Muscle contraction

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Muscle contraction is site activation that produces tension in muscle fibers. In physiology, muscle contraction does not necessarily mean muscle shortening because muscle tension can be produced without changes in muscle length such as holding a heavy book or dumbbell in the same position. The termination of muscle contraction is followed by muscle relaxation , which is the return of muscle fibers to a low voltage state.

Muscle contractions can be described based on two variables: length and tension. Muscle contraction is described as isometric if muscle tension changes but muscle length remains the same. Conversely, isotonic muscle contraction if muscle tension remains the same throughout the contraction. If muscle length is shortened, contraction is concentric; if the length of the muscle lengthens, the contraction becomes eccentric. In the natural movement underlying locomotor activity, muscle contraction is multifaceted because they are able to produce length and tension changes in varying time. Therefore, either the length or the tension tend to remain the same in the muscle contracting during locomotor activity.

In vertebrates, skeletal muscle contraction is neurogenic because it requires synaptic input from motor neurons to produce muscle contraction. A single motor neuron is able to menginstervasi some muscle fibers, thus causing the fibers to contract at the same time. Once conserved, the protein filaments in each skeletal muscle fiber shift past each other to produce contraction, which is explained by the theory of shear filaments. The resulting contractions can be described as twitch, addition, or tetanus, depending on the frequency of the action potential. In the skeletal muscle, the muscle tension is greatest when the muscle is stretched to the intermediate length as described by the long voltage relationship.

Unlike skeletal muscle, the contraction of the smooth muscles and the heart is myogenic (meaning that they are initiated by the smooth muscle cells or the heart itself instead of being stimulated by external events such as nerve stimulation), although they can be modulated by stimulation of the autonomic nervous system. The mechanism of contraction in muscle tissue is similar to skeletal muscle tissue.

Video Muscle contraction

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Muscle contractions can be described based on two variables: force and length. The power itself can be distinguished as tension or burden. Muscle tension is the force given by the muscles on the object while the load is the force given by the object on the muscle. When muscle tension changes without appropriate change in muscle length, muscle contraction is described as isometric. If muscle length changes when muscle tension remains the same, then muscle contraction is isotonic. In isotonic contraction, muscle length can shorten to produce concentric or elongated contractions to produce eccentric contractions. In the natural movement underlying locomotor activity, muscle contraction is multifaceted because they are able to produce changes in length and tension over time. Therefore, both the length and the stress tend to remain constant when the muscle is active during the locomotor activity.

Isometric contraction

Muscle isometric contractions produce tension without changing the length. Examples can be found when the muscles of the hand and forearm hold an object; the hand joint does not move, but the muscle produces enough strength to prevent it from falling.

Isotonic contractions

In isotonic contractions, the tension in the muscle remains constant despite changes in muscle length. This occurs when the muscle strength of the contraction corresponds to the total load on the muscle.

Concentric contractions

In concentric contractions, the muscle tension is sufficient to overcome the load, and the muscle shortens as it contracts. This occurs when the force generated by the muscle exceeds the load opposite to the contraction.

During concentric contractions, the muscles are stimulated to contract according to the shear filament theory. This occurs along the muscles, producing forces at the origin and insertion, causing the muscles to shorten and alter the angle of the joint. In relation to the elbow, the concentric contraction of the biceps will cause the arm to bend the elbow as the hand moves from foot to shoulder (biceps curl). The concentric contraction of the tricep will change the angle of the joint in the opposite direction, straightening the arms and moving the hands toward the feet.

Eccentric contractions

In the eccentric contraction , the resulting tension is not sufficient to overcome the external burden on the muscle and the muscle fibers extend as they contract. Instead of working to pull the joint toward muscle contraction, the muscles act to reduce joint speed at the end of the motion or otherwise control the repositioning of the load. This can happen unconsciously (for example, when trying to move a load that is too heavy to lift muscle) or voluntarily (for example, when the muscle 'smooths' the movement). During the short term, strength training involving eccentric and concentric contractions seems to increase muscle strength more than training with concentric contractions only. However, muscle damage due to exercise is also greater during prolonged contractions.

