Reflecting on the title of the future article, it was not by chance that I chose the option that is written just above - the reader can easily recognize in it a collage made up of the titles of two, perhaps, the most popular books about bodybuilding among amateur athletes. “Think! Bodybuilding without Steroids” by Stuart McRobert and “Supertraining” by Mike Mentzer shook up the world of amateur sports and upended what seemed to be established ideas about the theory of training. It would be more accurate to say that Mentzer for the first time tried to create at least some kind of theory; before him, most popular books and articles about bodybuilding were just collections of various and often contradictory principles of training, and catalogs of well-known exercises with weights. Mentzer called for bodybuilding to be viewed as a science, but for some reason he chose philosophy and logic rather than physiology as the basis. Just as Euclid once created his geometry based on a number of axioms about the properties of space, Mentzer created his “Supertraining” based on the axiom about the role of the last “failure” repetition in the mechanism of triggering muscle growth, without bothering to give any physiological explanation to his hypothesis. But, as we know, in addition to the geometry of Euclid, there are geometries of Lobachevsky and Minkowski, based on other axioms, but also internally completely non-contradictory and logical. Inspired by the excellent style and unshakable confidence of the author of “Supertraining” in his rightness, having built up, following his advice, 10 kilograms of “natural” muscles in six months, I became an ardent supporter of Mentzer’s ideas. Deciding to find physiological confirmation of the “teacher” axiom, I plunged headlong into a new field of knowledge for myself - human physiology and biochemistry. The result was unexpected for me, but more on that later.
Let me draw the readers’ attention to the monstrous situation in which the theory of modern “iron” sports finds itself. All sports magazines are full of articles with new, trendy training systems. “The movement must be powerful and explosive,” some say. “Only slow, controlled movement,” others contradict them. “If you want to gain mass, work with heavy weights.” “The weight of the projectile does not matter - the main thing is technique and the feeling of the muscle working.” Arnold Schwarzenegger advises training six times a week, morning and evening. Mike Mentzer forbids his students to appear in the gym more than twice a week. The pros describe a set of six exercises for biceps. McRobert urges not to train your arms with isolated exercises at all. Powerlifters almost never work to failure during their cycles. Mentzer assures that working too hard is a waste of time. The pros on Joe Weider's team advise going much beyond failure with forced reps and stripteases. This list can be continued indefinitely, but what is striking is not the abundance of mutually exclusive training principles, but the fact that each of them has its own supporters who have managed to get results from their use. This fact allowed the opinion to spread in wide circles that there was no system. I claim that there is a system! And the patient reader will soon be able to see for himself.
And so, I managed to create a more or less integral theory of training, which explains at the physiological level (in general terms, of course) the effect of training on the human muscular system and allows one to find answers to most of the questions that interest the reader.
You just didn't read it, I might say...Functional hypertrophy of skeletal muscles. Local mechanisms of adaptation of skeletal muscles to load
V.A.Protasenko
The structural basis of all tissues of living organisms is proteins, therefore the hypertrophy of any tissue, including muscle, is closely related to the intensity of protein synthesis and catabolism in a given tissue. It has been reliably established that regular training causes hypertrophy of skeletal muscles, accompanied by an increase in dry muscle mass (N.N. Yakovlev et al. 1957). Under the influence of training, the content of contractile proteins in the muscles increases - myosin and actin, sarcoplasmic and mitochondrial proteins, as well as muscle enzymes (N.N. Yakovlev 1974).
It has been established that physical activity inhibits protein synthesis in muscle tissue directly during exercise and activates protein catabolism in the initial recovery period (N.N. Yakovlev 1974), (A.A. Viru, N.N. Yakovlev 1988). Consequently, functional muscle hypertrophy occurs precisely due to the activation of protein synthesis, but not as a result of a decrease in the intensity of protein breakdown while maintaining the same level of intensity of protein synthesis.
However, the mechanisms of the effect of training on the intensity of protein synthesis in muscles have not yet been fully studied.
Regulation of protein synthesis at the level of mRNA transcription
The intensity of protein synthesis can depend on many factors and is regulated at all stages of its biosynthesis. However, the key stage in the regulation of protein synthesis is considered to be the stage of mRNA transcription - the first stage of protein biosynthesis, during which information about the sequence of amino acids in the protein molecule is read from the DNA of the cell nucleus and this information is recorded in the messenger RNA molecule, on the basis of which assembly is then carried out in the cell cytoplasm protein molecule.According to the concept generally accepted today by F. Jacob and J. Monod (explained according to T.T. Berezov and B.F. Korovkin 1998, M. Singer and P. Berg 1998), the DNA molecule contains not only structural genes (that is, those genes that encode proteins that ensure the functioning of the cell), but also genes that regulate the activity of the structural genes themselves - that is, the so-called “operator genes” and “regulator genes” (see Fig. 1).
Picture 1
A complex of genes consisting of an operator gene and one or more structural genes, the expression (that is, the process of activating the transcription of mRNA on a given gene and the synthesis of ready-made mRNA) of which is regulated jointly, is called an operon. Transcription of mRNA on the structural genes of the operon is possible only when the operator gene is in an active state. The operator gene can be affected by specific proteins expressed by the regulator gene, which can either block the operator gene (in this case the regulatory protein is called a repressor, and the regulatory pattern is called negative regulation) or activate the operator gene (in this case the regulatory protein is called a transcription activator, and the regulatory pattern is called positive regulation).
In turn, regulatory proteins are exposed to the influence of certain low-molecular substances, which, when combined with the regulatory protein, change its structure so that it either becomes able to contact the operator gene, or the ability of the regulatory protein to bind to the operator gene is blocked. The set of regulatory proteins, as well as low-molecular substances that induce or inhibit mRNA transcription, is individual for each operon and has not yet been precisely determined for most human genes.
The regulation of enzyme transcription has been most fully studied in the cells of prokaryotes, that is, the simplest nuclear-free single-celled living beings. As a rule, inducers of mRNA transcription of a particular enzyme in prokaryotes are substrates - initial substances that undergo certain transformations in the cell under the action of the enzyme. And the products of chemical reactions occurring in the cell, resulting from the processing of substrates, can act as inhibitors of enzyme mRNA transcription. Thus, when substrates that require further processing appear in the cell, the synthesis of enzymes that carry out such processing is induced, and when the concentration of substrates decreases and reaction products accumulate, enzyme transcription is blocked.
For example, if E. coli bacteria get into a glucose solution, then they adapt to digesting glucose, that is, these bacteria do not produce enzymes that break down more complex carbohydrates. If glucose in the nutrient solution is replaced with milk sugar - lactose, then E. coli cannot feed and reproduce for some time, since the lactase gene - the enzyme that breaks down lactose into glucose and galactose - is blocked in these bacteria by a repressor protein, and they do not synthesize this enzyme. However, already some time after replacing the nutrient medium, lactose absorbed by E. coli bacteria combines with the repressor protein of the gene encoding lactase, and the repressor loses the ability to bind to DNA and ceases to block the synthesis of lactase mRNA. As a result of such processes, the synthesis of the necessary enzyme is activated in the bacterial cell, the bacteria are able to digest milk sugar, and begin to multiply again. In this case, the repressor protein continues to be constantly produced by the bacterial cell, but new lactose molecules bind to the repressor and inactivate it. Once the bacteria have processed all the lactose, inactivation of the repressor protein by lactose becomes impossible and the active repressor again blocks the gene encoding lactase, an enzyme that is no longer needed. This is the mechanism by which the adaptive response of a cell to changes in the conditions of its existence is regulated through gene activity.
Regulation of transcription in eukaryotic cells, that is, living creatures whose cells have nuclei, can occur according to fundamentally similar, but much more complex schemes, since the processes of mRNA transcription and assembly of a protein molecule based on it are separated both by the nuclear membrane and by the time interval ( In eukaryotes, mRNA synthesis occurs in the cell nucleus, and protein molecule assembly occurs outside the nucleus, directly in the cytoplasm). In multicellular organisms, positive regulation of gene activity predominates, and for each operon there are at least five DNA sections to which specific regulatory proteins must bind in order for transcription of the structural genes of this operon to begin. For a number of operons, steroid hormones can act as inducers of mRNA transcription.
Modern concept of the effect of physical activity on the intensity of protein synthesis by the cell
When modeling the impact of training load on the functional state of muscles in general and on their hypertrophy in particular, modern sports theory is based on the concept of immediate and long-term adaptation of muscles to load (Kalinsky et al. 1986), (A.A. Viru, N.N. Yakovlev 1988 ), (F.Z. Meerson, M.G. Pshennikova 1988), (F.Z. Meerson 1993), which has already been included in textbooks (N.I. Volkov et al. 2000). According to this concept, physical activity causes significant changes in the internal environment of the muscles, and these changes are associated mainly with an imbalance in energy balance (that is, with a decrease in the content of ATP, creatine phosphate, glycogen in the muscles, as well as with the accumulation of energy metabolism products - ADP, AMP, free creatine, orthophosphate, lactic acid, etc.). These changes in the internal environment of the muscles stimulate the processes of adaptation of the body to new conditions of existence.The body's primary reaction to stress, called the urgent adaptation reaction, comes down mainly to changes in energy metabolism in the muscles and the body as a whole, as well as changes in the system of its vegetative maintenance. During urgent adaptation processes, substances accumulate in muscles that activate the transcription of mRNA of structural genes, either directly or through the induction of the synthesis of regulatory proteins that control the activity of genes for structural muscle proteins. With repeated training loads, due to regular activation of the genetic apparatus of muscle cells, the content of structural proteins in the muscles increases, as a result of which the muscles become more resistant to the given load - this is how long-term adaptation develops in the muscles. A schematic diagram of the relationship between the links of urgent and long-term adaptation is shown in Figure 2 (borrowed from the work of Kalinsky et al. 1986, N.I. Volkova and others 2000).
The primary cause that triggers the mechanisms of action on the genetic apparatus of the muscle cell and ultimately activates the synthesis of mRNA for structural proteins is most often considered to be depletion of intracellular energy resources, a decrease in the concentration of ATP and creatine phosphate in the sarcoplasm and an increase in the content of ADP, AMP and creatine.
F.Z. Meerson notes that what kind of intracellular signal has a direct effect on the genetic apparatus of the cell has not been reliably established, and as a hypothesis puts forward the role of this primary signal as an increase in the concentration of hydrogen ions in the sarcoplasm - that is, muscle acidosis caused by the accumulation acidic metabolic products (F.Z. Meyerson 1993). In Meyerson's concept of long-term adaptation, acidosis affects the synthesis of mRNA of structural proteins not directly, but through the activation of the proto-oncogenes c-myc and c-foc - early genes expressing regulatory proteins, which, in turn, activate the genes of structural proteins.
A number of sports methodologists, when justifying their training concepts, also consider muscle acidosis as an important factor in triggering protein synthesis - however, from their point of view, acidosis exerts its influence on the activity of the genetic apparatus of the cell through facilitating access of other transcription factors to hereditary information (V.N. Seluyanov 1996 ), (E.E. Arakelyan et al. 1997). The latter, according to the mentioned authors, is achieved by increasing the permeability of cell membranes, including nuclear membranes, unwinding of the DNA helix and a number of other processes that are activated in the cell with increasing H+ concentration. According to the same authors, a direct effect on cell DNA, inducing the synthesis of contractile proteins, is exerted by creatine, the concentration of which increases in the sarcoplasm of working muscles due to the intensive restoration of ATP due to creatine phosphate. Creatine as a factor-activator of protein synthesis is also indicated in modern textbooks on the biochemistry of sports (N.I. Volkov et al. 2000).
A fundamentally similar concept of regulation of protein synthesis was considered by J. McComas - with the only difference that the role of the trigger mechanism, including the transcription of mRNA of contractile muscle proteins, in this concept is not the factors associated with muscle fatigue, but the mechanical stretching of the fibers that occurs in the process motor activity of muscles (A.J. McComas 2001). It is assumed that tension of the muscle fiber cytoskeleton, especially during the eccentric phase of movement (that is, when the tense muscle fiber is lengthened under the influence of an external force), causes the release of a number of factors (possibly including prostaglandins), which activate the induction of early genes, the proteins of which, in turn, activate the genes of muscle contractile proteins.
Meyerson also considers increased mechanical tension of the heart muscle with increased blood pressure as a possible factor activating the expression of regulatory genes in cardiomyocytes. However, the latter, due to the fact that mechanical factors influence the activity of regulatory genes only in the beating, working heart, tends to predominate precisely metabolic factors in the activation of regulatory genes (F.Z. Meyerson 1993). According to Meyerson, hypertrophy of the heart muscle with increased mechanical stress develops according to the following scheme:
Load -> increase in mechanical activity -> energy deficit -> decrease in pH -> activation of proto-oncogene expression -> synthesis of regulatory proteins -> activation of synthesis of contractile proteins -> compensatory hypertrophy.
