Name: Human Physiology.
The first volume of the textbook, taking into account the latest advances in the field of normal physiology, outlines a brief history, subject and methods physiological research, as well as the physiology of excitable tissues, regulatory mechanisms physiological functions, physiology of the central nervous system, blood system, circulatory system, respiration. The second volume of the textbook, taking into account the latest advances in the field of normal physiology, covers issues of digestion, metabolism, thermoregulation, excretion and kidney function, as well as sexual behavior, reproduction and lactation; outlines the physiology of sensory systems and integrative brain activity.
PREFACE
Chapter 1. PHYSIOLOGY. SUBJECT AND METHODS. IMPORTANCE FOR MEDICINE. BRIEF HISTORY. - G. I. Kositsky, V. M. Pokrovsky, G. F. Korotko.
1.1. Physiology, its subject and role in the medical education system
1.2. Physiological research methods
1.3. Physiology of the whole organism
1.4. Organism and external environment. Adaptation
1.5. Brief history physiology
Chapter 2. EXCITABLE TISSUE
2.1. Physiology of excitable tissues. - V.I. Kobrin
2.1.1. Structure and basic properties of cell membranes and ion channels
2.1.2. Methods for studying excitable cells
2.1.3. Resting potential
2.1.4. Action potential
2.1.5. Action electric current on excitable tissues 48
2.2. Physiology of nervous tissue. - G. A. Kuraev
2.2.1. Structure and morphofunctional classification neurons
2.2.2. Receptors. Receptor and generator potentials
2.2.3. Afferent neurons, their functions
2.2.4. Interneurons, their role in formation neural networks
2.2.5. Efferent neurons
2.2.6. Neuroglia
2.2.7. Conducting stimulation along nerves
2.3. Physiology of synapses. - G. A. Kuraev
2.4. Physiology of muscle tissue
2.4.1. Skeletal muscles. - V.I. Kobrin
2.4.1.1. Classification of skeletal muscle fibers
2.4.1.2. Functions and properties of skeletal muscles
2.4.1.3. Mechanism of muscle contraction
2.4.1.4. Modes of muscle contraction
2.4.1.5. Muscle work and power
2.4.1.6. Energy of muscle contraction
2.4.1.7. Heat generation during muscle contraction
2.4.1.8. Musculoskeletal interaction
2.4.1.9. Assessment of the functional state of the human muscular system
2.4.2. Smooth muscles. - R. S. Orlov
2.4.2.1. Classification of smooth muscles
2.4.2.2. The structure of smooth muscles
2.4.2.3. Innervation of smooth muscles
2.4.2.4. Functions and properties of smooth muscles
2.5.1. Secretion
2.5.2. Multifunctionality of secretion
2.5.3. Secretory cycle
2.5.4. Biopotentials of glandulocytes
2.5.5. Regulation of glandulocyte secretion
Chapter 3. PRINCIPLES OF ORGANIZATION OF FUNCTION MANAGEMENT. - V. P. Degtyarev
3.1. Control in living organisms
3.2. Self-regulation of physiological functions
3.3. System organization management. Functional systems and their interaction
Chapter 4. NERVOUS REGULATION OF PHYSIOLOGICAL FUNCTIONS
4.1. Mechanisms of activity of the central nervous system. - O. G. Chorayan
4.1.1. Methods for studying the functions of the central nervous system
4.1.2. Reflex principle of regulation of functions
4.1.3. Inhibition in the central nervous system
4.1.4. Properties of nerve centers
4.1.5. Principles of integration and coordination in the activity of the central nervous system
4.1.6. Neuronal complexes and their role in the activity of the central nervous system
4.1.7. Blood-brain barrier and its functions
4.1.8. Cerebrospinal fluid
4.1.9. Elements of cybernetics of the nervous system
4.2. Physiology of the central nervous system. - G. A. Kuraev 134
4.2.1. Spinal cord
4.2.1.1. Morphofunctional organization spinal cord
4.2.1.2. Features of the neural organization of the spinal cord
4.2.1.3. Spinal cord pathways
4.2.1.4. Reflex functions of the spinal cord
4.2.2. Brain stem
4.2.2.1. Medulla oblongata
4.2.2.2. Bridge
4.2.2.3. Midbrain
4.2.2.4. Reticular formation of the brainstem
4.2.2.5. Diencephalon
4.2.2.5.1. Thalamus
4.2.2.6. Cerebellum
4.2.3. Limbic system
4.2.3.1. Hippocampus
4.2.3.2. Amygdala
4.2.3.3. Hypothalamus
4.2.4. Basal ganglia
4.2.4.1. Caudate nucleus. Shell
4.2.4.2. Pale ball
4.2.4.3. Fence
4.2.5. Cerebral cortex
4.2.5.1. Morphofunctional organization
4.2.5.2. Sensory areas
4.2.5.3. Motor areas
4.2.5.4. Associative areas
4.2.5.5. Electrical manifestations of cortical activity
4.2.5.6. Interhemispheric relationships
4.2.6. Coordination of movements. - V. S. Gurfinkel, Yu. S. Levik
4.3. Physiology of the autonomic (vegetative) nervous system. - A. D. Nozdrachev
4.3.1- Functional structure of the autonomic nervous system
4.3.1.1. The sympathetic part
4.3.1.2. Parasympathetic part
4.3.1.3. Metasympathetic part
4.3.2. Features of the design of the autonomic nervous system
4.3.3. Autonomic (vegetative) tone
4.3.4. Synaptic transmission of excitation in the autonomic nervous system
4.3.5- Influence of the autonomic nervous system on the functions of tissues and organs
Chapter 5. HORMONAL REGULATION OF PHYSIOLOGICAL FUNCTIONS. - V. A. Tachuk, O. E. Osadchiy
5.1. Principles of hormonal regulation
5.2. Endocrine glands
5.2.1. Research methods
5.2.2. Pituitary
5.2.3. Thyroid gland
5.2.4. Parathyroid glands
5.2.5. Adrenal glands
5.2.6. Pancreas
5.2.7. Gonads
5.3. Education, secretion and mechanisms of action of hormones 264
5.3.1. Regulation of hormone biosynthesis
5.3.2. Secretion and transport of hormones
5.3.3. Mechanisms of action of hormones on cells
Chapter 6. BLOOD. - B.I. Kuzink
6.1. Concept of the blood system
6.1.1. Basic functions of blood
6.1.2. Amount of blood in the body
6.1.3. Blood plasma composition
6.1.4. Physico-chemical properties blood
6.2. Formed elements of blood
6.2.1. Red blood cells
6.2.1.1. Hemoglobin and its compounds
6.2.1.2. Color index
6.2.1.3. Hemolysis
6.2.1.4. Functions of red blood cells
6.2.1.5. Erythron. Regulation of erythropoiesis
6.2.2. Leukocytes
6.2.2.1. Physiological leukocytosis. Leukopenia 292
6.2.2.2. Leukocyte formula
6.2.2.3. Characteristics of individual types of leukocytes
6.2.2.4. Regulation of leukopoiesis
6.2.2.5. Nonspecific resistance and immunity
6.2.3. Platelets
6.3. Blood groups
6.3.1. AVO system
6.3.2. Rhesus system (Rh-hr) and others
6.3.3. Blood groups and morbidity. Hemostasis system
6.4.1. Vascular-platelet hemostasis
6.4.2. Blood clotting process
6.4.2.1. Plasma and cellular coagulation factors
6.4.2.2. Blood clotting mechanism
6.4.3. Natural anticoagulants
6.4.4. Fibrniolysis
6.4.5. Regulation of blood coagulation and fibrinolysis
Chapter 7. BLOOD AND LYMPH CIRCULATION. - E. B. Babsky, G. I. Kositsky, V. M. Pokrovsky
7.1. Heart activity
7.1.1. Electrical phenomena in the heart, conducting excitation
7.1.1.1. Electrical activity of myocardial cells
7.1.1.2. Functions of the conduction system of the heart. . .
7.1.1.3. Refractory phase of the myocardium and extrasystole
7.1.1.4. Electrocardiogram
7.1.2. Pumping function of the heart
7.1.2.1. Phases of the cardiac cycle
7.1.2.2. Cardiac output
7.1.2.3. Mechanical and abnormal manifestations of cardiac activity
7.1.3. Regulation of heart activity
7.1.3.1. Intracardiac regulatory mechanisms
7.1.3.2. Extracardiac regulatory mechanisms. .
7.1.3.3. Interaction of intracardiac and extracardiac nervous regulatory mechanisms
7.1.3.4. Reflex regulation of heart activity
7.1.3.5. Conditioned reflex regulation of heart activity
7.1.3.6. Humoral regulation heart activity
7.1.4. Endocrine function of the heart
7.2. Functions of the vascular system
7.2.1. Basic principles of hemodynamics. Classification of vessels
7.2.2. Movement of blood through vessels
7.2.2.1. Blood pressure
7.2.2.2. Arterial pulse
7.2.2.3. Volumetric blood flow velocity
7-2.2.4. Movement of blood in capillaries. Microcirculation
7.2.2.5. Movement of blood in veins
7.2.2.6. Blood circulation time
7.2.3. Regulation of blood movement through vessels
7.2.3.1. Innervation of blood vessels
7.2.3.2. Vasomotor center
7.2.3.3. Reflex regulation of vascular tone
7.2.3.4. Humoral influences on blood vessels
7.2.3.5. Local mechanisms of blood circulation regulation
7.2.3.6. Regulation of circulating blood volume.
7.2.3.7. Blood depots
7.2.4. Regional blood circulation. - Y. A. Khananashvili 390
7.2.4.1. Cerebral circulation
7.2.4.2. Coronary circulation
7.2.4.3. Pulmonary circulation
7.3. Lymph circulation. - R. S. Orlov
7.3.1. Structure of the lymphatic system
7.3.2. Lymph formation
7.3.3. Composition of lymph
7.3.4. Lymph movement
7.3.5. Functions of the lymphatic system
Chapter 8. BREATHING. - V. CD. Pyatin
8.1. The essence and stages of breathing
8.2. External breathing
8.2.1. Biomechanics of respiratory movements
8.3. Pulmonary ventilation
8.3.1. Lung volumes and capacities
8.3.2. Alveolar ventilation
8.4. Mechanics of breathing
8.4.1. Lung compliance
8.4.2. Airway resistance
8.4.3. Work of breathing
8.5. Gas exchange and gas transport
8.5.1. Diffusion of gases through the airborne barrier. . 415
8.5.2. Content of gases in alveolar air
8.5.3. Gas exchange and O2 transport
8.5.4. Gas exchange and CO2 transport
8.6. Regulation of external respiration
8.6.1. Respiratory center
8.6.2. Reflex regulation of breathing
8.6.3. Coordination of breathing with other body functions
8.7. Peculiarities of breathing during physical exertion and with altered partial pressure of O2
8.7.1. Breathing during physical exertion
8.7.2. Breathing when climbing to altitude
8.7.3. Breathing at high blood pressure
8.7.4. Breathing pure O2
8.8. Dyspnea and pathological types of breathing
8.9. Non-respiratory functions of the lungs. - E. A. Maligonov, A. G. Pokhotko
8.9.1. Protective functions respiratory system
8.9.2. Metabolism of biologically active substances in the lungs
Chapter 9. DIGESTION. G. F. Korotko
9.1. Physiological basis of hunger and satiety
9.2. The essence of digestion. Conveyor principle of organizing digestion
9.2.1. Digestion and its importance
9.2.2. Types of digestion
9.2.3. Conveyor principle of organizing digestion
9.3. Digestive functions digestive tract
9.3.1. Secretion of the digestive glands
9.3.2. Motor function of the digestive tract
9.3.3. Suction
9.3.4. Study methods digestive functions
9.3.4.1. Experimental methods
9.3.4.2. Study of digestive functions in humans?
9.3.5. Regulation of digestive functions
9.3.5.1. Systemic mechanisms for controlling digestive activity. Reflex mechanisms
9.3.5.2. The role of regulatory peptides in the activity of the digestive tract
9.3.5.3. Blood supply and functional activity of the digestive tract
9.3.5.4. Periodic activity of the digestive organs
9.4. Oral digestion and swallowing
9.4.1. Eating
9.4.2. Chewing
9.4.3. Salivation
9.4.4. Swallowing
9.5. Digestion in the stomach
9.5.1. Secretory function of the stomach
9.5.2. Motor function of the stomach
9.5.3. Evacuation of stomach contents into the duodenum
9.5.4. Vomit
9.6. Digestion in the small intestine
9.6.1. Pancreatic secretion
9.6.2. Bile secretion and bile secretion
9.6.3. Intestinal secretion
9.6.4. Cavity and parietal digestion in the small intestine
9.6.5. Motor function of the small intestine
9.6.6. Absorption of various substances in the small intestine
9.7. Functions of the colon
9.7.1. Entry of intestinal chyme into the large intestine
9.7.2. The role of the colon in digestion
9.7.3. Motor function of the colon
9.7.4. Defecation
9.8. Microflora of the digestive tract
9.9. Liver functions
9.10. Non-digestive functions of the digestive tract 87
9.10.1. Excretory activity of the digestive tract
9.10.2. Participation of the digestive tract in water-salt metabolism
9.10.3. Endocrine function of the digestive tract and the release of biologically active substances in secretions
9.10.4. Increment (endosecretion) of enzymes by the digestive glands
9.10.5. Immune system digestive tract
Chapter 10. METABOLISM AND ENERGY. NUTRITION. E. B. Babsky V. M. Pokrovsky
10.1. Metabolism
10.1.1. Protein metabolism
10.1.2. Lipid metabolism
10.1.3. Carbohydrate metabolism
10.1.4. Exchange mineral salts and water
10.1.5. Vitamins
10.2. Energy conversion and general metabolism
10.2.1. Methods for studying energy exchange
10.2.1.1. Direct calorimetry
10.2.1.2. Indirect calorimetry
10.2.1.3. Gross Exchange Study
10.2.3. BX
10.2.4. Surface rule
10.2.5. Energy exchange during physical labor
10.2.6. Energy exchange during mental work
10.2.7. Specific dynamic action of food
10.2.8. Regulation of energy metabolism
10.3. Nutrition. G. F. Korotko
10.3.1. Nutrients
10.3.2. Theoretical foundations of nutrition
10.3.3. Nutrition standards
Chapter 11. THERMOREGULATION. E. B. Babsky, V. M. Pokrovsky
11.1. Body temperature and isothermia
11.2. Chemical thermoregulation
11.3. Physical thermoregulation
11.4. Isotherm regulation
11.5. Hypothermia and hyperthermia
Chapter 12. ALLOCATION. KIDNEY PHYSIOLOGY. Yu. V. Natochin.