During the eccentric contraction of the biceps muscles, the elbows begin movement while bending and then straightening as the hand moves away from the shoulder. During the eccentric contraction of the triceps muscle, the elbow initiates a straight movement and then bends as the hand moves toward the shoulder. Desmin, titin, and other z-line proteins are involved in eccentric contractions, but the mechanism is poorly understood compared to crossbridge cycling in concentric contractions.

Although muscles do a negative amount of mechanical work, (work is being done on muscle), chemical energy (in fat, glucose or ATP) is still consumed, although less than will be consumed during concentric contractions of the same force. For example, someone spends more energy going up the stairs than going down with the same flight.

Severe eccentric loading muscles experience greater damage when overloaded (such as during muscle-building exercises or strength training) than with concentric loads. When eccentric contractions are used in weight training, they are usually called negative . During concentric contractions, muscle fibers shift to each other, drawing a Z-line together. During eccentric contractions, filaments shift past each other in opposite ways, although the actual movement of the myosin head during eccentric contraction is unknown. Exercise displaying a heavy eccentric load can actually support greater weight (muscles about 40% stronger during eccentric contractions than during concentric contractions) and also result in greater muscle damage and delayed onset of muscle pain one to two days after training. Exercises that combine eccentric and concentric contraction of muscles (ie, involving strong contractions and controlled weight loss) can result in a greater increase in strength than concentric contractions alone. While unusual heavy eccentric contractions can easily lead to excessive training, moderate training can provide protection against injury.

Eccentric contractions in motion

Eccentric contractions usually occur as braking forces in opposition to concentric contractions to protect the joint from damage. During almost every routine motion, eccentric contractions help keep the movement smooth, but can also slow down fast movements such as punches or throws. Part of the training for rapid movements such as throwing a ball during baseball involves the reduction of eccentric braking that allows greater force to be developed throughout the movement.

Eccentric contractions are being investigated for their ability to speed up the rehabilitation of weak tendons or injuries. Achilles tendinitis and patellar tendonitis (also known as jumper's knee or patellar tendonosis) have proven beneficial from the high-burden eccentric contractions.

Maps Muscle contraction

Vertebrate animals

In vertebrate animals, there are three types of muscle tissue: skeletal, smooth, and heart. Skeletal muscle is the majority of muscle mass in the body and is responsible for locomotor activity. Smooth muscles form blood vessels, digestive tracts, and other areas of the body that produce continuous contractions. The heart muscle forms the heart, which pumps blood. Skeletal and heart muscles are called striated muscles because of their striped appearance under a microscope, which is due to the alternating pattern of band A and band I that are highly organized.

Skeletal muscle

Excluding reflexes, all skeletal muscle contractions occur as a result of conscious effort coming from the brain. The brain sends electrochemical signals through the nervous system to motor neurons that supply several muscle fibers. In the case of some reflexes, the signal to contract can come from the spinal cord through feedback with gray matter. Other actions such as mover, breathing, and chewing have a reflexive aspect on them: contractions can be started consciously or unconsciously.

