Watch this video that explains how to report muscle contraction. Muscle contraction is the activation of tension-generating sites in muscle cells. [1] [2] In physiology, muscle contraction does not necessarily mean muscle shortening, as muscle tension can be generated without a change in muscle length, for example when. B`a heavy book or dumbbell is held in the same position. [1] The end of muscle contraction is followed by muscle relaxation, which is a return of the muscle fibers to their low-tension state. [1] Cytoplasmic calcium binds to troponin C and moves the tropomyosin complex from the actin binding site so that the myosin head can bind to the actin filament. From this point on, the contractile mechanism is essentially the same as in skeletal muscle (above). In short, using ATP hydrolysis, the myosin head pulls the actin filament towards the center of the sarcomere. Although the term excitation-contraction coupling confuses or frightens some students, it boils down to this: for a skeletal muscle fiber to contract, its membrane must first be «excited» – in other words, it must be stimulated to trigger an action potential.

The action potential of muscle fibers, which sweeps like a wave along the sarcolemma, is «coupled» to the actual contraction by the release of calcium ions ((text{Ca}^{++})) from the SR. After release, the (text{Ca}^{++}) interacts with the shielding proteins, troponin and tropomyosin complex, forcing them to move to the side so that actin binding sites are available for fixation by myosin heads. The myosin then pulls the actin filaments towards the center, shortening the muscle fiber. Skeletal muscle fibers are red and white. They look striped or striped, so they are often called striped muscles. Heart muscles are also scratched, but smooth muscles are not. Duchenne muscular dystrophy (DMD) is a progressive weakening of skeletal muscle. It is one of many diseases collectively called «muscular dystrophy». DMD is caused by a deficiency of protein dystrophin, which helps the thin filaments of myofibrils bind to the sarcolemma. Without adequate dystrophin, muscle contractions cause the sarcolemma to rupture, leading to an influx of Ca++, leading to cell damage and breakdown of muscle fibers. Over time, as muscle damage accumulates, muscle mass is lost and greater functional impairments develop. 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] The length-tension relationship refers to the strength of an isometric contraction at the length of the muscle at which 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. The ability of cells to communicate electrically requires cells to use energy to create an electrical gradient across their cell membranes. This charge gradient is supported by ions that are distributed differently across the membrane. Each ion exerts an electrical influence and a concentration influence. Just as milk eventually mixes with coffee without the need to stir, ions distribute equally evenly if they allow it. In this case, they should not return to a uniformly mixed state. After contraction, muscle relaxation occurs when Ca2+ reassembles via the Ca2+ ATPase active pump (SERCA) on the membrane of the sarcoplasmic reticulum in the sarcoplasmic reticulum. This pump carries intracellular Ca2+ into the sarcoplasmic reticulum, which maintains a low intracellular Ca2+ when the muscle is relaxed. Inside the sarcoplasmic reticulum is a Ca2+ binding protein called calequesterin, which is used to decrease the free concentration of Ca2+ to reduce the work required by the SERCA pump. When the intracellular concentration of Ca2+ decreases, the Ca2+ of troponin C dissociates so that tropomyosin can again block myosin binding sites to F-actin.

[5] The area where the thick and thin filaments overlap has a dense appearance due to the lack of space between the filaments. This area, where thin and thick filaments overlap, is very important for muscle contraction because it is where the movement of the filament begins. Thin filaments anchored at their ends through the Z disks do not extend completely into the central zone, which contains only thick filaments anchored to their bases in a place called the M line. A myofibril consists of many sarcomeres that run along its length; Thus, myofibrils and muscle cells contract when sarcomeres contract. 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. Creatine phosphate is a molecule that can store energy in its phosphate bonds. In a resting muscle, excess ATP transfers its energy to creatine and produces ADP and creatine phosphate. This acts as an energy reserve that can be used to quickly generate more ATP. When the muscle contracts and needs energy, creatine phosphate transfers its phosphate to ADP to make ATP and creatine. This reaction is catalyzed by the enzyme creatine kinase and occurs very quickly; Thus, ATP derived from creatine phosphate causes the first few seconds of muscle contraction.

However, creatine phosphate can only provide energy worth about 15 seconds, after which another energy source must be used (Figure 10.12). Invertebrates such as annelids, molluscs and nematodes have oblique striped muscles that contain thick, thin filament bands arranged spirally rather than transversely, as in the skeletal or cardiac muscles of vertebrates. [44] In mussels, obliquely striped muscles can maintain tension for long periods of time without consuming too much energy. Mussels use these muscles to keep their shells closed. Motor neurons that tell skeletal muscle fibers to contract come from the spinal cord, with a smaller number in the brain stem to activate the skeletal muscles of the face, head, and neck. These neurons have long processes, called axons, that specialize in transmitting action potentials over long distances – in this case, all the way from the spinal cord to the muscle itself (which can be up to three feet away). The axons of several neurons group together in nerves, like wires grouped together in a cable. Muscle fatigue occurs when a muscle can no longer contract in response to signals from the nervous system. The exact causes of muscle fatigue are not fully known, although some factors have been correlated with the decrease in muscle contraction that occurs during fatigue. ATP is necessary for normal muscle contraction, and when ATP stores are reduced, muscle function may decrease. This may be more of a factor in short, intense muscle performance than in sustained, less intense exertion.

The accumulation of lactic acid can lower intracellular pH and affect the activity of enzymes and proteins. Imbalances in the Na+ and K+ levels resulting from membrane depolarization can disrupt the Ca++ flow of the SR. . . .