the formation of new muscle fibers in human muscles requires further study. Recently, the press began to skip reports of hyperplasia of human muscles under the influence of hormones, as an established fact, so in the fourth issue of this year, Muscular Development published an article by Dan Guartney with the loud name Hyperplasia. The literature to which this author refers when making his statements about the discovery of the fact of hyperplasia is well known to me – in these studies, we are not talking about muscle fiber hyperplasia at all. It seems that the author of the article simply mixed (I don’t know whether I was unaware or intentionally, for the sensational headline) division of satellite cells with fiber hyperplasia. In some sense, the division of satellite cells and an increase in their number can be called hyperplasia, hyperplasia of satellite cells, but the fact is that, traditionally speaking of muscle tissue, hyperplasia means only an increase in the number of muscle fibers, and not nuclei in of them. The increase in the number of fibers in humans, I repeat, was not reliably recorded. At this stage of development of our knowledge about intramuscular processes activated by exercise, we can only confine ourselves to a general, but completely reliable statement:

Any significant hypertrophy of human skeletal muscles under the influence of regular exercise is a consequence of cell division of satellites and an increase in the number of cell nuclei in the muscles.

Whether an increase in the content of nuclei in muscles occurs only due to an increase in the number of nuclei in pre-existing fibers, or the number of nuclei in muscles increases also due to the nuclei of newly formed muscle fibers – all this can not be specifically decided until the final resolution of the question of the possibility of muscle hyperplasia in humans. to negotiate Moreover, for the practice of sports, the possibility or impossibility of hyperplasia of muscle fibers does not matter in principle, since in both cases the goal of an athlete who wants to gain muscle mass should be to stimulate the division of satellite cell muscle fibers. It depends on whether muscle fiber hyperplasia is possible or not, except perhaps our assessment of the potential development of human muscles. If hyperplasia of fibers in the muscles of a person takes place – the development of the muscles of an athlete is virtually unlimited, otherwise every person has his own individual limit of muscle development, in overcoming which no hormone therapy can help.

Why is this so? What caused the limit of muscle development in case of impossibility of fiber hyperplasia? Does it really matter whether the muscles increase their size – by increasing the cross-section of the muscle fibers or by increasing their number? To understand what is the fundamental difference between the hypertrophy of muscle fibers and their hyperplasia, it is enough to look at a schematic representation of the transverse incision of muscle fibers (see Fig. 1).

As I mentioned earlier, the muscle fiber nuclei are not evenly distributed throughout the entire volume of the muscle fiber, but are located along the fiber perimeter, directly under the shell (apparently, this arrangement of the nuclei is explained by the need for the genetic apparatus of the muscle fibers concentrated in the nucleus to respond quickly to chemical signals of various kinds, which enter the fibers from the outside, through its shell). Muscle proteins are rather unstable substances and require constant replacement, because for the normal functioning of cellular structures located deep in the muscle fiber, it is necessary to constantly deliver there either RNA or already synthesized proteins from the nuclei, and this is in conditions of tight packaging throughout the entire volume of myofibril fibers serving as a barrier to the transported substances. The greater the muscle fiber in diameter – the longer distances forced to overcome the matter transported deep into the fiber, and the more difficult it is for such a fiber to ensure timely replacement of protein molecules in contractile structures located in the central regions of the fiber.

Hence the conclusion that there should be a limiting fiber size, on reaching which no matter how many you increase the number of nuclei in the fiber, and the volume of the fiber can no longer increase, because the nuclei are located too far from the inner regions of the fiber to ensure normal metabolism. If fiber hyperplasia is impossible, then when all fibers reach their maximum size, any workouts and doses of hormones will be useless. If the division of satellite cells can lead not only to an increase in the number of nuclei in existing fibers, but also to the formation of new fibers, then in this case, with muscle growth, a critical increase in transport distances between the nuclei and the cellular structures served by them does not occur. Restrictions on the size of the muscles, in this case, if they exist, it is not from the internal mechanisms of muscle growth, but from the rest of the body’s systems that ensure the vital activity of the muscle tissue.

