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Taiko Dojo | What Shortens When a Muscle Is Contracted
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What Shortens When a Muscle Is Contracted

What Shortens When a Muscle Is Contracted

Unlike smooth muscle cells with one unit, smooth muscle cells with multiple units are located in the eye muscle and at the base of the hair follicles. Smooth muscle cells in several parts contract by being stimulated separately by the nerves of the autonomic nervous system. As such, they allow fine control and progressive reactions, similar to the recruitment of motor units in skeletal muscle. In bright animals such as earthworms and bloodsuckers, circular and longitudinal muscle cells form the body wall of these animals and are responsible for their movement. [42] In an earthworm moving in soil, for example, contractions of the circular and longitudinal muscles occur reciprocally, while the coelomaal fluid serves as a hydroskeleton maintaining the turgor of the earthworm. [43] When the circular muscles of the anterior segments contract, the anterior part of the animal`s body begins to shrink radially, pushing the incompressible coelomaal fluid forward and increasing the length of the animal. As a result, the front end of the animal advances. When the front end of the earthworm is anchored and the circular muscles of the anterior segments are relaxed, a wave of longitudinal muscle contractions runs backwards, pulling the rest of the animal`s dragging body forward. [42] [43] These alternating waves of circular and longitudinal contractions are called peristalsis, which underlies the creeping movement of earthworms. Huxley, H. E.

& Hanson, J. Changes in the transverse bands of muscles during contraction and stretching and their structural interpretation. Nature 173, 973–976 (1954) doi:10.1038/173973a0. Although smooth muscle contractions are myogenic, the speed and strength of their contractions can be modulated by the autonomic nervous system. Postnodal nerve fibers in the parasympathetic nervous system release the neurotransmitter acetylcholine, which binds to muscarinic acetylcholine receptors (mAChR) on smooth muscle cells. These receptors are metabotropic or G protein-coupled receptors that initiate a second cascade of messengers. Conversely, the postnodal nerve fibers of the sympathetic nervous system release the neurotransmitters epinephrine and norepinephrine, which bind to adrenergic receptors that are also metabotropic. The exact effects on smooth muscle depend on the specific characteristics of the activated receptor — parasympathetic input and sympathetic entry can be excitatory (contractile) or inhibitory (relaxing). When calcium is released into muscle cells, it binds to troponin.

This binding allows tropomyosin to change orientation, exposing the binding sites of myosin to actin. The myosin heads can then bind to the actin, and a contraction can occur. Unlike skeletal muscle, it is thought that E-C coupling in the heart muscle depends primarily on a mechanism called calcium-induced calcium release,[33] which is based on the connection structure between the T tubule and the sarcoplasmic reticulum. Junctophilin-2 (JPH2) is important for maintaining this structure as well as the integrity of the T tubule. [34] [35] [36] Another protein, receptor actuator protein 5 (REEP5), works to maintain the normal morphology of junctional SR. [37] Junctional coupling defects can result from defects in one of the two proteins. During the calcium-induced calcium release process, RyR2 is activated by a calcium trigger caused by the flow of Ca2+ through L-type calcium channels. After that, the heart muscle tends to show diade structures rather than triads. Ions are the key to mediating muscle contraction. Which of the following structures interacts directly with ions to expose actin binding sites in contracting muscles? Goody, R.S.

The missing link in the cycle of the transverse muscular bridge. Nature Structural Molecular Biology 10, 773–775 (2003) doi:10.1038/nsb1003-773. After depolarization, the membrane returns to its resting state. This is called repolarization, in which voltage-dependent sodium channels close. Potassium channels remain at 90% conductivity. Since the sodium-potassium atPase plasma membrane always carries ions, the resting state (negatively charged inside relative to the outside) is restored. The period immediately after the transmission of an impulse into a nerve or muscle, in which a neuron or muscle cell regains its ability to transmit another impulse, is called the refractory period. During the refractory period, the membrane can no longer generate action potential. The refractory period allows voltage-sensitive ion channels to return to their resting configurations. Sodium-potassium ATPase continuously moves Na+ out of the cell and K+ into the cell, and K+ exits, leaving a negative charge. Very quickly, the membrane repolarizes so that it can be depolarized again. Excitation-contraction coupling is the process by which a potential for muscle action in the muscle fiber causes the myofibrils to contract.

