Why Muscles Contract and Relax
Because DMD is caused by a mutation in the gene that codes for dystrophin, it was thought that introducing healthy myoblasts into patients could be an effective treatment. Myoblasts are the embryonic cells responsible for muscle development and, ideally, they would carry healthy genes that could produce the dystrophin needed for normal muscle contraction. This approach has been largely unsuccessful in humans. A more recent approach was to increase the production of utrophin in muscle, a dystrophin-like protein that could potentially play the role of dystrophin and prevent cell damage. Passive stretching. This type of muscle contraction occurs when your muscle is passively elongated. For example, bend over to touch your toes. There is no extra weight that your thigh muscle needs to hold or lift by exerting strength, but it still stretches from movement. Although the muscle performs a negative amount of mechanical work (the work is done on the muscle), chemical energy (originally released by oxygen, by fat or glucose and temporarily stored in ATP) is still consumed, although less than would be consumed during a concentric contraction of the same force. For example, you use more energy when you climb a flight of stairs than when you go down the same flight.
The force-speed relationship refers to the speed at which a muscle changes its length (usually regulated by external forces such as tension or other muscles) with the amount of force it generates. The force decreases hyperbolically relative to the isometric force as the shortening rate increases, and eventually reaches zero at maximum speed. The opposite is true when the muscle is stretched – the force increases beyond the isometric maximum until an absolute maximum is finally reached. This intrinsic property of active muscle tissue plays a role in the active cushioning of joints operated by simultaneously active counter-muscles. In such cases, the force-speed profile amplifies the force generated by the lengthening muscle at the expense of the shortening muscle. This favor of the muscle, which balances the joint, effectively increases the cushioning of the joint. In addition, the strength of the cushioning increases with muscle strength. The motor system can thus actively control joint damping via the simultaneous contraction (co-contraction) of opposing muscle groups.  The mechanism of muscle contraction has eluded scientists for years and requires further research and updating.  The sliding wire theory was developed independently by Andrew F.
Huxley and Rolf Niedergerke, as well as Hugh Huxley and Jean Hanson. Their results were published as two consecutive papers published in the May 22, 1954 issue of Nature under the common theme “Structural Changes in Muscles During Contraction.”   How would muscle contractions be affected if the ATP in a muscle fiber were completely depleted? The contractile activity of smooth muscle cells can be tonic (persistent) or phasic (temporary) and is affected by multiple inputs such as spontaneous electrical activity, neuronal and hormonal inputs, local changes in chemical composition, and stretching.  This contrasts with the contractile activity of skeletal muscle cells, which is based on a single neuronal input. Some types of smooth muscle cells are able to spontaneously generate their own action potentials, which usually occur after pacemaker potential or slow wave potential. These action potentials are generated by the influx of extracellular Ca2+ and not Na+. Like skeletal muscles, cytosolic Ca2+ ions are also needed for the transverse bridge cycle in smooth muscle cells. Concentric and eccentric muscle contractions. These two types of contractions often go hand in hand. A concentric muscle contraction will help you lift something heavy.
We often talk about positive work. Passive stretching. This type of muscle contraction is useful for gently lengthening your muscles. You can passively contract your muscles by stretching them as far as they can physically walk. This lengthens your muscles in a way that activates them without the effort required. Excitation-contraction coupling is the process by which a potential for muscle action in the muscle fiber causes the myofibrils to contract.  In skeletal muscle, excitation-contraction coupling is based on direct coupling between key proteins, the sarcoplasmic reticulum (SR) calcium release channel (identified as ryanodine 1 receptor, RYR1) and voltage-controlled L-type calcium channels (identified as dihydropyridine receptors, DHPR). DHPR are located on the sarcolemma (which includes the surface sarcolemma and transverse tubules), while RyRs are located across the SR membrane. The narrow arrangement of a transverse tubule and two SR regions containing RyRs is described as a triad and is primarily the place where the excitation-contraction coupling takes place.
Excitation-contraction coupling occurs when depolarization of the skeletal muscle cell leads to a muscle action potential that spreads through the cell surface and into the tubular T network of the muscle fiber, thereby depolarizing the inner part of the muscle fiber. Depolarization of the internal parts activates dihydropyridine receptors in terminal cisterns, which are located near ryanodine receptors in the adjacent sarcoplasmic reticulum. Activated dihydropyridine receptors physically interact with ryanodine receptors to activate them via foot processes (with conformational changes that activate ryanodine receptors allosterically). When the ryanodine receptors open, Ca2+ is released from the sarcoplasmic reticulum into the local connection space and diffuses into the bulk cytoplasm to cause a spark of calcium. Note that the sarcoplasmic reticulum has a high calcium buffering capacity, which is partly due to a calcium-binding protein called calequesterin. The almost synchronous activation of thousands of calcium sparks by the action potential causes an increase in calcium at the cell level, which leads to the increase in calcium transient. The Ca2+ released in the cytosol binds to troponin C through the actin filaments to allow the transverse bridge cycle, which generates strength and movement in certain situations. Calcium ATPase of the endoplasmic sarco/reticulum (SERCA) actively pumps Ca2+ into the sarcoplasmic reticulum.
When Ca2+ falls back to the level of rest, strength decreases and relaxation occurs. During a concentric contraction, a muscle is stimulated to contract according to the sliding wire theory. This happens along the entire length of the muscle, creating strength at the origin and beginning, shortening the muscle and changing the angle of the joint. As for the elbow, a concentric contraction of the biceps would cause the arm to bend to the elbow when the hand passes from the leg to the shoulder (a bicepslock). A concentric contraction of the triceps would change the angle of the joint in the opposite direction, stretching the arm and moving the hand towards the leg. (2) Chemical reactions cause the reorganization of muscle fibers in such a way that the muscle shortens – this is contraction. In eccentric contraction, the tension generated during isometry is not enough to overcome the external load on the muscle, and the muscle fibers lengthen as they contract.  Instead of working to pull a joint towards muscle contraction, the muscle acts to slow down the joint at the end of a movement or otherwise control the repositioning of a load. This can happen unintentionally (for example. B when trying to move a weight too heavy to lift the muscle) or voluntarily (for example.
B when the muscle “smoothes” a movement or resists gravity, by. B example during the descent). In the short term, strength training, which involves both eccentric and concentric contractions, seems to increase muscle strength more than training with concentric contractions alone.  However, exercise-induced muscle damage is greater even with prolonged contractions.  A multi-step molecular process in muscle fibers begins when acetylcholine binds to receptors in the membrane of muscle fibers. 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 of contraction of a relaxed muscle fiber begins: when a muscle is at rest, the concentration of calcium in the sarcoplasm (the cytoplasm of a muscle cell) is very low and prevents the bridges from attaching to actin. .