If you look at the development of the muscles of modern elite bodybuilders and compare their muscles with the muscles of ordinary visitors to the gym, it is hard to believe that there was no hyperplasia of muscle fibers. On the other hand, the experience of the same bodybuilders shows that the limit of muscle development does exist, few of the athletes storming the summits of Olympia from year to year show an increase in muscle mass.

Summarizing the above, I made the following statement:

Any significant hypertrophy of human skeletal muscles is a consequence of the division of satellite cells and an increase in the number of cell nuclei in the muscles.

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Those readers who were interested in theory, and not just the practice of “iron sport”, should have paid attention to the fact that my statement asserted differs from the generally accepted ideas about the mechanisms of the effects of exercise on protein synthesis, both prevalent among athletes and textbooks. If you look at modern textbooks, in most of them you can find a description of the following mechanism of the effect of exercise on protein synthesis (see Figure 1): vigorous muscle activity leads to energy muscle exhaustion, manifested in a decrease in the content in the muscles that serve as sources of fast-available energy (such as ATP and creatine phosphate), and the accumulation in the muscles of their breakdown products (ADP, creatine, phosphoric acid); In turn, the accumulation of energy metabolism products directly or indirectly affects the DNA of muscle cells, which stimulates RNA synthesis and, as a result, muscle protein synthesis (see the description of the protein synthesis mechanism in the first part of this article).

At first glance, it may seem that the concept described in the textbooks fundamentally contradicts my conclusions about the causes of hypertrophy of human muscles. But, as will be shown later, this contradiction is, in fact, only apparent. The fact is that the mechanisms of protein synthesis were studied first on the simplest unicellular organisms that do not even have nuclei, whose DNA is located directly in the cell body (bacteria). Later, scientists began to study the mechanisms of protein regulation in more complex single-celled organisms with nuclei, and now the regulation of protein synthesis in multicellular organisms is being actively studied. It is easy to see that in the overwhelming majority of cases, the regulation of protein synthesis was studied in cells either with no nuclei at all or with only one nucleus. It is clear that the intensity of protein synthesis in such cells can be regulated only by controlling the intensity of RNA synthesis on the DNA of a given cell. Muscle fiber is a rare exception, a cell that has not one, but many nuclei, and, moreover, has the potential to increase their number. Only in such a cell is it possible to enhance protein synthesis not only by increasing the synthesis of RNA by the cell nuclei, but also by increasing the number of nuclei in the cell. This potential ability of muscle cells to increase the number of nuclei has been neglected by sports researchers for a long time, and muscle hypertrophy has been attributed solely to increased RNA synthesis by muscle nuclei.

Now that we know that muscle size increases due to an increase in the number of nuclei in muscles, we should not make a new mistake and completely forget about the possibility of regulating protein synthesis by controlling the intensity of RNA synthesis in the nuclei of muscle cells, because such regulation mechanisms, as I will show below, play an equally important role in the development of the functional properties of the muscles under the influence of training.

The number of nuclei in a muscle determines the size of the muscle, but cannot determine its “content”. What muscle proteins fill this volume, given by the number of nuclei, just depends on what RNA of which proteins and in what quantity is synthesized by the nuclei of the given muscle. But the intensity of the synthesis of RNA of various types of protein is influenced by intracellular factors associated with the mode of muscle functioning. And to understand the ways in which training affects the intensity of the synthesis of a particular type of protein, it is worth referring to the results of many years of research into the mechanisms of regulation of protein synthesis in the simplest organisms.

First, these studies have shown that the regulation of all types of protein is carried out according to a unified concept. Practically for each structural protein in cells, certain regulatory proteins are produced, which, combining with a number of substances entering the cell from the outside or forming inside the cell during its vital activity, interact with the DNA of the cell, act on the genes and either launch or alternatively block the synthesis of the corresponding proteins. Secondly, studies have shown that, despite the fact that for each type of protein there is an individual set of substances that initiate protein synthesis (synthesis activators) or block synthesis (synthesis inhibitors), which particular substances activate the synthesis of a particular type of protein There is some general rule.