Thus, at present, there is no consensus among researchers about exactly which processes accompanying physical activity act as a trigger for the transcription of mRNA of structural muscle proteins. What unites all the above concepts is that functional muscle hypertrophy is considered in them as a consequence of the intensification of the synthesis of mRNA for structural proteins in the nuclei of muscle cells.
A significant and fundamental drawback of all such concepts is that with the described approach, the most important factor that determines the volume of protein synthesized in muscle tissue either remains in the shadows or completely falls out of the field of view of researchers, namely: the number of DNA molecules on which this occurs. mRNA transcription.
Meerson notes that the DNA content in muscle is an important parameter influencing protein synthesis, but considers this parameter mainly as a genetic determinant closely related to the functional purpose of a particular muscle tissue. Thus, Meerson notes that for skeletal muscles, for the left and right ventricles of the heart muscle, the mass of muscle tissue per DNA molecule is different (F.Z. Meerson 1993). In other words, the more intensely muscle tissue functions during the life of the body, the higher its DNA density.
Meerson also notes that in the body of young animals, functional adaptation of the heart is possible through the activation of cardiomyocyte division and their hyperplasia, however, Meerson’s awareness of the possibility of this way of adaptation of the heart muscle to physical activity does not change his ideas about the fundamental scheme of regulation of protein synthesis in muscle tissue.
A.A.Viru and N.N.Yakovlev mention the inclusion of labeled atoms in the DNA of muscle cells after training (A.A.Viru, N.N. Yakovlev 1988), which is evidence of the new formation of DNA molecules. However, when considering the biochemical pathways of the impact of training load on muscles, these researchers also focus on the intensification of RNA transcription of structural proteins under the influence of energy metabolism products.
N.N. Seluyanov does not consider an increase in the amount of DNA in skeletal muscles as a possible factor in muscle hypertrophy at all. The volume of protein synthesized by a muscle cell, in the model of the effect of training on the human body developed by Seluyanov, is a function of the activation time of transcription of the mRNA of contractile proteins under the influence of increased concentrations of creatinine and H+ during muscle activity (V.N. Seluyanov 1996).
The possibility of increasing the DNA content in skeletal muscles as a factor in skeletal muscle hypertrophy remains practically unconsidered in modern textbooks (N.I. Volkov et al. 2000), (A.J. McComas 2001).
An increase in the number of nuclei in muscle fiber as a factor in skeletal muscle hypertrophy
Muscle fibers are multinucleated cells formed during the development of the embryo by the fusion of embryonic myoblasts into long elongated tubular structures - myotubes, which later, after contact with the sprouting axons of motor neurons and the synthesis of myofibrils in the myotubes, are transformed into muscle fibers (R.K. Danilov 1994 ), (E.G. Ulumbekov, Yu.A. Chelyshev 1998), (A.J. McComas 2001), (E.A. Shubnikova et al. 2001). The number of nuclei in a muscle fiber is determined by the number of myoblasts that formed it and, as a number of studies discussed below show, the number of nuclei in already formed muscle fibers is not constant.It is well known that the muscles of animals and humans radically increase their size, mass and strength during the growth of the body. To reach the size characteristic of an adult's muscles, the child's muscle belly must increase approximately 20 times (A. J. McComas 2001). Back in the 60s of the last century, it was found that as animals grow, the number of nuclei in their muscle fibers increases dramatically (M.Enesco, D.Puddy 1964), (F.P.Moss 1968). It was found that for people aged one to seventy-one years, muscle fiber volume correlates well with the number of nuclei per muscle fiber, and muscle fiber volume per nucleus is virtually constant throughout the age range studied (D. Vassilopoulos et al. al. 1977).
At first, the reason for the increase in the number of nuclei in muscle fibers remained not entirely clear, since it was known that the nuclei of myoblasts, after merging into muscle fibers, lose the ability to divide. At the same time, it was known that not all muscle fiber nuclei have the same properties; in particular, a small part of the nuclei (3-10%) differs from their main mass - the nuclei from this small part are located in the fiber membrane between the plasma membrane and the basement membrane, that is, they are separated from the sarcoplasm by their own membrane and are, in fact, individual cells ( A. Mauro 1961). These cells are called satellite cells or myosatellite cells. Subsequently, it was discovered that it is the division of myosatellite cells and their subsequent fusion with the main muscle fiber that causes the increase in the number of nuclei in the muscle fiber as the body grows (F.P.Moss, C.P.Leblond 1970).
An increase in the number of nuclei in muscle fibers occurs in an adult, already formed body under the influence of training. It was found that muscle hypertrophy in rats caused by forced swimming or overload due to cutting off synergistic muscles is not accompanied by a change in the density of nuclei in muscle fibers (D. Seiden 1976), which is evidence of an increase in the number of nuclei in proportion to the increase in the volume of muscle fibers. It was recorded that after swimming training twice a week for thirty-five days, the number of cell nuclei in the extensor digitorum longus of rats increased by 30% (N.T.James, M.Cabric 1981). Then the same researchers found an increase in the number of nuclei in the vastus lateralis of dogs trained in running (M.Cabric, N.T.James 1983). Overload of the muscles of the hind limbs of cats, caused by cutting off the gastrocnemius and soleus, is accompanied by significant hypertrophy of the plantaris and within three months leads to an almost fourfold increase in the number of nuclei in the fast fibers and a twofold increase in the number of nuclei in the slow fibers of this muscle (D. L. Allen et al. 1995). An increase in the number of nuclei was also noted in the muscles of people after electrically stimulated muscle contraction (M.Cabric et al. 1987), aerobic (exercise bike) and anaerobic (lifting legs with weights) training (P.J.Pacy et al. 1987), barbell training (F. Kadi et al. 1999 a), (F. Kadi et al. 1999 b).
The source of new nuclei that appear in muscle fibers under the influence of training, as well as as a result of age-related muscle hypertrophy, are satellite cells. Thus, it was noticed that long-term intensive movement on a treadmill with a downward slope (with a predominance of muscle work in a yielding mode) causes damage to part of the muscle fibers in rats and activates proliferation (that is, massive division and subsequent differentiation of cells towards specialization in performing a certain task). functions) of satellite cells with a peak of activity of these cells 24-76 hours after exercise. At the same time, the level of activation of satellite cells was higher than what would be required to restore damaged fibers, that is, satellite cells were activated not only in damaged fibers, but also in those fibers that did not show external signs of damage (K.C. Darr, E Schultz 1987). A twofold increase in the activity of satellite cell division was recorded in the muscles of rats after ten weeks of running training (K.M. McCormick, D.P. Thomas 1992). Cutting off the synergist muscles (plantaris and gastrocnemius) in rats causes overload of the soleus, which activates cell division - satellite cells in a given muscle in the first week after the onset of overload and subsequently leads to significant hypertrophy of the soleus (M.H. Snow 1990). The processes of activation of satellite cells and their fusion with muscle fibers were noted in the muscles of people during regular training on an exercise bike (H.J. Appell et al. 1988 ). Resistance training has been found to increase the proportion of satellite cells in human muscle and to increase the percentage of morphologically active satellite cells (Roth SM et al. 2001).
The influence of the intensity of mRNA synthesis in the cell nucleus on the size of the muscle fiber
As mentioned above, a number of studies have noted that the increase in the number of nuclei in muscle fibers during their hypertrophy occurs in such a way that the volume of fiber per nucleus remains practically unchanged (D. Seiden 1976), (D. Vassilopoulos et al . 1977). It has been suggested that the ratio of the volume of a muscle fiber to the number of nuclei in it, that is, the volume of a muscle cell controlled by one nucleus (the so-called DNA-unit), is a constant value, and the body has mechanisms to maintain its constancy (D.B. Cheek 1985). Subsequently, this point of view was repeatedly confirmed. Thus, it was shown that the muscles of rats that were subjected to functional overload as a result of the removal of synergistic muscles demonstrate significantly greater hypertrophy with regular injections of growth hormone in comparison with the muscles of rats that did not receive injections of the hormone. However, the ratio of fiber volume to the number of nuclei in it turned out to be the same not only in rats that received and did not receive hormone injections, but also in those rats whose muscles were not subjected to functional overload and did not increase (G.E. McCall et al. 1998). It was found that the increased volume of muscle fibers in the trapezius muscles of highly trained powerlifters relative to the control group (composed of people who did not lift weights) correlates well with the increased number of nuclei in these muscles - that is, the size of the DNA unit in the muscles of athletes does not exceed the size of the DNA unit in the muscles of representatives of the control group (F. Kadi et al. 1999 a). A comparison of the muscles of powerlifters, who, by their own admission, had taken anabolic steroids over the past several years, with the muscles of athletes who abstained from using these drugs, showed that there was no significant difference in the size of the DNA unit between these groups of athletes (F. Kadi et al. 1999 b).However, from the fact that muscle fiber hypertrophy is usually accompanied by a proportional increase in the number of nuclei in it, one cannot conclude that the size of the muscle fiber in all cases is determined only by the number of nuclei. A limited increase in the size of a DNA unit occurs early in the development of an organism. It was found that in the body of young growing rats, muscles in which the division of myosatellitocytes is blocked by radiation still slightly increase their size and mass, although they are significantly lagging in growth from non-irradiated muscles, in which the division of myosatellitocytes occurs in the usual manner (P.E. Mozdziak et al 1997). In the same experiments, it was shown that in muscles subjected to irradiation and in non-irradiated muscles, the size of the DNA unit increases to the same extent, that is, the increase in the size of the DNA unit in the early stages of the development of the organism is physiologically programmed. This increase in the volume of fiber served by one nucleus is apparently due to the fact that the size of the DNA unit of a muscle fiber in a young organism is smaller than the size of the DNA unit characteristic of the muscles of a mature organism. It is possible that an increase in the size of a DNA unit in the early stages of development of the organism is associated with an increase in muscle motor activity after birth - this is indicated by the fact that removing the load from growing muscles interrupts the increase in the size of the DNA unit (P.E. Mozdziak et al. 2000). At the same time, the possibilities of increasing the size of the DNA unit are apparently limited, since in irradiated muscles there is no additional increase in the size of the DNA unit, compensating for the lag in muscle development due to the smaller number of nuclei (P.E. Mozdziak et al. 1997).
However, a decrease in the size of a DNA unit is possible in an aging organism. Contrary to studies in which constancy of DNA unit size was observed in the muscles of people aged one to seventy-one years (D. Vassilopoulos et al. 1977), similar studies of the muscles of people in the age range from seventeen to eighty-two years found a decrease in the size of a DNA unit in the muscles of people over sixty years of age (P. Manta et al. 1987), that is, in the muscles of older people there was a decrease in the average size of fibers while the number of nuclei remained the same. Perhaps this decrease in DNA units is associated with a decrease in people’s motor activity with age.
With muscle atrophy caused by a significant decrease in motor activity, a decrease in the size of the DNA unit is also noted. For example, after denervation of rabbit muscles, muscle atrophy was observed, accompanied by a decrease in the size of the DNA unit (J.A. Gustafsson et al. 1984). When the load was removed from the muscles of the hind limb of rats for twenty-eight days, the number of nuclei in the muscles of rats did not decrease, while the size of the fibers decreased significantly (up to 70% of the control level in fast ones and up to 45% of the control level in slow ones). Consequently, the size of the DNA unit in atrophied muscles decreased noticeably - especially in slow fibers (C.E. Kasper, L. Xun 1996). Compliance by a group of volunteers with long-term (up to four months) bed rest led to a significant (35% of the initial level) a decrease in the cross-section of muscle fibers in the soleus muscle (95% of soleus muscle fibers are slow), while the number of nuclei in the fibers remained unchanged, that is, muscle inactivity led to a significant decrease in the size of the DNA unit of slow fibers (Y. Ohira et al. 1999). In these experiments, muscle atrophy was not accompanied by a decrease in the number of cell nuclei in muscle fibers, but in some cases, with muscle atrophy, both a decrease in the size of the DNA unit and a decrease in the number of nuclei were observed. For example, in the muscles of the hind limb of cats after six months of inactivity (due to spinoisolation, that is, isolation of the spinal cord from the influence of the brain), both a decrease in the size of the DNA unit and a decrease in the number of nuclei were noted (D. L. Allen et al. 1995). In the muscles of rats after a two-week stay in weightlessness, both a decrease in the number of nuclei in slow muscle fibers and a decrease in the size of the DNA unit of the slow fiber were recorded, while the number of nuclei and the size of the DNA unit in fast fibers remained unchanged (D. L. Allen et al. 1996). Signs of apoptosis (that is, self-destruction of DNA) of nuclei were found in the muscles of rats both after a two-week space flight (D.L. Allen et al. 1997) and after several days of fixation of rabbit muscles in a contracted state (H.K. Smith et al. 2000).
So, a decrease in the intensity of protein synthesis and a decrease in the size of the DNA unit is the main factor in the atrophy of muscle fibers during their long-term inactivity, however, a certain contribution to the atrophy of skeletal muscles can also be made by the suspension of the division of satellite cells and the death of existing nuclei. It is known that muscle atrophy caused by hypokinesia is reversible (X.J.Musacchia et al. 1980), (Y.Ohira et al. 1999). When recovering from atrophy, the size of the DNA unit is restored and even slightly increased (Y. Ohira et al. 1999).
