How does excitation spread along the muscle fiber? Satellites What types of muscle tissue have a cellular structure.
A- In the perimysium.
B- In the endomysium.
B- Between the basement membrane and the plasmolemma of the symplast.
G- Under the sarcolemma
48. What is characteristic of cardiac muscle tissue?
A- Muscle fibers are made up of cells.
B- Good cellular regeneration.
B- Muscle fibers anastomose with each other.
G- Regulated by the somatic nervous system.
49. In which part of the sarcomere are there no thin actin myofilaments?
A- In disc I.
B- In disk A.
B- In the overlap area.
G- In the H-band area.
50. How does smooth muscle tissue differ from striated skeletal tissue?
A- Consists of cells.
B- Part of the walls of blood vessels and internal organs.
B- Consists of muscle fibers.
D- Develops from myotomes of somites.
D- Does not have striated myofibrils.
1.What intercellular contacts are present in intercalary discs:
A- desmosomes
B- intermediate
B- slotted
G-hemidesmosomes
2.Types of cardiomyocytes:
A- secretory
B- contractile
B - transitional
G-sensory
D- conductive
3. Secretory cardiomyocytes:
A- localized in the wall of the right atrium
B- secrete corticosteroids
B- secrete natriuretic hormone
G- affect diuresis
D- promote myocardial contraction
4. Determine the correct sequence and reflect the dynamics of the process of histogenesis of striated skeletal muscle tissue: 1 - formation of the myotube, 2 - differentiation of myoblasts into symplast precursors and satellite cells, 3 - migration of myoblast precursors from the myotome, 4 - formation of symplast and satellite cells, 5- union of symplast and satellite cells to form skeletal muscle fiber
5.What types of muscle tissue have a cellular structure:
A - smooth
B- cardiac
B- skeletal
6.Sarcomere structure:
A - section of the myofibril located between two H-bands
B- consists of an A-disc and two halves of I-discs
B- when contracting the muscle does not shorten
G- consists of actin and myosin filaments
8.Smooth muscle cells:
A- synthesizes components of the basement membrane
B- caveolae - an analogue of the sarcoplasmic reticulum
B-myofibrils are oriented along the longitudinal axis of the cell
G-dense bodies – an analogue of T-tubules
D-actin filaments consist only of actin filaments
9.White muscle fibers:
A- large diameter with strong development of myofibrils
B - lactate dehydrogenase activity is high
B - a lot of myoglobin
D - long contractions, low strength
10. Red muscle fibers:
A - fast, high contraction force
B - a lot of myoglobin
B- few myofibrils, thin
G- high activity of oxidative enzymes
D - few mitochondria
11.During the reparative histogenesis of skeletal muscle tissue, the following occurs:
A - division of nuclei of mature muscle fibers
B- myoblast division
B- sarcomerogenesis inside myoblasts
G- formation of symplast
12. What do muscle fibers of skeletal and cardiac muscle tissue have in common:
A- triads
B- transversely striated myofibrils
B-insert discs
G-satellite cells
D-sarcomere
E - arbitrary type of contraction
13. Indicate the cells between which gap junctions are present:
A- cardiomyocytes
B- myoepithelial cells
B-smooth myocytes
G-myofibroblasts
14. Smooth muscle cell:
A- synthesizes collagen and elastin
B- contains calmodulin – an analogue of troponin C
B- contains myofibrils
G-sarcoplasmic reticulum is well developed
15. The role of the basement membrane in muscle fiber regeneration:
A- prevents the proliferation of surrounding connective tissue and scar formation
B - maintains the necessary acid-base balance
B-components of the basement membrane are used to restore myofibrils
G- ensures correct orientation of myotubes
16. Name the signs of skeletal muscle tissue:
A- Formed by cells
B- The nuclei are located along the periphery.
B- Consist of muscle fibers.
G- Has only intracellular regeneration.