Neuromuscular junction

A neuromuscular junction is a chemical synapse formed by contact between motor neurons and muscle fibers. This is the site where motor neurons transmit signals to muscle fibers to initiate muscle contraction. The sequence of events resulting in depolarization of muscle fibers at the neuromuscular junction begins when the action potential begins in the body of the motor neuron, which is then propagated by salt conduction along its axon to the neuromuscular junction. After reaching the terminal bouton, the action potential causes Ca ² the entry of the ion into the terminal through the voltage-gated calcium channel. The size of Ca ²
Entry causes synaptic vesicles containing acetylcholine neurotransmitters to fuse with the plasma membrane, releasing acetylcholine into the synaptic cleft between the motor neuron terminals and the neuromuscular junction of skeletal muscle fibers. Acetylcholine diffuses across the synapse and binds and activates nicotinic acetylcholine receptors at the neuromuscular junction. Activation of the nicotinic receptor opens its intrinsic sodium/potassium channel, causing sodium to flow profusely and potassium out. As a result, the sarcolemma reverses the polarity and the tension quickly jumps from the resting membrane potential to -90mV to as high as 75mV when sodium enters. The membrane potential then becomes hyperpolarized when the potassium exits and then adjusts back to the resting membrane potential. This rapid fluctuation is called the potential of the end plate. The voltage-gated sarcolemma ion channel next to the open plate is in response to the potential end plate. This voltage-gated channel is specific sodium and potassium and only allows one through. This ion motion wave creates a spreading action potential from the end plate of the motor in all directions. If the action potential stops, acetylcholine is no longer released from the bouton terminal. Acetylcholine remaining in the synaptic cleft is degraded by active acetylcholine esterase or reabsorbed by the synaptic button and there is nothing left to replace the degraded acetylcholine.

Merging contractions-excitation

Coupling contractions are the process by which muscle action potential in muscle fibers causes myofibrils to contract. In skeletal muscles, the excitation-contraction clutch relies on direct coupling between key proteins, calcium sarkoplasma calcium (SR) removal channels (identified as ryanodine receptors, RyR) and Gated-gated type calcium channels (identified as dihydropyridine receptors, DHPR). DHPR is located in the sarcolemma (which includes the surface sarcolemma and transverse tubules), whereas RyRs is across the SR membrane. The close apposition of the transverse tubules and the two SR regions containing RyR are described as triads and particularly where the excitation-contraction coupling takes place. Clutch excitations occur when skeletal muscle cell depolarization produces muscle action potential, which spreads across the cell surface and into T-tubular muscle fiber tissue, resulting in depolarization of the inner muscle fibers. Internal depolarization activates the dihydropyridine receptor in the terminal cisternae, which is close to the ryanodine receptor in the adjacent sarcoplasmic reticulum. The physically activated dihydropyridine receptors interact with the ryanodine receptors to activate them through the leg process (involves conformational changes that activate allosteric ryanodine receptors). When the ryanodine receptor opens, Ca ² is released from the sarcoplasmic reticulum into the local junctional space, which then diffuses into the mass cytoplasm to cause calcium spark. Note that the sarcoplasmic reticulum has a large capacity of the calcium buffer in part because of a calcium-binding protein called calsequestrin. The close synchronous activation of thousands of calcium sparks by action potential causes an increase in the cells in calcium which causes the rise of transient calcium. The Ca ² released to in the cytosol binds to Troponin C by actin filaments, to enable cross-bridge cycling, produce strength and, in some situations, motion. The sarco/endoplasmic reticulum calcium-ATPase (SERCA) actively pumps Ca ² < br> back to the sarcoplasmic reticulum. Like Ca ² drop back to resting level, decreasing style and relaxation occur.

The sliding filament theory

The shear filament theory describes a process used by muscles to contract. This is a recurring event cycle that causes the thin filaments to slide over the thick filaments and produce tension in the muscles. It was developed independently by Andrew Huxley and Rolf Niedergerke and by Hugh Huxley and Jean Hanson in 1954. Physiologically, this contraction is not uniform in the sarcomom; the central position of the thick filaments becomes unstable and may shift during contraction. However, the action of elastic proteins such as titin is hypothesized to maintain uniform tension in the sarcoma and to pull the thick filaments to a central position.