A moderate increase in the size of a DNA unit can occur not only in the postnatal (postpartum) period or during muscle recovery after atrophy, but also during functional muscle hypertrophy. Thus, in the already mentioned experiments (D.L. Allen et al. 1995), hypertrophy of slow fibers in overloaded cat muscles was accompanied by an increase in the size of the DNA unit by approximately 28%. However, the increase in DNA unit size did not make a significant contribution to muscle hypertrophy, since the observed increment in DNA unit size could increase the cross-sectional area of the slow fibers by only 28%, while the overall cross-sectional area increased by approximately 2.5 times (mainly way due to almost doubling the number of cores).
The circumstances that the size of a DNA unit depends on the level of motor activity of muscles, but the possibility of increasing the size of a DNA unit with increasing load on the muscles at the same time is very limited, apparently indicate that there is a limiting volume of muscle fiber, which can serve one core.
There is an assumption that the limited size of a DNA unit may be associated with the distances from the nucleus to which effective delivery of mRNA or synthesized proteins is possible (R.R. Roy et al. 1999).
Thus, in vitro it was shown that in multinucleated cells, mRNA is concentrated in a limited volume around the nucleus expressing it (E. Ralston, Z. W. Hall 1992), while proteins synthesized on the basis of the mRNA expressed are localized around the nucleus and at a certain distance from it are not found core (G.K. Pavlath et al. 1989).
At the same time, the limiting factor for the size of a DNA unit can be reaching the limit of the capabilities of one nucleus to synthesize certain types of RNA. The latter is supported by the fact that slow fibers, with the same or even smaller size as fast fibers, have a larger number of nuclei - accordingly, the density of nuclei in slow fibers is higher, and the size of the DNA unit is smaller than in fast fibers (I.G. Burleigh 1977 ), (J.A. Gustafsson et al. 1984), (B.S. Tseng et al. 1994), (C.E. Kasper, L. Xun 1996), (R. Roy et al. 1999). Perhaps the high density of nuclei in slow fibers is due to the fact that the turnover of protein in slow fibers is approximately two times higher than in fast fibers (F.J. Kelly et al. 1984), and the limit of the nuclear ability to synthesize certain types of RNA in slow fibers is easily achievable , and therefore the nuclei of slow fibers are able to serve a smaller volume of sarcoplasm than the nuclei of fast fibers. Statistical analysis of the distribution of nuclei in muscle fibers of various diameters showed that in slow fibers, as their diameter increases, there is a tendency to maintain the volume of the fiber served by one nucleus, and in fast fibers there is a tendency to maintain the surface area of the fiber (nuclei in mature fibers are located directly under shell) per core (J.C. Bruusgaard etal. 2003). The latter observation suggests that in slow fibers the limiter of the size of a DNA unit is largely the ability of the nucleus to synthesize RNA, while in fast fibers the limiter is transport distances.
When deciding whether it is necessary to revise the concept linking skeletal muscle hypertrophy with the activation of mRNA transcription of structural proteins, you should first of all find out the answer to this question: is the increase in the number of nuclei in muscle fibers the primary cause of fiber hypertrophy or is it a consequence of the same processes intensification of mRNA synthesis? At the first stage of muscle adaptation to load, an intensification of mRNA transcription and an increase in protein synthesis can occur and, as a result, an increase in the size of the DNA unit can be observed. And after this, as an adaptation to the increased size of the DNA unit, activation of satellite cells and an increase in the number of nuclei in the fiber can occur, that is, restoration of the optimal size of the DNA unit. A number of the following facts below testify against the latter assumption.
It has been found that activation and rapid expansion of satellite cells in muscle fibers is a primary response to various types of overload of animal muscles, such as stretching of quail muscles by attaching weights to the wings (M.H. Snow 1990) or overload of rat muscles caused by the removal of synergistic muscles. (P.K. Winchester et al. 1991). Activation of myosatellite cells is observed in the first days after the onset of muscle overload, but significant muscle hypertrophy is observed subsequently.
A number of studies have noted that muscle hypertrophy is not only not a consequence of an increase in the size of the DNA unit, but, on the contrary, the size of the DNA unit may even decrease during muscle hypertrophy. Thus, in fast fibers of cats subjected to functional overload due to the removal of synergistic muscles, a decrease in the size of the DNA unit is observed against the background of an almost fourfold increase in the number of nuclei (D. L. Allen et al. 1995).
Injections of testosterone for twenty weeks at a dosage of 300-600 mg per week led to hypertrophy of the human vastus lateralis, while the size of the DNA unit in the muscle fibers of this muscle not only was not increased, but, on the contrary, decreased (I. Sinha-Hikim et al. 2003), that is, hormonally induced hypertrophy of muscle fibers occurred solely due to an increase in the number of nuclei.
Cutting off certain muscles in animals causes compensatory hypertrophy of synergistic muscles - for example, removal of the tibialis anterior in rats causes hypertrophy of the extensor digitorum longus, however, if, before removing the tibialis anterior in the digitorum longus, the possibility of dividing satellite cells is blocked by treating the muscles of rats with radiation, then compensatory hypertrophy of the extensor digitorum longus is not observed (J.D. Rosenblatt et al. 1994). This indicates that any significant hypertrophy of muscle fibers only due to the intensification of mRNA synthesis without increasing the number of nuclei in the fiber is simply impossible.
Muscle fiber hyperplasia as a possible mechanism of skeletal muscle adaptation
Due to the fact that training activates the division of satellite cells and their subsequent fusion with the “mother” fiber, the question arises: is it possible for satellite cells to unite into new fibers, as happens with myoblasts during the embryonic formation of skeletal muscles? That is, is hyperplasia of muscle fibers possible?It is well known that when muscles are damaged, satellite cells, released from the membrane of fibers dying for one reason or another, merge into new fibers, due to which the regeneration of damaged tissue occurs (E.V. Dmitrieva 1975), (M.H. Snow 1977), (W.E. Pullman , G.C.Yeoh 1978), (R.K.Danilov 1994), (A.V. Volodina 1995), (E.G. Ulumbekov, Yu.A. Chelyshev 1998), (E.A. Shubnikova et al. 2001) . As a rule, while the muscle structure is preserved, new muscle fibers form in the area limited by the basement membrane of the old fiber, that is, they replace damaged fibers. Such regenerative processes after training occur in the muscles of all animals. This is evidenced by studies in which, with various types of functional overload of animal muscles, damage to muscle fibers and subsequent regenerative processes associated with the activation of satellite cells were recorded (K.C. Darr, E. Schultz 1987), (M.H. Snow 1990), (K.M. McCormick, D.P. Thomas 1992), (P.K. Winchester, W.J. Gonyea 1992), (T. Tamaki et al. 1997), as well as studies that, after various types of functional overload of the muscles of both laboratory animals and humans, revealed thin fibers in these muscles with the formation of contractile apparatus (A.Salleo et al. 1980), (C.J.Giddings, W.J.Gonyea 1992), (P.K.Winchester, W.J.Gonyea 1992), (K.M.McCormick, D.P.Thomas 1992), (T.Tamaki et al. 1997), (V.F. Kondalenko et al. 1981), (H.J. Appell et al. 1988), (F. Kadi et al 1999 a).
But can young muscle fibers be considered evidence of hyperplasia, that is, an increase in the number of fibers in the muscle? Isn't the appearance of these fibers the result of solely replacement regeneration? A. Salleo et al. recorded in the muscles of rats that experienced overload after cutting off the synergistic muscles, the separation of satellite cells from the muscle fiber membrane, their subsequent intensive division and then fusion into elongated structures, which then became new muscle fibers (A. Salleo et al. 1980). The formation of new fibers in the intercellular space was also recorded in overloaded muscles of chickens (J.M. Kennedy et al. 1988) and rats (T. Tamaki et al. 1997). Since young muscle fibers can be formed either in addition to existing fibers or to replace fibers that have undergone necrosis, the presence of such fibers in animal or human muscles after exercise cannot be considered sufficient evidence of fiber hyperplasia. The fact of fiber hyperplasia can be stated with confidence only in cases where it is possible to record an actual increase in the number of fibers in the muscle.
An increase in the number of muscle fibers in the muscles of rats is observed in the first weeks after birth (J. Rayne, G. N. Crawford 1975), (T. Tamaki 2002). However, many researchers are inclined to believe that muscle hypertrophy in animals in adulthood is not associated with hyperplasia and is completely explained by the hypertrophy of existing fibers. Thus, in a number of experiments, an increase in the number of fibers during muscle hypertrophy in rats caused by the removal of synergist muscles was not recorded (P.D. Gollnick et al. 1981), (B.F. Timson et al. 1985), (M.H. Snow, B.S. Chortkoff 1987). Long-term stretching of the muscles of flightless birds, carried out by attaching a weight to the wings, accompanied by muscle hypertrophy, also did not lead to an increase in the number of fibers (P.D. Gollnick et al. 1983), (J. Antonio, W. J. Gonyea 1993 a).
At the same time, despite the negative results of a number of the experiments mentioned above, it was possible to record fiber hyperplasia in the muscles of birds subjected to chronic stretching. In experiments by S.E.Alway et al., a load equal to 10% of the bird’s body weight was attached to one wing of a quail, and after a month of overload, the number of fibers in the stretched muscle was 51.8% higher than the number of fibers in the unloaded muscle used as a control object (S.E.Alway et al. al. 1989 b). Similar experiments, but with a progressive increase in the mass of the load, led to an even greater increase in the number of fibers - by 82% after twenty-eight days of overload (J. Antonio, W. J. Gonyea 1993 b).
Evidence of hyperplasia of muscle fibers in trained mammalian muscles has also been found. W. Gonyea and his co-authors were among the first to record hyperplasia in mammalian muscles (W. J. Gonyea et al. 1977). In this experiment, cats were trained to lift a weight with one of their paws, and the incentive to lift the load was a food reward. After forty-six weeks of training, the muscles of the trained and untrained cats' paws were subjected to histochemical analysis. The total number of muscle fibers in the trained paws was 19.3% greater than in the untrained paws. The results of these studies were subsequently confirmed by similar experiments (W.J. Gonyea et al. 1986). An increase of 14% in the number of muscle fibers was also recorded in the muscles of the hind limbs of rats that regularly (4-5 times a week) for 12 weeks performed an exercise similar to squats with weight using a specially designed device (T. Tamaki et al. 1992). However, despite advances in animal experiments, direct evidence of an increase in the number of muscle fibers in human muscles has not yet been found.
According to a number of researchers, hypertrophy of human muscles as a result of training is completely explained by the hypertrophy of existing fibers, while new fibers are not formed as a result of training (B.S. Shekman 1990), (G.E. McCall et al. 1996). At the same time, G.E. McCall and co-authors did not dare to draw an unambiguous conclusion that hyperplasia in humans is fundamentally impossible, since in a number of individuals the increase in the cross-section of the muscle caused by training did not correlate with an increase in the average cross-section of the fibers (G.E. McCall et al. 1996) .
The fact that direct evidence of fiber hyperplasia in human muscles has not yet been discovered may be due to the limitations of functional overload methods applicable to humans and methods for assessing the number of fibers in muscles: after all, such methods of functional overload as long-term multi-day muscle stretching (to the greatest extent causing fiber hyperplasia in animals), it is quite difficult to apply to humans. Significant hypertrophy of human muscles (as in the case of extreme muscle development of professional bodybuilders, weightlifters and powerlifters) occurs over many years of training; A comparison of the number of fibers in the muscles of athletes before the start of training and after a long period of training has never been carried out.
If the manifestations of fiber hyperplasia in humans are limited in nature, and it, hyperplasia, makes a significant contribution to muscle hypertrophy only in an accumulative mode within the framework of a long-term training period, then the detection of manifestations of hyperplasia after a relatively short period of training, limited by the time frame of the experiment, will be very problematic - especially given the limited fiber counting methods applicable to humans. Experiments in which muscle hyperplasia was found in animals were usually accompanied by killing the experimental animals and counting the total number of fibers in the muscles. Thus, in the already mentioned experiments (W.J.Gonyea et al. 1977), (W.J.Gonyea et al. 1986) fiber hyperplasia was discovered by comparing the total number of fibers in muscles extracted from trained and untrained limbs of the same animal. It is clear that such direct methods for detecting hyperplasia are not applicable to humans.
However, there are experiments in which the manifestations of hyperplasia in humans were studied using a similar method. Counting the total number of fibers in the anterior tibialis of the left and right human legs was carried out in muscles removed from the corpses of previously healthy young people (M. Sjostrom et al. 1991). The muscles of the dominant supporting limb (left for right-handed people) had a slightly larger size and a larger number of fibers - despite the fact that the average cross-section of fibers in the muscles of both limbs was the same. These data provide the most convincing evidence that functional hypertrophy of human muscles may still be associated with fiber hyperplasia (although initial genetic differences in the muscles of the dominant and non-dominant limbs cannot be ruled out).