D- Develops from myotomes
1. Embryonic myogenesis of skeletal muscle (all are true except):
A-myoblast of the limb muscles originate from the myotome
B- part of the proliferating myoblasts form satellite cells
B- during mitosis, daughter myoblasts are connected by cytoplasmic bridges
G- the assembly of myofibrils begins in the myotubes
D-nuclei move to the periphery of the myosymplast
2. Triad of skeletal muscle fiber (all are true except):
A-T-tubules are formed by invaginations of the plasmalemma
B- the membranes of the terminal cisterns contain calcium channels
B-excitation is transmitted from T-tubules to terminal cisterns
G-activation of calcium channels leads to a decrease in Ca2+ in the blood
3.Typical cardiomyocyte (all are true except):
B - contains one or two centrally located nuclei
B-T-tubule and cisterna terminalis form a dyad
D- together with the axon of the motor neuron forms the neuromuscular synapse
4. Sarcomere (all are true except):
A-thick filaments consist of myosin and C protein
B- thin filaments consist of actin, tropomyosin, troponin
B- the sarcomere consists of one A-disc and two halves of the I-disc
G- in the middle of the I-disc there is a Z-line
D - contraction reduces the width of the A-disc
5. Structure of a contractile cardiomyocyte (all are correct except):
A - ordered arrangement of bundles of myofibrils, layered with chains of mitochondria
B- eccentric location of the core
B- presence of anastomosing bridges between cells
G- intercellular contacts – intercalary discs
D - centrally located nuclei
6. During muscle contraction occurs (everything is true except):
A - sarcomere shortening
B- shortening of muscle fiber
B- shortening of actin and myosin myofilaments
G- shortening of myofibrils
7. Smooth myocyte (all are true except):
A - spindle-shaped cell
B- contains a large number of lysosomes
B-nucleus is located in the center
D - presence of actin and myosin filaments
D - contains desmin and vimentin intermediate filaments
8. Cardiac muscle tissue (all are true except):
A - incapable of regeneration
B- muscle fibers form functional fibers
B-pacemakers trigger contraction of cardiomyocytes
D - the autonomic nervous system regulates the frequency of contractions
D - cardiomyocyte is covered with sarcolemma, there is no basement membrane
9. Cardiomyocyte (all are correct except):
A - cylindrical cell with branched ends
B - contains one or two nuclei in the center
B-myofibrils consist of thin and thick filaments
G-intercalated discs contain desmosomes and gap junctions
D - together with the axon of the motor neuron of the anterior horns of the spinal cord, it forms a neuromuscular synapse
10. Smooth muscle tissue (all are true except):
A - involuntary muscle tissue
B- is under the control of the autonomic nervous system
B- contractile activity does not depend on hormonal influences
- (lat. satellites bodyguards, satellites). 1. S. cells (syn. amphocytes, perineuronal cells, Trabantenzel len), the name given by Ramon and Cajal (Ramon in Cajal) to special cells located in the nerve nodes of the cerebrospinal system between ... ...
Scheme of chromosome structure in late prophase and metaphase of mitosis. 1 chromatid; 2 centromeres; 3 short shoulder; 4 long shoulder. Chromosome set (Karyotype) of a human (female). Chromosomes (Greek χρώμα color and ... Wikipedia
NERVE CELLS- NERVE CELLS, the main elements of nervous tissue. Discovered by N. K. Ehrenberg and first described by him in 1833. More detailed data about N. to. with an indication of their shape and the existence of an axial-cylindrical process, as well as ... ... Great Medical Encyclopedia
Viral particles that are unable to build capsids on their own. They infect cells that do not naturally die from old age (for example, amoebas, bacteria). When a cell infected with a satellite virus is infected by a regular virus, then... ... Wikipedia
- (textus nervosus) a set of cellular elements that form the organs of the central and peripheral nervous system. Possessing the property of irritability, N.t. ensures the receipt, processing and storage of information from the external and internal environment,... ... Medical encyclopedia
Neuroglia, or simply glia (from other Greek νεῦρον “fiber, nerve” and γλία “glue”) is a collection of auxiliary cells of nervous tissue. Makes up about 40% of the volume of the central nervous system. The term was introduced in 1846 by Rudolf Virchow. Glial cells ... Wikipedia
- (from Neuro... and Greek glía glue) glia, cells in the brain, with their bodies and processes filling the spaces between nerve cells Neurons and brain capillaries. Each neuron is surrounded by several N. cells, which are evenly... ... Great Soviet Encyclopedia
Adaptation (adaptation) to changing conditions of existence is the most common property of living organisms. All pathological processes can essentially be divided into two groups: (1) damage processes (alterative processes) and (2) ... ... Wikipedia
- (s) (gliocytus, i, LNH; Glio + hist. cytus cell; synonym: glial cell, neuroglial cell) general name for the cellular elements of neuroglia. Mantle gliocytes (g. mantelli, LNH; synonym satellite cells) G., located on the surface of the body... ... Medical encyclopedia
- (g. mantelli, LNH; synonymous satellite cells) G., located on the surface of the neuron bodies ... Large medical dictionary
Restoration of damaged muscle tissue occurs thanks to satellite cells. And they cannot function without a special protein, scientists have found.
