Muscle contraction is the activation of tension-generating sites within muscle cells.[1][2] In physiology, muscle contraction does not necessarily mean muscle shortening because muscle tension can be produced without changes in muscle length, such as when holding something heavy in the same position.[1] The termination of muscle contraction is followed by muscle relaxation, which is a return of the muscle fibers to their low tension-generating state.[1]

The major constituent of thin filaments is a chain formed by helical coiling of two strands of actin, and thick filaments dominantly consist of chains of the motor-protein myosin. Together, these two filaments form myofibrils - the basic functional organelles in the skeletal muscle system.


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In vertebrates, skeletal muscle contractions are neurogenic as they require synaptic input from motor neurons. A single motor neuron is able to innervate multiple muscle fibers, thereby causing the fibers to contract at the same time. Once innervated, the protein filaments within each skeletal muscle fiber slide past each other to produce a contraction, which is explained by the sliding filament theory. The contraction produced can be described as a twitch, summation, or tetanus, depending on the frequency of action potentials. In skeletal muscles, muscle tension is at its greatest when the muscle is stretched to an intermediate length as described by the length-tension relationship.

Unlike skeletal muscle, the contractions of smooth and cardiac muscles are myogenic (meaning that they are initiated by the smooth or heart muscle cells themselves instead of being stimulated by an outside event such as nerve stimulation), although they can be modulated by stimuli from the autonomic nervous system. The mechanisms of contraction in these muscle tissues are similar to those in skeletal muscle tissues.

Muscle contraction can also be described in terms of two variables: length and tension.[1] In natural movements that underlie locomotor activity, muscle contractions are multifaceted as they are able to produce changes in length and tension in a time-varying manner.[3] Therefore, neither length nor tension is likely to remain the same in skeletal muscles that contract during locomotion. Contractions can be described as isometric if the muscle tension changes but the muscle length remains the same.[1][4][5][6] In contrast, a muscle contraction is described as isotonic if muscle tension remains the same throughout the contraction.[1][4][5][6] If the muscle length shortens, the contraction is concentric;[1][7] if the muscle length lengthens, the contraction is eccentric.

Muscle contractions can be described based on two variables: force and length. Force itself can be differentiated as either tension or load. Muscle tension is the force exerted by the muscle on an object whereas a load is the force exerted by an object on the muscle.[1] When muscle tension changes without any corresponding changes in muscle length, the muscle contraction is described as isometric.[1][4][5][6] If the muscle length changes while muscle tension remains the same, then the muscle contraction is isotonic.[1][4][5][6] In an isotonic contraction, the muscle length can either shorten to produce a concentric contraction or lengthen to produce an eccentric contraction.[1][7] In natural movements that underlie locomotor activity, muscle contractions are multifaceted as they are able to produce changes in length and tension in a time-varying manner.[3] Therefore, neither length nor tension is likely to remain constant when the muscle is active during locomotor activity.

An isometric contraction of a muscle generates tension without changing length.[1][4][5][6] An example can be found when the muscles of the hand and forearm grip an object; the joints of the hand do not move, but muscles generate sufficient force to prevent the object from being dropped.

In isotonic contraction, the tension in the muscle remains constant despite a change in muscle length.[1][4][5][6] This occurs when a muscle's force of contraction matches the total load on the muscle.

In concentric contraction, muscle tension is sufficient to overcome the load, and the muscle shortens as it contracts.[8] This occurs when the force generated by the muscle exceeds the load opposing its contraction.

During a concentric contraction, a muscle is stimulated to contract according to the sliding filament theory. This occurs throughout the length of the muscle, generating a force at the origin and insertion, causing the muscle to shorten and changing the angle of the joint. In relation to the elbow, a concentric contraction of the biceps would cause the arm to bend at the elbow as the hand moved from the leg to the shoulder (a biceps curl). A concentric contraction of the triceps would change the angle of the joint in the opposite direction, straightening the arm and moving the hand towards the leg.

In eccentric contraction, the tension generated while isometric is insufficient to overcome the external load on the muscle and the muscle fibers lengthen as they contract.[9] Rather than working to pull a joint in the direction of the muscle contraction, the muscle acts to decelerate the joint at the end of a movement or otherwise control the repositioning of a load. This can occur involuntarily (e.g., when attempting to move a weight too heavy for the muscle to lift) or voluntarily (e.g., when the muscle is 'smoothing out' a movement or resisting gravity such as during downhill walking). Over the short-term, strength training involving both eccentric and concentric contractions appear to increase muscular strength more than training with concentric contractions alone.[10] However, exercise-induced muscle damage is also greater during lengthening contractions.[11]

During an eccentric contraction of the biceps muscle, the elbow starts the movement while bent and then straightens as the hand moves away from the shoulder. During an eccentric contraction of the triceps muscle, the elbow starts the movement straight and then bends as the hand moves towards the shoulder. Desmin, titin, and other z-line proteins are involved in eccentric contractions, but their mechanism is poorly understood in comparison to cross-bridge cycling in concentric contractions.[9]

Though the muscle is doing a negative amount of mechanical work, (work is being done on the muscle), chemical energy (of fat or glucose, or temporarily stored in ATP) is nevertheless consumed, although less than would be consumed during a concentric contraction of the same force. For example, one expends more energy going up a flight of stairs than going down the same flight.