In most cases, the change in the number of fibers in a person under the influence of training must be judged only on the basis of indirect estimates made by comparing the size of the muscle and the average cross-section of the fibers in biopsies taken from this muscle. But the results of even such studies are very contradictory.
For example, when comparing the muscles of elite male and female bodybuilders, a correlation was found between muscle size and the number of fibers in it (S. E. Alway et al. 1989 a). Men's muscles were on average twice as large as women's muscles. Part of the larger muscle size of men is due to the larger cross-section of muscle fibers in their muscles, but at the same time, men's muscles also had a larger number of fibers than women's muscles. The latter may be both a consequence of fiber hyperplasia and a consequence of genetic differences between the sexes. A comparison of samples taken from the triceps of two international powerlifters and five elite bodybuilders with samples taken from the muscles of a control group who practiced weight training for only six months showed that despite large differences in arm strength and girth between elite athletes, and control groups there was no significant difference in muscle fiber cross-section (J.D. MacDougall et al. 1982). These data are confirmed by a study by L. Larsson and P. A. Tesch, which found that the cross-section of fibers in biopsies taken from the thigh and biceps muscles of four bodybuilders did not differ from the cross-section of fibers of ordinary physically active people (L. Larsson, P. A. Tesch 1986) . These studies indicate that bodybuilders' greater muscle volume is associated with a greater number of fibers in their muscles. An explanation for this phenomenon can be found either in a genetically determined difference in the number of muscle fibers in elite bodybuilders and powerlifters, or in fiber hyperplasia as a result of training. The genetic explanation seems the least convincing in this case, since it should follow that the athletes initially had very thin fibers and many years of training could only lead to the fact that their fibers reached the size characteristic of an ordinary averagely trained person.
Studies by J.D. MacDougall et al. and L. Larsson with P.A. Tesch could be considered reliable evidence of muscle fiber hyperplasia in humans as a result of training, if not for a similar, but more representative study by J.D. MacDougall et al. (J.D. MacDougall et al. 1984). This study looked at fiber counts in the biceps muscles of five elite bodybuilders, seven intermediate bodybuilders, and thirteen non-bodybuilders. Although the number of fibers in the muscles of athletes varied greatly from individual to individual, and athletes with greater muscle development had a higher number of fibers in their muscles, the study authors concluded that such differences in the number of fibers are a consequence of genetic predisposition and not at all hyperplasia, since a variation in the number of fibers was observed within each group, but the average number of fibers in the muscles of representatives of all three groups did not differ significantly.
So, the totality of experimental facts indicates that hyperplasia of muscle fibers in animals is possible and it is apparently associated with damage to muscle fibers as a result of functional overload, proliferation of satellite cells and subsequent regeneration processes. However, the possibility of human muscle hyperplasia is still questionable. Perhaps the regenerative potential of human muscles is not so great that microtrauma of fibers during training could cause their hyperplasia, but the injection use of cell division stimulators such as growth hormone and anabolic steroids can significantly increase the regenerative capabilities of human muscles. It is known that growth hormone, through its intermediary - insulin-like growth factor (IGF-1) - stimulates the proliferation of poorly differentiated cells - such as chondrocytes, fibroblasts, etc. (M.I. Balabolkin 1998). It has been established that IGF-1 stimulates proliferation and further differentiation of myosatellite cells as well (R.E. Allen, L.L. Rankin 1990), (G.E. McCall et al. 1998). Injections of anabolic steroids also stimulate proliferation of satellite cells (I. Sinha-Hikim et al. 2003). It is no secret that professional bodybuilders often resort to injections of growth hormone and anabolic steroids in their practice; accordingly, the division and differentiation of satellite cells should occur in their muscles much more intensely than in athletes who do not use these drugs. The question of whether such pharmacological intensification of myosatellite cell activity can contribute to fiber hyperplasia in humans requires further study.
At this level of existing knowledge about intramuscular processes activated by training, when constructing a new and more adequate concept of long-term muscle adaptation to load, it is necessary to limit ourselves to a more general conclusion, which can be considered quite substantiated in the course of this study: any significant hypertrophy of human skeletal muscles under the influence of regular training is a consequence of the proliferation of satellite cells and an increase in DNA content in the muscles. Whether an increase in the DNA content in muscles occurs only due to an increase in the number of nuclei in pre-existing fibers, or whether the DNA content in a muscle also increases due to the nuclei of newly formed muscle fibers - all this cannot be specifically decided before the final decision on the possibility of hyperplasia of muscle fibers in humans discuss.
Outlines of a new concept
As shown in the analysis undertaken above, hypertrophy and atrophy of skeletal muscles in the general case can be a consequence of both changes in the intensity of mRNA transcription in the nuclei of muscle cells, and a consequence of changes in the number of nuclei in the muscle - but the final contribution of these factors is the result of two antagonistic adaptive processes quite different.During the development of functional muscle hypertrophy, the following sequence of events dominates:
Increased load on muscles -> activation of myosatellite cell proliferation -> increase in the number of nuclei in the muscle -> RNA synthesis on new nuclei -> synthesis of new contractile structures -> muscle hypertrophy
A decrease in muscle motor activity, in turn, activates the following sequence of events leading to muscle atrophy:
Decrease in muscle motor activity -> decrease in the intensity of transcription of mRNA of structural proteins and decrease in the proliferative activity of myosatellite cells -> decrease in the size of the DNA unit and a decrease in the number of nuclei as they undergo apoptosis -> muscle atrophy
Due to the limited size of the DNA unit, changes in the intensity of mRNA transcription of structural proteins play an important role in the processes of muscle atrophy, but not in the processes of muscle hypertrophy. At the same time, it should be noted that not only the size of the DNA unit depends on the intensity of transcription of the mRNA of structural proteins. By controlling the intensity of gene expression, the spectrum of synthesized proteins is regulated, which has a dramatic impact on the functional properties of muscles.
A comparison of the muscle composition of rats after compensatory hypertrophy caused by cutting off synergistic muscles and after functional hypertrophy caused by regular forced swimming showed that compensatory hypertrophy is accompanied by an increase in mitochondrial density, a decrease in myofibril density and an unchanged sarcoplasmic reticulum density. In turn, functional hypertrophy is accompanied by an increase in the density of the sarcoplasmic reticulum, while the density of mitochondria and myofibrils remains unchanged (D. Seiden 1976).
As a result of training in muscles, the concentration of some enzymes that ensure energy reproduction may increase, while the concentration of other enzymes remains unchanged - as a result of which the muscles change their oxidative or glycolytic capabilities (N. Wang et al. 1993).
Under the influence of training, it is possible to change the characteristic properties of muscle fibers, up to a change in the type of fibers (F. Ingjer 1979), (R. S. Staron et al. 1990), (N. Wang et al. 1993).
Changes in the structure and properties of muscles under the influence of training are not limited to the above examples, but consideration of these changes is not the topic of this study. These examples were given only to show that changes occurring in muscle fibers as a result of training may be associated with changes in the protein composition of the fibers, that is, they may be a consequence of changes in the intensity of mRNA transcription of various types of structural proteins. Accordingly, the effect of training on the genetic apparatus of a muscle cell cannot be reduced to enhancing general protein synthesis through a regulatory factor common to all structural proteins. Moreover, the intensification of the synthesis of certain types of contractile proteins occurs not only with an increase in muscle motor activity. Thus, a decrease in the load on the muscles of rats, caused by the animals being in weightlessness, reduces the synthesis of myosin chains in a number of slow fibers, characteristic of slow fibers, but increases the expression of some forms of fast myosin (D. L. Allen et al 1996). Conversely, functional overload of feline muscles reduces the expression of some forms of fast myosin in slow fibers (D. L. Allen et al 1995). These facts do not fit into the concept of a direct activating effect of energy depletion factors on the expression of mRNA of contractile proteins. Even if the expression of muscle contractile protein mRNA depends on metabolic factors, this dependence appears to manifest itself in a more complex manner.
As noted at the beginning of this text, some sports researchers assign the role of a regulator of mRNA transcription of contractile muscle proteins to creatine, but the role of creatine in the regulation of the synthesis of contractile proteins cannot be considered unambiguously established. Indeed, in a number of studies (J.S. Ingwall et al. 1972), (J.S. Ingwall et al. 1974), (M.L. Zilber et al. 1976) it was shown that increasing the concentration of creatine intensifies the synthesis of specific muscle proteins (myosin and actin) in developing muscle tissues cells in vitro. These observations were taken as important evidence that creatine is an inducer of contractile protein transcription. However, subsequently, in contrast to the studies mentioned above, the effect of creatine on myosin synthesis was not found (D.M.Fry, M.F.Morales 1980), (R.B.Young, R.M.Denome 1984). R.B.Young and R.M.Denome suggested that the level of creatine can regulate myosin synthesis only in the early stages of embryonic development of muscle cells, but cannot be a regulator of the synthesis of contractile proteins in already formed muscle fibers.
Thus, the hypothesis about the role of creatine in the regulation of contractile protein synthesis requires further testing. However, based on general considerations, it should be recognized that the concept according to which the inducer of mRNA transcription of structural proteins is creatine or some other factor associated with the depletion of muscle energy seems quite convincing only in relation to the regulation of the synthesis of muscle enzymes - if we assume that the regulation of enzyme synthesis in complex multicellular organisms is carried out according to the same principle as in prokaryotes. Metabolyls such as ADP, AMP, orthophosphate, creatine, etc., which accumulate in actively contracting muscle fibers, are themselves substrates for reactions that restore the supply of energy phosphates in the fiber. Accordingly, the accumulation of these metabolyls in the muscles should stimulate the transcription of mRNA of enzymes that ensure the occurrence of energy-restoring reactions that use these metabolyls as substrates. Regular work to the point of muscle fatigue should be accompanied by regular activation of enzyme synthesis and ultimately lead to their accumulation in the muscles. Conversely, a decrease in muscle motor activity should reduce the frequency of activation of enzyme mRNA synthesis. Accordingly, the content of enzymes in the muscles should decrease as the latter undergo natural catabolism. The assumption that the accumulation of enzymes in muscles occurs due to a substrate-induced increase in the synthesis of these enzymes was put forward by N.N. Yakovlev (N.N. Yakovlev 1974). F.Z. Meyerson, in support of the hypothesis about the effect of muscle acidosis on the induction of mRNA of structural proteins, gave arguments that also relate to the induction of the synthesis of proteins responsible specifically for the energy supply of muscles. Meyerson noted that muscle acidosis is an early signal of energy deficiency, and therefore, from the standpoint of evolutionary theory, it would be justified to assume that this same signal could well be used as an activator of the genetic apparatus of the cell. Ultimately, this should lead to the growth of structures that are designed to eliminate energy deficiency - and the body thereby becomes generally more resistant to changed environmental conditions (F.Z. Meyerson 1993).
This argument can be considered very convincing, but the expansion of this principle to regulate the synthesis of other types of muscle proteins, especially contractile ones (as is the case in the concept of the same Meyerson and many other researchers), seems not entirely justified from an evolutionary point of view. A high concentration of macroenergetic phosphate breakdown products in the sarcoplasm is a signal that the muscle fiber’s ability to restore ATP levels due to oxidative processes and glycolysis is insufficient for a given contraction intensity. In such a situation, adaptation of the muscle fiber should be directed towards increasing the power of energy-restoring reactions. The synthesis of contractile proteins (the main energy consumers) can only contribute to an increase in the rate of ATP consumption in the fiber and lead to an even greater drop in the level of ATP under new similar loads - therefore, adaptation in this direction cannot make muscle fibers more resistant to the changed requirements for motor activity of the muscles .
Thus, the incentives for the development of muscle energy and the incentives for the extensive development of the muscle contractile apparatus should and seem to be of a different nature.
As noted above, improving the energy capabilities of muscles is closely related to an increase in the content of enzymes in muscles, that is, it is a consequence of substrate-induced activation of mRNA transcription of these types of proteins. It is likely that the synthesis of mRNA for other types of protein associated with the energy supply of muscles (for example, myoglobin or mitochondrial proteins) can occur according to a similar pattern. But, as shown above, the size of the DNA unit is limited and each cell nucleus is responsible for maintaining the functioning of a strictly defined volume of muscle fiber. To radically increase muscle volume and build new contractile structures in them, new cell nuclei are needed in addition to existing ones, that is, extensive muscle development is associated primarily with the activation of proliferation of satellite cells. At the same time, it is obvious that since the protein composition of contractile structures is different for different types of fibers and depends on the mode of muscle functioning, signals of some other kind affecting the genetic apparatus of muscle cells must additionally regulate the spectrum of expressed contractile proteins.
The analysis presented in this text showed that the generally accepted diagram of the relationship between the links of immediate and long-term muscle adaptation to load (see Fig. 2)
Figure 2In relation to skeletal muscles, it describes only part of the adaptation processes, namely, the adaptation of the muscle energy system. This scheme ignores a number of important mechanisms of long-term adaptation of skeletal muscles to load, and therefore requires significant clarification (see Fig. 3).