Generally speaking, all cellular proteins can be divided into two large classes: these are the proteins used as the building material of the cell, mainly myofibrillary (proteins forming chains of myofibrils — cell structures that reduce it) and sarcoplasma proteins, mainly enzymes or In other words, enzymes are proteins that ensure the flow of various chemical reactions in the muscle cell, which provide the contractile activity of the muscle cell and its very life. The content of enzymes in the muscles reaches up to 35% of the total mass of muscle protein. It is interesting that the above described mechanism of regulation of protein synthesis through regulation of RNA synthesis by substances that are activators or inhibitors of synthesis was studied just by the example of enzyme synthesis. It was found that in most cases the synthesis of enzymes is activated when substances that are processed by the action of these enzymes enter the cell.

If we now consider the mechanisms of muscle contraction and the mechanisms of energy recovery, wasted during contractile activity of muscles, it turns out that the substances that accumulate in the muscle cell during its contraction and are the decay products of high-energy substances that serve the muscle as energy sources are themselves the starting substances for reactions that testosterone cypionate injection restore energy stores in the muscle cell. Since ATP (ternary phosphate), giving up the energy stored in it, decomposes into ADP (double phosphate) and a free phosphate group, the recovery of ATP reserves occurs by reattaching the phosphate group to ADP, that is, ATP is the starting material for chemical reactions that restore stocks ATP. Or, for example, creatine phosphate – with intensive muscle contraction, the substance, giving away the energy stored in it, is decomposed to creatine, and creatine is the starting material for producing creatine phosphate. Reactions, restoring stocks of high-energy substances, occur in the muscle cell during the rest period after the load, and they proceed under the action of specific enzymes. The synthesis of enzymes, as was established in experiments with bacteria, is activated by substances that are basic for chemical reactions activated by this enzyme. That is: the consumption of energy reserves in the muscles in the process of their reduction and the accumulation in the muscle of the decay products of energy-containing substances activates the synthesis of enzymes that ensure the restoration of energy reserves.

So the contraction of muscles in almost any regimes leads to the consumption of ATP, which should activate the production of enzymes that ensure the recovery of ATP (including, apparently, oxidative cycle enzymes), but the synthesis of creatine kinase – an enzyme that restores creatine phosphate reserves, should activate only the work of the muscles in a fairly intensive mode, contributing to the consumption of creatine phosphate.

Thus, training of muscles in one mode or another should activate the synthesis of enzymes that ensure energy recovery when working in this mode, which during regular trainings should contribute to the accumulation of corresponding enzymes in muscles and, as a result, lead to an increase in performance (endurance) of muscles in this mode.

The absence of a certain mode of working for a long time means the absence of the breakdown of energetic substances that provide this mode of contraction and, as a result, the absence of stimuli to synthesize the corresponding enzymes, and the natural breakdown of previously synthesized enzymes leads to a gradual decrease in the content of enzymes in the muscles. It is for this reason that if a muscle that has not worked in a certain mode for a long time is forced to contract in this mode, then a low level of enzymes will not allow energy to be restored at the desired speed, which naturally leads to rapid muscle fatigue.

The life of enzymes is relatively short – from several hours to several days, therefore, without regular activation of the synthesis of enzymes, their content in the muscles is rather quickly depleted. That is why in sports, in order to achieve high results in which endurance of muscles is very important, regular and relatively frequent trainings are so important. In the practice of sports of higher achievements, the number of training sessions can reach up to two, and in exceptional cases – up to three per day. I am not sure that such a frequent load on muscles is fully justified even in sports requiring the development of muscle endurance and, accordingly, maintaining a high level of enzymes in muscles, but in any case, for such sports, coaches’ desire to increase the frequency of training is at least understandable. But how justified is the high frequency of muscle training in bodybuilding?

