The structure and mechanism of contraction of skeletal muscles. Skeletal muscle contraction and its mechanisms What causes skeletal muscle contraction

31.07.2024

Mobility is a characteristic property of all life forms. Directed movement occurs during the divergence of chromosomes during cell division, active transport of molecules, movement of ribosomes during protein synthesis, contraction and relaxation of muscles. Muscle contraction is the most advanced form of biological mobility. Any movement, including muscle movement, is based on general molecular mechanisms.

In humans, there are several types of muscle tissue. Striated muscle tissue makes up the skeletal muscles (skeletal muscles that we can contract voluntarily). Smooth muscle tissue is part of the muscles of internal organs: the gastrointestinal tract, bronchi, urinary tract, blood vessels. These muscles contract involuntarily, regardless of our consciousness.

In this lecture we will look at the structure and processes of contraction and relaxation of skeletal muscles, since they are of greatest interest for the biochemistry of sports.

Mechanism muscle contraction has not yet been fully disclosed.

The following is known for certain.

1. The source of energy for muscle contraction is ATP molecules.

2. ATP hydrolysis is catalyzed during muscle contraction by myosin, which has enzymatic activity.

3. The trigger mechanism for muscle contraction is an increase in the concentration of calcium ions in the sarcoplasm of myocytes, caused by a nerve motor impulse.

4. During muscle contraction, cross bridges or adhesions appear between thin and thick strands of myofibrils.

5. During muscle contraction, thin filaments slide along thick filaments, which leads to shortening of myofibrils and the entire muscle fiber as a whole.

There are many hypotheses explaining the mechanism of muscle contraction, but the most substantiated is the so-called hypothesis (theory) of “sliding threads” or “rowing hypothesis”.

In a resting muscle, thin and thick filaments are in a separated state.

Under the influence of a nerve impulse, calcium ions leave the cisterns of the sarcoplasmic reticulum and attach to the thin filament protein, troponin. This protein changes its configuration and changes the configuration of actin. As a result, a cross bridge is formed between the actin of the thin filaments and the myosin of the thick filaments. This increases the ATPase activity of myosin. Myosin breaks down ATP and, due to the energy released, the myosin head rotates like a hinge or oar of a boat, which leads to the sliding of muscle filaments towards each other.

Having made a turn, the bridges between the threads are broken. The ATPase activity of myosin decreases sharply, and ATP hydrolysis stops. However, with the further arrival of the nerve impulse, the cross bridges are formed again, since the process described above is repeated again.

Each contraction cycle uses up 1 molecule of ATP.

Muscle contraction is based on two processes:

helical coiling of contractile proteins;

cyclically repeating formation and dissociation of a complex between the myosin chain and actin.

Muscle contraction is initiated by the arrival of an action potential at the end plate of the motor nerve, where the neurohormone acetylcholine is released, the function of which is to transmit impulses. First, acetylcholine interacts with acetylcholine receptors, which leads to propagation of an action potential along the sarcolemma. All this causes an increase in the permeability of the sarcolemma for Na + cations, which rush into the muscle fiber, neutralizing the negative charge on the inner surface of the sarcolemma. Connected to the sarcolemma are the transverse tubes of the sarcoplasmic reticulum, through which the excitation wave propagates. From the tubes, the excitation wave is transmitted to the membranes of the vesicles and cisterns, which entwine the myofibrils in the areas where the interaction of actin and myosin filaments occurs. When a signal is transmitted to the cisterns of the sarcoplasmic reticulum, the latter begin to release the Ca 2+ contained in them. The released Ca 2+ binds to Tn-C, which causes conformational shifts that are transmitted to tropomyosin and then to actin. Actin seems to be released from the complex with the components of thin filaments in which it was located. Next, actin interacts with myosin, and the result of this interaction is the formation of adhesions, which makes it possible for the thin filaments to move along the thick ones.

The generation of force (shortening) is due to the nature of the interaction between myosin and actin. The myosin rod has a movable hinge, in the area of which rotation occurs when the globular head of myosin binds to a certain area of actin. It is these turns, occurring simultaneously in numerous areas of interaction between myosin and actin, that cause the retraction of actin filaments (thin filaments) into the H-zone. Here they contact (at maximum shortening) or even overlap each other, as shown in the figure.

Drawing. Reduction mechanism: A– state of rest; b– moderate reduction; V– maximum reduction

The energy for this process is supplied by the hydrolysis of ATP. When ATP attaches to the head of the myosin molecule, where the active center of myosin ATPase is localized, no connection is formed between the thin and thick filaments. The resulting calcium cation neutralizes the negative charge of ATP, promoting proximity to the active center of myosin ATPase. As a result, myosin phosphorylation occurs, i.e., myosin is charged with energy, which is used to form adhesions with actin and to advance the thin filament. After the thin filament advances one “step,” ADP and phosphoric acid are split off from the actomyosin complex. A new ATP molecule then attaches to the myosin head, and the whole process is repeated with the next head of the myosin molecule.

ATP consumption is also necessary for muscle relaxation. After the cessation of the motor impulse, Ca 2+ passes into the cisterns of the sarcoplasmic reticulum. Tn-C loses the calcium bound to it, resulting in conformational shifts in the troponin-tropomyosin complex, and Tn-I again closes the active centers of actin, making them unable to interact with myosin. The Ca 2+ concentration in the region of contractile proteins becomes below the threshold, and muscle fibers lose their ability to form actomyosin.

Under these conditions, the elastic forces of the stroma, deformed at the time of contraction, take over, and the muscle relaxes. In this case, thin threads are removed from the space between the thick threads of disk A, zone H and disk I acquire their original length, lines Z move away from each other to the same distance. The muscle becomes thinner and longer.

Hydrolysis rate ATP during muscular work it is huge: up to 10 micromol per 1 g of muscle in 1 minute. General reserves ATP small, therefore, to ensure normal muscle function ATP must be restored at the same rate at which it is consumed.

Muscle relaxation occurs after the cessation of a long-term nerve impulse. At the same time, the permeability of the wall of the sarcoplasmic reticulum tanks decreases, and calcium ions, under the action of the calcium pump, using the energy of ATP, go into the tanks. The removal of calcium ions into the reticulum tanks after the cessation of the motor impulse requires significant energy expenditure. Since the removal of calcium ions occurs towards a higher concentration, i.e. against the osmotic gradient, then two molecules of ATP are spent on removing each calcium ion. The concentration of calcium ions in the sarcoplasm quickly decreases to the initial level. The proteins again acquire the conformation characteristic of the resting state.

Introduction

All life activity of animals and humans is inextricably linked with mechanical movement carried out by muscles. All body movements, blood circulation, breathing and other acts are possible due to the presence in the body of muscles that have a special protein contractile complex - actomyosin.

However, the presence of contractile elements is important not only when performing the above macro movements. Currently, more and more data are accumulating on the role of contractile elements in microprocesses, in particular during the active transport of substances through membranes and during the movement of the cytoplasm. It has been established that the cytoplasm of all cells is in constant motion. According to Kamiya, the cytoplasm has oscillatory, circulating, gushing and other types of movement, which undoubtedly plays a large role in the course of metabolic processes in cells. Currently, there is no single point of view on the reasons for the origin of these movements of the cytoplasm, but the most likely hypothesis is the functioning of contractile elements similar to muscle ones.

Skeletal muscle contraction

smooth muscle contraction excitability

The main physiological properties of muscles are their excitability, conductivity and contractility. The latter manifests itself either in muscle shortening or in the development of tension.

Myography To record muscle contraction, the myography technique is used, i.e. graphically recording the contraction using a lever attached to one end of the muscle. The free end of the lever draws a contraction curve - a myogram - on the kymograph tape. This method of recording muscle contraction is simple and does not require complex equipment, but it has the disadvantage that the inertia of the lever and its friction on the surface of the kymograph tape somewhat distorts the recording. To avoid this drawback, a special sensor is now used that converts mechanical changes (linear movements or muscle efforts) into fluctuations in the strength of the electric current. The latter are recorded using a loop or cathode oscilloscope.