[20] In skeletal muscle, excitation-contraction coupling is based on direct coupling between key proteins, the sarcoplasmic reticulum (SR) calcium release channel (identified as ryanodine 1 receptor, RYR1) and voltage-controlled L-type calcium channels (identified as dihydropyridine receptors, DHPR). DHPR are located on the sarcolemma (which includes the surface sarcolemma and transverse tubules), while RyRs are located across the SR membrane. The narrow arrangement of a transverse tubule and two SR regions containing RyRs is described as a triad and is primarily the place where the excitation-contraction coupling takes place. Excitation-contraction coupling occurs when depolarization of the skeletal muscle cell leads to a muscle action potential that spreads through the cell surface and into the tubular T network of the muscle fiber, thereby depolarizing the inner part of the muscle fiber. Depolarization of the internal parts activates dihydropyridine receptors in terminal cisterns, which are located near ryanodine receptors in the adjacent sarcoplasmic reticulum. Activated dihydropyridine receptors physically interact with ryanodine receptors to activate them via foot processes (with conformational changes that activate ryanodine receptors allosterically). When the ryanodine receptors open, Ca2+ is released from the sarcoplasmic reticulum into the local connection space and diffuses into the bulk cytoplasm to cause a spark of calcium. Note that the sarcoplasmic reticulum has a high calcium buffering capacity, which is partly due to a calcium-binding protein called calequesterin. The almost synchronous activation of thousands of calcium sparks by the action potential causes an increase in calcium at the cell level, which leads to the increase in calcium transient.

The Ca2+ released in the cytosol binds to troponin C through the actin filaments to allow the transverse bridge cycle, which generates strength and movement in certain situations. Calcium ATPase of the endoplasmic sarco/reticulum (SERCA) actively pumps Ca2+ into the sarcoplasmic reticulum. When Ca2+ falls back to the level of rest, strength decreases and relaxation occurs. An experimental drug prevents the contraction of skeletal muscles by preventing the hydrolysis of ATP at the active center of muscle tissue. Where is this drug most likely to work? To understand the relationship between sl and tension, it is important to understand the sarcomere. Sarcoma is the basic unit of myocyte contraction. Sarcomeres are recognizable as the well-known band pattern observed when striped muscles are seen through the optical microscope. Figure 3(a) shows a part of a ventricular myocyte from a bluefin tuna in which the regular band pattern of the sarcomeres is clearly visible. A diagram of a mammalian sarcoma and its compound proteins is shown in Figure 3(b). The morphology of rainbow trout sarcoma is similar to that of mammalian sarcoma, and the length of the thin filament is about 0.95 μm in rat and ventricular myocytes of rainbow trout. A sarcoma is defined as the distance between the Z lines. The Z lines are brought closer together during contraction and move further apart during relaxation.

The Z lines are closer during contraction because the interaction between actin and myosin creates transverse bridges that allow myofilaments to slide over each other. During relaxation, myosin and actin dissolve and the Z lines move apart again. The role of myofilament overlap in shortening sarcoma is explained in more detail in the next section (see also DESIGN AND PHYSIOLOGY OF THE HEART | Excitation-cardiac contraction coupling: calcium and contractile element). The mechanism of muscle contraction has eluded scientists for years and requires continuous research and updating. [48] The sliding wire theory was developed independently by Andrew F. Huxley and Rolf Niedergerke, as well as Hugh Huxley and Jean Hanson. Their results were published as two consecutive papers published in the May 22, 1954 issue of Nature under the common theme «Structural Changes in Muscles During Contraction.» [22] [23] Fig. 3.5 illustrates a sarcoma and focuses on the physical orientation of actin and myosin filaments. .

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