Where Does Muscle Contraction Begin

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  • Post published:April 18, 2022
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ATP provides the energy needed for muscle contraction. In addition to its direct role in the transverse bridge cycle, ATP also provides energy for the Na+/K+ and Ca2+ active transport pumps. Muscle contraction does not occur without sufficient amounts of ATP. The amount of ATP stored in the muscle is very small and enough to cause contractions for a few seconds. Therefore, when decomposed, ATP must be rapidly regenerated and replaced to allow for prolonged contraction. The action potentials produced by pacemaker cells in the heart muscle are longer than those of motor neurons, which stimulate skeletal muscle contraction. Thus, heart contractions are about ten times longer than skeletal muscle contractions. Due to long periods of refractory, a new action potential cannot reach a heart muscle cell until it has entered the relaxation phase, so persistent tetanus contractions are impossible. If tetanus were to occur, the heart would not beat regularly and would not interrupt blood flow in the body. • Calcium ions and the proteins tropomyosin and troponin control muscle contractions Finally, when the frequency of muscle action potentials increases so that the muscle contraction reaches its maximum strength and reaches a plateau at this level, then the contraction is tetanus. Most muscles (organs) have a mixture of each type of fiber (cell). The predominant type of fiber in a muscle is determined by the primary function of the muscle. Large muscles used for powerful movements contain more fast fiber than slow fiber.

Therefore, different muscles have different speeds and different abilities to maintain contraction over time. The proportion of these different types of muscle fibers varies between different people and can change in a person with conditioning. Figure 3. A sarcomere is the area from one Z line to the next Z line. Many sarcomeres are present in a myofibrill, which leads to the characteristic scratch pattern of skeletal muscles. It is possible to distinguish two main types of muscle fibers in pathological and physiological studies: muscle contraction requires adenosine triphosphate (ATP). This can be produced either by carbohydrate degradation (glycogenolysis and glycolysis) or by lipid degradation (beta-oxidation). These oxygen-free processes produce only a limited amount of ATP, but also produce acetyl-Co-A, which is further metabolized in the presence of oxygen by the Krebs cycle in the mitochondria. This process provides even larger amounts of ATP. FG fibers primarily use anaerobic glycolysis as a source of ATP. They have a large diameter and possess large amounts of glycogen, which is used in glycolysis to quickly produce ATP; In this way, they generate a high degree of tension. Since they do not mainly use aerobic metabolism, they do not possess a significant number of mitochondria or large amounts of myoglobin, and therefore have a white color.

FG fibers are used to create fast and powerful contractions to make fast and powerful movements. However, these fibers get tired quickly, so they can only be used for a short time. Once the available ATP of creatine phosphate is depleted, the muscles produce ATP through glycolysis. Glycolysis is an anaerobic process that breaks down glucose (sugar) to produce ATP; However, glycolysis cannot produce ATP as quickly as creatine phosphate. The sugar used in glycolysis can be provided by blood sugar or by metabolizing glycogen stored in the muscle. Each glucose molecule produces two ATP molecules and two pyruvate molecules that can be used in aerobic respiration or converted into lactic acid. Muscle contraction begins with a neural signal, an action potential that travels along a long neural fiber (the axon) from a neuron in the spinal cord (or brain stem for the muscles of the neck and face), a neuron called alpha-motor, to a target muscle fiber (Figure 3.2A). When an action potential arrives at the junction between the nerve fiber and a muscle cell, it triggers a sequence of physico-chemical effects that ultimately lead to changes in the membrane potential in the muscle cell.

These compounds are called neuromuscular synapses (Figure 3.2B). Neuromuscular synapses are mandatory: this means that an action potential that arrives along a neuronal fiber always leads to the generation of an action potential in the muscle cell that innervates the fiber. A multi-step molecular process in muscle fiber begins when acetylcholine binds to receptors in the muscle fiber membrane. Proteins in muscle fibers are organized into long chains that can interact with each other and reorganize to shorten and relax. When acetylcholine reaches the receptors on the membranes of muscle fibers, the membrane channels open and the process that contracts a relaxed muscle fiber begins: The following list gives an overview of the sequence of events involved in the cycle of contraction of skeletal muscle: A contraction can last from a few milliseconds to 100 milliseconds, depending on the type of muscle. The voltage generated by a single contraction can be measured by a myogram that creates a graph that illustrates the amount of voltage generated over time. In combination with an electrical signaling diagram, the myogram shows three phases that each contraction goes through. The first period is the latency period during which the action potential propagates along the membrane and Ca2+ ions are released from the sarcoplasmic reticulum (SR). At this point, no tension or contraction is generated, but the conditions of contraction are defined. This is the phase where excitation and contraction are coupled, but contraction has not yet taken place.

The contraction phase occurs after the latency period, when calcium is used to trigger the formation of transverse bridges. This period lasts from the beginning of the contraction to the point of maximum stress. The last phase is the relaxation phase, where the tension decreases when the contraction stops. Calcium is pumped out of the sarcoplasm, back into the SR, and cycling across the bridge stops. The muscle returns to a resting state. There is a very short refractory period after the relaxation phase (check the previous material on the physiology of a neuromuscular compound) To allow muscle contraction, tropomyosin must modify the conformation, expose the myosin binding site to an actin molecule and allow the formation of transverse bridges. This can only occur in the presence of calcium, which is maintained in the sarcoplasm at extremely low concentrations. 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. Transverse cycling will continue until Ca2+ ions and ATP are no longer available and tropomyosin again covers actin binding sites. (2) Chemical reactions cause the reorganization of muscle fibers in such a way that the muscle is shortened – this is contraction. Figure 6.

It shows the muscular contraction cycle of the transverse bridge triggered by the binding of Ca2+ to the active center of actin. With each cycle of contraction, actin moves relative to myosin. Acetylcholine binds to the receptors of the end plate with the entry of Na+ into the muscle. Postsynaptic depolarization triggers an action potential that spreads along the sarpolmatous membrane. The length-tension relationship relates the force of an isometric contraction to the length of the muscle where the contraction occurs. Muscles work with the greatest active tension when they approach an ideal length (often their length at rest). In addition, if stretching or shortening is carried out (whether due to the action of the muscle itself or an external force), the maximum active tension generated decreases. [29] This decrease is minimal for small deviations, but the voltage decreases rapidly as the length continues to deviate from the ideal. Due to the presence of elastic proteins in a muscle cell (such as titin) and the extracellular matrix, when the muscle is stretched beyond a certain length, there is a completely passive tension that counteracts the elongation. In combination, there is a strong resistance to the elongation of an active muscle well beyond the peak of active tension. Muscle contractions can be described using two variables: length and tension.

[1] Muscle contraction is described as isometric when muscle tension changes but muscle length remains the same. [1] [3] [4] [5] In contrast, estotonic muscle contraction when muscle tension remains the same throughout the contraction. [1] [3] [4] [5] When muscle length shortens, the contraction is concentric; [1] [6] When muscle length lengthens, the contraction is eccentric. In the natural movements that underlie the activity of the musculoskeletal system, muscle contractions are diverse, since they are able to produce changes in length and tension in a way that varies over time. [7] Therefore, it is likely that neither the length nor the tension in the muscles that contract during the activity of the musculoskeletal system remain the same. 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.

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