Muscles undergoing heavy eccentric loading suffer greater damage when overloaded (such as during muscle building or strength training exercise) as compared to concentric loading. When eccentric contractions are used in weight training, they are normally called negatives. During a concentric contraction, contractile muscle myofilaments of myosin and actin slide past each other, pulling the Z-lines together. During an eccentric contraction, the myofilaments slide past each other the opposite way, though the actual movement of the myosin heads during an eccentric contraction is not known. Exercise featuring a heavy eccentric load can actually support a greater weight (muscles are approximately 40% stronger during eccentric contractions than during concentric contractions) and also results in greater muscular damage and delayed onset muscle soreness one to two days after training. Exercise that incorporates both eccentric and concentric muscular contractions (i.e., involving a strong contraction and a controlled lowering of the weight) can produce greater gains in strength than concentric contractions alone.[10][12] While unaccustomed heavy eccentric contractions can easily lead to overtraining, moderate training may confer protection against injury.[10]

Eccentric contractions normally occur as a braking force in opposition to a concentric contraction to protect joints from damage. During virtually any routine movement, eccentric contractions assist in keeping motions smooth, but can also slow rapid movements such as a punch or throw. Part of training for rapid movements such as pitching during baseball involves reducing eccentric braking allowing a greater power to be developed throughout the movement.

Eccentric contractions are being researched for their ability to speed rehabilitation of weak or injured tendons. Achilles tendinitis[13][14] and patellar tendonitis[15] (also known as jumper's knee or patellar tendonosis) have been shown to benefit from high-load eccentric contractions.

In vertebrate animals, there are three types of muscle tissues: skeletal, smooth, and cardiac. Skeletal muscle constitutes the majority of muscle mass in the body and is responsible for locomotor activity. Smooth muscle forms blood vessels, gastrointestinal tract, and other areas in the body that produce sustained contractions. Cardiac muscle make up the heart, which pumps blood. Skeletal and cardiac muscles are called striated muscle because of their striped appearance under a microscope, which is due to the highly organized alternating pattern of A bands and I bands.

Excluding reflexes, all skeletal muscles contractions occur as a result of signals originating in the brain. The brain sends electrochemical signals through the nervous system to the motor neuron that innervates several muscle fibers.[16] In the case of some reflexes, the signal to contract can originate in the spinal cord through a feedback loop with the grey matter. Other actions such as locomotion, breathing, and chewing have a reflex aspect to them: the contractions can be initiated both consciously or unconsciously.

A neuromuscular junction is a chemical synapse formed by the contact between a motor neuron and a muscle fiber.[17] It is the site in which a motor neuron transmits a signal to a muscle fiber to initiate muscle contraction. The sequence of events that results in the depolarization of the muscle fiber at the neuromuscular junction begins when an action potential is initiated in the cell body of a motor neuron, which is then propagated by saltatory conduction along its axon toward the neuromuscular junction. Once it reaches the terminal bouton, the action potential causes a Ca2+

 ion influx into the terminal by way of the voltage-gated calcium channels. The Ca2+

 influx causes synaptic vesicles containing the neurotransmitter acetylcholine to fuse with the plasma membrane, releasing acetylcholine into the synaptic cleft between the motor neuron terminal and the neuromuscular junction of the skeletal muscle fiber. Acetylcholine diffuses across the synapse and binds to and activates nicotinic acetylcholine receptors on the neuromuscular junction. Activation of the nicotinic receptor opens its intrinsic sodium/potassium channel, causing sodium to rush in and potassium to trickle out. As a result, the sarcolemma reverses polarity and its voltage quickly jumps from the resting membrane potential of -90mV to as high as +75mV as sodium enters. The membrane potential then becomes hyperpolarized when potassium exits and is then adjusted back to the resting membrane potential. This rapid fluctuation is called the end-plate potential[18] The voltage-gated ion channels of the sarcolemma next to the end plate open in response to the end plate potential. They are sodium and potassium specific and only allow one through. This wave of ion movements creates the action potential that spreads from the motor end plate in all directions.[18] If action potentials stop arriving, then acetylcholine ceases to be released from the terminal bouton. The remaining acetylcholine in the synaptic cleft is either degraded by active acetylcholine esterase or reabsorbed by the synaptic knob and none is left to replace the degraded acetylcholine. 2351a5e196

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