The lifetime of contractile proteins is much longer than the lifetime of enzymes – something about a month against several days in the case of enzymes, but, as I have repeatedly repeated, muscle volume is determined, first of all, not by the frequency of activation of protein synthesis in muscles, but by the number of nuclei muscle The lifespan of the nuclei is not exactly established, but it does not amount to hours and days, but months and even years. Of course, one should not assume that the content of the number of nuclei in the muscles will be unchanged when idle for months or even years, no, the self-destruction of unwanted nuclei is a completely natural process observed in a long time inactive muscles. But at the same time, the frequency of workouts that activate cell division, required to maintain and even develop muscle volumes, is significantly lower than the frequency of workouts that activate the synthesis of muscle enzymes, which are required to maintain and especially the development of muscle performance.

This is my statement is confirmed by the practice of bodybuilding. If twenty or thirty years ago in competitive bodybuilding, training each muscle 3 times a week was practically the accepted norm, then today it is considered permissible to load one muscle group no more than once every 4-8 days, and the muscle volumes of the athletes performing do not diminish . That’s right, endurance, muscle performance and muscle volume – this is not the same thing. But, at the same time, the saturation of muscles with enzymes, nevertheless, to some extent affects the volume of muscles.

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The fact is that the main volume of the muscles is not at all created by the protein itself, but by the water that is retained by the proteins inside the muscle fibers. Proteins together with lipids create the skeleton of muscle fibers, its shell, but it is the water that fills the fiber with a volume. Muscle fiber is surrounded by a shell, which is a stretching membrane with a selective ability to skip certain types of substances. Water can freely circulate through such a membrane back and forth, setting the volume of muscle fibers. It determines how much water is inside the muscle fiber, the amount of substances dissolved in water, inside the muscle fiber, all sorts of ions, including enzymes. The more solutes inside the muscle fiber, the more water passes inside the cell fiber through the membrane and the stronger the muscle fibers swell. All transient effects, expressed in an increase in muscle volume already during exercise or in the first few days after it, are not associated with increased protein synthesis, but with the accumulation in the muscle of the breakdown products of energetic substances (and in certain cases, the internal structures of the cell). An increase in soluble muscle fibers causes an instantaneous influx of water into the fibers, resulting in muscle fibers, followed by muscle swelling before the eyes.

But back to the enzymes. The saturation of muscle fibers with enzymes can not affect the volume of the muscles, the more enzymes in the muscle fibers, the larger will be the muscles with the same number of nuclei and contractile elements. But the saturation of the muscles with enzymes has a certain limit, and no matter how often you train, after reaching a certain state of muscles, there will be no further increase in the number of enzymes in the muscles, and therefore there will be no muscle growth without the appearance of new nuclei in the muscles. This picture of the lack of muscle growth in seemingly regular workouts is well known to athletes called the “training plateau” (not to be confused with the state of overtraining). Upon reaching a certain condition of the muscles, the increase in the results and volumes of the muscles ceases without stress training, which activates the division of satellite cells in the muscles.

So, the effect of training on muscles is realized not by any one, but at least two alternative ways, and the scheme of the influence of training on the mechanisms of protein synthesis, taken by me from modern textbooks on sports biochemistry (see Fig. 1), would be replaced by more complete (see fig. 2).

Fig. 1. (scheme taken from the textbook “Biochemistry of muscular activity” N.I. Volkov, E.N. Nesen, A.A. Osipenko, S.N. Korsun. The publishing house “Olympic literature”, 2000)

Fig. 2

In the above diagram, the reason for the activation of satellite cells is marked with a question mark. It’s not that at the present stage of the development of science these factors were not known to scientists at all, just modern knowledge in this area does not allow one to make definite conclusions. It has been reliably established that the activation of satellite cells is carried out by factors produced in the event of muscle damage – this is how the muscle repair mechanism is implemented. Damage to the muscles immediately causes the activation of satellite cells, which provides a sharp increase in protein synthesis in the muscle cell, the protein needed to “patch up” the damage. But whether this mechanism is dominant during muscle training, and even more so – is this path the only way to activate satellite cells – that is a question for which there is no exact answer yet.