Crossbridge cycling

Crossbridge cycling is a sequence of molecular events underlying the theory of shear filaments. Crossbridge is a projection of myosin, which consists of two myosin heads, which extend from thick filaments. Each myosin head has two binding sites: one for ATP and one for actin. The binding of ATP to the myosin head releases the myosin from actin, thus allowing myosin to bind to other actin molecules. Once installed, ATP is hydrolyzed by myosin, which uses the energy released to move to the "sloping position" which binds it weakly to the part of the actin-binding site. The remainder of the actin binding site is blocked by tropomiosin. With hydrolyzed ATP, the tilted myosin head now contains ADP P _i. Two Ca ² ion bind to troponin C on actin filaments. Troponin- Ca ² causing the tropomyosin to shift and unblock the rest of the actin binding site. Unblocking the rest of the actin binding site allows two myosin heads to close and myosin is strongly bound to act. The myosin head then releases inorganic phosphate and initiates a power stroke , that produces a force of 2 pN. The power stroke moves the actin filament inward, thus shortening the sarcoma. Myosin then releases the ADP but is still firmly bound to act. At the end of the power stroke, ADP is released from the myosin head, leaving the myosin attached to the actin in a tight state until the other ATP binds to myosin. Lack of ATP will result in rigor mortis stiffness characteristics. After the other ATP binds to myosin, the myosin head will be released from the actin and other crossbridges cycles occur.

Crossbridge cycling may continue for as long as there is an amount of ATP and Ca ² span> in the cytoplasm. Termination crossbridge cycling can occur when Ca ² is actively pumped back into the sarcoplasmic reticulum. When Ca ² is not again present on thin filaments, the tropomiosin converts the conformation back to its previous state thus blocking the binding site again. Myosin stops binding thin filaments, and muscles relax. The Ca ²
ion let molecules troponin to maintain ² ion concentration in sarcoplasm. Active pumping Ca ²
ion to the sarcoplasmic reticulum creating a lack of fluid around myofibrils. This causes the removal of Ca ² ion from troponin. Thus, the tropomycin-troponin complex again includes the binding sites in actin filaments and contraction stops.

Gradation of skeletal muscle contraction

The strength of skeletal muscle contraction can be widely separated into twitch, addition, and tetanus. Twitch is a single contraction and relaxation cycle generated by the action potential within the muscle fiber itself. The time between the stimulus to the motor nerve and the subsequent contraction of the conserved muscle is called latent period , which usually takes about 10 ms and is caused by the time taken for the nerve action potential to spread, the time for chemical transmission at the intersection neuromuscular, then the next step in excitation-contraction coupling.

If another muscle action potential must be produced before the muscle twitch relaxation, then the next twitch will only summarize the previous twitch, resulting in the summation of . . The summation can be achieved in two ways: the sum of frequencies and the double fiber addition . In frequency addition , the force given by the skeletal muscle is controlled by varying the frequency at which the action potential is sent to the muscle fibers. The potential action does not arrive at the muscles simultaneously, and, during contraction, some fractions of the fibers in the muscle will be fired at a given time. Under typical circumstances, when a man exerts a muscle as hard as he can consciously, about one-third of the fibers in the muscle will shoot at once, although this ratio can be affected by various physiological and psychological factors. (Including Golgi tendon organs and Renshaw cells). This 'low' contraction rate is a protective mechanism for preventing tendon-style avulsion produced by a 95% contraction of all fibers sufficient to damage the body. In the double fiber addition , if the central nervous system sends a weak signal to contract the muscle, the smaller motor unit, becomes more energized than the larger, stimulated first. As signal strength increases, more motor units are excited than larger ones, with the largest motor units having as much as 50 times the contractile force as smaller. As more and more motor units are activated, the strength of muscle contraction becomes stronger. A concept known as the principle of size, allows for gradation of muscle strength during weak contractions occurring in small steps, which then becomes progressively larger when a greater amount of force is required.

Finally, if the potential frequency of muscle action increases in such a way that muscle contraction reaches peak strength and plateau at this level, then the contraction is tetanus .