Muscles have a remarkable ability to heal themselves. With the help of training, you can restore them after injury, and age-related atrophy can be overcome with an active lifestyle. When a muscle is sprained, it hurts, but the pain usually goes away after a few days.
The muscles owe this ability to satellite cells - special cells of muscle tissue that are adjacent to myocytes, or muscle fibers. The muscle fibers themselves - the main structural and functional elements of the muscle - are long multinucleated cells that have the property of contraction, since they contain contractile protein filaments - myofibrils.
Satellite cells are, in fact, stem cells of muscle tissue. When muscle fibers are damaged, which occurs due to injury or with age, satellite cells rapidly divide.
They repair damage by fusing together to form new multinucleated muscle fibers.
With age, the number of satellite cells in muscle tissue decreases, and accordingly, the ability of muscles to recover, as well as muscle strength, decreases.
Scientists from the Max Planck Institute for Heart and Lung Research (Germany) have elucidated the molecular mechanics of muscle self-healing using satellite cells, which until now was not thoroughly known. They wrote about the results in the journal Cell Stem Cell.
Their discovery, according to scientists, will help create a muscle restoration technique that could someday be transferred from the laboratory to the clinic for the treatment of muscular dystrophy. Or maybe muscle aging.
Researchers have identified a key factor, a protein called Pax7, which plays a major role in muscle regeneration.
Actually, this protein in satellite cells has been known for a long time, but experts believed that the protein plays the main role immediately after birth. But it turned out that it is indispensable at all stages of the body’s life.
To pinpoint its role, biologists created genetically altered mice in which the Pax7 protein in satellite cells did not work. This led to a radical reduction in the satellite cells themselves in muscle tissue. The scientists then caused damage to the mouse muscles by injecting the toxin. In normal animals, the muscles began to regenerate intensively, and the damage healed. But in genetically altered mice without the Pax7 protein, muscle regeneration became almost impossible. As a result, biologists observed large numbers of dead and damaged muscle fibers in their muscles.
Scientists regarded this as evidence of the leading role of the Pax7 protein in muscle regeneration.
The muscle tissue of the mice was examined under an electron microscope. In mice without the Pax7 protein, biologists found very few surviving satellite cells, which were very different in structure from normal stem cells. Damage to organelles was noted in the cells, and the state of chromatin—DNA combined with proteins, which is normally structured in a certain way—was disrupted.
Interestingly, similar changes appeared in satellite cells that were cultured for a long time in the laboratory in an isolated state, without their “hosts” - myocytes. The cells degraded in the same way as in the bodies of genetically modified mice. And scientists found in these degraded cells signs of deactivation of the Pax7 protein, which was observed in mutant mice. Further - more: isolated satellite cells stopped dividing after some time, that is, stem cells ceased to be stem cells.
If, on the contrary, the activity of the Pax7 protein in satellite cells is increased, they begin to divide more intensively. Everything points to the key role of the Pax7 protein in the regenerative function of satellite cells. All that remains is to figure out how to use it in potential cell therapy for muscle tissue.
“When muscles deteriorate, such as in muscular dystrophy, implanting muscle stem cells will stimulate regeneration,” explains Thomas Brown, director of the institute.
Understanding how Pax7 works will help modify satellite cells to make them as active as possible.
This could lead to a revolution in the treatment of muscular dystrophy and may help maintain muscle strength in old age."
And healthy muscles and physical activity in old age are the best way to delay age-related diseases.
47.2.Sources of development
Division of cells into neurons and glia.
Nervous tissue was the last to arise in embryogenesis. It is formed at the 3rd week of embrygenesis, when the neural plate is formed, which turns into the neural groove, then into the neural tube. Ventricular stem cells proliferate in the wall of the neural tube, from which neuroblasts are formed - from which nerve cells are formed. Neuroblasts give rise to a huge number of neurons (10-12), but soon after birth they lose the ability to divide.
and glioblasts - from which glial cells are formed - these are astrocytes, oligodendrocytes and ependymocytes. Thus, nervous tissue includes nerve and glial cells.