An accurate technique is also optical registration, performed using a beam of light reflected from a mirror glued to the belly of the muscle.

According to their own mechanical properties of the muscle belong to elastomers - materials with elasticity (stretchability and elasticity). If a muscle is subjected to external mechanical force, it stretches. The amount of muscle stretch in accordance with Hooke's law will be proportional to the amount of deforming force (within certain limits):

where Dl is the absolute lengthening of the muscle; l -- initial muscle length; F-- deforming force; S -- cross-sectional area of the muscle; b - elasticity coefficient. Magnitude of ratio F/S is called mechanical stress, and the value l/b is called the elastic modulus; it shows the amount of stress required to elongate a body by 2 times its original length.

In terms of its properties, muscle is close to rubber; the elastic modulus for both of these materials is approximately 10 kgf/cm2. Muscles also have other properties inherent in rubber. As with rubber stretching, when a muscle is strongly stretched, local crystallization is observed (ordering of the macromolecular protein structure of the fibrillar type). This phenomenon was studied by X-ray diffraction analysis. This releases crystallization heat, causing the muscle temperature to increase during stretching.

Once the external force is removed, the muscle regains its length. However, recovery is not complete. The presence of residual deformation characterizes the plasticity of the muscle - the ability to maintain its shape after the cessation of force. Thus, the muscle is not an absolutely elastic body, but has viscoelastic properties. When stretched very strongly, the muscle behaves like a normal elastic body. In this case, when stretched, the temperature of the muscle decreases.

When a muscle contracts, tension develops and work is done. Muscles have contractile and elastic elements. Therefore, the tension that arises and the work done is caused not only by the active contraction of the contractile complex, but also by passive contraction, determined by the elasticity or the so-called sequential elastic component of the muscle. Due to the sequential elastic component, work is performed only if the muscle has been previously stretched, and the amount of this work is proportional to the amount of muscle stretch. This largely explains the fact that the most powerful movements are performed with a large amplitude, which provides preliminary stretching of the muscles.

Muscle contractions are divided into isometric- occurring at a constant muscle length, and isotonic- occurring at constant voltage. Purely isometric or purely isotonic contractions with greater or lesser approximation can only be obtained in laboratory conditions when working on isolated muscles. In the body, muscle contractions are never purely isometric or purely isotonic.

Skeletal muscles are attached to bones using tendons, which form a system of levers. In most cases, muscles are attached to bones in such a way that when they contract, there is a gain in range of motion and an equivalent loss in strength. The lever arm of a muscle is in most cases smaller than the lever arm of the corresponding bone. According to Ackerman, the mechanical gain in range of motion of most human limbs ranges from 2.5 to 20. For the biceps brachii, it is approximately 10. As bones move, the ratio of the muscle's lever arms to the bones changes, resulting in changes in muscle tension. For this reason, isotonic contractions are not observed under natural conditions. For the same reason, the above-mentioned values of the mechanical gain in the amplitude of movements change during the contraction process.

Depending on the amount of force that the muscle overcomes, the speed of contraction (shortening) of the muscle varies. Hill, based on experimental data obtained when working on isolated muscles, derived the so-called basic equation of muscle contraction. According to Hill, the speed of muscle contraction v is hyperbolically dependent on the magnitude of the load F:

(F + a) (v + b) = const,

Where A and b -- constants approximately equal? F and accordingly? v.

Fig.1. Dependence of the speed of contraction of the frog muscle on the magnitude of the load

Bayer made interesting comments on the equation. The equation is reduced to the form

F" v" = const,

if accepted F" = F + a And v" = v + b. Work F x v" represents the total power developed by a muscle during contraction. Because Fv less F"v", i.e. external power is less than the total power, then it should be assumed that the muscle performs not only external work, but also some internal work, manifested in the fact that the load seems to increase by A, and the speed of contraction by the amount b . This internal work can be interpreted as energy loss due to intramolecular friction in the form of thermal dissipation. Then, taking into account the comments made, it can be noted that the total muscle power within physiological limits is a constant value that does not depend on the magnitude of the load and the speed of contraction.

From a thermodynamic point of view, muscle is a system that converts chemical energy (ATP energy) into mechanical work, i.e. muscle is a chemo-mechanical machine.

As already noted, when a muscle contracts, heat is generated. Hill, using thermoelectric methods, established that with each stimulation, the heat of activation Q, which is constant in value and independent of the load, is first released, and then the heat of contraction kD l, proportional to muscle contraction Dl and load independent (k-proportionality coefficient). If the contraction is isotonic, then the muscle produces work A equal to the product of the load F by the magnitude of the contraction: A = FDl. According to the first law of thermodynamics, the change in internal energy DU of the muscle will be equal to the sum of the heat released and the work done:

-ДU = Q + kДl + FДl = Q + Дl (F + k)

Then the efficiency of muscle contraction will be equal to:

Considering that the values of Q and k do not depend on F, it follows from the last equation that, within certain limits, the efficiency of muscle contraction will increase with increasing load.

Hill, based on the data he obtained in experiments, determined that the efficiency of muscle contraction is approximately 40%. If a muscle worked like a heat engine with an efficiency of 40%, then at an environmental temperature of 20 0 C, the temperature of the muscle should be equal to 215 0 C. The efficiency value of 40% shows the efficiency of converting ATP energy into mechanical energy. If we take into account that the efficiency of oxidative phosphorylation, during which ATP is synthesized, is about 50%, then the total efficiency of converting nutrient energy into mechanical energy will be approximately 20%.

Methods of muscle irritation. In order to cause muscle contraction, it is subjected to irritation. Direct irritation of the muscle itself (for example, by electric current) is called direct irritation; irritation of a motor nerve leading to contraction of a muscle innervated by this nerve is called indirect irritation. Due to the fact that the excitability of muscle tissue is less than that of nervous tissue, the application of irritating current electrodes directly to the muscle does not yet provide direct irritation: the current, spreading through the muscle tissue, acts primarily on the endings of the motor nerves located in it and excites them, which leads to muscle contraction. To obtain muscle contraction under the influence of direct stimulation, it is necessary to either turn off the motor nerve endings in it with curare poison, or apply a stimulus through a microelectrode inserted into the muscle fiber.

Introduction

The basis of all types of muscle contraction is the interaction of actin and myosin. In skeletal muscle, myofibrils (about two-thirds of the dry weight of muscle) are responsible for contraction. Myofibrils are structures 1 - 2 microns thick, consisting of sarcomeres - structures about 2.5 microns long, consisting of actin and myosin (thin and thick) filaments and Z-disks connected to actin filaments. Contraction occurs with an increase in the concentration of Ca 2+ ions in the cytoplasm as a result of the sliding of myosin filaments relative to actin filaments. The source of contraction energy is ATP. The efficiency of a muscle cell is about 50%.

Myosin sliding relative to actin

Myosin heads break down ATP and, due to the released energy, change conformation, sliding along actin filaments. The cycle can be divided into 4 stages:

The free myosin head binds to ATP and hydrolyzes it to ADP and phosphate and remains associated with them. (A reversible process - the energy released as a result of hydrolysis is stored in the changed conformation of myosin).
The heads bind weakly to the next actin subunit, the phosphate is released, and this leads to strong binding of the myosin head to the actin filament. This reaction is already irreversible.
The head undergoes a conformational change that pulls the thick filament toward the Z-disc (or, equivalently, the free ends of the thin filaments toward each other).
ADP is released, due to this the head is separated from the actin filament. A new ATP molecule attaches.