Long-voltage relationship

The long voltage relationship connects the strength of isometric contraction to the length of the muscle in which contraction occurs. The muscle operates with the largest active stress when it is close to the ideal length (often the length of their rest). When stretched or shortened beyond this (whether due to the action of the muscle itself or by external forces), the maximum active voltage generated decreases. This decrease is minimal for small deviations, but the tension decreases rapidly because the length of the deviates is further than ideal. Due to the presence of elastic proteins in muscle cells (such as titin) and extracellular matrix, because the muscle is stretched beyond the given length, there is a completely passive tension, which opposes elongation. When combined together, there is a strong resistance to prolong the active muscle far beyond the peak of active tension.

The relationship of the velocities

The velocity relation connects the speed at which the muscle changes its length (usually governed by an external force, such as a load or other muscle) by the amount of force it produces. The force decreases hyperbolic relative to the isometric force as the shortening velocity increases, eventually reaching zero at some maximum speed. The converse is true for when the muscles are stretched - the power rises above the isometric maximum, until it finally reaches the absolute maximum. The intrinsic properties of this active muscle tissue play a role in the attenuation of the active joints that are activated by simultaneously active opponent muscles. In such cases, the force profile profile increases the force produced by the elongation muscle at the expense of shortening muscles. It supports which muscles restore joints to equilibrium effectively increases joint damping. In addition, the damping strength increases with muscle strength. The motor system can thus actively control the damping of the joint through simultaneous contraction (co-contraction) of the opposite muscle group.

Smooth muscle

The smooth muscles can be divided into two subgroups: single unit (unitary) and multi-unit. Single-cell smooth muscle cells can be found in the intestines and blood vessels. Because these cells are connected together by gap junctions, they can contract as syncytium. Single-unit smooth muscle cells contract miogenically, which can be modulated by the autonomic nervous system.

Unlike smooth single-cell muscle cells, multi-unit smooth muscle cells are found in the muscles of the eye and at the base of the hair follicle. Multi-unit smooth muscle cells contract by being stimulated separately by the nerves of the autonomic nervous system. Thus, they allow for good control and gradual response, such as recruitment of motor units in skeletal muscle.

Plain muscle contraction mechanism

The contractile activity of smooth muscle cells is influenced by several inputs such as spontaneous electrical activity, nerve and hormonal inputs, local changes in chemical composition, and stretching. This is in contrast to the contractile activity of skeletal muscle cells, which depend on a single neural input. Some types of smooth muscle cells are capable of generating their own spontaneous action potential, which usually follows the pacemaker's potential or slow-wave potential. The potential action is generated by the inclusion of extracellular Ca ² instead of Na . Like skeletal muscle, cytosolic Ca ² ion is also required for cross-bridge cycling in smooth muscle cells.

Two sources for cytosolic Ca ² in smooth muscle cells is Ca ² enter through the calcium channel and Ca ² ions released from the sarcoplasmic reticulum. The height of cytosolic Ca ² many Ca ² bind to calmodulin, which then binds and activates myosin light-chain kinase. Complex kinase light chain of calcium-kaldosulin-myosin phosphorylates myosin in kilosalton kilogram chains (kDa) myosin on serine amino acid residue 19, initiates contraction and activates myosin ATPase. Unlike skeletal muscle cells, smooth muscle cells are deprived of troponin, although they contain thin-film protein troposaosin and other important proteins - caldesmon and calponin. Thus, smooth muscle contraction is initiated by Ca ²
-otomes myosin phosphorylation instead of ²
binds to the troponin complex that regulates the myosin binding sites in actin such as skeletal and cardiac muscle.

The termination of crossbridge cycling (and leaving the muscle in the latch-state) occurs when the myosin light chain phosphatase removes the phosphate group from the myosin head. Phosphorylation in the 20 kDa myosin light chain correlates well with smooth muscle shortening speeds. During this period, there was a rapid burst of energy consumption measured by oxygen consumption. Within minutes of initiation, the calcium level decreased markedly, the 20 kDa myosin light chain phosphorylation decreased, and the energy usage decreased; However, the strength in tonic smooth muscle is maintained. During muscle contraction, fast cycling forms a cross between actin activated and myosin phosphorylated, producing strength. It is hypothesized that the maintenance strength results from dephosphorylated "latch-bridges" which slowly cycle and maintain strength. A number of kinases such as rho kinase, zip kinase, and protein kinase C are believed to participate in a continuous contraction phase, and Ca ²
flux may be significant.