Glioblasts, maintaining proliferative activity for a long time, differentiate into gliocytes (some of which are also capable of division).
At the same time, i.e. in the embryonic period, a significant part (up to 40-80%) of the resulting nerve cells die by apoptosis. It is believed that these are, firstly, cells with serious damage to chromosomes (including chromosomal DNA) and, secondly, cells whose processes could not establish a connection with the corresponding structures (target cells, sensory organs, etc.). d.)
47.3.Localization of various types of glial cells
Glia of the central nervous system:
macroglia - comes from glioblasts; these include oligodendroglia, astroglia and ependymal glia;
microglia - comes from promonocytes.
Glia of the peripheral nervous system (often considered a type of oligodendroglia): mantle gliocytes (satellite cells, or ganglion gliocytes),
neurolemmocytes (Schwann cells).
47.4.Structure of various types of glial cells
Briefly: 
Details:Astroglia- represented by astrocytes, the largest of the glial cells that are found in all parts of the nervous system. Astrocytes are characterized by a light oval nucleus, cytoplasm with moderately developed essential organelles, numerous glycogen granules and intermediate filaments. The last cells from the body penetrate into the processes and contain a special glial fibrillary acidic protein (GFAP), which serves as a marker of astrocytes. At the ends of the processes there are lamellar extensions (“legs”), which, connecting to each other, surround vessels or neurons in the form of membranes. Astrocytes form gap junctions among themselves, as well as with oligodendrocytes and ependymal glia.
Astrocytes are divided into two groups:
Protoplasmic (plasmatic) astrocytes are found predominantly in the gray matter of the central nervous system; they are characterized by the presence of numerous branched short relatively thick processes and a low content of GFCB.
Fibrous (fibrous) astrocytes are located mainly in the white matter of the central nervous system. Long, thin, slightly branched processes extend from their bodies. Characterized by a high content of GFCB.
Functions of astroglia
supporting formation of the supporting frame of the central nervous system, within which other cells and fibers are located; During embryonic development, they serve as supporting and guiding elements along which the migration of developing neurons occurs. The guiding function is also associated with the secretion of growth factors and the production of certain components of the intercellular substance, recognized by embryonic neurons and their processes.
demarcation, transport and barrier (aimed at ensuring an optimal microenvironment of neurons):
metabolic and regulatory is considered one of the most important functions of astrocytes, which is aimed at maintaining certain concentrations of K + ions and mediators in the microenvironment of neurons. Astrocytes, together with oligodendroglial cells, take part in the metabolism of mediators (catecholamines, GABA, peptides).
protective (phagocytic, immune and reparative) participation in various protective reactions when nerve tissue is damaged. Astrocytes, like microglial cells, are characterized by pronounced phagocytic activity. Like the latter, they also have the characteristics of APCs: they express MHC class II molecules on their surface, are able to capture, process and present antigens, and also produce cytokines. At the final stages of inflammatory reactions in the central nervous system, astrocytes proliferate and form a glial scar at the site of damaged tissue.
Ependymal glia, or ependyma formed by cubic or cylindrical cells (ependymocytes), single-layer layers of which line the cavities of the ventricles of the brain and the central canal of the spinal cord. A number of authors also include flat cells that form the lining of the meninges (meningothelium) as ependymal glia.
The nucleus of ependymocytes contains dense chromatin, the organelles are moderately developed. The apical surface of some ependymocytes bears cilia, which move cerebrospinal fluid (CSF) with their movements, and a long process extends from the basal pole of some cells, extending to the surface of the brain and being part of the superficial limiting glial membrane (marginal glia).
Since ependymal glia cells form layers in which their lateral surfaces are connected by intercellular connections, according to their morphofunctional properties they are classified as epithelia (ependymoglial type according to N.G. Khlopin). The basement membrane, according to some authors, is not present everywhere. In certain areas, ependymocytes have characteristic structural and functional features; Such cells, in particular, include choroid ependymocytes and tanycytes.