The cycle is then repeated until the concentration of Ca 2+ ions decreases or the ATP supply is exhausted (as a result of cell death). The speed of myosin sliding along actin is ≈15 μm/sec. There are many (about 500) myosin molecules in the myosin filament and, therefore, during contraction, the cycle is repeated by hundreds of heads at once, which leads to fast and strong contraction. It should be noted that myosin behaves like an enzyme - an actin-dependent ATPase. Since each repetition of the cycle is associated with ATP hydrolysis, and therefore with a positive change in free energy, the process is unidirectional. Myosin moves along actin only towards the plus end.

Successive stages

Source of energy for reduction

To contract a muscle, the energy of ATP hydrolysis is used, but the muscle cell has an extremely efficient system for regenerating the ATP reserve, so that in a relaxed and working muscle the ATP content is approximately equal. The enzyme phosphocreatine kinase catalyzes the reaction between ADP and creatine phosphate, the products of which are ATP and creatine. Creatine phosphate contains more stored energy than ATP. Thanks to this mechanism, during a burst of activity in the muscle cell, the content of creatine phosphate drops, but the amount of the universal energy source - ATP - does not change. Mechanisms for regenerating ATP reserves may vary depending on the partial pressure of oxygen in surrounding tissues (see Anaerobic Organisms).

Regulatory mechanism

Mostly neurons are involved in the regulation of muscle activity, but there are cases where hormones (for example, adrenaline and oxytocin) also control smooth muscle contraction. The contraction signal can be divided into several stages:

From cell membrane to sarcoplasmic reticulum

The effect of a transmitter released from a motor neuron causes an action potential on the cell membrane of the muscle cell, which is transmitted further using special membrane invaginations called T-tubules, which extend from the membrane into the cell. From the T-tubules, the signal is transmitted to the sarcoplasmic reticulum - a special compartment of flattened membrane vesicles (endoplasmic reticulum of the muscle cell) surrounding each myofibril. This signal causes the opening of Ca 2+ channels in the reticulum membrane. Back Ca 2+ ions enter the reticulum with the help of membrane calcium pumps - Ca 2+ -ATPase.

From the release of Ca 2+ ions to the contraction of myofibrils

The mechanism of muscle contraction taking into account troponin and tropomyosin

In order to control contraction, the protein tropomyosin and a complex of three proteins - troponin (the subunits of this complex are called troponins T, I and C) are attached to the actin filament. Troponin C is a close homologue of another protein, calmodulin. There is only one troponin complex located every seven actin subunits. The binding of actin to troponin I moves tropomyosin to a position that interferes with the binding of myosin to actin. Troponin C binds to four Ca 2+ ions and weakens the effect of troponin I on actin, and tropomyosin occupies a position that does not interfere with the connection of actin with myosin.

Major proteins of myofibrils

Protein	Protein %	His pier. mass, kDa	Its function
Myosin	44	510	Main component of thick filaments. Forms bonds with actin. Moves along actin due to ATP hydrolysis.
Actin	22	42	Main component of thin filaments. During muscle contraction, myosin moves along it.
Titin	9	2500	A large flexible protein that forms a chain to bind myosin to the Z-disc.
Troponin	5	78	A complex of three proteins that regulates contraction when bound to Ca 2+ ions.
Tropomyosin	5	64	A rod-shaped protein associated with actin filaments that blocks myosin movement.
Nebulin	3	600	A long, inextensible protein associated with the Z-disk and running parallel to actin filaments.

Literature

B. Alberts, D. Bray, J. Lewis, M. Reff, K. Roberts, J. Watson, Molecular biology of the cell - In 3 volumes - Trans. from English - T.2. - M.: Mir, 1994. - 540 p.
M. B. Berkinblit, S. M. Glagolev, V. A. Furalev, General biology - In 2 parts - Part 1. - M.: MIROS, 1999. - 224 p.: ill.

MUSCLE CONTRACTION- shortening or tension of muscles in response to irritation caused by motor discharge. neurons. The M. s model has been adopted, according to which, when the surface of the muscle fiber membrane is excited, the action potential first spreads through the system... ... Biological encyclopedic dictionary

muscle contraction- raumens susitraukimas statusas T sritis Kūno kultūra ir sportas apibrėžtis Raumens ilgio kitimas cheminei energijai virstant mechanine ir šilumine. Skiriamas auksotoninis, izometrinis, izotoninis, maksimalusis ir pavienis raumens… … Sporto terminų žodynas

muscle contraction- raumens susitraukimas statusas T sritis Kūno kultūra ir sportas apibrėžtis Raumenį sudarančių skaidulų patrumpėjimas arba įtampos kitimas atliekant judesį (veiksmą). atitikmenys: engl. muscle contraction vok. Muskelkontraktion, f rus. muscular… …Sporto terminų žodynas

muscle contraction- see Abbreviation... Large medical dictionary

Muscle contraction- shortening of a muscle, as a result of which it produces mechanical work. M. s. provides the ability of animals and humans to voluntary movements. The most important component of muscle tissue (See Muscle tissue) proteins (16.5... ...

MUSCLE CONTRACTION- the main function of muscle tissue is the shortening or tension of muscles in response to irritation caused by the discharge of motor neurons. M. s. underlies all movements of the human body. There are M. s. isometric, when the muscle develops force... ... Psychomotorics: dictionary-reference book

Isometric muscle contraction- contraction of a muscle, expressed in an increase in its tension with a constant length (for example, contraction of a muscle of a limb, both ends of which are fixed motionless). In the body to I. m.s. the tension developed by the muscle when attempting... is approaching. Great Soviet Encyclopedia

Isotonic muscle contraction- contraction of a muscle under constant tension, expressed in a decrease in its length and an increase in cross-section. In the body I. m.s. is not observed in its pure form. To purely I. m.s. movement of the unloaded limb is approaching; at… … Great Soviet Encyclopedia

Lecture notes| Lecture summary | Interactive test | Download abstract

» Structural organization of skeletal muscle
» Molecular mechanisms of skeletal muscle contraction
» Coupling of excitation and contraction in skeletal muscle
» Relaxation of skeletal muscle
»
» Skeletal muscle work
» Structural organization and contraction of smooth muscle
» Physiological properties of muscles

Muscle contraction is a vital function of the body associated with defensive, respiratory, nutritional, sexual, excretory and other physiological processes. All types of voluntary movements - walking, facial expressions, movements of the eyeballs, swallowing, breathing, etc. are carried out by skeletal muscles. Involuntary movements (except for heart contraction) - peristalsis of the stomach and intestines, changes in the tone of blood vessels, maintenance of bladder tone - are caused by contraction of smooth muscles. The work of the heart is ensured by the contraction of the cardiac muscles.

Structural organization of skeletal muscle

Muscle fiber and myofibril (Fig. 1). Skeletal muscle consists of many muscle fibers that have points of attachment to bones and are located parallel to each other. Each muscle fiber (myocyte) includes many subunits - myofibrils, which are built from blocks (sarcomeres) repeating in the longitudinal direction. The sarcomere is the functional unit of the contractile apparatus of skeletal muscle. The myofibrils in the muscle fiber lie in such a way that the location of the sarcomeres in them coincides. This creates a pattern of cross striations.

Sarcomere and filaments. Sarcomeres in the myofibril are separated from each other by Z-plates, which contain the protein beta-actinin. Thin actin filaments extend from the Z plate in both directions. In the spaces between them are thicker myosin filaments.

Actin filament externally resembles two strings of beads twisted into a double helix, where each bead is an actin protein molecule. In the recesses of actin helices, at equal distances from each other, lie molecules of the protein troponin, connected to filamentous molecules of the protein tropomyosin.

Myosin filaments are formed by repeating molecules of the myosin protein. Each myosin molecule has a head and a tail. The myosin head can bind to an actin molecule, forming a so-called cross bridge.