Figure 3 (EOS - energy supply systems)It should be noted that the proposed block diagram of the mechanisms of muscle adaptation to load is also not exhaustive, since it does not include quite important mechanisms of hormonal adaptation of the body to load - it takes into account only the main local (intramuscular) adaptation processes, which were the only subject of consideration of this study.
The question arises: what are the consequences of such a change in the fundamental scheme of adaptation for the theory of sports training, that is, does it matter for the development of training methods and load planning due to which specific processes muscle adaptation occurs? The answer to this question is: yes, apparently, changing ideas about the pattern of muscle adaptation to load is of considerable importance.
The fact is that intense contractile muscle activity blocks protein synthesis in the muscles and even activates its catabolism. Therefore, a training regime in which a new training session is combined in time with the shutdown of adaptive protein synthesis after the previous training session or with a significant decrease in its intensity (A.A. Viru, N.N. Yakovlev 1988) should be considered rational. If, when implementing this principle, we assume that the training effect is reduced only to the activation of the transcription of mRNA structural proteins under the influence of a single factor-regulator, then the maximum effect will occur as a result of using an extremely simple training scheme with training sessions following each other at equal rest intervals , the intensity of which increases as the body is trained. However, unfortunately, the low effectiveness of this kind of training methods, especially for well-trained athletes, is well known from sports practice.
From the scheme for the development of long-term adaptation of skeletal muscles proposed in this text (see Fig. 3), it is clear that the adaptive increase in protein synthesis is associated not only with the processes of activating the transcription of mRNA of structural proteins, but also with an increase in the volume of synthesized protein due to protein synthesis on mRNA, expressed by newly formed DNA. Moreover, post-training activation of mRNA transcription plays the most important role in regulating the synthesis of proteins associated with muscle energy supply. To increase the energy capacity of muscles, training sessions that activate the transcription of mRNA of proteins of energy supply systems should be carried out during a period when the adaptive synthesis of these proteins caused by the previous training session is close to completion or, in any case, has passed the phase of highest activity.
Adaptive enhancement of protein synthesis due to mRNA expressed by newly formed nuclei can be considered complete only when the construction of new contractile structures based on newly formed nuclei is completed, that is, when the characteristic size of the DNA unit is restored in the muscles after an increase in the number of nuclei. The construction of contractile structures from scratch, in contrast to the synthesis of enzymes, is a very lengthy process, therefore the optimal frequency of training sessions that activate the proliferation of myosatellite cells may differ radically from the optimal frequency of training that ensures maximum synthesis of proteins in the energy-supplying systems of muscles.
In the proposed block diagram of local mechanisms of long-term adaptation of skeletal muscles, two blocks are marked with a question mark, and the regulatory factors are not identified. As noted above, the regulatory factors for the synthesis of enzymes are the products of energy metabolism, but the set of factors that influence the spectrum of expressed contractile proteins, as well as factors that activate the proliferation of myosatellite cells, have not yet been fully established. Advancement of research in these areas will make it possible in the future to develop more specialized training methods that specifically stimulate various adaptive processes in muscles. In turn, a clearer division of the training impact will allow optimizing the dosage of the load in the training microcycle.
Literature:
1. Arakelyan E.E., Zbarsky V.A., Shevchenko T.N., Seluyanov V.N.
"Formation of sprint running technique through
targeted development of strength of individual muscle groups in young
athletes" Physical culture: upbringing, education,
training. 1997 N 32. Berezov T.T., Korovkin B.F. "Biological Chemistry"
Ed. "Medicine" Moscow 1998 704 pp.3. Balabolkin M.I. "Endocrinology" Moscow "Universum"
publishing" 19984. Viru A.A., Yakovlev N.N. "Chapters from sports physiology"
Ed. Tartu State University. Tartu 1988
134 pp.5. Volkov N.I., Nessen E.N., Osipenko A.A., Korsun S.N.
"Biochemistry of muscle activity" Ed. "Olympic Literature"
Kyiv 2000, 503 pp.6. Volodina A.V. "Post-traumatic regeneration of skeletal
muscles" Dissertation of Doctor of Biological Sciences. Moscow 1995.7. Danilov R.K. "Essays on the histology of muscle tissue" Ufa
1994 49 pp.8. Kalinsky M.I., Kursky M.D., Osipenko A.A. "Biochemical
mechanisms of adaptation during muscle activity" Kyiv. Ed.
"Vysha School" 1986 183 pp.9. McComas A.J. "Skeletal muscles" Ed. "Olympic
literature" Kyiv 2001 407 pp.10. Meerson F.Z. “Adaptive medicine: concept
long-term adaptation" Moscow. Publishing house "Delo" 1993.
138 pp.11. Meerson F.Z. Pshennikova M.G. "Adaptation to stressful
situations and physical activity" Moscow. Publishing house "Medicine"
1988 253 pp.12. Seluyanov V.N. "Development of methods and plans for physical
training of athletes based on simulation modeling"
From the collection "Theory and practice of didactics"
developmental training in training specialists in
physical education" Publishing house "Physical education, education and
science". Works of employees of the problematic scientific research
laboratory / Scientific supervisor V.N. Seluyanov. - M:
Physical education, education and science, 1996. - 106 pp.13. Singer M., Berg P. “Genes and Genomes” in 2 volumes Ed. "World"
Moscow 1998 764 pp.14. Ulumbekov E.G., Chelyshev Yu.A. "Histology, introduction to
pathology", Moscow "GEOTAR Medicine" 199815. Shekman B.S. "The influence of training on muscle composition, size
and oxidative potential of muscle fibers in humans"
Dissertation. Moscow 199016. Shubnikova E.A., Yurina N.A., Gusev N.B., Balezina O.P.,
Bolshakova G.B. "Muscle tissue" Moscow "Medicine" 200117. Yakovlev N.N. "Biochemistry of Sports" Ed. "Physical education and sports".
Moscow 1974, 288 pp.18. Yakovlev N.N., Korobkov A.V., Yananis S.V. "Physiological
and biochemical foundations of the theory and methodology of sports
training" Publishing house "Physical culture and sport". Moscow 1957
323 pp.19. Allen DL, Linderman JK, Roy RR, Bigbee AJ, Grindeland RE,
Mukku V, Edgerton VR (1997) "Apoptosis: a mechanism
contributing to remodeling of skeletal muscle in response to
hindlimb unweighting" Am J Physiol. 1997
Aug; 273(2 Pt 1):C579-87.20. Allen DL, Monke SR, Talmadge RJ, Roy RR, Edgerton VR
(1995) "Plasticity of myonuclear number in hypertrophied and
atrophied mammalian skeletal muscle fibers" J Appl Physiol 78:
1969-1976, 1995;21. Allen DL, Yasui W, Tanaka T, Ohira Y, Nagaoka S,
Sekiguchi C, Hinds WE, Roy RR, Edgerton VR (1996) "Myonuclear
number and myosin heavy chain expression in rat soleus single
muscle fibers after spaceflight" J Appl Physiol.
1996 Jul;81(1):145-51.22. Allen RE, Rankin LL (1990) "Regulation of satellite cells
during skeletal muscle growth and development" Proc Soc Exp
Biol Med. 1990 Jun;194(2):81-6.23. Alway SE, Grumbt WH, Gonyea WJ, Stray-Gundersen J (1989a)
"Contrasts in muscle and myofibers of elite male and female
bodybuilders" J Appl Physiol. 1989 Jul;67(1):24-3124. Alway SE, Winchester PK, Davis ME, Gonyea WJ (1989b)
"Regionalized adaptations and muscle fiber proliferation in
stretch-induced enlargement" J Appl Physiol. 1989
Feb;66(2):771-81.25. Antonio J, Gonyea WJ (1993 a) "Role of muscle fiber
hypertrophy and hyperplasia in intermittently stretched avian
muscle" J Appl Physiol. 1993 Apr;74(4):1893-826. Antonio J, Gonyea WJ (1993 b) "Progressive stretch
overload of skeletal muscle results in hypertrophy before
hyperplasia" J Appl Physiol. 1993 Sep;75(3):1263-71.27. Appell HJ, Forsberg S, Hollmann W (1988) "Satellite cell
activation in human skeletal muscle after training: evidence
for muscle fiber neoformation" Int J Sports Med. 1988
Aug;9(4):297-9.28. Bruusgaard JC, Liestol K, Ekmark M, Kollstad K,
Gundersen K (2003) "Number and spatial distribution of nuclei
in the muscle fibers of normal mice studied in vivo"
J Physiol. 2003 Sep 1;551(Pt 2):467-78. Epub 2003 Jun 17.29. Burleigh IG (1977) "Observations on the number of
nuclei within the fibers of some red and white muscles"
J Cell Sci. 1977 Feb;23:269-84.30. Cabric M, Appell HJ, Resic A (1987) "Effects of
electrical stimulation of different frequencies on the
myonuclei and fiber size in human muscle" Int J Sports Med.
1987 Oct;8(5):323-6.31. Cabric M, James NT (1983) "Morphometric analyzes on
the muscles of exercise trained and untrained dogs" Am J
Anat.166(3):359-68.32. Cheek DB (1985) "The control of cell mass and
replication. The DNA unit - a personal 20-year study" Early
Hum Dev. 1985 Dec;12(3):211-39.33. Darr KC, Schultz E (1987) "Exercise-induced satellite
cell activation in growing and mature skeletal muscle" J
Appl Physiol. 1987 Nov;63(5):1816-2134. Dmitrieva EV (1975) "The role of the buds and myoblasts
in reparative regeneration of muscle fibers of the skeletal
type" Arkh Anat Gistol Embriol. 1975 Feb;68(2):37-43.35. Enesco M, Puddy D "Increase in the number of nuclei
and weight in skeletal muscle of rats of various ages"
(1964) Amer. J Anat.114:23536. Fry DM, Morales MF (1980) "A reexamination of the
effects of creatine on muscle protein synthesis in tissue
culture" J Cell Biol. 1980 Feb;84(2):294-7.37. Giddings CJ, Gonyea WJ (1992) "Morphological observations
supporting muscle fiber hyperplasia following weight-lifting
exercise in cats" Anat Rec.1992 Jun;233(2):178-9538. Gollnick PD, Timson BF, Moore RL, Riedy M (1981)
"Muscular enlargement and number of fibers in skeletal muscles
of rats" J Appl Physiol. 1981 May;50(5):936-43.39. Gollnick PD, Parsons D, Riedy M, Moore RL (1983) "Fiber
number and size in overloaded chicken anterior latissimus
dorsi muscle" J Appl Physiol. 1983 May;54(5):1292-7.40. Gonyea W, Ericson GC, Bonde-Petersen F "Skeletal muscle
fiber splitting induced by weight-lifting exercise in cats"
Acta Physiol Scand. 1977 Jan;99(1):105-9.41. Gonyea WJ, Sale DG, Gonyea FB, Mikesky A (1986)
"Exercise induced increases in muscle fiber number" Eur
J Appl Physiol Occup Physiol. 1986;55(2):137-41.42. Gustafsson JA, Saartok T, Dahlberg E, Snochowski M,
Haggmark T, Eriksson E (1984) "Studies on steroid receptors
in human and rabbit skeletal muscle - clues to the
understanding of the mechanism of action of anabolic steroid"
Prog Clin Biol Res. 1984;142:261-9043. Ingjer F (1979) "Effects of endurance training on muscle
fiber ATP-ase activity, capillary supply and mitochondrial
content in man" J Physiol. 1979 Sep;294:419-32.44. Ingwall JS, Morales MF, Stockdale FE (1972) "Creatine and
the control of myosin synthesis in differentiating skeletal
muscle" Proc Natl Acad Sci USA. 1972 Aug;69(8):2250-3.45. Ingwall JS, Weiner CD, Morales MF, Davis E, Stockdale FE
(1974) "Specificity of creatine in the control of muscle
protein synthesis" J Cell Biol. 1974 Jul;62(1):145-5146. James NT, Cabric M (1981) "Quantitative studies on the
numerical frequency of myonuclei in the muscles of
exercised rats: evidence against the occurrence of
fiber-splitting" Br J Exp Pathol. 1981 Dec;62(6):600-5.47. Kadi F, Eriksson A, Holmner S, Butler-Browne GS,
Thornell LE (1999a) "Cellular adaptation of the trapezius
muscle in strength-trained athletes" Histochem Cell Biol.
1999 Mar;111(3):189-95.48. Kadi F, Eriksson A, Holmner S, Thornell LE (1999b)
"Effects of anabolic steroids on the muscle cells of
strength-trained athletes" Med Sci Sports Exerc.