Choroid ependymocytes- ependymocytes in the area of the choroid plexus where CSF is formed. They have a cubic shape and cover protrusions of the pia mater, protruding into the lumen of the ventricles of the brain (the roof of the III and IV ventricles, sections of the wall of the lateral ventricles). On their convex apical surface there are numerous microvilli, the lateral surfaces are connected by complexes of compounds, and the basal surfaces form protrusions (pedicles), which intertwine with each other, forming the basal labyrinth. The layer of ependymocytes is located on the basement membrane, separating it from the underlying loose connective tissue of the pia mater, which contains a network of fenestrated capillaries that are highly permeable due to numerous pores in the cytoplasm of the endothelial cells. Ependimopitis of the choroid plexus is part of the hematocerebrospinal fluid barrier (barrier between blood and CSF), through which ultrafiltration of blood occurs with the formation of CSF (about 500 ml/day).
Tanycytes- specialized ependymal cells in the lateral areas of the wall of the third ventricle, infundibular recess, and median eminence. They have a cubic or prismatic shape, their apical surface is covered with microvilli and individual cilia, and a long process extends from the basal surface, ending in a lamellar extension on the blood capillary. Tanycytes absorb substances from the CSF and transport them along their process into the lumen of blood vessels, thereby providing a connection between the CSF in the lumen of the ventricles of the brain and the blood.
Functions of ependymal glia:
neurocerebrospinal fluid (with high permeability),
hematocerebrospinal fluid
supporting (due to the basal processes);
formation of barriers:
ultrafiltration of CSF components
Oligodendroglia(from the Greek oligo few, dendron tree and glia glue, i.e. glia with a small number of processes) a large group of various small cells (oligodendrocytes) with short, few processes that surround the bodies of neurons, are part of nerve fibers and nerve endings. Found in the central nervous system (gray and white matter) and PNS; characterized by a dark nucleus, dense cytoplasm with a well-developed synthetic apparatus, high content of mitochondria, lysosomes and glycogen granules.
Satellite cells(mantle cells) envelop the cell bodies of neurons in the spinal, cranial and autonomic ganglia. They have a flattened shape, a small round or oval core. They provide a barrier function, regulate neuronal metabolism, and capture neurotransmitters.
Lemmocytes(Schwann cells) in the PNS and oligodendrocytes in the CNS participate in the formation of nerve fibers, isolating the processes of neurons. They have the ability to produce myelin sheath.
Microglia- a collection of small elongated stellate cells (microgliocytes) with dense cytoplasm and relatively short branching processes, located mainly along the capillaries in the central nervous system. Unlike macroglial cells, they are of mesenchymal origin, developing directly from monocytes (or perivascular macrophages of the brain) and belong to the macrophage-monopitary system. They are characterized by nuclei with a predominance of heterochrome! ina and high content of lysosomes in the cytoplasm.
The function of microglia is protective (including immune). Microglial cells are traditionally considered as specialized macrophages of the central nervous system - they have significant mobility, becoming activated and increasing in number during inflammatory and degenerative diseases of the nervous system, when they lose processes, become rounded and phagocytose the remains of dead cells. Activated microglial cells express MHC class I and II molecules and the CD4 receptor, perform the function of dendritic APCs in the central nervous system, and secrete a number of cytokines. These cells play a very important role in the development of nervous system lesions in AIDS. They are credited with the role of a “Trojan horse”, carrying (together with hematogenous monocytes and macrophages) HIV throughout the central nervous system. Increased activity of microglial cells, which release significant amounts of cytokines and toxic radicals, is also associated with increased death of neurons in AIDS by the mechanism of apoptosis, which is induced in them due to disruption of the normal balance of cytokines.
Aagaard P. Hyperactivation of myogenic satellite cells with blood flow restricted exercise // 8th International Conference on Strength Training, 2012 Oslo, Norway, Norwegian School of Sport Sciences. – P.29-32.
