• What Stimulates a Skeletal Muscle Cell to Contract

What Stimulates a Skeletal Muscle Cell to Contract

The opening of voltage-controlled sodium channels, followed by the influx of Na+, transmits an action potential once the membrane is sufficiently depolarized. The delayed opening of the potassium channels allows K+ to leave the cell, repolarize the membrane. The structural organization of the T tubules collapses in heart failure. This degradation, caused, among other things, by myocardial toads (such as myocardial infarction, which causes ischemia), leads to impaired contractility due to reduced, asynchronous and chaotic calcium release. Several signaling pathways are compromised in heart failure. First of all, there may be a reorganization of the β-adrenergic system. Activation of the β2-adrenergic receptor is usually limited to the T-tubule, while heart failure involves a redistribution of the receptor over the entire plasma membrane (Nikolaev et al. 2010). With chronic adrenergic activation, hyperphosphorylation of RyR leads to leakage of RyR channels, resulting in a reduction in SR calcium and therefore weaker contractions. Calcium triggers a contraction in the striated muscle. (A) Actomyosin in striated muscles. (1) The striped muscle in the relaxed state has tropomyosin, which covers the sites of binding to myosin on actin. (2) Calcium binds to troponin C, which induces a conformational change in the troponin complex.

This causes tropomyosin to penetrate deeper into the actinrillilla and expose the myosin binding sites. (B) Transverse bridge cycle in striated muscles. (1) Calcium binds to troponin C and causes conformational displacement to tropomyosin, which reveals myosin binding sites to actin. (2) ATP then binds to myosin. (3) The ATP is then hydrolyzed. (4) A transverse bridge forms and myosin binds to a new position on actin. (5) Pi is released and the myosin changes the conformation, resulting in the force impact that causes the filaments to slide over each other. (6) ADP is then released. (C) Contraction in smooth muscles.

In smooth muscle, calcium binds to calmodulin and causes activation of myosin light chain kinase (MLC) (MLCK). This phosphorylate MLC, which then binds to actin to form phosphorylated actomyosine, allowing the transverse bridge cycle to begin. Skeletal muscles contain connective tissue, blood vessels and nerves. There are three layers of connective tissue: epimysium, perimisium and endomysium. Skeletal muscle fibers are organized into groups called fascicles. Blood vessels and nerves enter the connective tissue and branch out into the cell. The muscles connect directly or through tendons or fascia on the bones. Skeletal muscle maintains posture, stabilizes bones and joints, controls internal movements and generates heat. Malignant hyperthermia is a life-threatening disease that occurs mainly in people with a genetic predisposition with a mutation in the ryanodine receptor of the sarcoplasmic reticulum. When these people are exposed to volatile anesthetics or the muscle relaxant succinylcholine, there is a massive release of intracellular Ca2+ from ryanodine receptors and insufficient sequestration of Ca2+ by the SERCA pump.

This mechanism leads to muscle contraction, rhabdomyolysis, severe hyperthermia and eventually death. The only treatment for malignant hyperthermia is dantrolene, which binds to the ryanodine receptor to prevent the release of Ca2+. [8] The assessment of muscle strength and muscle contraction is a routine procedure in the physical examination of the patient. The Medical Research Council`s Manual Muscle Test Scale is the most commonly used muscle strength assessment system, where scores from 0 to 5 are assigned based on the patient`s abilities. A score of 0 does not refer to muscle activation. A score of 1 means that there is only a slight contractility of the muscle. A score of 2 is when muscle activation is tested in the absence of severity. 3 refers to muscle activation against gravity, but not resistance. 4 is muscle activation against gravity and some resistance and 5 is muscle activation against gravity and total resistance. The main purpose of muscle strength tests during physical examination is to assess and determine a differential diagnosis when a patient has discomfort of weakness, often as part of a neurological disorder. [12] Muscles would lose their integrity during strong movements, resulting in muscle damage. Myasthenia gravis is an autoimmune disease that affects the neuromuscular connection.

It is characterized by tiring skeletal muscle weakness, which worsens with repetitive movements and improves with rest. Most often, myasthenia gravis initially involves weakness of the eye muscles with possible progression to the muscles of the limbs. Most patients with this disease have autoantibodies against the nicotinic ACh receptors of the neuromuscular compound, which leads to endocytosis and receptor breakdown. Without ACh binding to receptors, action potentials cannot spread into the muscle fiber and, as a result, muscle weakness occurs. Acetylcholinesterase inhibitors prevent the breakdown of ACh and are used to increase neuromuscular transmission for the treatment of myasthenia gravis. [9] Neurons and skeletal muscle cells are electrically excitable, meaning they are able to generate action potentials. An action potential is a special type of electrical signal that can travel in wave form along a cell membrane. As a result, a signal can be transmitted quickly and faithfully over long distances. Excitation-contraction coupling is the link (transduction) between the action potential generated in the sarkolemma and the onset of muscle contraction. The trigger for the release of calcium from the sarcoplasmic reticulum into the sarcoplasm is a neural signal. Each skeletal muscle fiber is controlled by a motor neuron that transmits signals from the brain or spinal cord to the muscle. The area of the sarcolemma on the muscle fiber that interacts with the neuron is called the motor end plate.

The end of the neuron`s axon is called the synaptic terminal and does not really touch the end plate of the motor. A small space called the synaptic space separates the synaptic terminal from the end plate of the motor. .