The cell membrane of the muscle fiber forms invaginations (transverse tubules), which perform the function of conducting excitation to the membrane of the sarcoplasmic reticulum. The sarcoplasmic reticulum (longitudinal tubes) is an intracellular network of closed tubes and performs the function of depositing Ca++ ions.

Motor unit. The functional unit of skeletal muscle is the motor unit (MU). MU is a set of muscle fibers that are innervated by the processes of one motor neuron. Excitation and contraction of the fibers that make up one motor unit occur simultaneously (when the corresponding motor neuron is excited). Individual motor units can be excited and contracted independently of each other.

Molecular mechanisms of contractionskeletal muscle

According to the sliding filament theory, muscle contraction occurs due to the sliding movement of actin and myosin filaments relative to each other. The thread sliding mechanism involves several sequential events.

Myosin heads attach to actin filament binding centers (Fig. 2, A).

The interaction of myosin with actin leads to conformational rearrangements of the myosin molecule. The heads acquire ATPase activity and rotate 120°. Due to the rotation of the heads, the actin and myosin filaments move “one step” relative to each other (Fig. 2, B).

Disconnection of actin and myosin and restoration of the head conformation occurs as a result of the attachment of an ATP molecule to the myosin head and its hydrolysis in the presence of Ca++ (Fig. 2, B).

The cycle “binding – change in conformation – disconnection – restoration of conformation” occurs many times, as a result of which actin and myosin filaments are displaced relative to each other, the Z-disks of sarcomeres come closer and the myofibril is shortened (Fig. 2, D).

Pairing of excitation and contractionin skeletal muscle

In the resting state, thread sliding in the myofibril does not occur, since the binding centers on the actin surface are closed by tropomyosin protein molecules (Fig. 3, A, B). Excitation (depolarization) of the myofibril and muscle contraction itself are associated with the process of electromechanical coupling, which includes a series of sequential events.

As a result of the activation of a neuromuscular synapse on the postsynaptic membrane, an EPSP arises, which generates the development of an action potential in the area surrounding the postsynaptic membrane.

Excitation (action potential) spreads along the myofibril membrane and, through a system of transverse tubules, reaches the sarcoplasmic reticulum. Depolarization of the sarcoplasmic reticulum membrane leads to the opening of Ca++ channels in it, through which Ca++ ions enter the sarcoplasm (Fig. 3, B).

Ca++ ions bind to the protein troponin. Troponin changes its conformation and displaces the tropomyosin protein molecules that covered the actin binding centers (Fig. 3, D).

Myosin heads attach to the opened binding centers, and the contraction process begins (Fig. 3, E).

The development of these processes requires a certain period of time (10–20 ms). The time from the moment of excitation of the muscle fiber (muscle) to the beginning of its contraction is called the latent period of contraction.

Skeletal muscle relaxation

Muscle relaxation is caused by the reverse transfer of Ca++ ions through the calcium pump into the channels of the sarcoplasmic reticulum. As Ca++ is removed from the cytoplasm, there are fewer and fewer open binding sites, and eventually the actin and myosin filaments are completely disconnected; muscle relaxation occurs.

Contracture is a persistent, prolonged contraction of a muscle that persists after the cessation of the stimulus. Short-term contracture can develop after tetanic contraction as a result of the accumulation of large amounts of Ca++ in the sarcoplasm; long-term (sometimes irreversible) contracture can occur as a result of poisoning and metabolic disorders.

Phases and modes of skeletal muscle contraction

Phases of muscle contraction

When a skeletal muscle is irritated by a single pulse of electric current of suprathreshold strength, a single muscle contraction occurs, in which 3 phases are distinguished (Fig. 4, A):

latent (hidden) contraction period (about 10 ms), during which the action potential develops and electromechanical coupling processes occur; muscle excitability during a single contraction changes in accordance with the phases of the action potential;

shortening phase (about 50 ms);

relaxation phase (about 50 ms).

Modes of muscle contraction

Under natural conditions, a single muscle contraction is not observed in the body, since a series of action potentials occur along the motor nerves innervating the muscle. Depending on the frequency of nerve impulses coming to the muscle, the muscle can contract in one of three modes (Fig. 4, B).

Single muscle contractions occur at a low frequency of electrical impulses. If the next impulse enters the muscle after the completion of the relaxation phase, a series of successive single contractions occurs.

At a higher impulse frequency, the next impulse may coincide with the relaxation phase of the previous contraction cycle. The amplitude of contractions will be summed up, and serrated tetanus will appear - a long contraction interrupted by periods of incomplete relaxation of the muscle.

With a further increase in the frequency of impulses, each subsequent impulse will act on the muscle during the shortening phase, resulting in smooth tetanus - a long contraction not interrupted by periods of relaxation.

Optimum and pessimum frequency

The amplitude of tetanic contraction depends on the frequency of impulses irritating the muscle. The optimum frequency is the frequency of irritating impulses at which each subsequent impulse coincides with the phase of increased excitability (Fig. 4, A) and, accordingly, causes tetanus of the greatest amplitude. Frequency pessimum is a higher frequency of stimulation at which each subsequent current pulse falls into the refractory phase (Fig. 4, A), as a result of which the amplitude of the tetanus decreases significantly.

Skeletal muscle work

The strength of skeletal muscle contraction is determined by 2 factors:

- the number of units involved in the reduction;

frequency of contraction of muscle fibers.

The work of skeletal muscle is accomplished through a coordinated change in tone (tension) and length of the muscle during contraction.

Types of skeletal muscle work:

dynamic overcoming work is performed when a muscle, contracting, moves the body or its parts in space;

static (holding) work is performed if, due to muscle contraction, parts of the body are maintained in a certain position;

dynamic yielding work is performed if the muscle functions, but at the same time stretches, since the force it makes is not enough to move or hold parts of the body.

During work, the muscle can contract:

isotonic – the muscle shortens under constant tension (external load); isotonic contraction is reproduced only in experiment;

isometrics - muscle tension increases, but its length does not change; the muscle contracts isometrically when performing static work;

auxotonic - muscle tension changes as it shortens; auxotonic contraction is performed during dynamic overcoming work.

Rule of average loads– the muscle can perform maximum work under moderate loads.

Fatigue is a physiological state of a muscle that develops after prolonged work and is manifested by a decrease in the amplitude of contractions, an extension of the latent period of contraction and the relaxation phase. The causes of fatigue are: depletion of ATP reserves, accumulation of metabolic products in the muscle. Muscle fatigue during rhythmic work is less than synapse fatigue. Therefore, when the body performs muscular work, fatigue initially develops at the level of the synapses of the central nervous system and neuromuscular synapses.

Structural organization and reductionsmooth muscles

Structural organization. Smooth muscle consists of single spindle-shaped cells (myocytes), which are located more or less chaotically in the muscle. Contractile filaments are arranged irregularly, as a result of which there is no transverse striation of the muscle.

The mechanism of contraction is similar to that of skeletal muscle, but the rate of filament sliding and the rate of ATP hydrolysis are 100–1000 times lower than in skeletal muscle.

The mechanism of coupling of excitation and contraction. When the cell is excited, Ca++ enters the cytoplasm of the myocyte not only from the sarcoplasmic reticulum, but also from the intercellular space. Ca++ ions, with the participation of the calmodulin protein, activate the enzyme (myosin kinase), which transfers the phosphate group from ATP to myosin. Phosphorylated myosin heads acquire the ability to attach to actin filaments.

Contraction and relaxation of smooth muscles. The rate of removal of Ca++ ions from the sarcoplasm is much less than in skeletal muscle, as a result of which relaxation occurs very slowly. Smooth muscles perform long tonic contractions and slow rhythmic movements. Due to the low intensity of ATP hydrolysis, smooth muscles are optimally adapted for long-term contraction, which does not lead to fatigue and high energy consumption.