Neuromodulation

Although smooth muscle contraction is myogenic, their level and strength of contraction can be modulated by the autonomic nervous system. Postganglionic nerve fibers of the parasympathetic nervous system release the acetylcholine neurotransmitter, which binds to muscarinic acetylcholine receptors (mAChRs) in smooth muscle cells. These receptors are metabotropic, or G-protein paired receptors that start the second messenger cascade. In contrast, postganglionic nerve fibers of the sympathetic nervous system secrete neurotransmitters epinephrine and norepinephrine, which bind to the metabotropic, adrenergic receptors. The exact effect on smooth muscle depends on the specific characteristics of the activated receptor - both parasympathetic and sympathetic input may be stimulated (contractile) or inhibition (relaxed).

Cardiac muscle

There are two types of heart muscle cells: autorhythmic and contractile. The autorhythmic cells do not contract, but instead regulate the rate of contraction for other cardiac muscle cells, which can be modulated by the autonomic nervous system. Conversely, contractile muscle cells (cardiomyocytes) constitute the majority of cardiac muscle and are able to contract.

Contraction-Excitation coupling

Unlike skeletal muscles, the excitation-contraction clutch in the heart muscle is considered to be highly dependent on a mechanism called calcium-induced release of calcium. Although the proteins involved are similar, the L type calcium channels and ryanodine receptors (RyRs) are not physically combined. In contrast, RyR is activated by calcium triggers, caused by the flow of Ca ² > through the L-type calcium channel. Furthermore, the heart muscle tends to show the structure of the dyad (or dyad), rather than the triads.

The clutch exclusions in the heart muscle cells occur when the action potential is initiated by pacemaker cells in the sinoatrial node or Atrioventricular node and is performed for all cells in the heart through the gap junction. The potential action goes along the surface membrane to the T tube (the latter is not seen in all types of heart cells) and depolarization causes extracellular Ca ²
to enter the cell through an L-type calcium channel and possibly a sodium-calcium exchanger (NCX) during the early part of the upland phase. The size of Ca ²
small in ² . Increase Ca ² detected by receptors of ryanodine in the sarcoplasmic reticulum membrane that releases Ca ²
in the positive feedback physiological response. This positive feedback is known as calcium-induced calcium release and gives rise to a sponge of calcium ( Ca ² sparks). Spatial and temporal summation ~ 30.000 Ca ² sparks provides increased cytoplasmic calcium concentrations in cells. Increased calcium cytosolic follows the flow of calcium through cell membranes and the sarcoplasmic reticulum is moderated by calcium buffers that bind most of intracellular calcium. As a result, a large increase in total calcium leads to a relatively small increase in ² < br> .

Calcium cytoplasm binds Troponin C, removes the tropomiosin complex from the actin binding site which allows the myosin head to bind to the actin filament. From this point, the contractile mechanism is essentially the same as the skeletal muscle (above). Briefly, using ATP hydrolysis, the myosin head pulls the actin filament toward the center of the sarcomere.

After systole, intracellular calcium is taken by the sarco/endoplasmic reticulum ATPase (SERCA) pump back to the sarcoplasmic reticulum ready for the next cycle to begin. Calcium is also excreted from cells primarily by sodium-calcium exchanger (NCX) and, to a lesser extent, calcium plasma membrane ATPase. Some calcium is also taken by mitochondria. Enzyme, phospholamban, serves as a brake for SERCA. At low heart rate, active phosphorous and slow ATPase activity so that Ca ² > should not leave the cell completely. At high heart rate, phosphorus is phosphorylated and deactivated thus taking most of the Ca ² < br> from the cytoplasm back to the sarcoplasmic reticulum. Again, the calcium buffer moderates this decrease in ²
concentration, allowing a relatively small decrease in ²
Concentration in response to major changes in total calcium. The fall Ca ² allowing the complex troponin to dissociate from the actin filament thereby terminating the contraction. The heart relaxes, allowing the ventricles to fill with blood and start the heart cycle again.