12.1. Selection
12.2. Kidneys and their functions
12.2.1. Methods for studying kidney function
12.2.2. Nephron and its blood supply
12.2.3. The process of urine formation
12.2.3.1. Glomerular filtration
12.2.3.2. Kayalceous reabsorption
12.2.3.3. Kayal secretion
12.2.4. Determination of the magnitude of renal plasma and blood flow
12.2.5. Synthesis of substances in the kidneys
12.2.6. Osmotic dilution and concentration of urine
12.2.7. Homeostatic functions of the kidneys
12.2.8. Excretory function of the kidneys
12.2.9. Endocrine function of the kidneys
12.2.10. Metabolic kidney function
12.2.11. Principles of regulation of reabsorption and secretion of substances in renal tubular cells
12.2.12. Regulation of kidney activity
12.2.13. Quantity, composition and properties of urine
12.2.14. Urination
12.2.15. Consequences of kidney removal and artificial kidney
12.2.16. Age-related features of the structure and function of the kidneys
Chapter 13. SEXUAL BEHAVIOR. REPRODUCTIVE FUNCTION. LACTATION. Yu. I. Savchenkov, V. I. Kobrin
13.1. Sexual development
13.2. Puberty
13.3. Sexual behavior
13.4. Physiology of sexual intercourse
13.5. Pregnancy and maternal relations
13.6. Childbirth
13.7. Major changes in the body of a newborn
13.8. Lactation
Chapter 14. SENSORY SYSTEMS. M. A. Ostrovsky, I. A. Shevelev
14.1. General physiology sensory systems
14.1.1. Methods for studying sensory systems
4.2. General principles of the structure of sensory systems
14.1.3. Basic functions of the sensor system
14.1.4. Mechanisms of information processing in the sensory system
14.1.5. Adaptation of the sensory system
14.1.6. Interaction of sensory systems
14.2. Particular physiology of sensory systems
14.2.1. Visual system
14.2.2. Auditory system
14.2.3. Vestibular system
14.2.4. Somatosensory system
14.2.5. Olfactory system
14.2.6. Taste system
14.2.7. Visceral system
Chapter 15. INTEGRATIVE ACTIVITY OF THE HUMAN BRAIN. O. G. Chorayan
15.1. Conditioned reflex basis of higher nervous activity
15.1.1. Conditioned reflex. Education mechanism
15.1.2. Methods for studying conditioned reflexes
15.1.3. Stages of formation of a conditioned reflex
15.1.4. Types of conditioned reflexes
15.1.5. Inhibition of conditioned reflexes
15.1.6. Dynamics of basic nervous processes
15.1.7. Types of higher nervous activity
15.2. Physiological mechanisms of memory
15.3. Emotions
15.4. Sleep and hypnosis. V. I. Kobrin
15.4.1. Dream
15.4.2. Hypnosis
15.5. Basics of psychophysiology
15.5.1. Neurophysiological foundations of mental activity
15.5.2. Psychophysiology of the decision-making process. . 292
15.5.3. Consciousness
15.5.4. Thinking
15.6. Second signaling system
15.7. The principle of probability and “fuzziness” in the higher integrative functions of the brain
15.8. Interhemispheric asymmetry
15.9. Influence motor activity on the functional state of a person. E. K. Aganyats
15.9.1. General physiological mechanisms of the influence of physical activity on metabolism
15.9.2. Autonomic support of motor activity 314
15.9.3. The influence of physical activity on the regulatory mechanisms of the central nervous system and hormonal link
15.9.4. The influence of physical activity on the functions of the neuromuscular system
15.9.5. Physiological significance of fitness
15.10. Fundamentals of the physiology of mental and physical labor. E. K. Aganyants
15.10.1. Physiological characteristics mental labor
15.10.2. Physiological characteristics of physical labor
15.10.3. The relationship between mental and physical labor
15.11. Fundamentals of chronophysiology. G. F. Korotko, N. A. Agad-zhanyan
15.11.1. Classification biological rhythms
15.11.2. Circadian rhythms in humans
15.11.3. Ultradian rhythms in humans
11/15/4. Infradian rhythms in humans
15.11.5. Biological clock
11/15/6. Pacemakers of mammalian biological rhythms
Basic quantitative physiological indicators of the body
List of recommended literature.
ORGANISM AND EXTERNAL ENVIRONMENT. ADAPTATION.
A complete organism is inextricably linked with its external environment, and therefore, as I.M. Sechenov wrote, the scientific definition of an organism should also include the environment that influences it. The physiology of the whole organism studies not only the internal mechanisms of self-regulation physiological processes, but also mechanisms that ensure continuous interaction and inextricable unity of the body with environment. An indispensable condition and manifestation of such unity is the adaptation of the body to these conditions. However, the concept of adaptation also has a broader meaning and significance.
Adaptation (from the Latin adaptatio - adaptation) - all types of congenital and acquired adaptive activities that are provided on the basis of physiological processes occurring at the cellular, organ, systemic and organismal levels. This term is used to describe wide range adaptive processes: from adaptive protein synthesis in the cell and adaptation of receptors to a long-acting stimulus to human social adaptation and the adaptation of peoples to certain climatic conditions. At the level of the human body, adaptation is understood as its adaptation to constantly changing conditions of existence.
The human body is adapted to adequate environmental conditions as a result of long-term evolution and ontogenesis, the creation and improvement of their adaptive mechanisms (adaptogenesis) in response to pronounced and fairly long-term changes in the environment. The body is fully adapted to some environmental factors, partially adapted to others, and cannot adapt to others due to their extreme nature. Under these conditions, a person dies without special means life support (for example, in space without a spacesuit outside a spacecraft). A person can adapt to less severe—subextreme—influences, but prolonged exposure of a person to subextreme conditions leads to overstrain of adaptation mechanisms, illness, and sometimes death.
n1.doc
Human physiology
Edited by V.M. Pokrovsky, G.F. Korotko
Chapter 1. EXCITABLE TISSUE
PHYSIOLOGY OF NERVOUS TISSUE
Conducting stimulation along nerves
The main function of axons is to conduct impulses arising in a neuron. Axons may be covered with a myelin sheath (myelinated fibers) or lack it (unmyelinated fibers). Myelinated fibers are more common in motor nerves, while non-myelinated fibers predominate in the autonomic (autonomic) nervous system.
An individual myelinated nerve fiber consists of an axial cylinder covered by a myelin sheath formed by Schwann cells. The axial cylinder has a membrane and axoplasm. The myelin sheath is a product of the activity of the Schwann cell and consists of 80% lipids with high ohmic resistance and 20% protein.
The myelin sheath does not cover the axial cylinder with a continuous cover, but is interrupted, leaving open areas of the axial cylinder, called nodes of Ranvier. The length of the sections between these interceptions is different and depends on the thickness of the nerve fiber: the thicker it is, the longer the distance between the interceptions
Unmyelinated nerve fibers are covered only by the Schwann sheath.
The conduction of excitation in unmyelinated fibers differs from that in myelinated fibers due to the different structure of the membranes. In unmyelinated fibers, excitation gradually covers adjacent sections of the membrane of the axial cylinder and thus spreads to the end of the axon. The speed of excitation propagation along the fiber is determined by its diameter.
In nerve fibers without myelin, where metabolic processes do not provide rapid compensation for energy expenditure on excitation, the spread of this excitation occurs with a gradual weakening - with decrement. Decremental conduction of excitation is characteristic of a low-organized nervous system.
In higher animals, thanks primarily to the presence of the myelin sheath and the perfection of metabolism in the nerve fiber, excitation passes without fading, without decrement. This is facilitated by the presence of fiber throughout the membrane equal charge and its rapid recovery after the passage of excitation.
In myelinated fibers, excitation covers only areas of nodal interceptions, that is, it bypasses areas covered with myelin. This conduction of excitation along the fiber is called saltatory (saccade-like). In the nodes, the number of sodium channels reaches 12,000 per 1 µm, which is significantly more than in any other part of the fiber. As a result, the nodal interceptions are the most excitable and provide a greater speed of excitation. The conduction time of excitation along the myelin fiber is inversely proportional to the length between interceptions.
The conduction of excitation along the nerve fiber is not disrupted for a long time (many hours). This indicates low fatigue of the nerve fiber. It is believed that the nerve fiber is relatively tireless due to the fact that the processes of energy resynthesis in it proceed at a sufficiently high speed and manage to restore the energy expenditure that occurs during the passage of excitation.
At the moment of excitation, the energy of the nerve fiber is spent on the operation of the sodium-potassium pump. Particularly large amounts of energy are wasted at the nodes of Ranvier due to the high density of sodium-potassium channels here.
J. Erlanger and H. Gasser (1937) were the first to classify nerve fibers based on the speed of excitation. A different speed of excitation along the fibers of the mixed nerve occurs when using an extracellular electrode. The potentials of fibers conducting excitation at different speeds are recorded separately (Fig. 2.18).
Depending on the speed of excitation, nerve fibers are divided into three types: A, B, C. In turn, type A fibers are divided into four groups: A?, A?, A?, A?. The highest conduction speed (up to 120 m/s) is possessed by fibers of group A?, which consists of fibers with a diameter of 12-22 microns. Other fibers have a smaller diameter and, accordingly, excitation through them occurs at a lower speed (Table 2.4).
The nerve trunk is formed a large number fibers, however, the excitation going along each of them is not transmitted to the neighboring ones. This feature of the conduction of excitation along a nerve is called the law of isolated conduction of excitation along a separate nerve fiber. The possibility of such conduct is of great physiological importance, since it ensures, for example, the isolation of the contraction of each neuromotor unit.
The ability of a nerve fiber to conduct excitation in isolation is due to the presence of membranes, as well as the fact that the resistance of the fluid filling the interfiber spaces is significantly lower than the resistance of the fiber membrane. Therefore, the current, leaving the excited fiber, is shunted in the liquid and turns out to be weak for exciting neighboring fibers. A necessary condition for the conduction of excitation in a nerve is not just its anatomical continuity, but also its physiological integrity. In any metal conductor, electric current will flow as long as the conductor maintains physical continuity. For a nerve “conductor” this condition is not enough: the nerve fiber must also maintain physiological integrity. If the properties of the fiber membrane are violated (ligation, blockade with novocaine, ammonia, etc.), the conduction of excitation along the fiber stops. Another property characteristic of the conduction of excitation along a nerve fiber is the ability for bilateral conduction. Applying stimulation between two output electrodes on the surface of a fiber will induce electrical potentials beneath each electrode.
PHYSIOLOGY OF SYNAPSES
Synapses are the contacts that establish neurons as independent entities. The synapse is a complex structure and consists of a presynaptic part (the end of the axon that transmits the signal), a synaptic cleft and a postsynaptic part (the structure of the receiving cell).
Classification of synapses. Synapses are classified by location, nature of action, and method of signal transmission.
Based on location, neuromuscular synapses and neuroneuronal synapses are distinguished, the latter in turn divided into axosomatic, axoaxonal, axodendritic, and dendrosomatic.
According to the nature of the effect on the perceptive structure, synapses can be excitatory or inhibitory.
According to the method of signal transmission, synapses are divided into electrical, chemical, and mixed.
The nature of the interaction of neurons. It is determined by the method of this interaction: distant, adjacent, contact.
Distant interaction can be ensured by two neurons located in different structures of the body. For example, in the cells of a number of brain structures, neurohormones and neuropeptides are formed, which are able to have a humoral effect on neurons of other parts.
Adjacent interaction between neurons occurs when the membranes of neurons are separated only by intercellular space. Typically, such interaction occurs where there are no glial cells between the membranes of neurons. Such contiguity is characteristic of axons of the olfactory nerve, parallel fibers of the cerebellum, etc. It is believed that contiguous interaction ensures the participation of neighboring neurons in the performance of a single function. This occurs, in particular, because metabolites, products of neuron activity, entering the intercellular space, affect neighboring neurons. Adjacent interaction can, in some cases, ensure the transfer of electrical information from neuron to neuron.
Contact interaction is caused by specific contacts of neuron membranes, which form so-called electrical and chemical synapses.
Electrical synapses. Morphologically they represent a fusion, or convergence, of membrane sections. In the latter case, the synaptic cleft is not continuous, but is interrupted by full contact bridges. These bridges form a repeating cellular structure of the synapse, with the cells limited by areas of adjacent membranes, the distance between which in mammalian synapses is 0.15-0.20 nm. At membrane fusion sites there are channels through which cells can exchange certain products. In addition to the described cellular synapses, among the electrical synapses there are others - in the form of a continuous gap; the area of each of them reaches 1000 μm, as, for example, between the neurons of the ciliary ganglion.