Physiological properties of muscles

Common physiological properties of skeletal and smooth muscles are excitability and contractility. Comparative characteristics of skeletal and smooth muscles are given in table. 6.1. The physiological properties and characteristics of the cardiac muscle are discussed in the section “Physiological mechanisms of homeostasis”.

Table 7.1. Comparative characteristics of skeletal and smooth muscles

Property	Skeletal muscles	Smooth muscle
Depolarization rate		slow
Refractory period	short	long
Nature of contraction	fast phasic	slow tonic
Energy costs
Plastic
Automatic
Conductivity
Innervation	motor neurons of the somatic NS	postganglionic neurons of the autonomic nervous system
Performed movements	arbitrary	involuntary
Chemical sensitivity
Ability to divide and differentiate

The plasticity of smooth muscles is manifested in the fact that they can maintain constant tone both in a shortened and in an extended state.

The conductivity of smooth muscle tissue is manifested in the fact that excitation spreads from one myocyte to another through specialized electrically conductive contacts (nexuses).

The property of smooth muscle automaticity is manifested in the fact that it can contract without the participation of the nervous system, due to the fact that some myocytes are able to spontaneously generate rhythmically repeating action potentials.

All muscles of the body are divided into smooth and striated.

Mechanisms of skeletal muscle contraction

Striated muscles are divided into two types: skeletal muscles and myocardium.

The structure of muscle fiber

The muscle cell membrane, called the sarcolemma, is electrically excitable and capable of conducting action potentials. These processes in muscle cells occur according to the same principle as in nerve cells. The resting potential of a muscle fiber is approximately -90 mV, that is, lower than that of a nerve fiber (-70 mV); the critical depolarization at which an action potential occurs is the same as that of a nerve fiber. Hence: the excitability of the muscle fiber is somewhat lower than the excitability of the nerve fiber, since the muscle cell needs to be depolarized by a greater amount.

The muscle fiber's response to stimulation is reduction, which is performed by the contractile apparatus of the cell - myofibrils. They are cords consisting of two types of threads: thick - myosin, and thin - actin. Thick filaments (15 nm in diameter and 1.5 µm in length) contain only one protein - myosin. Thin filaments (7 nm in diameter and 1 µm in length) contain three types of proteins: actin, tropomyosin and troponin.

Actin is a long protein thread that consists of individual globular proteins linked together in such a way that the entire structure is an elongated chain. Molecules of globular actin (G-actin) have lateral and terminal binding centers with other similar molecules. As a result, they come together in such a way that they form a structure that is often compared to two strands of beads joined together. The ribbon formed from G-actin molecules is twisted into a spiral. This structure is called fibrillar actin (F-actin). The helix pitch (turn length) is 38 nm; for each turn of the helix there are 7 pairs of G-actin. The polymerization of G-actin, that is, the formation of F-actin, occurs due to the energy of ATP, and, conversely, when F-actin is destroyed, energy is released.

Fig.1. Association of individual G-actin globules into F-actin

The protein tropomyosin is located along the spiral grooves of actin filaments. Each tropomyosin filament, 41 nm long, consists of two identical α-chains twisted together into a spiral with a turn length of 7 nm. Along one turn of F-actin there are two tropomyosin molecules. Each tropomyosin molecule connects, slightly overlapping, to the next, resulting in a tropomyosin filament extending continuously along the actin.

Fig.2. The structure of a thin filament of myofibril

In striated muscle cells, the thin filaments, in addition to actin and tropomyosin, also contain the protein troponin. This globular protein has a complex structure. It consists of three subunits, each of which performs a different function during the contraction process.

Thick thread consists of a large number of molecules myosin, collected in a bundle. Each myosin molecule, 155 nm long and 2 nm in diameter, consists of six polypeptide threads: two long and four short. The long chains are twisted together into a spiral with a pitch of 7.5 nm and form the fibrillar part of the myosin molecule. At one end of the molecule, these chains unwind and form a forked end. Each of these ends forms a complex with two short chains, that is, there are two heads on each molecule. This is the globular part of the myosin molecule.

Fig.3. The structure of the myosin molecule.

Myosin has two fragments: light meromyosin (LMM) and heavy meromyosin (HMM), between them there is a hinge. TMM consists of two subfragments: S1 and S2. The LMM and subfragment S2 are embedded in a bundle of threads, and subfragment S1 protrudes above the surface. This protruding end (myosin head) is able to bind to the active site on the actin filament and change the angle of inclination to the myosin filament bundle. The combination of individual myosin molecules into a bundle occurs due to electrostatic interactions between the LMMs. The central part of the thread has no heads. The entire complex of myosin molecules extends over 1.5 µm. It is one of the largest biological molecular structures known in nature.

When viewing a longitudinal section of striated muscle through a polarizing microscope, light and dark areas are visible. Dark areas (disks) are anisotropic: in polarized light they appear transparent in the longitudinal direction and opaque in the transverse direction, designated by the letter A. Light areas are isotropic and designated by the letter I. Disc I includes only thin threads, and disc A includes both thick and thin. In the middle of disk A there is a bright stripe called the H-zone. It does not have thin threads. Disc I is separated by a thin stripe Z, which is a membrane containing structural elements that hold the ends of thin filaments together. The area between two Z-lines is called sarcomere.

Fig.4. Myofibril structure (cross section)

Fig.5. Structure of striated muscle (longitudinal section)

Each thick thread is surrounded by six thin ones, and each thin thread is surrounded by three thick ones. Thus, in a cross section, the muscle fiber has a regular hexagonal structure.

Muscle contraction

When a muscle contracts, the length of actin and myosin filaments does not change. There is only a displacement of them relative to each other: thin threads move into the gap between the thick ones. In this case, the length of disk A remains unchanged, but disk I is shortened, and the H strip almost disappears. Such sliding is possible due to the existence of cross bridges (myosin heads) between thick and thin filaments. During contraction, the length of the sarcomere can change from approximately 2.5 to 1.7 μm.

The myosin filament has many heads with which it can bind to actin. The actin filament, in turn, has sections (active centers) to which myosin heads can attach. In a resting muscle cell, these binding centers are covered by tropomyosin molecules, which prevents the formation of bonds between thin and thick filaments.

In order for actin and myosin to interact, the presence of calcium ions is necessary. At rest they reside in the sarcoplasmic reticulum. This organelle is a membrane cavity containing a calcium pump, which, using the energy of ATP, transports calcium ions into the sarcoplasmic reticulum. Its inner surface contains proteins capable of binding Ca2+, which somewhat reduces the difference in the concentrations of these ions between the cytoplasm and the reticulum cavity. An action potential propagating along the cell membrane activates the reticulum membrane located close to the cell surface and causes the release of Ca2+ into the cytoplasm.

The troponin molecule has a high affinity for calcium.

Under its influence, it changes the position of the tropomyosin filament on the actin filament in such a way that the active center, previously covered by tropomyosin, opens. A cross bridge is attached to the opened active center. This leads to the interaction of actin with myosin. After bond formation, the myosin head, previously located at right angles to the filaments, tilts and pulls the actin filament relative to the myosin filament by approximately 10 nm. The resulting atin-myosin complex prevents further sliding of the threads relative to each other, so its separation is necessary. This is only possible due to the energy of ATP. Myosin has ATPase activity, that is, it is capable of causing ATP hydrolysis. The energy released in this case breaks the bond between actin and myosin, and the myosin head is able to interact with a new part of the actin molecule. The work of the bridges is synchronized in such a way that the binding, tilting and breaking of all bridges of one thread occurs simultaneously. When the muscle relaxes, the calcium pump is activated, which reduces the concentration of Ca2+ in the cytoplasm; consequently, connections between thin and thick threads can no longer be formed. Under these conditions, when the muscle is stretched, the threads slide smoothly relative to each other. However, such extensibility is only possible in the presence of ATP. If there is no ATP in the cell, then the actin-myosin complex cannot break. The threads remain rigidly linked to each other. This phenomenon is observed in rigor mortis.