1999 Nov;31(11):1528-34.49. Kasper CE, Xun L (1996) "Cytoplasm-to-myonucleus ratios
in plantaris and soleus muscle fibers following hindlimb
suspension" J Muscle Res Cell Motil. 1996 Oct;17(5):603-1050. Kelly FJ, Lewis SE, Anderson P, Goldspink DF (1984)
"Pre- and postnatal growth and protein turnover in four
muscles of the rat" Muscle Nerve. 1984 Mar-Apr;7(3):235-42.51. Kennedy JM, Eisenberg BR, Reid SK, Sweeney LJ, Zak R
(1988) "Nascent muscle fiber appearance in overloaded chicken
slow-tonic muscle" Am J Anat. 1988 Feb;181(2):203-15.52. Kondalenko VF, Sergeev IP, Ivanitskaia VV (1981)
"Electron microscopic study of signs of skeletal muscle fiber
hyperplasia in athletes" Arkh Anat Gistol Embriol. 1981
Jun;80(6):66-70.53. Larsson L., Tesch PA (1986) "Motor unit fiber density in
extremely hypertriphied skeletal muscles in man" Eur J Appl
Physiol Occup Physiol. 1986;55(2):130-6.54. MacDougall JD, Sale DG, Elder GC, Sutton JR (1982)
"Muscle ultrastructural characteristics of elite powerlifters
and bodybuilders" Eur J Appl Physiol Occup Physiol.
1982;48(1):117-26.55. MacDougall JD, Sale DG, Alway SE, Sutton JR (1984)
"Muscle fiber number in biceps brachii in bodybuilders and
control subjects" J Appl Physiol. 1984 Nov;57(5):1399-403.56. Manta P, Vassilopoulos D, Spengos M (1987)
"Nucleo-cytoplasmic ratio in aging skeletal muscle" Eur Arch
Psychiatry Neurol Sci. 1987;236(4):235-6.57. Mauro A (1961) "Satellite cell of skeletal muscle fibers"
J Biophys Biochem Cytol 9:493-498, 196158. McCall, GE, Allen DL, Linderman JK, Grindeland RE, Roy RR,
Mukku VR, and Edgerton VR (1998) "Maintenance of myonuclear
domain size in rat soleus after overload and growth
hormone/IGF-I treatment" J Appl Physiol 84: 1407-1412, 199859. McCall GE, Byrnes WC, Dickinson A, Pattany PM, Fleck SJ
(1996) "Muscle fiber hypertrophy, hyperplasia, and capillary
density in college men after resistance training" J Appl
Physiol. 1996 Nov;81(5):2004-12.60. McCormick KM, Thomas DP (1992) "Exercise-induced
satellite cell activation in senescent soleus muscle"
J Appl Physiol. 1992 Mar;72(3):888-93.61. Moss FP (1968) "The relationship between the dimensions
of the fibers and the number of nuclei during normal growth
of skeletal muscle in the domestic fowl" Amer. J.
Anat. 122:555.62. Moss FP, Leblond CP (1970) "Nature of dividing nuclei
in skeletal muscle of growing rats" J Cell Biol.
44(2):459-62.63. Mozdziak PE, Schultz E, Cassens RG (1997) "Myonuclear
accretion is a major determinant of avian skeletal muscle
growth" Am J Physiol. 1997 Feb;272(2Pt1):C565-71.64. Mozdziak PE, Pulvermacher PM, Schultz E (2000) "Unloading
of juvenile muscle results in a reduced muscle size 9 wk after
reloading" J Appl Physiol 88:158-164, 200065. Musacchia XJ, Deavers DR, Meininger GA, Davis TP (1980)
"A model for hypokinesia: effects on muscle atrophy in the
rat" J Appl Physiol. 1980 Mar;48(3):479-86.66. Ogilvie RW, Armstrong RB, Baird KE, Bottoms CL (1988)
"Lesions in the rat soleus muscle following eccentrically
biased exercise" Am J Anat. 1988 Aug; 182(4):335-46.67. Ohira Y, Yoshinaga T, Ohara M, Nonaka I, Yoshioka T,
Yamashita-Goto K, Shenkman BS, Kozlovskaya IB, Roy RR,
Edgerton VR (1999) "Myonuclear domain and myosin phenotype in
human soleus after bed rest with or without loading" J Appl
Physiol. 1999 Nov;87(5):1776-8568. Pacy PJ, Evans RH, Halliday D (1987) "Effect of anaerobic
and aerobic exercise promoted by computer regulated functional
electrical stimulation (FES) on muscle size, strength and
histology in paraplegic males" Prosthet Orthot Int.
1987 Aug;11(2):75-9.69. Pavlath GK, Rich K, Webster SG, Blau HM (1989)
"Localization of muscle gene products in nuclear domains"
Nature. 1989 Feb 9;337(6207):570-3.70. Pullman WE, Yeoh GC (1977) "The role of myonuclei in
muscle regeneration: an in vitro study" J Cell Physiol.
1978 Aug;96(2):245-51.71. Ralston E, Hall ZW (1992) "Restricted distribution
of mRNA produced from a single nucleus in hybrid myotubes"
The Journal of Cell Biology, Vol 119, 1063-106872. Rayne J, Crawford GN (1975) "Increase in fiber numbers
of the rat pterygoid muscles during postnatal growth" J Anat.
1975 Apr;119(2):347-57.73. Rosenblatt JD, Yong D, Parry DJ (1994) "Satellite cell
activity is required for hypertrophy of overloaded adults
rat muscle" Muscle Nerve. 1994 Jun;17(6):608-13.74. Roth SM, Martel GF, Ivey FM, Lemmer JT, Tracy BL,
Metter EJ, Hurley BF, Rogers MA (2001) "Skeletal muscle
satellite cell characteristics in young and older men and
women after heavy resistance strength training" J Gerontol
A Biol Sci Med Sci. 2001 Jun;56(6):B240-7.75. Roy RR, Monke SR, Allen DL, Edgerton VR (1999)
"Modulation of myonuclear number in functionally overloaded
and exercised rat plantaris fibers" J Appl Physiol.
1999 Aug;87(2):634-42.76. Salleo A, Anastasi G, La Spada G, Falzea G, Denaro MG
(1980) "New muscle fiber production during compensatory
hypertrophy" Med Sci Sports Exerc. 1980;12(4):268-73.77. Seiden D (1976) "Quantitative analysis of muscle cell
changes in compensatory hypertrophy and work-induced
hypertrophy" Am J Anat. 1976 Apr;145(4):459-65.78. Sinha-Hikim I, Roth SM, Lee MI, Bhasin S (2003)
"Testosterone-induced muscle hypertrophy is associated with
an increase in satellite cell number in healthy, young men"
Am J Physiol Endocrinol Metab 285: E197-E205, 2003. First
published April 1, 200379. Sjostrom M, Lexell J, Eriksson A, Taylor CC (1991)
"Evidence of fiber hyperplasia in human skeletal muscles
from healthy young men? A left-right comparison of the fiber
number in whole anterior tibialis muscles" Eur J Appl
Physiol Occup Physiol. 1991;62(5):301-4.80. Smith HK, Maxwell L, Martyn JA, Bass JJ (2000)
"Nuclear DNA fragmentation and morphological alterations in
adult rabbit skeletal muscle after short-term immobilization"
Cell Tissue Res. 2000 Nov;302(2):235-41.81. Snow MH (1977) "Myogenic cell formation in regenerating
rat skeletal muscle injured by mining. II. An
autoradiographic study" Anat Rec. 1977 Jun;188(2):201-1782. Snow MH (1990) "Satellite cell response in rat soleus
muscle undergoing hypertrophy due to surgical ablation of
synergists" Anat Rec. 1990 Aug;227(4):437-46.83. Snow MH, Chortkoff BS (1987) "Frequency of bifurcated
muscle fibers in hypertrophic rat soleus muscle" Muscle
Nerve. 1987 May;10(4):312-7.84. Staron RS, Malicky ES, Leonardi MJ, Falkel JE,
Hagerman FC, Dudley GA (1990) "Muscle hypertrophy and fast
fiber type conversions in heavy resistance-trained women"
Eur J Appl Physiol Occup Physiol. 1990; 60 (1):71-985. Tamaki T, Akatsuka A, Tokunaga M, Ishige K, Uchiyama S,
Shiraishi T (1997) "Morphological and biochemical evidence of
muscle hyperplasia following weight-lifting exercise in rats"
Am J Physiol. 1997 Jul;273(1 Pt 1):C246-56.86. Tamaki T, Akatsuka A, Yoshimura S, Roy RR, Edgerton VR
(2002) "New fiber formation in the interstitial spaces of
rat skeletal muscle during postnatal growth" J Histochem
Cytochem. 2002 Aug;50(8):1097-11187. Tamaki T, Uchiyama S, Nakano S (1992) "A weight-lifting
exercise model for inducing hypertrophy in the hindlimb
muscles of rats" Med Sci Sports Exerc. 1992 Aug;24(8):881-6.88. Timson BF, Bowlin BK, Dudenhoeffer GA, George JB (1985)
"Fiber number, area, and composition of mouse soleus muscle
following enlargement" J Appl Physiol. 1985 Feb;58(2):619-24.89. Tseng BS, Kasper CE, Edgerton VR (1994)
"Cytoplasm-to-myonucleus ratios and succinate dehydrogenase
activities in adult rat slow and fast muscle fibers" Cell
Tissue Res. 1994 Jan;275(1):39-4990. Vassilopoulos D, Lumb EM, Emery AE (1977) "Karyometric
changes in human muscle with age" Eur Neurol.
1977;16(1-6):31-4.91. Wang N, Hikida RS, Staron RS, Simoneau JA (1993)
"Muscle fiber types of women after resistance training -
quantitative ultrastructure and enzyme activity" Pflugers
Arch. 1993 Sep;424(5-6):494-502.92. Winchester PK, Davis ME, Alway SE, Gonyea WJ (1991)
"Satellite cell activation in the stretch-enlarged anterior
latissimus dorsi muscle of the adult quail" Am J Physiol
Cell Physiol 260: C206-C212, 199193. Winchester PK, Gonyea WJ (1992) "Regional injury and the
terminal differentiation of satellite cells in stretched
avian slow tonic muscle" Dev Biol. 1992 Jun;151(2):459-7294. Young RB, Denome RM (1984) "Effect of creatine on
contents of myosin heavy chain and myosin-heavy-chain mRNA
in steady-state chicken muscle-cell cultures" Biochem J.
1984 Mar 15;218(3):871-6.95. Zilber ML, Litvinova VN, Morozov VI, Pliskin AV,
Pshendin AI, Rogozkin VA (1976) "The creatine effect on RNA
and protein synthesis in growing culture of chick embryo
myoblasts" Biokhimiia. 1975 Jul-Aug;40(4):854-60
Books (1)
Think! Or “Supertraining” without misconceptions
“Think! Bodybuilding without Steroids” by Stuart McRobert and “Supertraining” by Mike Mentzer shook up the world of amateur sports and upended what seemed to be established ideas about the theory of training.
It would be more accurate to say that Mentzer for the first time tried to create at least some kind of theory; before him, most popular books and articles about bodybuilding were just collections of various and often contradictory principles of training, and catalogs of well-known exercises with weights.
Mentzer called for bodybuilding to be viewed as a science, but for some reason he chose philosophy and logic rather than physiology as the basis. Just as Euclid once created his geometry based on a number of axioms about the properties of space, Mentzer created his “Supertraining” based on the axiom about the role of the last “failure” repetition in the mechanism of triggering muscle growth, without bothering to give any physiological explanation to his hypothesis.
But, as we know, in addition to the geometry of Euclid, there are geometries of Lobachevsky and Minkowski, based on other axioms, but also internally completely non-contradictory and logical. Inspired by the excellent style and unshakable confidence of the author of “Supertraining” in his rightness, having built up, following his advice, 10 kilograms of “natural” muscles in six months, I became an ardent supporter of Mentzer’s ideas.
Having decided to find physiological confirmation of the “teacher” axiom, I plunged headlong into a new field of knowledge for myself - human physiology and biochemistry. The result was unexpected for me...
Reader comments
Kyzmadrom/ 11/18/2015 This is the best work in the world today on sports topics! I graduated from a Sports University but only began to understand it after reading Vadim’s Work!
Seryoga/ 08/16/2015 Super! Got to the point. Collected so many articles into one!
Novel/ 02/19/2015 The theory of training and muscle structure is excellently presented.
You won’t find ready-made training programs here, but reading this book will give you an understanding of all the mechanisms. You can create programs for yourself, depending on your individual characteristics.
Grishustrick/ 03/27/2014 This work does not pretend to have a title - it is a book because it is only a large summary.
Vladimir/ 01/17/2014 This is the best book on the topic.
Andrey/ 08/08/2012 Ilya, there are a lot of complexes on the Internet, but they are of no use. If you want to feed a person, don’t give him a fish, but a fishing rod.
Paul/ 10.15.2011 Well done! The only one who got to the bottom of it, now everything falls into place...Great job!)
Seva/ 06.26.2011 He is the only one who collected different studies and methods into one, processed them and presented them in an accessible form... and as for the complexes of classes, this is not a book for lamers, there is no need to write it...