P. Aagaard
HYPERACTIVATION OF MYOGENIC SATELLITE CELLS USING STRENGTH EXERCISES WITH BLOOD FLOW LIMITATION
Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark
Introduction
Blood Flow Restriction Exercises (BFRE)
Strength training with blood flow restriction at low to moderate intensity (20–50% of maximum) using parallel blood flow restriction (hypoxic strength training) is of increasing interest in both scientific and applied fields (Manini & Clarck 2009, Wernbom et al. 2008). The growing popularity is due to the fact that skeletal muscle mass and maximal muscle strength can be increased to an equal or greater extent by hypoxic strength training (Wernbom et al., 2008) compared to conventional resistance training with heavy resistance (Aagaard et al., 2008). 2001). Additionally, hypoxic strength training appears to result in enhanced hypertrophic responses and strength gains compared with exercise applying identical load and volume without cutting off blood flow (Abe et al. 2006, Holm et al. 2008), although the potential for hypertrophic a role for low-intensity strength training may also exist in its own right (Mitchell et al. 2012). However, the specific mechanisms responsible for adaptive changes in skeletal muscle morphology during hypoxic strength training remain largely unknown. Myofiber protein synthesis is increased during intense sessions of hypoxic resistance training, together with dysregulated activity in the AKT/mTOR pathway (Fujita et al. 2007, Fry et al. 2010). In addition, decreases in the expression of proteolysis genes (FOXO3a, Atrogin, MuRF-1) and myostatin, a negative regulator of muscle mass, were observed after intense hypoxic strength training (Manini et al. 2011, Laurentino et al. 2012).
The structure and functions of muscles are described in more detail in my books “Hypertrophy of Human Skeletal Muscles” and “Muscle Biomechanics”
Myogenic satellite cells
Effect of hypoxic strength training on muscle contractile functions
During hypoxic strength training with low to moderate training loads, significant increases in maximal muscle strength (MVC) were observed despite relatively short training periods (4–6 weeks) (e.g. Takarada et al. 2002, Kubo et al. 2006; reviewed by Wernbom et al. al. 2008). In particular, the adaptive effects of hypoxic strength training on muscle contractile function (MVC and power) are comparable to those achieved with heavy resistance training for 12–16 weeks (Wernbom et al. 2008). However, the effects of hypoxic strength training on skeletal muscle's rapid twitch capacity (RFD) remain largely unexplored, a phenomenon that has only recently gained interest (Nielsen et al., 2012).
Effect of Hypoxic Strength Training on Muscle Fiber Size
Hypoxic strength training using high-intensity light resistance training has been shown to significantly increase muscle fiber volume and cross-sectional area (CSA) of the entire muscle (Abe et al. 2006, Ohta et al. 2003, Kubo et al. 2006, Takadara et al. 2002 ). In contrast, light resistance training without ischemia typically results in no benefit (Abe et al. 2006, Mackey et al. 2010) or a small increase in (<5%) (Holm et al. 2008) роста мышечного волокна , хотя это недавно было оспорено (Mitchell et al. 2012). При гипоксической силовой тренировке большой прирост в объеме мышечного волокна частично объясняется распространением миогенных клеток-сателлитов и формированием новых миоядер .
Effect of hypoxic strength training on myogenic satellite cells and the number of myonuclei
We recently examined the involvement of myogenic satellite cells in myonuclei enlargement in response to hypoxic strength training (Nielsen et al. 2012). Evidence of satellite cell proliferation and an increase in myonuclei number was found at 3 weeks after hypoxic resistance training, which was accompanied by a significant increase in muscle fiber volume (Nielsen et al. 2012). (Fig.1).
Rice. 1. Muscle fiber cross-sectional area (CSA) measured before and after 19 days of light resistance training (20% of maximum) with blood flow restriction (BFRE) and resistance training without blood flow restriction in type I muscle fibers (left) and muscle type II fibers<0.001, ** p<0.01, межгрупповая разница: p<0.05. Адаптировано из Nielsen et al., 2012.
The density and number of Pax-7+ satellite cells increased 1-2 times (i.e., 100-200%) after 19 days of hypoxic strength training (Fig. 2). This significantly exceeds the 20-40% increase in satellite cell numbers observed after several months of traditional strength training (Kadi et al. 2005, Olsen et al. 2006, Mackey et al. 2007). The number and density of satellite cells increased similarly in type I and II muscle fibers (Nielsen et al. 2012) (Fig. 2). While during conventional strength training with heavy weights, a greater response is observed in the satellite cells of type II muscle fibers compared to type I (Verdijk et al. 2009). In addition, hypoxic strength training significantly increased the number of myonuclei (+22-33%), while the myonuclear domain (muscle fiber volume/number of myonuclei) remained unchanged (~1800-2100 μm2), although slight even temporary, a decrease on the eighth day of training (Nielsen et al. 2012).