Fig.6. Contraction of the sarcomere: 1 – myosin filament; 2 – active center; 3 – actin filament; 4 – myosin head; 5 - Z-line.

A) there is no interaction between thin and thick threads;

b) in the presence of Ca2+, the myosin head binds to the active center on the actin filament;

V) the cross bridges bend and pull the thin thread relative to the thick one, as a result of which the length of the sarcomere decreases;

G) the bonds between the threads are broken due to the energy of ATP, the myosin heads are ready to interact with new active centers.

There are two modes of muscle contraction: isotonic(the length of the fiber changes, but the voltage remains unchanged) and isometric(the ends of the muscle are fixed, as a result of which it is not the length that changes, but the tension).

Power and speed of muscle contraction

Important characteristics of a muscle are the strength and speed of contraction. The equations expressing these characteristics were empirically obtained by A. Hill and subsequently confirmed by the kinetic theory of muscle contraction (Deshcherevsky model).

Hill's equation, which relates the strength and speed of muscle contraction, has the following form: (P+a)(v+b) = (P0+a)b = a(vmax+b), where v is the speed of muscle shortening; P – muscle force or load applied to it; vmax — maximum speed of muscle shortening; P0 is the force developed by the muscle in the isometric contraction mode; a,b are constants. Total power, developed by the muscle, is determined by the formula: Ntotal = (P+a)v = b(P0-P). Efficiency muscles maintains a constant value ( about 40%) in the range of force values from 0.2 P0 to 0.8 P0. During muscle contraction, a certain amount of heat is released. This quantity is called heat production. Heat production depends only on changes in muscle length and does not depend on load. Constants a And b have constant values for a given muscle. Constant A has the dimension of force, and b– speed. Constant b depends largely on temperature. Constant A is in the range of values from 0.25 P0 to 0.4 P0. Based on these data, it is estimated maximum contraction speed for a given muscle: vmax = b (P0 / a).

Characteristics of muscle tissue.

Skeletal muscle contraction and its mechanisms

Types of muscle tissue. Actino-myosin complex and mechanisms of its functioning.

There are 3 types of animal tissues: 1) muscle, 2) nervous, 3) secretory. The first responds to stimulation by contracting and carrying out the work of displacement. The second is the ability to conduct and analyze impulses, the third is to isolate various secrets.

There are 3 types of muscle tissue: 1. striated, 2. smooth, 3. cardiac.

Characteristics	striped	smooth	cardiac
specialization	very high	least specialized	secondary specialized
structure	fibers up to 10 cm long, divided into subunits - sarcomeres. The fibers are connected to each other by connective tissue and blood vessels. Nerve endings approach the fibers, forming neuromuscular junctions	Consists of individual spindle-like. cells connected into bundles.	The cells branch at the ends and connect with others using processes.
core	Several cores at the periphery	1 core per cent	several cores in the center
cytoplasm	contains mitochondria, sarcoplasm. reticulum, T tubes, glycogen, fat drops	sod. mitochondria, sarcoplasm. reticulum, tubes,	sod. mitochondria, sarcoplasm. reticulum, T tube,
sarcolemma	There is	No	There is
regulation	neurogenic	neurogenic	neurog. and humoral
cross stripes	There is	No	There is
Compound activity.	powerful, fast contractions. The refractory period is short; rest time is short; fatigue is rapid.	slow rhythm	fast rhythm, long refractory time - no fatigue.

Actino-myosin complex. All muscle cells contain a large number of special contractile proteins - 60-80% of the total muscle proteins. Main contractiles

proteins are fibrillar proteins: - myosin- forms thick threads; — actin- forms thin threads. To regulate contraction, globular proteins are used: troponin-tropomyosin.

Myosin - 2-chain structure 1=180 nm and 0=2.5 nm. Actin is a 2-helix peptide chain.

Reduction mechanism: Actin and myosin are spatially separated in the fibril. The nerve impulse causes the release of acetylcholine into the synaptic cleft of the neuromuscular junction. This

causes depolarization of the postsynaptic membrane after binding of the transmitter and

propagation of the action potential across cell membranes and into the muscle

fibers through T tubes. As a result of actin-myosin interaction, fibril contraction occurs. This is achieved by the myosin head pushing the actin filament through the formation of a bridge. When the impulse disappears, Ca2+ is restored, the bridge between actin and myosin is destroyed and the muscle returns to its original state.

Troponin is a globular protein with 3 centers:

- T - binds to tropomyosin

- C - binds Ca2+

- 1 - inhibits actin-myosin interaction.

Contraction phases:

1. Latent period - 0.05 seconds.

2. Contraction phase - 0.1 sec

3. Relaxation period - 0.2 seconds.

Biochemistry of muscle function

1. ATP + myosin-actin complex——-ADP + Myosin + actin + F + energy

2. ADP + creatinine phosphate——ATP + creatine

3. Glycogen—Glucose——Glucose + O2—CO2 + H2O + 38 ATP (aerobic process)

4. Glucose—2 lactic acid + 2 ATP (anaerobic process—dissolves nerve endings—

5. Lactic acid + O2—CO2 + H2O (rest) or Molten acid—glucose—glycogen.

Mechanism of skeletal muscle contraction

Muscle shortening is the result of contraction of multiple sarcomeres. When shortening, the actin filaments slide relative to the myosin filaments, as a result of which the length of each sarcomere of the muscle fiber decreases. At the same time, the length of the threads themselves remains unchanged. Myosin filaments have transverse projections (cross bridges) about 20 nm long. Each protrusion consists of a head, which is connected to the myosin filament through a “neck” (Fig. 23).

In a relaxed state, the muscles of the heads of the cross bridges cannot interact with actin filaments, since their active sites (places of mutual contact with the heads) are isolated by tropomyosin. Shortening of the muscle is the result of conformational changes in the cross bridge: its head tilts by bending the “neck”.

Rice. 23. Spatial organization of contractile and regulatory proteins in striated muscle. The position of the myosin bridge is shown (raking effect, the neck is bent) during the interaction of contractile proteins in muscle fibers (fiber contraction)

Sequence of processes , providing muscle fiber contraction(electromechanical interface):

1. After occurrence PD in the muscle fiber near the synapse (due to the electric field of the PKP) excitation spreads across the myocyte membrane, including on transverse membranes T-tubules. The mechanism of conduction of action potentials along a muscle fiber is the same as through an unmyelinated nerve fiber - the emerging action potential near the synapse, through its electric field, ensures the emergence of new action potentials in the adjacent section of the fiber, etc. (continuous conduction of excitation).

2. Potential actions T-tubules due to its electric field, it activates voltage-gated calcium channels on SPR membrane, as a result of which Ca2+ leaves the SPR tanks according to an electrochemical gradient.

3. In the interfibrillar space Ca2+ contacts with troponin, which leads to its conformation and displacement of tropomyosin, resulting in actin filaments active areas are exposed, with which they connect heads of myosin bridges.

4. As a result of interaction with actin ATPase activity of myosin filament heads increases, ensuring the release of ATP energy, which is spent on bending of the myosin bridge, outwardly reminiscent of the movement of oars when rowing (stroke movement) (see Fig. 23), ensuring the sliding of actin filaments relative to myosin filaments. The energy of one ATP molecule is consumed to complete one rowing movement. In this case, the filaments of contractile proteins are displaced by 20 nm. The attachment of a new ATP molecule to another part of the myosin head leads to the cessation of its engagement, but the energy of ATP is not consumed. In the absence of ATP, myosin heads cannot detach from actin - the muscle is tense; This, in particular, is the mechanism of rigor mortis.