Electrical synapses have one-way conduction of excitation. This is easy to prove by recording the electrical potential at the synapse: when the afferent pathways are stimulated, the synapse membrane is depolarized, and when the efferent fibers are stimulated, it hyperpolarizes. It turned out that the synapses of neurons with same function have bilateral conduction of excitation (for example, synapses between two sensitive cells), and synapses between differently functional neurons (sensory and motor) have unilateral conduction. The functions of electrical synapses are primarily to ensure urgent reactions of the body. This apparently explains their location in animals in structures that provide the reaction of flight, salvation from danger, etc.
The electrical synapse is relatively less fatigued and is resistant to changes in the external and internal environment. Apparently, these qualities, along with speed, ensure high reliability of its operation.
Chemical synapses. Structurally represented by the presynaptic part, the synaptic cleft and the postsynaptic part. The presynaptic part of the chemical synapse is formed by the expansion of the axon along its course or termination (Fig. 2.19). The presynaptic part contains agranular and granular vesicles. Bubbles (quanta) contain a mediator. In the presynaptic expansion there are mitochondria that provide the synthesis of the transmitter, glycogen granules, etc. With repeated stimulation of the presynaptic ending, the reserves of the transmitter in the synaptic vesicles are depleted. It is believed that small granular vesicles contain norepinephrine, large ones contain other catecholamines. Agranular vesicles contain acetylcholine. Derivatives of glutamic and aspartic acids can also be excitation mediators.
Synaptic contacts can be between axon and dendrite (axodendritic), axon and cell soma (axosomatic), axons (axoaxonal), dendrites (dendrodendritic), dendrites and cell soma.
The effect of the mediator on the postsynaptic membrane is to increase its permeability to Na+ ions. The emergence of a flow of Na+ ions from the synaptic cleft through the postsynaptic membrane leads to its depolarization and causes the generation of an excitatory postsynaptic potential (EPSP) (see Fig. 2.19).
Synapses with a chemical method of excitation transmission are characterized by a synaptic delay in the conduction of excitation, lasting about 0.5 ms, and the development of a postsynaptic potential (PSP) in response to a presynaptic impulse. This potential, upon excitation, manifests itself in the depolarization of the postsynaptic membrane, and upon inhibition, in its hyperpolarization, resulting in the development of an inhibitory postsynaptic potential (IPSP). When excited, the conductivity of the postsynaptic membrane increases.
EPSP occurs in neurons under the action of acetylcholine, norepinephrine, dopamine, serotonin, glutamic acid, and substance P at the synapses.
IPSP occurs when glycine and gamma-aminobutyric acid act in synapses. IPSP can also develop under the influence of mediators that cause EPSP, but in these cases the mediator causes the postsynaptic membrane to transition to a state of hyperpolarization.
For the propagation of excitation through a chemical synapse, it is important that the nerve impulse traveling along the presynaptic part is completely extinguished in the synaptic cleft. However, the nerve impulse causes physiological changes in the presynaptic part of the membrane. As a result, synaptic vesicles accumulate at its surface, releasing the transmitter into the synaptic cleft.
The transition of the transmitter into the synaptic cleft is carried out by exocytosis: the vesicle with the transmitter comes into contact and merges with the presynaptic membrane, then the exit to the synaptic cleft opens and the transmitter enters it. At rest, the transmitter enters the synaptic cleft constantly, but in small quantities. Under the influence of the incoming excitement, the amount of mediator increases sharply. Then the transmitter moves to the postsynaptic membrane, acts on its specific receptors and forms a transmitter-receptor complex on the membrane. This complex changes the permeability of the membrane to K+ and Na+ ions, as a result of which its resting potential changes.
Depending on the nature of the transmitter, the resting potential of the membrane can decrease (depolarization), which is typical for excitation, or increase (hyperpolarization), which is typical for inhibition. The magnitude of the EPSP depends on the amount of released transmitter and can be 0.12-5.0 mV. Under the influence of EPSP, the areas of the membrane adjacent to the synapse are depolarized, then the depolarization reaches the axon hillock of the neuron, where excitation occurs, spreading to the axon.
In inhibitory synapses, this process develops as follows: the axon terminal of the synapse is depolarized, which leads to the appearance of weak electrical currents, causing the mobilization and release of a specific inhibitory transmitter into the synaptic cleft. It changes the ionic permeability of the postsynaptic membrane in such a way that pores with a diameter of about 0.5 nm open in it. These pores do not allow Na+ ions to pass through (which would cause depolarization of the membrane), but allow K+ ions to pass out of the cell, resulting in hyperpolarization of the postsynaptic membrane.
This change in membrane potential causes the development of IPSP. Its appearance is associated with the release of a specific transmitter into the synaptic cleft. In different synapses nerve structures The role of inhibitory mediator can be performed by various substances. In the ganglia of mollusks, the role of an inhibitory transmitter is played by acetylcholine, in the central nervous system of higher animals - gamma-aminobutyric acid, glycine.
Neuromuscular synapses ensure the conduction of excitation from the nerve fiber to the muscle fiber thanks to the mediator acetylcholine, which, when the nerve ending is excited, passes into the synaptic cleft and acts on the end plate of the muscle fiber. Therefore, like the interneuron synapse, the neuromuscular synapse has a presynaptic part belonging to the nerve ending, a synaptic cleft, and a postsynaptic part (end plate) belonging to the muscle fiber.
Acetylcholine is formed and accumulates in the form of vesicles in the presynaptic terminal. When excited by an electrical impulse traveling along the axon, the presynaptic part of the synapse becomes permeable to acetylcholine.
This permeability is possible due to the fact that as a result of depolarization of the presynaptic membrane, its calcium channels open. The Ca2+ ion enters the presynaptic part of the synapse from the synaptic cleft. Acetylcholine is released and enters the synaptic cleft. Here it interacts with its receptors on the postsynaptic membrane belonging to the muscle fiber. The receptors, when excited, open a protein channel embedded in the lipid layer of the membrane. Na+ ions penetrate into the muscle cell through the open channel, which leads to depolarization of the muscle cell membrane, resulting in the development of the so-called end plate potential (EPP). It causes the generation of an action potential in the muscle fiber.
The neuromuscular synapse transmits excitation in one direction: from the nerve ending to the postsynaptic membrane of the muscle fiber, which is due to the presence of a chemical link in the mechanism of neuromuscular transmission.
The speed of excitation through the synapse is much less than along the nerve fiber, since time is spent here on the activation of the presynaptic membrane, the passage of calcium through it, the release of acetylcholine into the synaptic cleft, the depolarization of the postsynaptic membrane, and the development of PPP.
Synaptic transmission of excitation has a number of properties:
1) the presence of a mediator in the presynaptic part of the synapse;
2) relative transmitter specificity of the synapse, i.e., each synapse has its own dominant transmitter;
3) transition of the postsynaptic membrane under the influence of mediators into a state of de- or hyperpolarization;
4) the possibility of action of specific blocking agents on the receptor structures of the postsynaptic membrane;
5) an increase in the duration of the postsynaptic membrane potential when the action of enzymes that destroy the synaptic transmitter is suppressed;
6) development of PSP in the postsynaptic membrane from miniature potentials caused by quanta of the transmitter;
7) dependence of the duration of the active phase of the action of the mediator in the synapse on the properties of the mediator;
8) one-sided conduction of excitation;
9) the presence of chemosensitive receptor-controlled channels of the postsynaptic membrane;
10) an increase in the release of transmitter quanta into the synaptic cleft is proportional to the frequency of impulses arriving along the axon;
11) the dependence of the increase in the efficiency of synaptic transmission on the frequency of synapse use (“training effect”);
12) fatigue of the synapse, which develops as a result of prolonged high-frequency stimulation. In this case, fatigue may be caused by exhaustion and untimely synthesis of the transmitter in the presynaptic part of the synapse or by deep, persistent depolarization of the postsynaptic membrane (pessimal inhibition).
The properties listed apply to chemical synapses. Electrical synapses have some features, namely: a short delay in the conduction of excitation; the occurrence of depolarization in both the pre- and postsynaptic parts of the synapse; the presence of a larger area of the synaptic cleft in an electrical synapse than in a chemical one.
Synaptic mediators are substances that have specific inactivators. For example, acetylcholine is inactivated by acetylcholinesterase, norepinephrine - by monoamine oxidase, catecholomethyltransferase.
Unused transmitter and its fragments are absorbed back into the presynaptic part of the synapse.
A number of chemicals in the blood and postsynaptic membrane change the state of the synapse, making it inactive. Thus, prostaglandins inhibit the secretion of transmitters at the synapse. Other substances, called chemoreceptor channel blockers, stop transmission at synapses. For example, botulinum toxin and manganese block the secretion of the transmitter at the neuromuscular synapse and at the inhibitory synapses of the central nervous system. Tubocurarine, atropine, strychnine, penicillin, picrotoxin, etc. block receptors in the synapse, as a result of which the transmitter, once in the synaptic cleft, does not find its receptor.
At the same time, substances are isolated that block systems that destroy mediators. These include eserine and organophosphorus compounds.
At the neuromuscular synapse, acetylcholine normally acts on the synaptic membrane short time(1-2 ms), as it immediately begins to be destroyed by acetylcholinesterase. In cases where this does not happen and acetylcholine is not destroyed within hundreds of milliseconds, its effect on the membrane stops and the membrane does not depolarize, but hyperpolarizes and excitation through this synapse is blocked.
Blockade of neuromuscular transmission can be caused by the following methods:
1) the effect of local anesthetic substances that block excitation in the presynaptic part;
2) blockade of transmitter release in the presynaptic part (for example, botulinum toxin);
3) disruption of mediator synthesis, for example under the action of hemicholinium;
4) blockade of acetylcholine receptors, for example under the action of bungarotoxin;
5) displacement of acetylcholine from receptors, for example, the effect of curare;
6) inactivation of the postsynaptic membrane with succinylcholine, decamethonium, etc.;
7) inhibition of cholinesterase, which leads to long-term preservation of acetylcholine and causes deep depolarization and inactivation of synaptic receptors. This effect is observed under the action of organophosphorus compounds.
Especially to reduce muscle tone, especially during operations, blockade of neuromuscular transmission with muscle relaxants is used; depolarizing muscle relaxants act on the receptors of the subsynaptic membrane (succinylcholine, etc.), non-depolarizing muscle relaxants that eliminate the effect of acetylcholine on the membrane by competition (drugs of the curare group).
PHYSIOLOGY OF MUSCLE TISSUE
Moving the body in space, maintaining a certain posture, the work of the heart and blood vessels and the digestive tract in humans and vertebrates is carried out by muscles of two main types: striated (skeletal, cardiac) and smooth, which differ from each other in cellular and tissue organization, innervation and in a certain way. degree of functioning mechanisms. At the same time, there are many similarities in the molecular mechanisms of muscle contraction between these types of muscles.
Skeletal muscles
Classification of skeletal muscle fibers
The skeletal muscles of humans and vertebrates consist of several types of muscle fibers that differ from each other in structural and functional characteristics. Currently, there are four main types of muscle fibers.
Slow phasic fibers of oxidative type. Fibers of this type are characterized by a high content of myoglobin protein, which is capable of binding O2 (close in its properties to hemoglobin). Muscles that are predominantly composed of this type of fiber are called red muscles because of their dark red color. They perform very important function maintaining the posture of humans and animals. Ultimate fiber fatigue of this type and, therefore, muscle contraction occurs very slowly, which is due to the presence of myoglobin and large number mitochondria. Recovery of function after fatigue occurs quickly. The neuromotor units of these muscles consist of a large number of muscle fibers.
Fast phasic fibers of oxidative type. Muscles that are predominantly composed of this type of fiber perform rapid contractions without noticeable fatigue, which is explained by the large number of mitochondria in these fibers and the ability to generate ATP through oxidative phosphorylation. As a rule, the number of fibers that make up the neuromotor unit in these muscles is less than in the previous group. The main purpose of this type of muscle fiber is to perform fast, energetic movements.
Fast phasic fibers with a glycolytic type of oxidation. Fibers of this type are characterized by the fact that ATP is formed in them due to glycolysis. The fibers of this group contain fewer mitochondria than the fibers of the previous group. Muscles containing these fibers develop fast and strong contractions, but fatigue relatively quickly. Myoglobin is absent in this group of muscle fibers, as a result of which muscles consisting of fibers of this type are called white.
Muscle fibers of all of these groups are characterized by the presence of one, or at least several end plates formed by one motor axon.
Tonic fibers. Unlike previous muscle fibers, in tonic fibers the motor axon forms many synaptic contacts with the muscle fiber membrane. The development of contraction occurs slowly, which is due to the low activity of myosin ATPase. Relaxation also occurs slowly. Muscle fibers of this type work effectively in isometric mode. These muscle fibers do not generate action potentials and do not obey the all-or-none law. A single presynaptic impulse causes a small contraction. A series of impulses will cause summation of the postsynaptic potential and a smoothly increasing depolarization of the muscle fiber. In humans, muscle fibers of this type are part of the external muscles of the eye.
There is a close relationship between the structure and function of muscle fibers. It has been shown that fast phasic fibers have a highly developed sarcoplasmic reticulum and an extensive T-system network, while slow fibers have a less developed sarcoplasmic reticulum and T-system network. In addition, there is a difference in the activity of calcium pumps in the sarcoplasmic reticulum: it is much higher in fast-twitch fibers, which allows these muscle fibers to relax quickly. Most human skeletal muscles consist of muscle fibers of various types, with a predominance of one type depending on the functions that a particular muscle performs.