Ilya/ 06/05/2011 The book is for reading in the toilet, so that after reading it can be used for its intended purpose. The author collected a bunch of theories and dumped them in his book. He didn’t even bother to write a set of classes, citing the fact that he was an amateur, and the sets should be written by professionals. If the author himself cannot create a complex, then what can he teach?! How does he train himself?! Anyone can write such a book by copying and pasting various techniques and dumping them in a heap. The book can be read for general development, nothing more. You won't find a set of workouts in it.
Introduction.
Reflecting on the title of the future article, it was not by chance that I chose the option that is written just above - the reader can easily recognize in it a collage made up of the titles of two, perhaps, the most popular books about bodybuilding among amateur athletes. “Think! Bodybuilding without Steroids” by Stuart McRobert and “Supertraining” by Mike Mentzer shook up the world of amateur sports and upended what seemed to be established ideas about the theory of training. It would be more accurate to say that Mentzer for the first time tried to create at least some kind of theory; before him, most popular books and articles about bodybuilding were just collections of various and often contradictory principles of training, and catalogs of well-known exercises with weights. Mentzer called for bodybuilding to be viewed as a science, but for some reason he chose philosophy and logic rather than physiology as the basis. Just as Euclid once created his geometry based on a number of axioms about the properties of space, Mentzer created his “Supertraining” based on the axiom about the role of the last “failure” repetition in the mechanism of triggering muscle growth, without bothering to give any physiological explanation to his hypothesis. But, as we know, in addition to the geometry of Euclid, there are geometries of Lobachevsky and Minkowski, based on other axioms, but also internally completely non-contradictory and logical. Inspired by the excellent style and unshakable confidence of the author of “Supertraining” in his rightness, having built up, following his advice, 10 kilograms of “natural” muscles in six months, I became an ardent supporter of Mentzer’s ideas. Deciding to find physiological confirmation of the “teacher” axiom, I plunged headlong into a new field of knowledge for myself - human physiology and biochemistry. The result was unexpected for me, but more on that later.
Let me draw the readers’ attention to the monstrous situation in which the theory of modern “iron” sports finds itself. All sports magazines are full of articles with new, trendy training systems. “The movement must be powerful and explosive,” some say. “Only slow, controlled movement,” others contradict them. “If you want to gain mass, work with heavy weights.” “The weight of the projectile does not matter - the main thing is technique and the feeling of the muscle working.” Arnold Schwarzenegger advises training six times a week, morning and evening. Mike Mentzer forbids his students to appear in the gym more than twice a week. The pros describe a set of six exercises for biceps. McRobert urges not to train your arms with isolated exercises at all. Powerlifters almost never work to failure during their cycles. Mentzer assures that working too hard is a waste of time. The pros on Joe Weider's team advise going much beyond failure with forced reps and stripteases. This list can be continued indefinitely, but what is striking is not the abundance of mutually exclusive training principles, but the fact that each of them has its own supporters who have managed to get results from their use. This fact allowed the opinion to spread in wide circles that there was no system. I claim that there is a system! And the patient reader will soon be able to see for himself.
And so, I managed to create a more or less integral theory of training, which explains at the physiological level (in general terms, of course) the effect of training on the human muscular system and allows one to find answers to most of the questions that interest the reader.
I foresee the doubts of skeptics - a person without special education climbs into the jungle of a new science, and even gains the audacity to present his own theories to the public. Well, if scientists don’t care about the problems of bodybuilding, then they have to rely on their own strengths, after all, “saving drowning people is the work of the drowning people themselves.” So, if you are ready, then go ahead!
Part 1. What you should know about the structure and principle of muscle function.
There are three types of muscle tissue: skeletal, smooth And cardiac. The function of cardiac tissue is clear from the name, and its role, I think, does not need to be explained. We often don’t even know about the existence of smooth muscles, since these are muscles of internal organs, and we are deprived of the ability to directly control them, as well as the heart muscle. Meanwhile, it is smooth muscles that contract the walls of blood vessels, contract the intestines, helping to move food, and perform many other vital functions. The job of skeletal muscles is to move parts of the skeleton relative to each other (hence the name). It is these muscles that we so persistently try to build on our body, and it is their structure and properties that we will consider in the future.
Current page: 1 (book has 9 pages in total)
Vadim Protasenko
Think! Or “Supertraining” without misconceptions
Introduction
Reflecting on the title of the future article, it was not by chance that I chose the option that is written just above - the reader can easily recognize in it a collage made up of the titles of two, perhaps, the most popular books about bodybuilding among amateur athletes. “Think! Bodybuilding without Steroids” by Stuart McRobert and “Supertraining” by Mike Mentzer shook up the world of amateur sports and upended what seemed to be established ideas about the theory of training. It would be more accurate to say that Mentzer for the first time tried to create at least some kind of theory; before him, most popular books and articles about bodybuilding were just collections of various and often contradictory principles of training, and catalogs of well-known exercises with weights. Mentzer called for bodybuilding to be viewed as a science, but for some reason he chose philosophy and logic rather than physiology as the basis. Just as Euclid once created his geometry based on a number of axioms about the properties of space, Mentzer created his “Supertraining” based on the axiom about the role of the last “failure” repetition in the mechanism of triggering muscle growth, without bothering to give any physiological explanation to his hypothesis. But, as we know, in addition to the geometry of Euclid, there are geometries of Lobachevsky and Minkowski, based on other axioms, but also internally completely non-contradictory and logical. Inspired by the excellent style and unshakable confidence of the author of “Supertraining” in his rightness, having built up, following his advice, 10 kilograms of “natural” muscles in six months, I became an ardent supporter of Mentzer’s ideas. Deciding to find physiological confirmation of the “teacher” axiom, I plunged headlong into a new field of knowledge for myself - human physiology and biochemistry. The result was unexpected for me, but more on that later.
Let me draw the readers’ attention to the monstrous situation in which the theory of modern “iron” sports finds itself. All sports magazines are full of articles with new, trendy training systems. “The movement must be powerful and explosive,” some say. “Only slow, controlled movement,” others contradict them. “If you want to gain mass, work with heavy weights.” “The weight of the projectile does not matter - the main thing is technique and the feeling of the muscle working.” Arnold Schwarzenegger advises training six times a week, morning and evening. Mike Mentzer forbids his students to appear in the gym more than twice a week. The pros describe a set of six exercises for biceps. McRobert urges not to train your arms with isolated exercises at all. Powerlifters almost never work to failure during their cycles. Mentzer assures that working too hard is a waste of time. The pros on Joe Weider's team advise going much beyond failure with forced reps and stripteases. This list can be continued indefinitely, but what is striking is not the abundance of mutually exclusive training principles, but the fact that each of them has its own supporters who have managed to get results from their use. This fact allowed the opinion to spread in wide circles that there was no system. I claim that there is a system! And the patient reader will soon be able to see for himself.
And so, I managed to create a more or less integral theory of training, which explains at the physiological level (in general terms, of course) the effect of training on the human muscular system and allows one to find answers to most of the questions that interest the reader.
I foresee the doubts of skeptics - a person without special education climbs into the jungle of a new science, and even gains the audacity to present his own theories to the public. Well, if scientists don’t care about the problems of bodybuilding, then they have to rely on their own strengths, after all, “saving drowning people is the work of the drowning people themselves.” So, if you are ready, then go ahead!
What you should know about the structure and principle of muscle function
There are three types of muscle tissue: skeletal, smooth And cardiac. The function of cardiac tissue is clear from the name, and its role, I think, does not need to be explained. We often don’t even know about the existence of smooth muscles, since these are muscles of internal organs, and we are deprived of the ability to directly control them, as well as the heart muscle. Meanwhile, it is smooth muscles that contract the walls of blood vessels, contract the intestines, helping to move food, and perform many other vital functions. The job of skeletal muscles is to move parts of the skeleton relative to each other (hence the name). It is these muscles that we so persistently try to build on our body, and it is their structure and properties that we will consider in the future.
Let's look into the cage.
As you know, all tissues of the body have a cellular structure, and muscles are no exception. Therefore, I will have to make a brief excursion into cytology - the science of the cell, and remind readers of the role and properties of the main structures of the cell.
To a rough approximation, the cell consists of two important, interconnected parts - cytoplasm And kernels.
Core- contains molecules DNA, which contain all hereditary information. DNA is a polymer twisted in the form of a double helix, each helix of which is made up of a huge number of four types of monomers called nucleotides. The sequence of nucleotides in the chain codes for all the proteins in the body.
The nucleus is responsible for cell reproduction - division. Cell division begins with the division of the DNA molecule into two helices, each of which is capable of completing a pair from a set of free nucleotides and again turns into a DNA molecule. Thus, the amount of DNA in the nucleus doubles, then the nucleus is divided into two parts, followed by the entire cell.
Cytoplasm- This is everything that surrounds the nucleus in a cell. It consists of cytosol (cellular fluid), which includes various organelles, such as mitochondria, lysosomes, ribosomes and others.
Mitochondria- These are the energy stations of the cell; in them, with the help of various enzymes, the oxidation of carbohydrates and fatty acids occurs. The energy released during the oxidation of substances goes to the addition of a third phosphate group to the molecule Adenesine diphosphate(ADF) with education Adenesine triphosphate(ATP) is a universal source of energy for all processes occurring in the cell. By detaching the third phosphate group and turning back into ADP, ATP releases previously stored energy.
Enzymes or Enzymes– substances of protein nature that increase the speed of chemical reactions hundreds and thousands of times. Almost all vital chemical processes in the body occur only in the presence of specific enzymes.
Lysosomes- round vesicles containing about 50 enzymes. Lysosomal enzymes break down the material absorbed by the cell and the cell's own internal structures (autolysis). Lysosomes, merging into phagosomes, are able to digest entire organelles that are subject to disintegration.
Ribosomes- organelles on which protein molecules are assembled.
Cell membrane– the cell membrane, it has selective permeability, that is, the ability to let some substances through and retain others. The task of the membrane is to maintain the constancy of the internal environment of the cell.
Muscle structure.
The structural and functional unit of skeletal muscle is simplast or muscle fiber– a huge cell in the shape of an extended cylinder with pointed edges (hereinafter the names symplast, muscle fiber, muscle cell should be understood as the same object). The length of the muscle cell most often corresponds to the length of the whole muscle and reaches 14 cm, and the diameter is equal to several hundredths of a millimeter. The muscle fiber, like any cell, is surrounded by a membrane - sarcolemoma. On the outside, individual muscle fibers are surrounded by loose connective tissue, which contains blood and lymphatic vessels, as well as nerve fibers. Groups of muscle fibers form bundles, which, in turn, are combined into a whole muscle, placed in a dense cover of connective tissue, which passes at the ends of the muscle into tendons attached to the bone.
Fig.1
The force caused by shortening the length of the muscle fiber is transmitted through the tendons to the bones of the skeleton and causes them to move.
The contractile activity of the muscle is controlled using a large number motor neurons(Fig. 2) - nerve cells, the bodies of which lie in the spinal cord, and long branches - axons as part of the motor nerve they approach the muscle. Having entered the muscle, the axon branches into many branches, each of which is connected to a separate fiber. Thus, one motor neuron innervates a whole group of fibers (the so-called neuromotor unit), which works as a single unit.
Fig.2
A muscle consists of many neuromotor units and is capable of working not with its entire mass, but in parts, which allows you to regulate the strength and speed of contraction.
To understand the mechanism of muscle contraction, it is necessary to consider the internal structure of the muscle fiber, which, as you already understand, is very different from an ordinary cell. Let's start with the fact that muscle fiber is multinucleated. This is due to the peculiarities of fiber formation during fetal development. Symplasts (muscle fibers) are formed at the stage of embryonic development of the body from precursor cells - myoblasts. Myoblasts (unformed muscle cells) intensively divide, merge and form muscular tubes with a central location of the nuclei. Then synthesis begins in the myotubes myofibrils(see below for the contractile structures of the cell), and the formation of the fiber is completed by the migration of nuclei to the periphery. By this time, the muscle fiber nuclei have already lost the ability to divide, and they only have the function of generating information for protein synthesis.
But not all myoblasts follow the path of fusion; some of them are isolated in the form of satellite cells located on the surface of the muscle fiber, namely in the sarcolemma, between the plasmolema and the basement membrane - the components of the sarcolemma. Satellite cells, unlike muscle fibers, do not lose the ability to divide throughout life, which ensures an increase in muscle fiber mass and their renewal. Restoration of muscle fibers in case of muscle damage is possible thanks to satellite cells. When the fiber dies, the satellite cells hidden in its shell are activated, divide and transform into myoblasts. Myoblasts fuse with each other and form new muscle fibers, in which the assembly of myofibrils then begins. That is, during regeneration, the events of embryonic (intrauterine) muscle development are completely repeated.