5. After this the heads of the cross bridges, due to their elasticity, return to their original position and establish contact with the next section of actin; then another rowing movement and sliding of actin and myosin filaments occurs again. Similar elementary acts are repeated many times. One rowing movement (one step) causes a decrease in the length of each sarcomere by 1%. When an isolated frog muscle contracts without a load of 50%, sarcomere shortening occurs in 0.1 s. To do this, you need to perform 50 rowing movements.

Mechanism of muscle contraction

Myosin bridges bend asynchronously, but due to the fact that there are many of them and each myosin filament is surrounded by several actin filaments, muscle contraction occurs smoothly.

Relaxation muscle growth occurs due to processes occurring in reverse order. Repolarization of the sarcolemma and T-tubules leads to the closure of voltage-gated calcium channels in the SPR membrane. Ca pumps return Ca2+ to the SPR (the activity of the pumps increases with increasing concentration of free ions).

A decrease in the Ca2+ concentration in the interfibrillar space causes a reverse conformation of troponin, as a result of which tropomyosin filaments isolate the active sites of actin filaments, which makes it impossible for the heads of myosin cross bridges to interact with them. Sliding of actin filaments along myosin filaments in the opposite direction occurs under the influence of gravity and elastic traction of muscle fiber elements, which restores the original dimensions of the sarcomeres.

The source of energy to ensure the work of skeletal muscles is ATP, the costs of which are significant. Even in conditions of basic metabolism, the body uses about 25% of all its energy resources for the functioning of muscles. Energy expenditure increases sharply during physical work.

ATP reserves in muscle fiber are insignificant (5 mmol/l) and can provide no more than 10 single contractions.

Energy consumption ATP is necessary for the following processes.

Firstly, ATP energy is spent to ensure the operation of the Na/K pump (it maintains the concentration gradient of Na+ and K+ inside and outside the cell, forming the PP and PD, which ensures electromechanical coupling) and the operation of the Ca pump, which reduces the concentration of Ca2+ in the sarcoplasm after contraction of the muscle fiber, which leads to relaxation.

Secondly, ATP energy is spent on the rowing movement of myosin bridges (bending them).

ATP resynthesis carried out using the three energy systems of the body.

1. The phosphogenic energy system ensures the resynthesis of ATP due to the highly energy-intensive CP present in the muscles and adenosine diphosphoric acid (adenosine diphosphate, ADP) formed during the breakdown of ATP with the formation of creatine (K): ADP + + CP → ATP + K. This is an instant resynthesis of ATP, while the muscle can develop greater power, but for a short time - up to 6 s, since the reserves of CP in the muscle are limited.

2. The anaerobic glycolytic energy system provides ATP resynthesis using the energy of anaerobic breakdown of glucose to lactic acid. This pathway of ATP resynthesis is fast, but also short-lived (1-2 min), since the accumulation of lactic acid inhibits the activity of glycolytic enzymes. However, lactate, causing a local vasodilator effect, improves blood flow in the working muscle and its supply of oxygen and nutrients.

3. The aerobic energy system ensures the resynthesis of ATP using oxidative phosphorylation of carbohydrates and fatty acids, which occurs in the mitochondria of muscle cells. This method can provide energy for muscle function for several hours and is the main way to provide energy for the work of skeletal muscles.

Types of muscle contractions

Depending on the nature of the abbreviations There are three types of muscles: isometric, isotonic and auxotonic.

Auxotonic muscle contraction involves a simultaneous change in muscle length and tension. This type of contraction is characteristic of natural motor acts and comes in two types: eccentric, when muscle tension is accompanied by its lengthening - for example, during the process of squatting (lowering), and concentric, when muscle tension is accompanied by its shortening - for example, when extending the lower limbs after squatting ( rise).

Isometric muscle contraction- when muscle tension increases, but its length does not change. This type of contraction can be observed in experiment, when both ends of the muscle are fixed and there is no possibility of their approach, and in natural conditions - for example, in the process of squatting and fixing the position.

Isotonic muscle contraction consists of shortening the muscle with constant tension. This type of contraction occurs when an unloaded muscle with one tendon attached contracts without lifting (moving) any external load or lifting a load without acceleration.

Depending on duration There are two types of muscle contractions: solitary and tetanic.

Single muscle contraction occurs when a single irritation of the nerve or muscle itself occurs. Typically the muscle shortens by 5-10% of its original length. There are three main periods on the single contraction curve: 1) latent- time from the moment of irritation to the onset of contraction; 2) period shortening (or development of tension); 3) period relaxation. The duration of single contractions of human muscles is variable. For example, in the soleus muscle it is 0.1 s. During the latent period, excitation of muscle fibers occurs and its conduction along the membrane. The relationship between the duration of a single contraction of a muscle fiber, its excitation and phase changes in the excitability of the muscle fiber are shown in Fig. 24.

The duration of muscle fiber contraction is much longer than that of the AP because time is required for the Ca-pumps to work to return Ca2+ to the SPR and the environment and the greater inertia of mechanical processes compared to electrophysiological ones.

Rice. 24. The ratio of the time of occurrence of AP (A) and a single contraction (B) of the slow fiber of the skeletal muscle of a warm-blooded animal. Arrow– moment of irritation. The contraction time of fast fibers is several times shorter

Tetanic contraction- this is a long-term contraction of a muscle that occurs under the influence of rhythmic stimulation, when each subsequent stimulation or nerve impulses arrive at the muscle while it has not yet relaxed. Tetanic contraction is based on the phenomenon of summation of single muscle contractions (Fig. 25) - an increase in the amplitude and duration of contraction when two or more rapidly successive stimuli are applied to a muscle fiber or a whole muscle.

Rice. Fig. 25. Summation of contractions of the frog gastrocnemius muscle: 1 – curve of a single contraction in response to the first stimulation of the relaxed muscle; 2 – curve of single contraction of the same muscle in response to the second stimulus; 3 – curve of the summed contraction obtained as a result of coupled stimulation of the contracting muscle ( indicated by arrows)

In this case, irritations should arrive during the period of the previous contraction. The increase in contraction amplitude is explained by an increase in the concentration of Ca2+ in the hyaloplasm upon repeated excitation of muscle fibers, since the Ca pump does not have time to return it to the SPR. Ca2+ ensures an increase in the number of zones of engagement of myosin bridges with actin filaments.

If repeated impulses or irritations occur during the muscle relaxation phase, serrated tetanus. If repeated stimulation occurs during the shortening phase, smooth tetanus(Fig. 26).

Rice. 26. Contraction of the frog gastrocnemius muscle at different frequencies of irritation of the sciatic nerve: 1 – single contraction (frequency 1 Hz); 2.3 – serrated tetanus (15-20 Hz); 4.5 – smooth tetanus (25-60 Hz); 6 – relaxation at pessimal frequency of stimulation (120 Hz)

The amplitude of contraction and the magnitude of tension developed by muscle fibers during smooth tetanus are usually 2-4 times greater than during a single contraction. Tetanic contraction of muscle fibers, unlike single contractions, causes them to fatigue more quickly.

As the frequency of nerve or muscle stimulation increases, the amplitude of smooth tetanus increases. Maximum tetanus is called optimum. The increase in tetanus is explained by the accumulation of Ca2+ in the hyaloplasm. With a further increase in the frequency of nerve stimulation (about 100 Hz), the muscle relaxes due to the development of a block in the conduction of excitation in the neuromuscular synapses - Vvedensky pessimum(irritation frequency pessimal) (see Fig. 26). Vvedensky's pessimum can also be obtained with direct, but more frequent irritation of the muscle (about 200 impulses/s), however, for the purity of the experiment, the neuromuscular synapses should be blocked. If, after the occurrence of a pessimum, the frequency of stimulation is reduced to the optimal one, the amplitude of muscle contraction instantly increases - evidence that the pessimum is not the result of muscle fatigue or depletion of energy resources.