Muscle fibers are not the functional unit of skeletal muscle. This role is performed by a neuromotor, or motor, unit, which includes a motor neuron and a group of muscle fibers innervated by the axon branches of this motor neuron located in the central nervous system. The number of muscle fibers that make up a motor unit varies (Table 2.5) and depends on the function performed by the muscle as a whole.
In the muscles that provide the most precise and rapid movements, the motor unit consists of several muscle fibers, while in the muscles involved in maintaining posture, the motor units include several hundred and even thousands of muscle fibers.
The resting potential of muscle fibers is approximately 90 mV, the action potential is 120-130 mV. The duration of the action potential is 1-3 ms, the value of the critical potential is 50 mV.
Skeletal muscles
Functions and properties of skeletal muscles
Skeletal muscles are integral part human musculoskeletal system. In this case, the muscles perform the following functions:
1) provide a certain posture of the human body;
2) move the body in space;
3) move individual parts of the body relative to each other;
4) are a source of heat, performing a thermoregulatory function.
In this chapter we will consider the functional properties of muscles associated with the participation of the musculoskeletal system. Skeletal muscle has the following essential properties:
1) excitability - the ability to respond to a stimulus by changing ionic conductivity and membrane potential. Under natural conditions, this stimulus is the neurotransmitter acetylcholine, which is released in the presynaptic endings of the axons of motor neurons. IN laboratory conditions often
Electrical muscle stimulation is used. With electrical stimulation of the muscle, nerve fibers are initially excited, which release acetylcholine, i.e. in this case indirect irritation of the muscle is observed. This is due to the fact that the excitability of nerve fibers is higher than muscle fibers. For direct muscle irritation, it is necessary to use muscle relaxants - substances that block the transmission of nerve impulse through the neuromuscular junction;
2) conductivity - the ability to conduct an action potential along and deep into the muscle fiber along the T-system;
3) contractility - the ability to shorten or develop tension when excited;
4) elasticity - the ability to develop tension when stretched.
Series: Educational literature for medical students
Mechanism of muscle contraction
Skeletal muscle is a complex system that converts chemical energy into mechanical work and heat. Currently, the molecular mechanisms of this transformation are well studied.
Structural organization of muscle fiber. Muscle fiber is a multinuclear structure surrounded by a membrane and containing a specialized contractile apparatus - myofibrils. In addition, the most important components of muscle fiber are mitochondria, a system of longitudinal tubes - the sarcoplasmic reticulum (reticulum) and a system of transverse tubes - the T-system. The functional unit of the contractile apparatus of a muscle cell is the sarcomere (Fig. 2.20, A); The myofibril consists of sarcomeres. Sarcomeres are separated from each other by Z-plates. Sarcomeres in the myofibril are arranged sequentially, so contraction of the sarcomeres causes contraction of the myofibril and overall shortening of the muscle fiber.
Studying the structure of muscle fibers in a light microscope revealed their transverse striations. Electron microscopic studies have shown that cross-striations are due to the special organization of the contractile proteins of myofibrils - actin (molecular weight 42,000) and myosin (molecular weight about 500,000). Actin filaments are represented by a double filament twisted into a double helix with a pitch of about 36.5 nm. These filaments are 1 µm long and 6-8 nm in diameter, the number of which reaches about 2000, and are attached at one end to the Z-plate. Filament-like molecules of the protein tropomyosin are located in the longitudinal grooves of the actin helix. In increments of 40 nm, a molecule of another protein, troponin, is attached to the tropomyosin molecule. Troponin and tropomyosin play an important role in the mechanisms of interaction between actin and myosin. In the middle of the sarcomere, between the actin filaments, there are thick myosin filaments about 1.6 µm long. In a polarizing microscope, this area is visible as a dark stripe (due to birefringence) - anisotropic A-disk. A lighter stripe H is visible in its center. At rest, there are no actin filaments in it. On both sides of the A-disk, light isotropic stripes are visible - I-disks formed by actin filaments. At rest, the actin and myosin filaments overlap each other slightly so that the total length of the sarcomere is about 2.5 μm. Electron microscopy revealed an M-line in the center of the H-band, a structure that holds myosin filaments. On a cross section of a muscle fiber, you can see the hexagonal organization of the myofilament: each myosin thread is surrounded by six actin threads (Fig. 2.20, B).
Electron microscopy shows that on the sides of the myosin filament there are protrusions called cross bridges. They are oriented relative to the axis of the myosin filament at an angle of 120°. According to modern concepts, the transverse bridge consists of a head and a neck. The head acquires pronounced ATPase activity upon binding to actin. The neck has elastic properties and is a hinged joint, so the head of the cross bridge can rotate around its axis.
The use of microelectrode technology in combination with interference microscopy has made it possible to establish that applying electrical stimulation to the Z-plate region leads to a contraction of the sarcomere, while the size of the A disk zone does not change, and the size of the H and I stripes decreases. These observations indicated that the length of myosin filaments does not change. Similar results were obtained when the muscle was stretched - the intrinsic length of actin and myosin filaments did not change. As a result of these experiments, it became clear that the area of mutual overlap of actin and myosin filaments changed. These facts allowed N. Huxley and A. Huxley to independently propose the theory of thread sliding to explain the mechanism of muscle contraction. According to this theory, during contraction, the size of the sarcomere decreases due to the active movement of thin actin filaments relative to thick myosin filaments. Currently, many details of this mechanism have been clarified and the theory has received experimental confirmation.
The mechanism of muscle contraction. During the process of muscle fiber contraction, the following transformations occur in it:
A. Electrochemical conversion:
1. Generation of PD.
2. Distribution of PD through the T-system.
3. Electrical stimulation of the contact zone between the T-system and the sarcoplasmic reticulum, activation of enzymes, formation of inositol triphosphate, increase in the intracellular concentration of Ca2+ ions.
B. Chemomechanical transformation:
4. Interaction of Ca2+ ions with troponin, release of active centers on actin filaments.
5. Interaction of the myosin head with actin, rotation of the head and development of elastic traction.
6. Sliding of actin and myosin filaments relative to each other, reducing the size of the sarcomere, developing tension or shortening of the muscle fiber.
The transfer of excitation from the motor neuron to the muscle fiber occurs with the help of the mediator acetylcholine (ACh). The interaction of ACh with the endplate cholinergic receptor leads to activation of ACh-sensitive channels and the appearance of an endplate potential, which can reach 60 mV. In this case, the area of the end plate becomes a source of irritating current for the muscle fiber membrane and in areas of the cell membrane adjacent to the end plate, an AP occurs, which spreads in both directions at a speed of approximately 3-5 m/s at a temperature of 36 oC. Thus, the generation of PD is the first stage of muscle contraction.
The second stage is the propagation of PD into the muscle fiber through the transverse system of tubules, which serves as a link between the surface membrane and the contractile apparatus of the muscle fiber. The T-system is in close contact with the terminal cisterns of the sarcoplasmic reticulum of two neighboring sarcomeres. Electrical stimulation of the contact site leads to the activation of enzymes located at the contact site and the formation of inositol triphosphate. Inositol triphosphate activates calcium channels in the membranes of the terminal cisterns, which leads to the release of Ca2+ ions from the cisterns and an increase in the intracellular Ca2+ concentration from 107 to 105 M. The set of processes leading to an increase in the intracellular Ca2+ concentration constitutes the essence of the third stage of muscle contraction. Thus, at the first stages, the electrical signal of the AP is converted into a chemical one - an increase in the intracellular concentration of Ca2+, i.e., an electrochemical transformation.
With an increase in the intracellular concentration of Ca2+ ions, tropomyosin shifts into the groove between the actin filaments, and areas on the actin filaments open with which myosin cross bridges can interact. This displacement of tropomyosin is due to a change in the conformation of the troponin protein molecule upon Ca2+ binding. Consequently, the participation of Ca2+ ions in the mechanism of interaction between actin and myosin is mediated through troponin and tropomyosin.
The essential role of calcium in the mechanism of muscle contraction was proven in experiments using the protein aequorin, which emits light when interacting with calcium. After injection of aequorin, the muscle fiber was subjected to electrical stimulation and simultaneously measured isometric muscle tension and aequorin luminescence. Both curves were completely correlated with each other (Fig. 2.21). Thus, the fourth stage of electromechanical coupling is the interaction of calcium with troponin.
The next, fifth, stage of electromechanical coupling is the attachment of the head of the cross bridge to the actin filament to the first of several sequentially located stable centers. In this case, the myosin head rotates around its axis, since it has several active centers that sequentially interact with the corresponding centers on the actin filament. Rotation of the head leads to an increase in the elastic traction of the neck of the cross bridge and an increase in tension. At each specific moment during the development of contraction, one part of the heads of the cross bridges is in connection with the actin filament, the other is free, i.e., there is a sequence of their interaction with the actin filament. This ensures a smooth reduction process. At the fourth and fifth stages, a chemomechanical transformation occurs.
The sequential reaction of connecting and disconnecting the heads of the cross bridges with the actin filament leads to the sliding of thin and thick filaments relative to each other and a decrease in the size of the sarcomere and the total length of the muscle, which is the sixth stage. The totality of the described processes constitutes the essence of the theory of thread sliding
It was initially believed that Ca2+ ions served as a cofactor for the ATPase activity of myosin. Further research refuted this assumption. In resting muscle, actin and myosin have virtually no ATPase activity. The attachment of the myosin head to actin causes the head to acquire ATPase activity.
Hydrolysis of ATP in the ATPase center of the myosin head is accompanied by a change in the conformation of the latter and its transfer to a new, high-energy state. Reattachment of the myosin head to a new center on the actin filament again leads to rotation of the head, which is provided by the energy stored in it. In each cycle of connection and separation of the myosin head with actin, one ATP molecule is cleaved per bridge. The speed of rotation is determined by the rate of ATP breakdown. It is clear that fast phasic fibers consume significantly more ATP per unit time and retain less chemical energy during tonic exercise than slow fibers. Thus, in the process of chemomechanical transformation, ATP provides the separation of the myosin head and the actin filament and provides energy for further interaction of the myosin head with another part of the actin filament. These reactions are possible at calcium concentrations above 106M.
The described mechanisms of muscle fiber shortening suggest that relaxation first requires a decrease in the concentration of Ca2+ ions. It has been experimentally proven that the sarcoplasmic reticulum has a special mechanism - a calcium pump, which actively returns calcium to the tanks. Activation of the calcium pump is carried out by inorganic phosphate, which is formed during the hydrolysis of ATP, and the energy supply for the operation of the calcium pump is also due to the energy generated during the hydrolysis of ATP. Thus, ATP is the second most important factor, absolutely necessary for the relaxation process. For some time after death, the muscles remain soft due to the cessation of the tonic influence of motor neurons (see Chapter 4). The ATP concentration then decreases below critical level and the possibility of disconnection of the myosin head from the actin filament disappears. The phenomenon of rigor mortis occurs with pronounced rigidity of skeletal muscles.
Modes of muscle contraction
The contractility of a skeletal muscle is characterized by the force of contraction that the muscle develops (usually the total force that the muscle can develop and the absolute force, i.e., the force per 1 cm2 of cross-section are assessed), the length of shortening, the degree of tension of the muscle fiber, the speed of shortening and development of tension, rate of relaxation. Since these parameters are largely determined by the initial length of muscle fibers and the load on the muscle, studies of muscle contractility are carried out in various modes.
Irritation of a muscle fiber by a single threshold or supra-threshold stimulus leads to the occurrence of a single contraction, which consists of several periods (Fig. 2.23). The first, the latent period, is the sum of time delays caused by the excitation of the muscle fiber membrane, the propagation of PD through the T-system into the fiber, the formation of inositol triphosphate, an increase in the concentration of intracellular calcium and activation of cross bridges. For the frog sartorius muscle, the latency period is about 2 ms.
The second is the period of shortening, or development of tension. In the case of free shortening of the muscle fiber, we speak of an isotonic contraction mode, in which the tension practically does not change, and only the length of the muscle fiber changes. If the muscle fiber is fixed on both sides and cannot freely shorten, then we speak of an isometric contraction mode. Strictly speaking, with this mode of contraction, the length of the muscle fiber does not change, while the size of the sarcomeres changes due to the sliding of actin and myosin filaments relative to each other. In this case, the resulting tension is transferred to elastic elements located inside the fiber. The cross-bridges of myosin filaments, actin filaments, Z-plates, longitudinally located sarcoplasmic reticulum and the sarcolemma of muscle fibers have elastic properties.
In experiments on an isolated muscle, stretching of the connective tissue elements of the muscle and tendons is revealed, to which the tension developed by the transverse bridges is transmitted.
In the human body, isotonic or isometric contraction does not occur in isolated form. As a rule, the development of tension is accompanied by a shortening of muscle length - auxotonic contraction mode
The third is a period of relaxation, when the concentration of Ca2+ ions decreases and the myosin heads are disconnected from the actin filaments.
It is believed that for a single muscle fiber the tension developed by any sarcomere is equal to the tension in any other sarcomere. Since the sarcomeres are connected in series, the rate at which a muscle fiber contracts is proportional to the number of its sarcomeres. Thus, during a single contraction, the rate of shortening of a long muscle fiber is higher than that of a shorter one. The amount of force developed by a muscle fiber is proportional to the number of myofibrils in the fiber. During muscle training, the number of myofibrils increases, which is the morphological substrate for increasing the force of muscle contraction. At the same time, the number of mitochondria increases, increasing the endurance of the muscle fiber during physical activity.