Probably, all readers know the expression “there is no growth without pain” existing among athletes. But pain is a signal of muscle damage, so it can be argued that bodybuilding experience, concentrated in this expression, shows that with a high probability muscle growth as a result of satellite cell activation can be associated with muscle microfractures, obtained during exercise. At the same time, one should be aware that this is so far only what is called a “working hypothesis”.

Let us see what conclusions about the basic principles of planning a training load follow from reliably established mechanisms of muscle hypertrophy, summarized in a single scheme in Figure 2, and this working hypothesis.

Heavy loads, destroying muscle tissue and activating cell division of satellite cells, require long-term recovery. So, only the cleansing of muscles from damaged tissue after heavy loads can last for several days, as evidenced by the peak of pain occurring in the muscles on the second day after exercise, and the peak of pain is just the peak of self-destruction of the tissue damaged during exercise. About one more day is required for one cycle of division of satellite cells, this division follows the self-cleaning of muscles from damage (there may be several such cycles after one workout). By this time, it is worthwhile to add the time required for the synthesis of RNA by the newly formed nuclei and the construction of the protein necessary for reconstructing the cell volume corresponding to each nucleus in a normal intact muscle fiber. Consequently, intensive loads, accompanied by the destruction of the muscle tissue, should not be applied too often. Apparently, such loads are allowed no more than once a week per muscle group, and even less. At the same time, to maintain a high level of enzymes in the muscles of a single muscle should be carried out much more often.

What are the ways to resolve this contradiction? With all the wealth of choice of possible options, most of which have already been implemented in the training methods of various practitioners, for bodybuilding I would single out two main approaches.

The first approach is to divide the annual training plan into periods (mesocycles) of various directions. In the simplest case, only two such mesocycles can be distinguished – let’s call them “basic” and “precompetitive.”

In the base period, heavy training should be applied, stimulating micro tissue damage of the muscles and subsequent regeneration processes in the muscles. Such training requires a long rest after exercise, and therefore should be held quite rarely, no more than once a week for each muscle (perhaps less often, depending on the individual recovery abilities of the athlete, and also depending on the pharmacological drugs used or not). By the end of the base period, the athlete is faced with the task of increasing the number of cell nuclei in the muscles, and, consequently, the “base” muscle volume associated with the number of nuclei.

The task of the precompetitive period should be to “squeeze out” the maximum of the achieved “basic” muscle volume by increasing the muscle volume even more by filling the muscle fibers with enzymes and, as a result, with water (water inside the muscle fibers, which actually contains there in the form of a gel, because of the high concentration of substances dissolved in it, you should not be confused with water in the intercellular space, which athletes just try to get rid of before the competition). Therefore, in the pre-competition period, the intensity of training should be reduced, and the frequency of training should be increased to several trainings per muscle per week. During this period, muscle damage during training is contraindicated, because it increases the requirements for muscle recovery time, and the athlete has the task only to bring the muscles to a moderate energy depletion than to stimulate the synthesis of enzymes in the muscles. Increasing the frequency of training and the overall energy consumption of the body is the best way to achieve another challenge facing the athlete – reducing the content of subcutaneous fat before the competition.

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There is also a second fundamental approach to training, which allows in one training program to combine the requirements for long-term muscle recovery after hard training, causing muscle tissue destruction and satellite cell division, with the requirements of a high frequency of training sessions to saturate muscles with enzymes. This approach is based on the introduction into training practice of training sessions of various orientations and intensities and then cycling such training sessions. The basic rule here is the following: after one or several hard intensive exercises, several lighter workouts should follow, which do not cause the destruction of muscle tissue and do not interfere with the recovery processes. A feature of such techniques is that when they are used, there are no pronounced peaks of fitness and its reduction, as in the first approach considered, which can be useful if you want to maintain a sufficiently high fitness form throughout the entire annual period. But, in my opinion, such an approach to training increases the requirements for the recovery capabilities of the body.

With this, I, perhaps, will complete my excursion into the biochemistry and physiology of muscular activity. I hope that the information presented in this article will help you, dear readers of Iron World, to better understand the variety of existing training systems and techniques, and will give you a criterion that allows you to choose among this diversity the methodology that best suits your goals.