Consequences of muscle fiber growth
The increase in satellite cell activity induced by hypoxic strength training (Fig. 2) was accompanied by significant muscle fiber hypertrophy (+30-40%) in muscle fibers I and II from biopsies taken 3-10 days after training (Fig. 1) . In addition, hypoxic strength training caused significant increases in maximal voluntary muscle contraction (MVC ~10%) and RFD (16-21%) (Nielsen et al., ICST 2012).
Rice. 2 Myogenic satellite cell counts measured before and after 19 days of light resistance training (20% of maximum) with blood flow restriction (BFRE) and resistance training without blood flow restriction (CON) in type I muscle fibers (left) and muscle fibers Type II (right). Changes are significant: *p<0.001, † p<0.01, межгрупповая разница: p<0.05. Адаптировано из Nielsen et al., 2012.
After hypoxic strength training, an increase in the number of satellite cells has a positive effect on muscle fiber growth. There was a positive correlation between changes before and after training in the average cross-sectional area of the muscle fiber and the increase in the number of satellite cells and the number of myonuclei, respectively (r = 0.51-0.58, p<0.01).
No changes in the parameters listed above were found in the control group performing a similar type of training without blood flow restriction, except for a temporary increase in the size of type I+II muscle fibers after eight days of training.
Potential adaptive mechanisms
Muscle fiber CSA was found to increase in both fiber types after only eight days of hypoxic strength training (10 training sessions) and remained elevated on the third and tenth days post-training (Nielsen et al., 2012). Surprisingly, muscle CSA also increased transiently in control subjects performing nonocclusive training on day eight, but returned to baseline levels after 19 days of training. These observations suggest that the rapid initial change in muscle fiber CSA is dependent on factors other than accumulation of myofibrillar proteins, such as muscle fiber swelling.
Short-term swelling of muscle fibers can be caused by changes in sarcolemmal channels caused by hypoxia (Korthuis et al. 1985), opening of membrane channels that is caused by stretch (Singh & Dhalla 2010) or microfocal damage to the sarcolemma itself (Grembowicz et al. 1999). In contrast, the later increase in muscle fiber CSA observed after 19 days of hypoxic strength training (Fig. 1) is likely due to the accumulation of myofibrillar proteins, as muscle fiber CSA remained elevated 3-10 days after training along with a 7-11% maintained increase in maximal resistance training. voluntary muscle contraction (MVC) and RFD.
The specific pathways by which hypoxic strength training stimulates the effects of myogenic satellite cells remain unexplored. Hypothetically, a decrease in the amount of myostatin released after hypoxic resistance training (Manini et al. 2011, Laurentino et al. 2012) may play an important role, since myostatin is a potent inhibitor of myogenic satellite cell activation (McCroskery et al. 2003, McKay et al. 2012) by suppressing Pax-7 signaling (McFarlane et al. 2008). Administration of the insulin-like growth factor (IFR) variant compounds IFR-1Ea and IFR-1Eb (mechano-dependent growth factor) after hypoxic resistance training may also potentially play an important role, as they are known to be potent stimuli for satellite cell proliferation and differentiation (Hawke & Garry 2001, Boldrin et al. 2010). Mechanical stress applied to muscle fibers can trigger satellite cell activation through the release of nitric oxide (NO) and hepatocyte growth factor (HGR) (Tatsumi et al. 2006, Punch et al. 2009). Therefore, NO may also be an important factor for the hyperactivation of myogenic satellite cells observed during hypoxic strength training, as transient elevations in NO values may likely occur as a result of the ischemic conditions of hypoxic strength training.
For further discussion of potential signaling pathways that may activate myogenic satellite cells during hypoxic strength training, see the Wernborn conference presentation (ICST 2012).
Conclusion
Short-term strength exercise, performed with light resistance and partial blood flow restriction, appears to induce significant proliferation of myogenic satellite stem cells and results in myonuclei enlargement in human skeletal muscle, which contributes to the acceleration and significant degree of muscle fiber hypertrophy observed with this type of training. Molecular signals that cause increased activity of satellite cells during hypertrophic strength training can be: an increase in intramuscular production of insulin-like growth factor, as well as local NO values; as well as a decrease in the activity of myostatin and other regulatory factors.
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