In an isolated muscle, the magnitude and speed of a single contraction are determined by a number of additional factors. The magnitude of a single contraction will primarily be determined by the number of motor units involved in the contraction. Since muscles are made up of muscle fibers with different levels excitability, there is a certain relationship between the magnitude of the stimulus and the response. An increase in contraction force is possible up to a certain limit, after which the contraction amplitude remains unchanged as the stimulus amplitude increases. In this case, all muscle fibers that make up the muscle take part in contraction.
The importance of the participation of all muscle fibers in contraction is shown by studying the dependence of the speed of shortening on the magnitude of the load. The graph of the dependence of the speed of contraction on the magnitude of the load approaches a hyperbola (Fig. 2.24). Since the force of contraction is equivalent to the load, it becomes clear that the maximum force that can be developed by a muscle occurs at very low speeds. A weightlifter can only “lift a record weight” with slow movements. On the contrary, fast movements are possible with lightly loaded muscles.
Changes in contraction force are observed with rhythmic stimulation of skeletal muscles.
In Fig. Figure 2.25 shows options for stimulating a muscle with two stimuli. If the second stimulus acts during the refractory period of the muscle fiber, then it will not cause repeated muscle contraction (Fig. 2.25, A). If the second stimulus acts on the muscle after the end of the relaxation period, then a single muscle contraction occurs again (Fig. 2.25, B).
When a second stimulus is applied during the period of shortening or development of muscle tension, the summation of two successive contractions occurs and the resulting response in amplitude becomes significantly higher than with a single stimulus; if a muscle fiber or muscle is stimulated with such a frequency that repeated stimuli occur during the period of shortening, or development of tension, then a complete summation of single contractions occurs and smooth tetanus develops (Fig. 2.25, B). Tetanus is a strong and prolonged muscle contraction. It is believed that this phenomenon is based on an increase in the concentration of calcium inside the cell, which allows the reaction of interaction between actin and myosin and the generation of muscle force by cross bridges to occur sufficiently long time. When the frequency of stimulation is reduced, it is possible that a repeated stimulus is applied during a period of relaxation. In this case, summation of muscle contractions will also occur, but a characteristic retraction on the muscle contraction curve will be observed (Fig. 2.25, D) - incomplete summation, or jagged tetanus.
With tetanus, summation of muscle contractions occurs, while the action potential of muscle fibers is not summed up.
Under natural conditions, single contractions of skeletal muscles do not occur. Addition, or superposition, of contractions of individual neuromotor units occurs. In this case, the force of contraction can increase both due to a change in the number of motor units involved in the contraction, and due to a change in the frequency of impulses of motor neurons. If the impulse frequency increases, a summation of contractions of individual motor units will be observed.
One of the reasons for the increase in contractile force in natural conditions is the frequency of impulses generated by motor neurons. The second reason for this is an increase in the number of excited motor neurons and synchronization of the frequency of their excitation. An increase in the number of motor neurons corresponds to an increase in the number of motor units involved in the contraction, and an increase in the degree of synchronization of their excitation contributes to an increase in the amplitude during the superposition of the maximum contraction developed by each motor unit separately.
The force of contraction of an isolated skeletal muscle, other things being equal, depends on the initial length of the muscle. Moderate stretching of a muscle causes the force it develops to increase compared to the force developed by an unstretched muscle. There is a summation of passive tension, caused by the presence of elastic components of the muscle, and active contraction. The maximum contractile force is achieved when the sarcomere size is 2-2.2 µm (Fig. 2.26). An increase in sarcomere length leads to a decrease in the force of contraction, since the area of mutual overlap of actin and myosin filaments decreases. With a sarcomere length of 2.9 µm, the muscle can develop a force equal to only 50% of the maximum possible.
Under natural conditions, the force of contraction of skeletal muscles when stretched, for example during massage, increases due to the work of gamma efferents.
Muscle work and power
Since the main task of skeletal muscles is to perform muscle work, in experimental and clinical physiology they evaluate the amount of work that a muscle does and the power it develops during work.
According to the laws of physics, work is the energy expended to move a body with a certain force over a certain distance: A = FS. If a muscle contraction occurs without load (in isotonic mode), then the mechanical work is zero. If at maximum load the muscle does not shorten (isometric mode), then the work is also zero. In this case, chemical energy is completely converted into thermal energy.
According to the law of average loads, a muscle can perform maximum work under average loads.
When contracting skeletal muscles in natural conditions, mainly in the mode of isometric contraction, for example, with a fixed position, they speak of static work; when performing movements, they speak of dynamic work.
The force of contraction and the work done by the muscle per unit time (power) do not remain constant during static and dynamic work. As a result of prolonged activity, the performance of skeletal muscles decreases. This phenomenon is called fatigue. At the same time, the force of contraction decreases, the latent period of contraction and the period of relaxation increase.
The static mode of operation is more tiring than the dynamic one. Fatigue of an isolated skeletal muscle is primarily due to the fact that in the process of performing work, products of oxidation processes accumulate in the muscle fibers - lactic and pyruvic acids, which reduce the possibility of generating PD. In addition, the processes of resynthesis of ATP and creatine phosphate, necessary for the energy supply of muscle contraction, are disrupted. Under natural conditions, muscle fatigue during static work is mainly determined by inadequate regional blood flow. If the contraction force in isometric mode is more than 15% of the maximum possible, then oxygen “starvation” occurs and muscle fatigue progressively increases.
IN real conditions it is necessary to take into account the state of the central nervous system - a decrease in the force of contractions is accompanied by a decrease in the frequency of neuronal impulses, due to both their direct inhibition and the mechanisms of central inhibition. Back in 1903, I.M. Sechenov showed that the restoration of the performance of tired muscles of one hand is significantly accelerated when performing work with the other hand during the rest period of the first. Unlike simple rest, such rest is called active.
The performance of skeletal muscles and the rate of development of fatigue depend on the level of mental activity: a high level of mental stress reduces muscle endurance.
Energy of muscle contraction
In dynamic mode, muscle performance is determined by the rate of breakdown and resynthesis of ATP. In this case, the rate of ATP breakdown can increase 100 times or more. ATP resynthesis can be achieved through the oxidative breakdown of glucose. Indeed, under moderate loads, ATP resynthesis is ensured by increased muscle consumption of glucose and oxygen. This is accompanied by an increase in blood flow through the muscles by approximately 20 times, an increase in cardiac output and respiration by 2-3 times. In trained individuals (for example, an athlete), an increase in the activity of mitochondrial enzymes plays a major role in ensuring the body’s increased need for energy.
At maximum physical activity, additional breakdown of glucose occurs through anaerobic glycolysis. During these processes, ATP resynthesis occurs several times faster and the mechanical work performed by the muscles is also greater than during aerobic oxidation. The maximum time for this type of work is about 30 seconds, after which lactic acid accumulates, i.e. metabolic acidosis, and fatigue develops.
Anaerobic glycolysis also occurs at the beginning of long-term physical work, until the rate of oxidative phosphorylation increases so that ATP resynthesis again equals its breakdown. After metabolic restructuring, the athlete gains a kind of second wind. Detailed diagrams metabolic processes are given in biochemistry manuals.
Heat generation during muscle contraction
According to the first law of thermodynamics, total energy system and its environment must remain constant.
Skeletal muscle converts chemical energy into mechanical work producing heat. A. Hill found that all heat generation can be divided into several components:
1. Heat of activation - the rapid release of heat in the early stages of muscle contraction, when there are no visible signs of shortening or development of tension. Heat formation at this stage is due to the release of Ca2+ ions from the triads and their combination with troponin.
2. Heat of shortening - the release of heat when doing work, if we are not talking about an isometric mode. Moreover, the more mechanical work is done, the more heat is released.
3. Heat of relaxation - the release of heat by the elastic elements of the muscle during relaxation. In this case, the release of heat is not directly related to metabolic processes.
As noted earlier, load determines the rate of shortening. It turned out that at a high speed of shortening the amount of heat released is small, and at a low speed it is large, since the amount of heat released is proportional to the load (Hill's law for the isotonic contraction regime).
Musculoskeletal interaction
When performing work, the force developed by the muscle is transferred to an external object using tendons attached to the bones of the skeleton. In any case, the load is overcome by rotating one part of the skeleton relative to another around the axis of rotation.
The transmission of muscle contraction to the bones of the skeleton occurs with the participation of tendons, which have high elasticity and extensibility. When a muscle contracts, the tendons are stretched and the kinetic energy developed by the muscle is converted into potential energy of the stretched tendon. This energy is used in such forms of movement as walking, running, i.e. when the heel lifts off the surface of the ground.
The speed and force with which one part of the body moves relative to another depends on the length of the lever, that is, the relative position of the muscle attachment points and the axis of rotation, as well as on the length, strength of the muscle and the magnitude of the load. Depending on the function performed by a particular muscle, speed or strength qualities may prevail. As already indicated in section 2.4.1.4, the longer the muscle, the higher the rate of its shortening. In this case, the parallel arrangement of muscle fibers relative to each other plays an important role. In this case, physiological cross section corresponds to the geometric one (Fig. 2.27, A). An example of such a muscle is the sartorius muscle. On the contrary, strength characteristics are higher in muscles with the so-called pennate arrangement of muscle fibers. With this arrangement of muscle fibers, the physiological cross-section is larger than the geometric cross-section (Fig. 2.27, B). An example of such a muscle in humans is the gastrocnemius muscle.
At the muscles spindle-shaped, for example, in the biceps brachii muscle, the geometric cross-section coincides with the physiological one only in the middle part; in other areas, the physiological cross-section is larger than the geometric one, so muscles of this type occupy an intermediate place in their characteristics
When determining the absolute strength of various muscles, the maximum force that the muscle develops is divided by the physiological cross-section. The absolute strength of the human gastrocnemius muscle is 5.9 kg/cm2, and the biceps brachii muscle is 11.4 kg/cm2.
Assessment of the functional state of the human muscular system
When assessing the functional state of the muscular system in humans, various methods are used.
Ergometric methods. These methods are used to determine physical performance. A person performs work under certain conditions and at the same time the magnitude of the work performed and various physiological parameters are recorded: respiratory rate, pulse, blood pressure, volume of circulating blood, the amount of regional blood flow, consumed O2, exhaled CO2, etc. With the help of special devices - bicycle ergometers or treadmills (treadmill) - it is possible to dose the load on the human body.
Electromyographic methods. These methods for studying human skeletal muscles have found wide application in physiological and clinical practice. Depending on the objectives of the study, the total electromyogram (EMG) or the potentials of individual muscle fibers are recorded and analyzed. When recording total EMG, cutaneous electrodes are more often used; when recording the potentials of individual muscle fibers, multichannel needle electrodes are used.
The advantage of total voluntary force electromyography is the non-invasiveness of the study and, as a rule, the absence of electrical stimulation of muscles and nerves. In Fig. Figure 2.28 shows the EMG of the muscle at rest and during voluntary effort. Quantitative EMG analysis consists of determining the frequencies of EMG waves, conducting spectral analysis, estimates of the average amplitude of EMG waves. One of the common methods for analyzing EMG is its integration, since it is known that the magnitude of the integrated EMG is proportional to the magnitude of the developed muscle effort.
Using needle electrodes, it is possible to record both the total EMG and the electrical activity of individual muscle fibers. The electrical activity recorded in this case is largely determined by the distance between the output electrode and the muscle fiber. Criteria for assessing the parameters of individual potentials of a healthy and sick person have been developed. In Fig. Figure 2.29 shows a recording of the potential of a human motor unit.
Smooth muscle
Smooth muscles are found in the walls of internal organs, blood and lymphatic vessels, in the skin and morphologically differ from skeletal and cardiac muscles in the absence of visible transverse striations.
Classification of smooth muscles
Smooth muscles are divided into visceral (unitary) and multiunitary (Fig. 2.30). Visceral smooth muscles are found in all internal organs, ducts of the digestive glands, blood and lymphatic vessels, and skin. Mulipunitary muscles include the ciliary muscle and the iris muscle. The division of smooth muscles into visceral and multiunitary is based on various densities their motor innervation. In visceral smooth muscle, motor nerve endings are present on a small number of smooth muscle cells. Despite this, excitement with nerve endings transmitted to all smooth muscle cells of the bundle due to tight contacts between neighboring myocytes - nexuses. Nexes allow action potentials and slow waves of depolarization to propagate from one muscle cell to another, so visceral smooth muscles contract simultaneously with the arrival of a nerve impulse.
The structure of smooth muscles
Smooth muscle consists of spindle-shaped cells with an average length of 100 µm and a diameter of 3 µm. The cells are located in muscle bundles and are closely adjacent to each other. The membranes of adjacent cells form nexuses, which provide electrical connection between cells and serve to transfer excitation from cell to cell. Smooth muscle cells contain actin and myosin myofilaments, which are arranged in a less orderly manner than in skeletal muscle fibers. The sarcoplasmic reticulum in smooth muscle is less developed than in skeletal muscle.
Innervation of smooth muscles
Visceral smooth muscle has dual innervation - sympathetic and parasympathetic, the function of which is to change the activity of the smooth muscle. Stimulation of one of the autonomic nerves usually increases smooth muscle activity, while stimulation of the other decreases it. In some organs, such as the intestines, stimulation of adrenergic nerves reduces, and cholinergic nerves increases, muscle activity; in others, for example, blood vessels, norepinephrine increases and ACh decreases muscle tone. The structure of nerve endings in smooth muscle differs from the structure of the neuromuscular synapse of skeletal muscle. Smooth muscle does not have end plates or separate nerve endings. Along the entire length of the branches of adrenergic and cholinergic neurons there are thickenings called varicosities. They contain granules with a mediator that is released from each varicose nerve fiber. Thus, along the path of the nerve fiber, many smooth muscle cells can be excited or inhibited. Cells deprived of direct contacts with varicosities are activated by action potentials propagating through the nexuses to neighboring cells. The speed of excitation in smooth muscle is low and amounts to several centimeters per second.
