Excitation-contraction coupling refers to the mechanism that converts the above action potentials in muscle fibers into contraction of muscle fibers. The action potentials at the level of the muscular cell membrane that surrounds the myofibrils migrate into the T-tubules, which are responsible for the propagation of the action potential from the surface inside the muscle fiber. The T tubules contain dihydropyridine receptors adjacent to the terminal cisterns of the sarcoplasmic reticulum of the muscle fiber. When T tubules are depolarized, their dihydropyridine receptors undergo a conformational change that mechanically interacts with ryanodine receptors on the sarcoplasmic reticulum. This interaction opens the ryanodine receptors, releasing Ca2+ from the sarcoplasmic reticulum. The resulting increase in intracellular Ca2+ binds to troponin C of the troponin complex on thin filaments. The interaction between Ca2+ and troponin C shows cooperation, which means that each Ca2+ that binds troponin C increases the affinity of the troponin C bond for the next Ca2+ molecule, up to a total of four Ca2+ ions per troponin C. As a result of ca2+ binding, the troponin complex undergoes a conformational change that leads to a displacement of tropomyosin from myosin binding sites to F-actin, allowing myosin from thick filaments to be bound. [2] [3] 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 adrenaline and norepinephrine, which also bind to metabotropic adrenergic receptors.
The exact effects on smooth muscles depend on the specific characteristics of the activated receptor – parasympathetic input and sympathetic entry can be excitatory (contractile) or inhibitory (relaxing). Botulinum toxin is a remedy that alters neuromuscular function. This toxin, produced by C. botulinum, prevents the release of ACh from the presynaptic membrane of the motor neuron. Therefore, skeletal muscles cannot contract, which leads to flaccid paralysis. [10] A muscle fiber creates tension through the transverse bridge cycle of actin and myosin. Under tension, the muscle can lengthen, shorten or remain the same. Although the term contraction implies a shortening, compared to the muscles, it means the generation of tension in a muscle fiber. Different types of muscle contractions occur and are defined by changes in muscle length during contraction. An eccentric contraction leads to the lengthening of a muscle while the muscle still generates strength; In fact, the resistance is greater than the force generated. Eccentric contractions can be both voluntary and involuntary. For example, a voluntary eccentric contraction would be the controlled lowering of the heavy weight increased during the above concentric contraction.
An involuntary eccentric contraction can occur when a weight is too big for a muscle to carry, and is therefore slowly lowered when it is energized. Transverse cycling occurs even though sarcomas, muscle fibers and muscles lengthen and control muscle stretching. To allow muscle contraction, tropomyosin must modify the conformation, reveal the binding site of myosin on an actin molecule and allow the formation of cross bridges. This can only occur in the presence of calcium, which is maintained at extremely low concentrations in the sarcoplasm. When present, calcium ions bind to troponin, resulting in conformational changes in troponin that allow tropomyosin to move away from myosin binding sites on actin. Once tropomyosin is eliminated, a transverse bridge can form between actin and myosin, triggering contraction. The transverse bridge cycle continues until Ca2+ ions and ATP are no longer available and tropomyosin again covers the binding sites on actin. The sliding filament theory describes a process used by muscles for contraction. It is a cycle of repetitive events that cause a thin filament to slide over a thick filament, creating tension in the muscle. It was developed independently in 1954 by Andrew Huxley and Rolf Niedergerke, as well as Hugh Huxley and Jean Hanson.[21] [22] [23] Physiologically, this contraction on the sarcoma is not uniform; The central position of thick filaments becomes unstable and can move during contraction. However, the action of elastic proteins such as titin is believed to maintain a uniform tension on the sarcomere, pulling the thick filament into a central position.
[24] Concentric contraction refers to the case where the contraction force exceeds the resistance force, resulting in muscle shortening and an approach to muscle origin and introduction. Eccentric contraction occurs when the contraction force is less than the resistance force. In other words, the strength of resistance is greater than that of contraction, which leads to muscle lengthening and increased distance between muscle origin and introduction. In annelids 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 coelomeral 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 coeloma 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. Explain the interaction of speed and duration in muscle contraction Muscles that are exposed to a strong eccentric load suffer from overload (e.B. during muscle building or strength training) more damage than with a concentric load. When eccentric contractions are used in strength training, they are usually called negative. During a concentric contraction, the muscle myofilaments slide over each other and contract the Z lines. During an eccentric contraction, the myofilaments slide on top of each other in the opposite direction, although the actual movement of the myosin heads during an eccentric contraction is not known. Exercise with a heavy eccentric load can actually support more weight (muscles are about 40% stronger during eccentric contractions than during concentric contractions) and also leads to greater muscle damage and delayed muscle pain one to two days after exercise. Exercises involving both eccentric and concentric muscle contractions (i.e. Strong contraction and controlled weight reduction) can lead to greater force gains than concentric contractions alone.
[10] [13] While unusual strong eccentric contractions can easily lead to overtraining, moderate exercise can provide protection from injury. [10] Figure 3. . .