Under natural conditions, individual muscle fibers often contract in the serrated tetanus mode, but the contraction of the whole muscle resembles smooth tetanus, due to the asynchrony of their contraction.

Structural organization of skeletal muscle

Sarcomere and filaments. Sarcomeres in the myofibril are separated from each other by Z-plates, which contain the protein beta-actinin. In both directions, thin actin filaments. In the spaces between them there are thicker myosin filaments.

Actin filament externally resembles two strings of beads twisted into a double helix, where each bead is a protein molecule actin. Protein molecules lie in the recesses of actin helices at equal distances from each other. troponin, connected to thread-like protein molecules tropomyosin.

Myosin filaments are formed by repeating protein molecules myosin. Each myosin molecule has a head and tail. The myosin head can bind to an actin molecule, forming a so-called cross bridge.

The cell membrane of the muscle fiber forms invaginations ( transverse tubules), which perform the function of conducting excitation to the membrane of the sarcoplasmic reticulum. Sarcoplasmic reticulum (longitudinal tubules) It is an intracellular network of closed tubes and performs the function of depositing Ca++ ions.

Motor unit. The functional unit of skeletal muscle is motor unit (MU). MU is a set of muscle fibers that are innervated by the processes of one motor neuron. Excitation and contraction of the fibers that make up one motor unit occur simultaneously (when the corresponding motor neuron is excited). Individual motor units can be excited and contracted independently of each other.

Molecular mechanisms of skeletal muscle contraction

According to thread sliding theory, muscle contraction occurs due to the sliding movement of actin and myosin filaments relative to each other. The thread sliding mechanism involves several sequential events.

Myosin heads attach to actin filament binding centers (Fig. 2 A).

The uncoupling of actin and myosin and the restoration of the head conformation occurs as a result of the attachment of an ATP molecule to the myosin head and its hydrolysis in the presence of Ca++ (Fig. 2, B).

The cycle “binding – change in conformation – uncoupling – restoration of conformation” occurs many times, as a result of which the actin and myosin filaments move relative to each other, the Z-disks of the sarcomeres come closer together and the myofibril shortens (Fig. 2, D).

Coupling of excitation and contraction in skeletal muscle

As a result of the firing of a neuromuscular synapse on the postsynaptic membrane, an EPSP arises, which generates the development of an action potential in the area surrounding the postsynaptic membrane.

Ca++ ions bind to the protein troponin. Troponin changes its conformation and displaces the tropomyosin protein molecules that covered the actin binding centers (Fig. 3, D).

Myosin heads attach to the opened binding centers, and the contraction process begins (Fig. 3, E).

The development of these processes requires a certain period of time (10–20 ms). The time from the moment of excitation of a muscle fiber (muscle) to the beginning of its contraction is called latent period of contraction.

Skeletal muscle relaxation

Contracture called a persistent, long-term contraction of a muscle that persists after the cessation of the stimulus. Short-term contracture can develop after tetanic contraction as a result of the accumulation of large amounts of Ca++ in the sarcoplasm; long-term (sometimes irreversible) contracture can occur as a result of poisoning and metabolic disorders.

Phases and modes of skeletal muscle contraction

Phases of muscle contraction

When a skeletal muscle is irritated by a single pulse of electric current of suprathreshold strength, a single muscle contraction occurs, in which 3 phases are distinguished (Fig. 4, A):

Latent (hidden) contraction period (about 10 ms), during which the action potential develops and electromechanical coupling processes occur; muscle excitability during a single contraction changes in accordance with the phases of the action potential;

Shortening phase (about 50 ms);

Relaxation phase (about 50 ms).

Modes of muscle contraction

Single muscle contractions occur at low frequency electrical impulses. If the next impulse enters the muscle after the completion of the relaxation phase, a series of successive single contractions occurs.

At a higher pulse frequency, the next pulse may coincide with the relaxation phase of the previous contraction cycle. The amplitude of contractions will be summed up, and there will be serrated tetanus- prolonged contraction, interrupted by periods of incomplete muscle relaxation.

With a further increase in the pulse frequency, each subsequent pulse will act on the muscle during the shortening phase, resulting in smooth tetanus- prolonged contraction, not interrupted by periods of relaxation.

Optimum and pessimum frequency

The amplitude of tetanic contraction depends on the frequency of impulses irritating the muscle. Optimum frequency they call the frequency of irritating impulses at which each subsequent impulse coincides with the phase of increased excitability (Fig. 4, A) and, accordingly, causes tetanus of the greatest amplitude. Pessimum frequency called a higher frequency of stimulation, at which each subsequent current pulse falls into the refractory phase (Fig. 4, A), as a result of which the amplitude of the tetanus decreases significantly.

Skeletal muscle work

The strength of skeletal muscle contraction is determined by 2 factors:

The number of units involved in the reduction;

Frequency of contraction of muscle fibers.

The work of skeletal muscle is accomplished through a coordinated change in tone (tension) and length of the muscle during contraction.

Types of skeletal muscle work:

dynamic overcoming work occurs when a muscle, contracting, moves the body or its parts in space;

static (holding) work performed if, due to muscle contraction, parts of the body are maintained in a certain position;

dynamic yielding operation occurs when a muscle functions but is stretched because the force it makes is not enough to move or hold parts of the body.

During work, the muscle can contract:

isotonic– the muscle shortens under constant tension (external load); isotonic contraction is reproduced only in experiment;

isometrics– muscle tension increases, but its length does not change; the muscle contracts isometrically when performing static work;

auxotonic– muscle tension changes as it shortens; auxotonic contraction is performed during dynamic overcoming work.

Rule of average loads– the muscle can perform maximum work under moderate loads.

Fatigue– a physiological state of a muscle that develops after prolonged work and is manifested by a decrease in the amplitude of contractions, an extension of the latent period of contraction and the relaxation phase. The causes of fatigue are: depletion of ATP reserves, accumulation of metabolic products in the muscle. Muscle fatigue during rhythmic work is less than synapse fatigue. Therefore, when the body performs muscular work, fatigue initially develops at the level of the synapses of the central nervous system and neuromuscular synapses.

Structural organization and contraction of smooth muscle

Structural organization. Smooth muscle consists of single spindle-shaped cells ( myocytes), which are located in the muscle more or less chaotically. Contractile filaments are arranged irregularly, as a result of which there is no transverse striation of the muscle.

The mechanism of contraction is similar to that of skeletal muscle, but the rate of filament sliding and the rate of ATP hydrolysis are 100–1000 times lower than in skeletal muscle.

Physiological properties of muscles

The general physiological properties of skeletal and smooth muscles are excitability And contractility. Comparative characteristics of skeletal and smooth muscles are given in table. 6.1. The physiological properties and characteristics of the cardiac muscle are discussed in the section “Physiological mechanisms of homeostasis”.

Table 7.1.Comparative characteristics of skeletal and smooth muscles

Property	Skeletal muscles	Smooth muscle
Depolarization rate		slow
Refractory period	short	long
Nature of contraction	fast phasic	slow tonic
Energy costs
Plastic
Automatic
Conductivity
Innervation	motor neurons of the somatic NS	postganglionic neurons of the autonomic nervous system
Performed movements	arbitrary	involuntary
Chemical sensitivity
Ability to divide and differentiate

Plastic smooth muscles is manifested in the fact that they can maintain constant tone both in a shortened and in an extended state.

Conductivity smooth muscle tissue is manifested in the fact that excitation spreads from one myocyte to another through specialized electrically conductive contacts (nexuses).

Property automation smooth muscle is manifested in the fact that it can contract without the participation of the nervous system, due to the fact that some myocytes are able to spontaneously generate rhythmically repeating action potentials.