Neuromuscular transmission. The excitatory influence of adrenergic or cholinergic nerves is electrically manifested in the form of separate waves of depolarization. With repeated stimulation, these potentials are summed up and upon reaching a threshold value, an AP occurs.
The inhibitory influence of adrenergic or cholinergic nerves manifests itself in the form of separate waves of hyperpolarization, called inhibitory postsynaptic potentials (IPSPs). During rhythmic stimulation, IPSPs are summed up. Excitatory and inhibitory postsynaptic potentials are observed not only in muscle cells in contact with varicose veins, but also at some distance from them. This is explained by the fact that postsynaptic potentials are transmitted from cell to cell through nexuses or through the diffusion of the transmitter from the sites of its release.
Functions and properties of smooth muscles
Electrical activity. Visceral smooth muscles are characterized by unstable membrane potential. Fluctuations in membrane potential, regardless of neural influences, cause irregular contractions that maintain the muscle in a state of constant partial contraction - tone. The tone of smooth muscles is clearly expressed in the sphincters of hollow organs: the gall bladder, bladder, at the junction of the stomach into the duodenum and the small intestine into the large intestine, as well as in the smooth muscles of small arteries and arterioles. The membrane potential of smooth muscle cells does not reflect the true value of the resting potential. When the membrane potential decreases, the muscle contracts; when it increases, it relaxes. During periods of relative rest, the membrane potential is on average - 50 mV. In visceral smooth muscle cells, slow wave-like fluctuations of the membrane potential of several millivolts are observed, as well as AP. The value of PD can vary widely. In smooth muscles, the AP duration is 50-250 ms; PDs of various shapes are found. In some smooth muscles, such as the ureter, stomach, and lymphatic vessels, APs have a prolonged plateau during repolarization, reminiscent of the potential plateau in myocardial cells. Plateau-shaped PDs ensure the entry into the cytoplasm of myocytes of a significant amount of extracellular calcium, which subsequently participates in the activation of contractile proteins of smooth muscle cells. The ionic nature of smooth muscle PD is determined by the characteristics of the smooth muscle cell membrane channels. The main role in the mechanism of occurrence of PD is played by Ca2+ ions. Calcium channels in the membrane of smooth muscle cells allow not only Ca2+ ions to pass through, but also other doubly charged ions (Ba2+, Mg2+), as well as Na+. The entry of Ca2+ into the cell during PD is necessary to maintain tone and develop contraction, therefore blocking calcium channels of the smooth muscle membrane, leading to a limitation of the entry of Ca2+ ion into the cytoplasm of myocytes of internal organs and blood vessels, is widely used in practical medicine to correct motility of the digestive tract and vascular tone in the treatment of patients with hypertension.
Automation. The action potentials of smooth muscle cells are autorhythmic (pacemaker) in nature, similar to the potentials of the conduction system of the heart. Pacemaker potentials are recorded in various areas of smooth muscle. This indicates that any visceral smooth muscle cells are capable of spontaneous automatic activity. Automaticity of smooth muscles, i.e. the ability for automatic (spontaneous) activity is inherent in many internal organs and vessels.
Tensile response. A unique feature of visceral smooth muscle is its response to stretch. In response to stretch, smooth muscle contracts. This is because stretching reduces the cell membrane potential, increases AP frequency and, ultimately, smooth muscle tone. In the human body, this property of smooth muscles serves as one of the ways to regulate motor activity internal organs. For example, when the stomach is filled, its wall stretches. An increase in the tone of the stomach wall in response to its stretching helps maintain the volume of the organ and better contact of its walls with incoming food. In blood vessels, distension created by fluctuations in blood pressure is a major factor in the myogenic self-regulation of vascular tone. Finally, stretching of the uterine muscles by the growing fetus is one of the reasons for the onset of labor.
Plastic. Another important specific characteristic of smooth muscle is the variability of tension without a natural connection with its length. Thus, if visceral smooth muscle is stretched, its tension will increase, but if the muscle is held in the state of elongation caused by stretching, then the tension will gradually decrease, sometimes not only to the level that existed before the stretch, but also below this level. This property is called smooth muscle plasticity. Thus, smooth muscle is more similar to a viscous plastic mass than to a poorly pliable structured tissue. The plasticity of smooth muscles contributes to the normal functioning of internal hollow organs.
Relationship between excitation and contraction. It is more difficult to study the relationship between electrical and mechanical manifestations in visceral smooth muscle than in skeletal or cardiac muscle, since visceral smooth muscle is in a state of continuous activity. Under conditions of relative rest, a single AP can be recorded. The contraction of both skeletal and smooth muscle is based on the sliding of actin in relation to myosin, where the Ca2+ ion performs a trigger function (Fig. 2.31).
The mechanism of contraction of smooth muscle has a feature that distinguishes it from the mechanism of contraction of skeletal muscle. This feature is that before smooth muscle myosin can exhibit its ATPase activity, it must be phosphorylated. Phosphorylation and dephosphorylation of myosin is also observed in skeletal muscle, but in it the phosphorylation process is not necessary to activate the ATPase activity of myosin. The mechanism of phosphorylation of smooth muscle myosin is as follows: the Ca2+ ion combines with calmodulin (calmodulin is a receptive protein for the Ca2+ ion). The resulting complex activates the enzyme myosin light chain kinase, which in turn catalyzes the process of myosin phosphorylation. Actin then slides against myosin, which forms the basis of contraction. Note that the trigger for smooth muscle contraction is the addition of Ca2+ ion to calmodulin, while in skeletal and cardiac muscle the trigger is the addition of Ca2+ to troponin.
Chemical sensitivity. Smooth muscles are highly sensitive to various physiologically active substances: adrenaline, norepinephrine, ACh, histamine, etc. This is due to the presence of specific receptors on the smooth muscle cell membrane. If you add adrenaline or norepinephrine to a preparation of intestinal smooth muscle, the membrane potential increases, the frequency of AP decreases and the muscle relaxes, i.e., the same effect is observed as when the sympathetic nerves are excited.
Norepinephrine acts on the β- and β-adrenergic receptors of the membrane of smooth muscle cells. The interaction of norepinephrine with β-receptors reduces muscle tone as a result of activation of adenylate cyclase and the formation of cyclic AMP and a subsequent increase in the binding of intracellular Ca2+. The effect of norepinephrine on β-receptors inhibits contraction by increasing the release of Ca2+ ions from muscle cells.
ACh has an effect on the membrane potential and contraction of intestinal smooth muscles, opposite action norepinephrine. The addition of ACh to an intestinal smooth muscle preparation reduces membrane potential and increases the frequency of spontaneous APs. As a result, the tone increases and the frequency of rhythmic contractions increases, i.e., the same effect is observed as when the parasympathetic nerves are excited. ACh depolarizes the membrane and increases its permeability to Na+ and Ca+.
The smooth muscles of some organs respond to various hormones. Thus, the smooth muscles of the uterus in animals during the periods between ovulation and when the ovaries are removed are relatively inexcitable. During estrus or in ovarian animals that have been given estrogen, smooth muscle excitability increases. Progesterone increases membrane potential even more than estrogen, but in this case the electrical and contractile activity of the uterine muscles is inhibited.
PHYSIOLOGY OF GLANDAL TISSUE
The classic cellular elements of excitable tissues (nervous and muscle) are neurons and myocytes. Glandular tissue is also excitable, but the glandulocytes that form it have significant morphofunctional specificity.
Secretion
Secretion is the process of formation inside a cell (glandulocyte) from substances entering it, and the release from the cell of a specific product (secret) of a certain functional purpose. Glandulocytes can be represented by individual cells and are combined into exocrine and endocrine glands.
The functional state of the glands is determined by the quantity and quality of their exosecretions (for example, digestive, sweat, etc.) and the content of products secreted by the glands in the blood and lymph. Less commonly used for this purpose are methods of tapping and recording secretory potentials from the surface of the body and mucous membranes; Registration of the potentials of glands, their fragments and individual glandulocytes is also used; In addition, morphological, including histo- and cytochemical methods for studying the secretory function of various glands are common.
Glandulocytes secrete products of various chemical natures: proteins, lipoproteins, mucopolysaccharides, solutions of salts, bases and acids. A secretory cell can synthesize and secrete one or more secretory products of the same or different chemical nature. The material secreted by the secretory cell may have a different relationship to intracellular processes. It is generally accepted that a secret is a product of the metabolism of a given cell, an excrete is a product of its catabolism, a recrete is a product absorbed by a cell from the blood and then excreted unchanged. The secretion can be removed from the cell through its apical membrane into the lumen of the acini, gland ducts, or the cavity of the digestive tract - external secretion, or exocretion. The removal of secretion from a cell through its basolateral membrane into the interstitial fluid, from where it enters the blood and lymph, is called internal secretion - endocretion, or incretion.
Exo- and endocretion have much in common at the level of synthesis and release of the secretory product. The secretion of secretions from a cell can be carried out in two ways, therefore, products of the exocretory glands can be found in the blood (for example, enzymes of the digestive glands), and hormones can be found in the exocrine secretions (small amounts of hormones are found in the secretions of the digestive glands). Some glands (for example, the pancreas) contain exocrine and endocrine cells. These phenomena are explained in the excretory theory of the origin of secretory processes (A. M. Ugolev). According to this theory, external and internal secretion of glands originated from a nonspecific function characteristic of all cells - excretion - the release of metabolic products from them.
Multifunctionality of secretion
In the process of exo- and endocretion, several functions are realized. Thus, as a result of external secretion of the glands of the digestive tract, solutions of enzymes and electrolytes are released into it, ensuring the digestion of food in the optimal physicochemical conditions created by them. The secretion of sweat glands acts as an important mechanism of thermoregulation (see Chapter 11). Secretion of the mammary glands is necessary for lactotrophic nutrition of children (see section 13.5). Exocretion of glands plays a large role in maintaining the relative constancy of the internal environment of the body, ensuring the release of endogenous and exogenous substances from the body (see Chapter 12). Products exocreted into the cavity of the digestive tract (H+ ions, enzymes, etc.) take part in the regulation of digestive functions (see Chapter 9). The mucus secreted by mucocytes plays a protective role, protecting the mucous membranes from excessive mechanical and chemical irritations. The secretions contain substances necessary for the body's immune defense.
Internal secretion products act as humoral regulators of metabolism and functions. The role of specific hormones is especially important in this (see Chapter 5). Enzymes produced and secreted by various glands are involved in tissue hydrolysis of nutrients, the formation of protective histohematic barriers, the formation of physiologically active substances (for example, regulatory peptides from proteins), and in other physiological processes (for example, blood coagulation and fibrinolysis). Examples of the secrets function will be added in the corresponding chapters.
Secretory cycle
The secretory cycle is a periodic change in the state of the secretory cell, caused by the formation, accumulation, secretion of secretion and the restoration of its further secretion. There are several phases in the secretory cycle: entry into the cell starting materials(diffusion, active transport and endocytosis are of key importance in this), synthesis and transport of the initial secretory product, formation of secretory granules, release of secretions from the cell - exocytosis. Non-granulated secretion products are also released from the cell. There are cells with different types of intracellular processes and types of secretion. Depending on the type of secretion, secretion is divided into holocrine, apocrine (macro- and micro-) and merocrine of two types, depending on the mechanism of release of secretion through the apical membrane: the secretion leaves the glandulocyte through the holes formed when the secretory granule comes into contact with it in the apical membrane, or through a membrane that does not change its structure.
Biopotentials of glandulocytes
The biopotentials of secretory cells have a number of features at rest and during secretion: low magnitude and rate of change, gradualism, different polarization of the basal and apical membranes, heterochronic changes in membrane polarization during secretion, etc.
The membrane potential of glandulocytes of various exocrine glands in a state of relative rest is from -30 to -75 mV. Stimulation of secretion changes the membrane potential. This change in membrane polarization is called secretory potential. It has significant differences in different glandulocytes, characterizes the secretory process, affects the secretory cycle and the conjugation of its phases, synchronization of the activity of glandulocytes within a given gland (this does not exclude their chemical interaction through intercellular contacts). A membrane polarization of -50 mV is considered optimal for the occurrence of secretory potentials.
The excitation of most types of glandulocytes is characterized by depolarization of their membranes, but glandulocytes have been described, upon excitation of which the membranes hyperpolarize, forming biphasic potentials. Membrane depolarization is caused by the flow of Na+ ions into the cell and the release of K+ ions from it. Hyperpolarization of the membrane is caused by the transport of Cl- ions into the cell and the release of Na+ and K+ ions from it. The difference in polarization of the basal and apical membranes is 2-3 mV, which creates a significant electric field (20-30 V/cm). When the secretory cell is excited, its tension approximately doubles, which promotes the movement of secretory granules to the apical pole of the cell and the release of secretory material from the cell.
Physiological secretory stimulants that increase the concentration of Ca2+ in glandulocytes affect potassium and sodium channels and cause secretory potential. A number of secretion stimulants that act through the activation of adenylate cyclase and do not affect the exchange of Ca2+ ions in glandulocytes do not cause electrical effects in them. Consequently, changes in the membrane potential and electrical conductivity of glandulocytes are mediated by an increase in intracellular calcium concentration.