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Animal invertebrates

Circular and elongated muscle

In annelids such as earthworms and leeches, circular and elongated muscle cells form the walls of the bodies of these animals and are responsible for their movements. In earthworms moving through the ground, for example, the contraction of the circular and elongated muscles occurs mutually while the coelomic fluid serves as a hydroskeleton by maintaining the turgidity of earthworms. When the circular muscles in the anterior segment contract, the anterior portion of the animal's body begins to narrow radially, which pushes the incompressible coelomic fluid forward and increases the animal's length. As a result, the front end of the animal moves forward. When the front end of the earthworm becomes anchored and the circular muscles in the anterior segment become relaxed, the waves of contraction of the longitudinal muscle pass backward, which draws the remaining body of the animal left behind. This alternating wave of circular and elongated contractions is called peristalsis, which underlies the movement of earthworm creeps.

Cluttered abrasions

Invertebrates such as annelids, molluscs and nematodes, have a sloping striated muscle, which contains thick and thin filaments that are arranged in a helical rather than transverse manner, as in vertebrates or heart muscle. In bivalves, striated lurik muscles can sustain long-standing tension without using too much energy. Bivalves use these muscles to keep their shells closed.

Asynchronous muscle

Sophisticated insects such as wasps, flies, bees, and beetles have asynchronous muscles that form flight muscles in these animals. These flight muscles are often called fibrillar muscles because they contain myofibrils that are thick and conspicuous. The remarkable feature of these muscles is that they do not require stimulation for any muscle contractions. Therefore, they are called asynchronous muscle because the amount of contraction in these muscles is not appropriate (or aligned) with the number of action potentials. For example, a tethered fly wing muscle can receive an action potential at a frequency of 3 Hz but capable of beating at a frequency of 120 Hz. High frequency beating is possible because the muscles connect to the resonance system, which is driven to the natural frequency of vibration.

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History

In 1780, Luigi Galvani discovered that the leg muscles of dead frogs twitched when struck by electric sparks. This is one of the first forays into the study of bioelectricity, a field that still studies electrical patterns and signals in tissues such as nerves and muscles.

In 1952, the term excitation-excitation coupling was created to describe the physiological processes of transforming electrical stimuli into mechanical responses. This process is essential for muscle physiology, where electrical stimulus is usually an action potential and a mechanical contraction response. The excitation-contraction clutch can be dysregulated in many diseases. Although the clutch of excitation contractions have been known for more than half a century, this is still an active area of â€‹â€‹biomedical research. A common scheme is that the action potential arrives to depolarize the cell membrane. With a special mechanism for muscle type, this depolarization results in an increase in calcium cytosol called temporary calcium. This increase in calcium activates calcium-sensitive contractile proteins which then use ATP to cause cell shortening.

The mechanisms for muscle contraction prevent scientists for years and require further research and updates. The shear filament theory was developed independently by Andrew F. Huxley and Rolf Niedergerke and by Hugh Huxley and Jean Hanson. Their findings were published as two consecutive papers published in the May 22, 1954 edition of Nature under the general theme of "Muscle Structural Changes During Contractions".

Muscle Fiber Contraction and Relaxation | Lifetime Fitness and ...

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References

Associate Degree Nursing Physiology Review

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External links

Sliding Filament of Muscle Contraction Model
Animation: Myofilament Contraction

Source of the article : Wikipedia

Muscle contraction

Minggu, 08 Juli 2018

Muscle contraction

Video Muscle contraction