What Happens When a Skeletal Muscle Fibre Contracts

Molecular events of muscle fiber shortening occur in fiber sarcomeres (see Figure 3). The contraction of a striated muscle fiber occurs when the sarcomeres, which are arranged linearly in the myofibrils, shorten when the myosin heads pull on the actin filaments. (2) Chemical reactions cause the reorganization of muscle fibers in such a way that the muscle is shortened - this is contraction. (3) When the signal from the nervous system is no longer present, the chemical process reverses, the muscle fibers rearrange and the muscle relaxes. Without ATP, myosin heads cannot detach from actin binding sites. All "stuck" transverse bridges cause muscle stiffness. In a living person, this can lead to such a condition as "writer`s cramps." In a recently deceased person, this leads to mortis rigor. When an event changes the permeability of the membrane for Na+ ions, they enter the cell. It changes the tension. This is an electrical event called action potential that can be used as a cellular signal. Communication between nerves and muscles is via neurotransmitters. The action potentials of neurons cause the release of neurotransmitters from the synaptic terminal into the synaptic cleft, where they can then diffuse through the synaptic cleft and bind to a receptor molecule on the motor end plate. The end plate of the motor has connecting folds - folds in the sarcolemma that create a large area for the neurotransmitter to bind to the receptors.

Receptors are actually sodium channels that open to allow Na+ to pass into the cell when they receive a neurotransmitter signal. When a sarcomere shortens, some regions shorten while others remain the same length. A sarcomere is defined as the distance between two successive Z disks or Z lines; When a muscle contracts, the distance between the intervertebral Z discs is reduced. Zone H – the central zone of zone A – contains only thick filaments and is shortened during contraction. The I strip contains only thin filaments and is also shortened. The A band does not shorten – it remains the same length – but the A bands of various sarcomeres get closer during contraction and eventually disappear. The thin filaments are pulled by the thick filaments towards the center of the sarcomere until the Z discs approach the thick filaments. The overlapping area, where thin filaments and thick filaments occupy the same surface, increases as thin filaments move inward. For a muscle cell to contract, the sarcomor must shorten. However, thick and thin filaments - the components of sarcomeres - do not shorten. Instead, they slide in front of each other, shortening the sarcomor while keeping the filaments of the same length. The sliding thread theory of muscle contraction was developed to adjust the differences observed in the ligaments mentioned on the sarcoma with different degrees of muscle contraction and relaxation.

The contraction mechanism is the binding of myosin to actin and forms transverse bridges that produce filament movements (Figure 6.7). The second work by Hugh Huxley and Jean Hanson is entitled "Changes in the crossed streaks of muscle during contraction and stretching and their structural interpretation". It is more complex and based on their study of rabbit muscle with phase contrast and electron microscopes. According to them:[19] This muscle fiber disorder triggers an increase in white blood cells after induced muscle pain, leading to the observation of the inflammatory response due to induced muscle pain. Increased plasma enzymes, myoglobinemia, and abnormal muscle histology and ultrastructure are associated with the inflammatory response. High tension in the contractile-elastic system of the muscle leads to structural damage to the muscle fiber and plasma lemma and its epimysium, perimysium and endomysium. Mysium damage interferes with calcium homeostasis in injured fibers and fiber bundles, resulting in necrosis that peaks about 48 hours after exercise. Products of macrophage activity and intracellular content (such as histamines, kinins and K+) accumulate outside the cells. These substances then stimulate the free nerve endings in the muscle; A process that seems accentuated by eccentric training, in which large forces are distributed over a relatively small cross-section of the muscle. Muscle contraction occurs when a muscle fiber or group of fibers is signaled by the brain via the nerves to activate and increase tension in the muscle. It is also called activation of muscle fibers.

Their body has three different types of muscles and they contract in three different ways. 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: neuronal control initiates the formation of actin-myosin transverse bridges, leading to the shortening of the sarcoma involved in muscle contraction. These contractions extend from the muscle fiber through the connective tissue to pull on the bone, resulting in skeletal movement. The pull exerted by a muscle is called tension, and the amount of force generated by this tension can vary. This allows the same muscles to move very light objects and very heavy objects. For individual muscle fibers, the amount of tension generated depends on the cross-section of the muscle fiber and the frequency of neuronal stimulation. concentric contraction: a type of muscle contraction in which muscles shorten while creating strength The nerves responsible for innerving muscle fibers are called motor neurons. A single motor neuron and the muscle fibers it innervates are collectively called the motor unit.

The number of muscle fibers in a motor unit varies predictably with muscle function. For example, the motor units responsible for the facial expression muscles contain far fewer muscle fibers than the motor units responsible for the muscles involved in activities such as swimming. Bridge cross-formation occurs when the myosin head binds to actin, while adenosine diphosphate (ADP) and inorganic phosphate (Pi) are always bound to myosin (Figure 4a,b). Pi is then released, which causes the formation of a stronger bond with the myosin, after which the head of the myosin moves to the M line, dragging the actin with it. When the actin is pulled, the filaments move about 10 nm in the direction of the M line. This movement is called force stroke because this step causes the thin filament to move (Figure 4c). In the absence of ATP, the myosin head does not detach from actin. Sarcoma: Delayed muscle pain is caused by structural damage to the Z-disc and myosin and actin filaments. 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] As organs that contain cells that can contract, muscles can produce strength and movement. Skeletal muscle works in conjunction with the bones of the skeleton to create body movements. In addition, it is also associated with the muscles of the diaphragm, esophagus and eyes. Thus, skeletal muscle serves a variety of purposes, including body movement, breathing, and swallowing. Unlike smooth muscles and heart muscles, skeletal muscle contracts mainly in response to a voluntary stimulus. Binding to ATP causes the myosin to release actin, allowing actin and myosin to detach from each other. After that, the newly bound ATP is converted to ADP and inorganic phosphate, Pi. The enzyme at the myosin binding site is called ATPase.

The energy released during ATP hydrolysis changes the angle of the myosin head to a "tense" position. The myosin head is then in position for further movement and has potential energy, but ADP and Pi are still linked. When actin binding sites are covered and unavailable, myosin remains in the high-energy configuration with hydrolyzed ATP, but still bound. Muscles cannot contract on their own. They need a stimulus from a nerve cell to "tell" them to contract. Let`s say you decide to raise your hand in class...