Regulation of glandulocyte secretion
The secretion of glands is controlled by nervous, humoral and paracrine mechanisms. As a result of the action of these mechanisms, excitation, inhibition and modulation of glandulocyte secretion occur. The effect depends on the type of efferent nerves, mediators, hormones and other physiologically active substances, the type of glandulocytes that make up the glandular tissue, membrane receptors on them, and the mechanism of action of these substances on intracellular processes. Synaptic endings on glandulocytes are characterized by open, relatively wide synaptic clefts filled with interstitial fluid. Mediators come here from the endings of neurons, hormones from the blood, parahormones from neighboring endocrine cells, and products of their activity from the glandulocytes themselves.
Mediators and hormones (primary messengers, or transmitters) interact with receptors on the basolateral membrane of the glandulocyte. The resulting signal is transmitted to a localized inside membrane adenylate cyclase, as a result of which its activity increases or decreases, and accordingly the formation of cyclic adenosine monophosphate cAMP increases or decreases. The process with guanylate cyclase and cyclic guanyl monophosphate cGMP develops similarly. These cyclic nucleotides, acting as secondary transmitters (messengers), influence the chain of intracellular enzymatic reactions characteristic of this type of glandulocyte through interaction with protein kinase.
In addition, the influence of secondary messengers is carried out by the calcium-calmodulin system, in which Ca2+ ions are of intra- and extracellular origin, and the activation of secretion depends on the concentration of calcium and calmodulin.
Glandulocytes in a state of relative rest secrete a small amount of secretion, which can gradually increase and decrease. On the membranes of glandulocytes there are excitatory and inhibitory receptors, with the participation of which the secretory activity of glandulocytes varies over a wide range.
Some substances change the activity of glandulocytes, penetrating into them through the basolateral membrane. Thus, secretion products themselves inhibit the secretory activity of glandulocytes according to the principle of negative feedback
2nd ed., revised. and additional - M.: 2003. - 656 p.
The second edition of the textbook (the first was published in 1997 and was printed three times in 1998, 2000 and 2001) has been revised in accordance with the latest scientific achievements. New facts and concepts are presented. The authors of the textbook are highly qualified specialists in relevant areas of physiology. Particular attention is paid to the description of methods for quantitative assessment of the functional state of the most important systems of the human body. The textbook corresponds to the program approved by the Ministry of Health of Russia.
For students of medical universities and faculties.
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VOLUME 1.
PREFACE
Chapter 1. PHYSIOLOGY. SUBJECT AND METHODS. IMPORTANCE FOR MEDICINE. BRIEF HISTORY. - G. I. Kositsky, V. M. Pokrovsky, G. F. Korotko. . .
1.1. Physiology, its subject and role in the medical education system
1.2. Physiological research methods
1.3. Physiology of the whole organism
1.4. Organism and external environment. Adaptation
1.5. A Brief History of Physiology
Chapter 2. EXCITABLE TISSUE
2.1. Physiology of excitable tissues. - V.I. Kobrin
2.1.1. Structure and basic properties of cell membranes and ion channels
2.1.2. Methods for studying excitable cells
2.1.3. Resting potential
2.1.4. Action potential
2.1.5. The effect of electric current on excitable tissues 48
2.2. Physiology of nervous tissue. - G. A. Kuraev
2.2.1. Structure and morphofunctional classification of neurons
2.2.2. Receptors. Receptor and generator potentials
2.2.3. Afferent neurons, their functions
2.2.4. Interneurons, their role in the formation of neural networks
2.2.5. Efferent neurons
2.2.6. Neuroglia
2.2.7. Conducting stimulation along nerves
2.3. Physiology of synapses. - G. A. Kuraev
2.4. Physiology of muscle tissue
2.4.1. Skeletal muscles. - V.I. Kobrin
2.4.1.1. Classification of skeletal muscle fibers
2.4.1.2. Functions and properties of skeletal muscles
2.4.1.3. Mechanism of muscle contraction
2.4.1.4. Modes of muscle contraction
2.4.1.5. Muscle work and power
2.4.1.6. Energy of muscle contraction
2.4.1.7. Heat generation during muscle contraction
2.4.1.8. Musculoskeletal interaction
2.4.1.9. Assessment of the functional state of the human muscular system
2.4.2. Smooth muscles. - R. S. Orlov
2.4.2.1. Classification of smooth muscles
2.4.2.2. The structure of smooth muscles
2.4.2.3. Innervation of smooth muscles
2.4.2.4. Functions and properties of smooth muscles
2.5.1. Secretion
2.5.2. Multifunctionality of secretion
2.5.3. Secretory cycle
2.5.4. Biopotentials of glandulocytes
2.5.5. Regulation of glandulocyte secretion
Chapter 3. PRINCIPLES OF ORGANIZATION OF FUNCTION MANAGEMENT. - V. P. Degtyarev
3.1. Control in living organisms
3.2. Self-regulation of physiological functions
3.3. System organization of management. Functional systems and their interaction
Chapter 4. NERVOUS REGULATION OF PHYSIOLOGICAL FUNCTIONS
4.1. Mechanisms of activity of the central nervous system. - O. G. Chorayan
4.1.1. Methods for studying the functions of the central nervous system
4.1.2. Reflex principle of regulation of functions
4.1.3. Inhibition in the central nervous system
4.1.4. Properties of nerve centers
4.1.5. Principles of integration and coordination in the activity of the central nervous system
4.1.6. Neuronal complexes and their role in the activity of the central nervous system
4.1.7. Blood-brain barrier and its functions
4.1.8. Cerebrospinal fluid
4.1.9. Elements of cybernetics of the nervous system
4.2. Physiology of the central nervous system. - G. A. Kuraev 134
4.2.1. Spinal cord
4.2.1.1. Morphofunctional organization of the spinal cord
4.2.1.2. Features of the neural organization of the spinal cord
4.2.1.3. Spinal cord pathways
4.2.1.4. Reflex functions of the spinal cord
4.2.2. Brain stem
4.2.2.1. Medulla oblongata
4.2.2.2. Bridge
4.2.2.3. Midbrain
4.2.2.4. Reticular formation of the brainstem
4.2.2.5. Diencephalon
4.2.2.5.1. Thalamus
4.2.2.6. Cerebellum
4.2.3. Limbic system
4.2.3.1. Hippocampus
4.2.3.2. Amygdala
4.2.3.3. Hypothalamus
4.2.4. Basal ganglia
4.2.4.1. Caudate nucleus. Shell
4.2.4.2. Pale ball
4.2.4.3. Fence
4.2.5. Cerebral cortex
4.2.5.1. Morphofunctional organization
4.2.5.2. Sensory areas
4.2.5.3. Motor areas
4.2.5.4. Associative areas
4.2.5.5. Electrical manifestations of cortical activity
4.2.5.6. Interhemispheric relationships
4.2.6. Coordination of movements. - V. S. Gurfinkel, Yu. S. Levik
4.3. Physiology of the autonomic (vegetative) nervous system. - A. D. Nozdrachev
4.3.1- Functional structure of the autonomic nervous system
4.3.1.1. The sympathetic part
4.3.1.2. Parasympathetic part
4.3.1.3. Metasympathetic part
4.3.2. Features of the design of the autonomic nervous system
4.3.3. Autonomic (vegetative) tone
4.3.4. Synaptic transmission of excitation in the autonomic nervous system
4.3.5- Influence of the autonomic nervous system on the functions of tissues and organs
Chapter 5. HORMONAL REGULATION OF PHYSIOLOGICAL FUNCTIONS. - V. A. Tachuk, O. E. Osadchiy
5.1. Principles of hormonal regulation
5.2. Endocrine glands
5.2.1. Research methods
5.2.2. Pituitary
5.2.3. Thyroid gland
5.2.4. Parathyroid glands
5.2.5. Adrenal glands
5.2.6. Pancreas
5.2.7. Gonads
5.3. Education, secretion and mechanisms of action of hormones 264
5.3.1. Regulation of hormone biosynthesis
5.3.2. Secretion and transport of hormones
5.3.3. Mechanisms of action of hormones on cells
Chapter 6. BLOOD. - B.I. Kuzink
6.1. Concept of the blood system
6.1.1. Basic functions of blood
6.1.2. Amount of blood in the body
6.1.3. Blood plasma composition
6.1.4. Physicochemical properties of blood
6.2. Formed elements of blood
6.2.1. Red blood cells
6.2.1.1. Hemoglobin and its compounds
6.2.1.2. Color index
6.2.1.3. Hemolysis
6.2.1.4. Functions of red blood cells
6.2.1.5. Erythron. Regulation of erythropoiesis
6.2.2. Leukocytes
6.2.2.1. Physiological leukocytosis. Leukopenia 292
6.2.2.2. Leukocyte formula
6.2.2.3. Characteristics of individual types of leukocytes
6.2.2.4. Regulation of leukopoiesis
6.2.2.5. Nonspecific resistance and immunity
6.2.3. Platelets
6.3. Blood groups
6.3.1. AVO system
6.3.2. Rhesus system (Rh-hr) and others
6.3.3. Blood groups and morbidity. Hemostasis system
6.4.1. Vascular-platelet hemostasis
6.4.2. Blood clotting process
6.4.2.1. Plasma and cellular coagulation factors
6.4.2.2. Blood clotting mechanism
6.4.3. Natural anticoagulants
6.4.4. Fibrniolysis
6.4.5. Regulation of blood coagulation and fibrinolysis
Chapter 7. BLOOD AND LYMPH CIRCULATION. - E. B. Babsky, G. I. Kositsky, V. M. Pokrovsky
7.1. Heart activity
7.1.1. Electrical phenomena in the heart, conduction of excitation
7.1.1.1. Electrical activity of myocardial cells
7.1.1.2. Functions of the conduction system of the heart. . .
7.1.1.3. Refractory phase of the myocardium and extrasystole
7.1.1.4. Electrocardiogram
7.1.2. Pumping function of the heart
7.1.2.1. Phases of the cardiac cycle
7.1.2.2. Cardiac output
7.1.2.3. Mechanical and abnormal manifestations of cardiac activity
7.1.3. Regulation of heart activity
7.1.3.1. Intracardiac regulatory mechanisms
7.1.3.2. Extracardiac regulatory mechanisms. .
7.1.3.3. Interaction of intracardiac and extracardiac nervous regulatory mechanisms
7.1.3.4. Reflex regulation of heart activity
7.1.3.5. Conditioned reflex regulation of heart activity
7.1.3.6. Humoral regulation of heart activity
7.1.4. Endocrine function of the heart
7.2. Functions of the vascular system
7.2.1. Basic principles of hemodynamics. Classification of vessels
7.2.2. Movement of blood through vessels
7.2.2.1. Blood pressure
7.2.2.2. Arterial pulse
7.2.2.3. Volumetric blood flow velocity
7-2.2.4. Movement of blood in capillaries. Microcirculation
7.2.2.5. Movement of blood in veins
7.2.2.6. Blood circulation time
7.2.3. Regulation of blood movement through vessels
7.2.3.1. Innervation of blood vessels
7.2.3.2. Vasomotor center
7.2.3.3. Reflex regulation of vascular tone
7.2.3.4. Humoral influences on blood vessels
7.2.3.5. Local mechanisms of blood circulation regulation
7.2.3.6. Regulation of circulating blood volume.
7.2.3.7. Blood depots
7.2.4. Regional blood circulation. - Y. A. Khananashvili 390
7.2.4.1. Cerebral circulation
7.2.4.2. Coronary circulation
7.2.4.3. Pulmonary circulation
7.3. Lymph circulation. - R. S. Orlov
7.3.1. Structure of the lymphatic system
7.3.2. Lymph formation
7.3.3. Composition of lymph
7.3.4. Lymph movement
7.3.5. Functions of the lymphatic system
Chapter 8. BREATHING. - V. CD. Pyatin
8.1. The essence and stages of breathing
8.2. External breathing
8.2.1. Biomechanics of respiratory movements
8.3. Pulmonary ventilation
8.3.1. Lung volumes and capacities
8.3.2. Alveolar ventilation
8.4. Mechanics of breathing
8.4.1. Lung compliance
8.4.2. Airway resistance
8.4.3. Work of breathing
8.5. Gas exchange and gas transport
8.5.1. Diffusion of gases through the airborne barrier. . 415
8.5.2. Content of gases in alveolar air
8.5.3. Gas exchange and O2 transport
8.5.4. Gas exchange and CO2 transport
8.6. Regulation of external respiration
8.6.1. Respiratory center
8.6.2. Reflex regulation of breathing
8.6.3. Coordination of breathing with other body functions
8.7. Peculiarities of breathing during physical exertion and with altered partial pressure of O2
8.7.1. Breathing during physical exertion
8.7.2. Breathing when climbing to altitude
8.7.3. Breathing at high pressure
8.7.4. Breathing pure O2
8.8. Dyspnea and pathological types of breathing
8.9. Non-respiratory functions of the lungs. - E. A. Maligonov,
A. G. Pokhotko
8.9.1. Protective functions of the respiratory system
8.9.2. Metabolism of biologically active substances in the lungs
VOLUME 2.