In addition to multinucleation, a distinctive feature of a muscle fiber is the presence in the cytoplasm (in muscle fibers it is usually called sarcoplasm) of thin fibers - myofibrils (Fig. 1), located along the cell and laid parallel to each other. The number of myofibrils in a fiber reaches two thousand. Myofibrils are contractile elements of the cell and have the ability to reduce their length when a nerve impulse arrives, thereby tightening the muscle fiber. Under a microscope, it can be seen that the myofibril has transverse striations - alternating dark and light stripes. When the myofibril contracts, the light areas reduce their length and disappear completely when the contraction is complete. To explain the mechanism of myofibril contraction, about fifty years ago, Hugh Huxley developed the sliding filament model, then it was confirmed in experiments and is now generally accepted.
Mechanism of fiber contraction.
The alternation of light and dark stripes in the myofibril filament is determined by the ordered arrangement along the length of the myofibril of thick filaments of the myosin protein and thin filaments of the actin protein; thick filaments are contained only in dark areas (A-disc) (Fig. 3), light areas (I-disc) do not contain thick filaments, in the middle of the I-disc there is a Z-line - thin actin filaments are attached to it. A section of myofibril consisting of an A-disc (dark stripe) and two halves of I-discs (light stripes) is called a sarcomere. The length of the sarcomere is shortened by drawing thin filaments of actin between thick filaments of myosin. The sliding of actin filaments along the myosin filaments occurs due to the presence of side branches called bridges on the myosin filaments. The head of the myosin bridge engages with actin and changes the angle of inclination to the axis of the filament, thereby, as it were, advancing the filament of myosin and actin relative to each other, then uncouples, engages again and makes movement again. The movement of myosin bridges can be compared to the strokes of oars on galleys. Just as the movement of a galley in water occurs due to the movement of the oars, so the sliding of the threads occurs due to the rowing movements of the bridges; the only significant difference is that the movement of the bridges is asynchronous.
Fig.3
The thin filament is made up of two helical strands of the actin protein. In the grooves of the helical chain lies a double chain of another protein - tropomyosin. In a relaxed state, myosin bridges are unable to contact actin, since the adhesion sites are blocked by tropomyosin. When a nerve impulse arrives along the axon of a motor motor neuron, the cell membrane changes the polarity of the charge, and calcium ions (Ca++) are released into the sarcoplasm from special terminal cisterns located around each myofibril along its entire length (Fig. 4).
Fig.4
Under the influence of Ca++, the tropomyosin filament enters deeper into the groove and frees up space for myosin to adhere to actin; the bridges begin the stroke cycle. Immediately after the release of Ca++ from the terminal cisterns, it begins to be pumped back, the concentration of Ca++ in the sarcoplasm drops, tropomyosin moves out of the groove and blocks the bonding sites of the bridges - the fiber relaxes. A new impulse again releases Ca++ into the sarcoplasm and everything repeats. With a sufficient impulse frequency (at least 20 Hz), individual contractions almost completely merge, that is, a state of stable contraction is achieved, called tetanic contraction or smooth tetanus.
Muscle energy.
Naturally, energy is required to move the bridge. As I mentioned earlier, the universal source of energy in a living organism is the ATP molecule. Under the action of the enzyme ATPase, ATP is hydrolyzed, detaching the phosphate group in the form of orthophosphoric acid (H3PO4), and converted into ADP, releasing energy.
ATP + H2O = ADP + H3PO4 + energy.
The head of the myosin bridge, when in contact with actin, has ATPase activity and, accordingly, the ability to break down ATP and obtain the energy necessary for movement.
The supply of ATP molecules in the muscle is limited, so energy consumption during muscle work requires its constant replenishment. The muscle has three sources of energy reproduction: the breakdown of creatine phosphate; glycolysis; oxidation of organic substances in mitochondria.
Creatine phosphate has the ability to detach a phosphate group and become creatine by attaching a phosphate group to ADP, which is converted to ATP.
ADP + creatine phosphate = ATP + creatine.
This reaction is called the Lohmann reaction. The reserves of creatine phosphate in the fiber are not large, so it is used as an energy source only at the initial stage of muscle work, until other more powerful sources are activated - glycolysis and oxygen oxidation. At the end of the muscle work, the Lohmann reaction goes in the opposite direction, and creatine phosphate reserves are restored within a few minutes.
Glycolysis - the process of decomposition of one glucose molecule (C6H12O6) into two molecules of lactic acid (C3H6O3) with the release of energy sufficient to “charge” two ATP molecules, occurs in the sarcoplasm under the influence of 10 special enzymes.
C6H12O6 + 2H3PO4 + 2ADP = 2C3H6O3 + 2ATP + 2H2O.
Glycolysis occurs without oxygen consumption (such processes are called anaerobic) and is able to quickly restore ATP reserves in the muscle.
Oxidation occurs in mitochondria under the influence of special enzymes and requires oxygen consumption and, accordingly, time for its delivery. Such processes are called aerobic. Oxidation occurs in several stages, first there is glycolysis (see above), but the two pyruvate molecules formed during the intermediate stage of this reaction are not converted into lactic acid molecules, but penetrate into the mitochondria, where they are oxidized in the Krebs cycle to carbon dioxide CO2 and water H2O and provide energy to produce 36 more ATP molecules. The overall equation for the glucose oxidation reaction looks like this:
C6H12O6 + 6O2 + 38ADP + 38H3PO4 = 6CO2 + 44H(2)O + 38ATP.
In total, the breakdown of glucose along the aerobic pathway provides energy for the reduction of 38 ATP molecules. That is, oxidation is 19 times more effective than glycolysis.
Types of muscle fibers.
Skeletal muscles and the muscle fibers that form them differ in many parameters: contraction speed, fatigue, diameter, color, etc. Traditionally, red and white, slow and fast, glycolytic and oxidative fibers are distinguished.
The rate of muscle fiber contraction is determined by the type of myosin. The isoform of myosin that provides a high rate of contraction, fast myosin, is characterized by high ATPase activity and, accordingly, the rate of ATP consumption. The myosin isoform with a slower contraction rate, slow myosin, is characterized by lower ATPase activity. Fibers with high ATPase activity and ATP consumption rate are usually called fast fibers, fibers characterized by low ATPase activity and a lower ATP consumption rate are called slow fibers.
To replenish energy costs, muscle fibers use the oxidative or glycolytic pathway of ATP formation.
Oxidative, or red, muscle fibers of small diameter are surrounded by a mass of capillaries and contain a lot of the protein myoglobin (it is the presence of this protein that gives the fibers their red color). Numerous red fiber mitochondria have high levels of oxidative enzyme activity. A powerful network of capillaries is necessary to deliver large amounts of oxygen through the blood, and myoglobin is used to transport oxygen within the fiber from the surface to the mitochondria. Red fibers obtain energy by oxidizing carbohydrates and fatty acids in mitochondria.
Glycolytic, or white, muscle fibers have a larger diameter, their sarcoplasm contains a significant amount of glycogen granules, mitochondria are not numerous, and the activity of oxidative enzymes is significantly inferior to the activity of glycolytic enzymes. Glycogen, also commonly called “animal starch,” is a complex polysaccharide with a high molecular weight that serves as a reserve nutrient for white fiber. Glycogen breaks down into glucose, which serves as fuel during glycolysis.
Fast fibers, which have high ATPase activity and, accordingly, a rate of energy consumption, require a high rate of ATP reproduction, which can only be provided by glycolysis, since, unlike oxidation, it occurs directly in the sarcoplasm and does not require time to deliver oxygen to mitochondria and deliver energy from them to myofibrils. Therefore, fast fibers prefer the glycolytic pathway for ATP reproduction and, accordingly, are classified as white fibers. For the high rate of energy production, white fibers pay with rapid fatigue, since glycolysis, as can be seen from the reaction equation, leads to the formation of lactic acid, the accumulation of which increases the acidity of the environment and causes muscle fatigue and ultimately stops its work.
Slow fibers, characterized by low ATPase activity, do not require such rapid replenishment of ATP reserves and use the oxidation pathway to meet energy needs, that is, they are classified as red fibers. Thanks to this, slow-twitch fibers are low-fatigue and are able to maintain relatively low but long-lasting tension.
There is an intermediate type of fiber with high ATPase activity and the oxidative-glycolytic pathway of ATP reproduction.
The type of muscle fiber depends on the motor neuron innervating it. All fibers of one motor neuron belong to the same type. An interesting fact is that when a slow motor neuron is connected to a fast axon fiber and vice versa, the fiber is degenerated, changing its type. Until recently, there were two points of view on the dependence of the type of fiber on the type of motor neuron, some researchers believed that the properties of the fiber are determined by the frequency of impulses of the motor neuron, others that the effect on the type of fiber is determined by hormone-like substances coming from the nerve (these substances have not yet been isolated) . Research in recent years shows that both points of view have a right to exist; the effect of a motor neuron on a fiber is carried out in both ways.
Regulation of the strength and speed of muscle contraction.
As you know from your own experience, a person has the ability to voluntarily regulate the strength and speed of muscle contraction. This possibility is implemented in several ways. You are already familiar with one of them - controlling the frequency of nerve impulses. By giving the fiber single commands to contract, you can achieve slight tension in it. For example, the muscles that support the posture are slightly tense, even when the person is resting. By increasing the frequency of impulses, it is possible to increase the force of contraction to the maximum possible for a given fiber under given operating conditions, which is achieved by merging individual impulses into the tetanus.
The force developed by the fiber in the tetanus state is not always the same and depends on the nature and speed of movement. Under static tension (when the length of the fiber remains constant), the force developed by the fiber is greater than when the fiber contracts, and the faster the fiber contracts, the less force it can develop. The fiber develops maximum force under conditions of negative movement, that is, when the fiber elongates.
In the absence of external load, the fiber contracts at maximum speed. As the load increases, the rate of fiber contraction decreases and, upon reaching a certain load level, drops to zero; with a further increase in load, the fiber lengthens.
The reason for the difference in fiber strength in different directions of movement is easy to understand by considering the previously given example of rowers and oars. The fact is that after the completion of the “stroke”, the myosin bridge is in a state of adhesion to the actin filament for some time; imagine that the oar, after the stroke, is also not immediately removed from the water, but remains submerged for some time. In the case when the rowers are swimming forward (positive movement), the oars remaining submerged in the water after completing the stroke slow down the movement and interfere with swimming, at the same time, if the boat is towed back and the rowers resist this movement, then the submerged oars also interfere movement, and the tug has to exert great effort. That is, when the fiber contracts, the linked bridges interfere with movement and weaken the strength of the fiber; during negative movement - lengthening of the muscle - uncoupled bridges also interfere with movement, but in this case they seem to support the descending weight, which allows the fiber to develop greater force. The easiest way to understand the differences between static tension, positive and negative movement is to look at Figure 5.
So, we have looked at the main factors influencing the strength and speed of contraction of an individual fiber. The strength of contraction of an entire muscle depends on the number of fibers involved in the work at a given time.
Fig.5
Involvement of fibers in work.
When an excitatory signal (triggering impulse) arrives from the CNS (central nervous system) to the motor neurons (located in the spinal cord), the membrane of the motor neuron is polarized, and it generates a series of impulses sent along the axon to the fibers. The stronger the effect on a motor neuron (membrane polarization), the higher the frequency of the impulse generated by it - from a low starting frequency (4–5 Hz) to the maximum possible frequency for a given motor neuron (50 Hz or more). Fast motor neurons are capable of generating a much higher frequency impulse than slow ones, so the force of contraction of fast fibers is much more subject to frequency regulation than the force of slow ones.
At the same time, there is feedback from the muscle, from which inhibitory signals are received that reduce the polarization of the motor neuron membrane and reduce its response.
Each motor neuron has its own excitability threshold. If the sum of excitatory and inhibitory signals exceeds this threshold and the required level of polarization is achieved on the membrane, then the motor neuron is involved in work. Slow motor neurons, as a rule, have a low threshold of excitability, and fast motor neurons have a high threshold. Motoneurons of the whole muscle have a wide range of values of this parameter. Thus, as the strength of the CNS signal increases, an increasing number of motor neurons are activated, and motor neurons with a low excitability threshold increase the frequency of the generated impulse.
When light effort is required, such as walking or jogging, a small number of slow motor neurons and a corresponding number of slow fibers are activated, and due to the high endurance of these fibers, such work can be maintained for a very long time. As the load increases, the central nervous system has to send an increasingly stronger signal, and a larger number of motor neurons (and, therefore, fibers) are involved in the work, and those that were already working increase the force of contraction, due to an increase in the frequency of impulses coming from the motor neurons. As the load increases, fast oxidative fibers are activated, and upon reaching a certain load level (20%-25% of the maximum), for example, during an uphill climb or the final spurt, the strength of the oxidative fibers becomes insufficient, and the signal sent by the central nervous system turns on fast work - glycolytic fibers. Fast-twitch fibers significantly increase the force of muscle contraction, but, in turn, quickly tire, and more and more of them are involved in the work. If the level of external load does not decrease, work will soon have to be stopped due to fatigue, as a result of the accumulation of lactic acid.
Loading...