Chapter 9. DIGESTION. G. F. Korotko
9.1. Physiological basis of hunger and satiety
9.2. The essence of digestion. Conveyor principle of organizing digestion
9.2.1. Digestion and its importance
9.2.2. Types of digestion
9.2.3. Conveyor principle of organizing digestion
9.3. Digestive functions of the digestive tract
9.3.1. Secretion of the digestive glands
9.3.2. Motor function of the digestive tract
9.3.3. Suction
9.3.4. Methods for studying digestive functions
9.3.4.1. Experimental methods
9.3.4.2. Study of digestive functions in humans?
9.3.5. Regulation of digestive functions
9.3.5.1. Systemic mechanisms for controlling digestive activity. Reflex mechanisms
9.3.5.2. The role of regulatory peptides in the activity of the digestive tract
9.3.5.3. Blood supply and functional activity of the digestive tract
9.3.5.4. Periodic activity of the digestive organs
9.4. Oral digestion and swallowing
9.4.1. Eating
9.4.2. Chewing
9.4.3. Salivation
9.4.4. Swallowing
9.5. Digestion in the stomach
9.5.1. Secretory function of the stomach
9.5.2. Motor function of the stomach
9.5.3. Evacuation of stomach contents into the duodenum
9.5.4. Vomit
9.6. Digestion in the small intestine
9.6.1. Pancreatic secretion
9.6.2. Bile secretion and bile secretion
9.6.3. Intestinal secretion
9.6.4. Cavity and parietal digestion in the small intestine
9.6.5. Motor function of the small intestine
9.6.6. Absorption of various substances in the small intestine
9.7. Functions of the colon
9.7.1. Entry of intestinal chyme into the large intestine
9.7.2. The role of the colon in digestion
9.7.3. Motor function of the colon
9.7.4. Defecation
9.8. Microflora of the digestive tract
9.9. Liver functions
9.10. Non-digestive functions of the digestive tract 87
9.10.1. Excretory activity of the digestive tract
9.10.2. Participation of the digestive tract in water-salt metabolism
9.10.3. Endocrine function of the digestive tract and the release of biologically active substances in secretions
9.10.4. Increment (endosecretion) of enzymes by the digestive glands
9.10.5. Immune system of the digestive tract
Chapter 10. METABOLISM AND ENERGY. NUTRITION. E. B. Babsky V. M. Pokrovsky
10.1. Metabolism
10.1.1. Protein metabolism
10.1.2. Lipid metabolism
10.1.3. Carbohydrate metabolism
10.1.4. Exchange of mineral salts and water
10.1.5. Vitamins
10.2. Energy conversion and general metabolism
10.2.1. Methods for studying energy exchange
10.2.1.1. Direct calorimetry
10.2.1.2. Indirect calorimetry
10.2.1.3. Gross Exchange Study
10.2.3. BX
10.2.4. Surface rule
10.2.5. Energy exchange during physical labor
10.2.6. Energy exchange during mental work
10.2.7. Specific dynamic action of food
10.2.8. Regulation of energy metabolism
10.3. Nutrition. G. F. Korotko
10.3.1. Nutrients
10.3.2. Theoretical foundations of nutrition
10.3.3. Nutrition standards
Chapter 11. THERMOREGULATION. E. B. Babsky, V. M. Pokrovsky
11.1. Body temperature and isothermia
11.2. Chemical thermoregulation
11.3. Physical thermoregulation
11.4. Isotherm regulation
11.5. Hypothermia and hyperthermia
Chapter 12. ALLOCATION. KIDNEY PHYSIOLOGY. Yu. V. Natochin.
12.1. Selection
12.2. Kidneys and their functions
12.2.1. Methods for studying kidney function
12.2.2. Nephron and its blood supply
12.2.3. The process of urine formation
12.2.3.1. Glomerular filtration
12.2.3.2. Kayalceous reabsorption
12.2.3.3. Kayal secretion
12.2.4. Determination of the magnitude of renal plasma and blood flow
12.2.5. Synthesis of substances in the kidneys
12.2.6. Osmotic dilution and concentration of urine
12.2.7. Homeostatic functions of the kidneys
12.2.8. Excretory function of the kidneys
12.2.9. Endocrine function of the kidneys
12.2.10. Metabolic kidney function
12.2.11. Principles of regulation of reabsorption and secretion of substances in renal tubular cells
12.2.12. Regulation of kidney activity
12.2.13. Quantity, composition and properties of urine
12.2.14. Urination
12.2.15. Consequences of kidney removal and artificial kidney
12.2.16. Age-related features of the structure and function of the kidneys
Chapter 13. SEXUAL BEHAVIOR. REPRODUCTIVE FUNCTION. LACTATION. Yu. I. Savchenkov, V. I. Kobrin
13.1. Sexual development
13.2. Puberty
13.3. Sexual behavior
13.4. Physiology of sexual intercourse
13.5. Pregnancy and maternal relations
13.6. Childbirth
13.7. Major changes in the body of a newborn
13.8. Lactation
Chapter 14. SENSORY SYSTEMS. M. A. Ostrovsky, I. A. Shevelev
14.1. General physiology of sensory systems
14.1.1. Methods for studying sensory systems
4.2. General principles of the structure of sensory systems
14.1.3. Basic functions of the sensor system
14.1.4. Mechanisms of information processing in the sensory system
14.1.5. Adaptation of the sensory system
14.1.6. Interaction of sensory systems
14.2. Particular physiology of sensory systems
14.2.1. Visual system
14.2.2. Auditory system
14.2.3. Vestibular system
14.2.4. Somatosensory system
14.2.5. Olfactory system
14.2.6. Taste system
14.2.7. Visceral system
Chapter 15. INTEGRATIVE ACTIVITY OF THE HUMAN BRAIN. O. G. Chorayan
15.1. Conditioned reflex basis of higher nervous activity
15.1.1. Conditioned reflex. Education mechanism
15.1.2. Methods for studying conditioned reflexes
15.1.3. Stages of formation of a conditioned reflex
15.1.4. Types of conditioned reflexes
15.1.5. Inhibition of conditioned reflexes
15.1.6. Dynamics of basic nervous processes
15.1.7. Types of higher nervous activity
15.2. Physiological mechanisms of memory
15.3. Emotions
15.4. Sleep and hypnosis. V. I. Kobrin
15.4.1. Dream
15.4.2. Hypnosis
15.5. Basics of psychophysiology
15.5.1. Neurophysiological foundations of mental activity
15.5.2. Psychophysiology of the decision-making process. . 292
15.5.3. Consciousness
15.5.4. Thinking
15.6. Second signaling system
15.7. The principle of probability and “fuzziness” in the higher integrative functions of the brain
15.8. Interhemispheric asymmetry
15.9. The influence of physical activity on the functional state of a person. E. K. Aganyats
15.9.1. General physiological mechanisms of the influence of physical activity on metabolism
15.9.2. Autonomic support of motor activity 314
15.9.3. The influence of physical activity on the regulatory mechanisms of the central nervous system and hormonal link
15.9.4. The influence of physical activity on the functions of the neuromuscular system
15.9.5. Physiological significance of fitness
15.10. Fundamentals of the physiology of mental and physical labor. E. K. Aganyants
15.10.1. Physiological characteristics of mental work
15.10.2. Physiological characteristics of physical labor
15.10.3. The relationship between mental and physical labor
15.11. Fundamentals of chronophysiology. G. F. Korotko, N. A. Agad-zhanyan
15.11.1. Classification of biological rhythms
15.11.2. Circadian rhythms in humans
15.11.3. Ultradian rhythms in humans
11/15/4. Infradian rhythms in humans
15.11.5. Biological clock
11/15/6. Pacemakers of mammalian biological rhythms
Basic quantitative physiological indicators of the body
List of recommended literature
Textbook for higher educational institutions physical culture. 7th edition
Approved by the Ministry of the Russian Federation for Physical Culture and Sports as a textbook for higher educational institutions of physical culture
The publication was prepared at the Department of Physiology of the National State University of Physical Culture, Sports and Health. P. F. Lesgafta, St. Petersburg
Reviewers:
V. I. Kuleshov, doctor med. sciences, prof. (VmedA named after S. M. Kirov)
I. M. Kozlov, Doctor of Biology and doctor ped. sciences, prof. (NSU named after P.F. Lesgaft, St. Petersburg)
© Solodkov A. S., Sologub E. B., 2001, 2005, 2008, 2015, 2017
© Publication, LLC Publishing House "Sport", 2017
Aleksey Sergeevich Solodkov – Professor of the Department of Physiology of the National State University of Physical Culture, Sports and Health named after. P. F. Lesgafta (head of the department for 25 years, 1986–2012).
Honored Scientist of the Russian Federation, Academician of the Petrovsky Academy of Sciences and Arts, Honorary Worker of Higher Professional Education of the Russian Federation, Chairman of the section “Physiology of Sports” and member of the Board of the St. Petersburg Physiological Society named after. I. M. Sechenov.
Sologub Elena Borisovna – doctor biological sciences, professor. Since 2002 he has lived in New York (USA).
At the Department of Physiology of the National State University of Physical Culture, Sports and Health. P.F. Lesgafta worked since 1956, from 1986 to 2002 - as a professor of the department. Was elected academician Russian Academy Medical and Technical Sciences, Honorary Worker higher education Russia, member of the Board of the St. Petersburg Society of Physiologists, Biochemists and Pharmacologists named after. I. M. Sechenov.
Preface
Human physiology is theoretical basis a number of practical disciplines (medicine, psychology, pedagogy, biomechanics, biochemistry, etc.). Without understanding the normal course of physiological processes and the constants that characterize them, various specialists cannot correctly assess the functional state of the human body and its performance in various operating conditions. Knowledge of the physiological mechanisms of regulation of various body functions is important in understanding the course of recovery processes during and after intense muscular labor.
By revealing the basic mechanisms that ensure the existence of an entire organism and its interaction with the environment, physiology makes it possible to clarify and study the conditions and nature of changes in the activity of various organs and systems in the process of human ontogenesis. Physiology is the science that carries out systematic approach in the study and analysis of the diverse intra- and intersystem relationships of the complex human body and their reduction into specific functional formations and a unified theoretical picture.
It is important to emphasize that in the development of modern scientific physiological ideas A significant role belongs to domestic researchers. Knowledge of the history of any science is a necessary prerequisite for a correct understanding of the place, role and significance of the discipline in the content of the socio-political status of society, its influence on this science, as well as the influence of science and its representatives on the development of society. Therefore, consideration of the historical path of development of individual sections of physiology, mention of its most prominent representatives and analysis of the natural science base on which the basic concepts and ideas of this discipline were formed make it possible to assess the current state of the subject and determine its further promising directions.
Physiological science in Russia in the 18th–19th centuries is represented by a galaxy of brilliant scientists - I. M. Sechenov, F. V. Ovsyannikov, A. Ya. Danilevsky, A. F. Samoilov, I. R. Tarkhanov, N. E. Vvedensky and etc. But only I.M. Sechenov and I.P. Pavlov deserve the credit for creating new directions not only in Russian, but also in world physiology.
Physiology as an independent discipline began to be taught in 1738 at the Academic (later St. Petersburg) University. The Moscow University, founded in 1755, also played a significant role in the development of physiology, where the Department of Physiology was opened within it in 1776.
In 1798, the Medical-Surgical (Military Medical) Academy was founded in St. Petersburg, which played an exceptional role in the development of human physiology. The Department of Physiology created under her was successively headed by P. A. Zagorsky, D. M. Vellansky, N. M. Yakubovich, I. M. Sechenov, I. F. Tsion, F. V. Ovsyannikov, I. R. Tarkhanov, I. P. Pavlov, L. A. Orbeli, A. V. Lebedinsky, M.P. Brestkin and other outstanding representatives of physiological science. Behind each named name there are discoveries in physiology that are of global significance.
Physiology was included in the curriculum of physical education universities from the first days of their organization. At the Higher Courses of Physical Education created by P. F. Lesgaft in 1896, a physiology office was immediately opened, the first head of which was Academician I. R. Tarkhanov. In subsequent years, physiology was taught here by N.P. Kravkov, A.A. Walter, P.P. Rostovtsev, V.Ya. Chagovets, A. G. Ginetsinsky, A. A. Ukhtomsky, L. A. Orbeli, I. S. Beritov, A. N. Krestovnikov, G. V. Folbort and others.
The rapid development of physiology and the acceleration of scientific and technological progress in the country led to the emergence in the 30s of the 20th century of a new independent section of human physiology - sports physiology, although individual works devoted to the study of body functions during exercise physical activity, published back in late XIX century (I. O. Rozanov, S. S. Gruzdev, Yu. V. Blazhevich, P. K. Gorbachev, etc.). It should be emphasized that systematic research and teaching of sports physiology began in our country earlier than abroad, and was more targeted. By the way, we note that only in 1989 the General Assembly International Union Physiological Sciences decided to create a commission under it “Physiology of Sports”, although similar commissions and sections in the system of the USSR Academy of Sciences, the USSR Academy of Medical Sciences, the All-Union Physiological Society named after. I. P. Pavlova of the USSR State Sports Committee have existed in our country since the 1960s.
The theoretical prerequisites for the emergence and development of sports physiology were created by the fundamental works of I. M. Sechenov, I. P. Pavlov, N. E. Vvedensky, A. A. Ukhtomsky, I. S. Beritashvili, K. M. Bykov and others. However, the systematic study of the physiological foundations of physical culture and sports began much later. Particularly great merit in the creation of this section of physiology belongs to L. A. Orbeli and his student A. N. Krestovnikov, and it is inextricably linked with the formation and development of the University of Physical Culture. P.F. Lesgaft and his department of physiology - the first such department among physical education universities in the country and in the world.
After the creation in 1919 of the Department of Physiology at the Institute of Physical Education named after. P. F. Lesgaft teaching this subject carried out by L. A. Orbeli, A. N. Krestovnikov, V. V. Vasilyeva, A. B. Gandelsman, E. K. Zhukov, N. V. Zimkin, A. S. Mozzhukhin, E. B. Sologub, A. . S. Solodkov and others. In 1938, A. N. Krestovnikov published the first “Textbook of Physiology” in our country and in the world for physical education institutes, and in 1939 – the monograph “Physiology of Sports”. Important role Three editions of the “Textbook of Human Physiology” edited by N.V. Zimkin (1964, 1970, 1975) played a role in the further development of teaching the discipline.
