|This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (May 2013)|
Muscle contraction is the activation of tension-generating sites within muscle fibers. In physiology, muscle contraction does not mean muscle shortening because muscle tension can be produced without changes in muscle length such as holding a heavy book or a dumbbell at the same position. The termination of muscle contraction is followed by muscle relaxation, which is a return of the muscle fibers to their low tension-generating state.
Muscle contractions can be described based on two variables: length and tension. A muscle contraction is described as isometric if the muscle tension changes but the muscle length remains the same. In contrast, a muscle contraction is isotonic if muscle length changes but the muscle tension remains the same. If the muscle length shortens, the contraction is concentric; if the muscle length lengthens, the contraction is eccentric. 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. Therefore neither length nor tension is likely to remain the same in muscles that contract during locomotor activity.
In vertebrates, skeletal muscle contractions are neurogenic as they require synaptic input from motor neurons to produce muscle contractions. 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 contractions that is 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.
Smooth and cardiac muscle contractions are myogenic and can be modulated by the autonomic nervous system. The mechanisms of contraction in these muscle tissues are similar to skeletal muscle tissues.
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. When muscle tension changes without any corresponding changes in muscle length, the muscle contraction is described as isometric. If the muscle length changes while muscle tension remains the same, then the muscle contraction is isotonic. In an isotonic contraction, the muscle length can either shorten to produce a concentric contraction or lengthen to produce an eccentric contraction. Furthermore, if the muscle length shortens, the contraction is concentric. But if the muscle length lengthens, then the contraction is eccentric. 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. 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. 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. 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. 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 is insufficient to overcome the external load on the muscle and the muscle fibers lengthen as they contract. 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). Over the short-term, strength training involving both eccentric and concentric contractions appear to increase muscular strength more than training with concentric contractions alone. However, exercise-induced muscle damage is also greater during lengthening contractions.
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.
Though the muscle is doing a negative amount of mechanical work, (work is being done on the muscle), chemical energy (in fat, glucose or 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, muscle fibers slide across each other, pulling the Z-lines together. During an eccentric contraction, the filaments 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. While unaccustomed heavy eccentric contractions can easily lead to overtraining, moderate training may confer protection against injury.
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  and patellar tendonitis  (also known as jumper's knee or patellar tendonosis) have been shown to benefit from high-load eccentric contractions.
For voluntary muscles, all contraction (excluding reflexes) occurs as a result of conscious effort originating in the brain. The brain sends signals, in the form of action potentials, through the nervous system to the motor neuron that innervates several muscle fibers. In the case of some reflexes, the signal to contract can originate in the spinal cord through a feedback loop with the grey matter. Involuntary muscles such as the heart or smooth muscles in the gut and vascular system contract as a result of non-conscious brain activity or stimuli endogenous to the muscle itself. Other actions such as locomotion, breathing, and chewing have a reflex aspect to them: the contractions can be initiated both consciously or unconsciously.
There are three general types of muscle tissues:
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 band and I band.
While nerve impulse profiles are, for the most part, always the same, skeletal muscles are able to produce varying levels of contractile force. This phenomenon can be best explained by Force Summation. Force Summation describes the addition of individual twitch contractions to increase the intensity of overall muscle contraction. This can be achieved in two ways: by increasing the number and size of contractile units simultaneously, called multiple fiber summation, and by increasing the frequency at which action potentials are sent to muscle fibers, called frequency summation.
Such a temporal summation occurs when a single synapse generates excitatory postsynaptic potentials (EPSP's), which occur when sodium enters the cell and neutralizes some of the cell's negative charge, at such a rate that a new potential is fired before the previous one has faded. This rapid buildup of EPSP's add together over time reaching a threshold voltage that triggers an action potential. The threshold that must be reached in order to produce an action potential is -55 mV. The depolarization that occurs is responsible for the all-or-nothing signal conducted through the postsynaptic membrane.  Temporal summation can occur if even a single presynaptic neuron stimulates a postsynaptic neuron at a fast enough rate.
Excitation–contraction coupling is the process by which a muscular action potential in the muscle fiber causes the myofibrils to contract. In skeletal muscle, excitation–contraction coupling relies on a direct coupling between key proteins, the sarcoplasmic reticulum (SR) calcium release channel (identified as the ryanodine receptor, RyR) and voltage-gated L-type calcium channels (identified as dihydropyridine receptors, DHPRs). DHPRs are located on the sarcolemma (which includes the surface sarcolemma and the transverse tubules), while the RyRs reside across the SR membrane. The close apposition of a transverse tubule and two SR regions containing RyRs is described as a triad and is predominantly where excitation–contraction coupling takes place. Excitation–contraction coupling proceeds as follows:
The sliding filament theory describes a process used by muscles to contract. It is a cycle of repetitive events that cause a thin filament to slide over a thick filament and generate tension in the muscle. It was independently developed by Andrew Huxley and Rolf Niedergerke and by Hugh Huxley and Jean Hanson in 1954.
The calcium ions leave the troponin molecule in order to maintain the calcium ion concentration in the sarcoplasm. The active pumping of calcium ions into the sarcoplasmic reticulum creates a deficiency in the fluid around the myofibrils. This causes the removal of calcium ions from the troponin. Thus, the tropomyosin-troponin complex again covers the binding sites on the actin filaments and contraction ceases.
Physiologically, this contraction is not uniform across the sarcomere; the central position of the thick filaments becomes unstable and can shift during contraction. However the actions of elastic proteins such as titin are hypothesised to maintain uniform tension across the sarcomere and pull the thick filament into a central position.
Latent period refers to the time between a stimulus to the motor nerve and the subsequent contraction of the innervated muscle. This delay is caused by the time taken for nerve action potential to propagate, the time for chemical transmission at the neuromuscular junction, then the subsequent steps in excitation-contraction coupling discussed above. This usually takes about 10ms.
Skeletal muscle contractions can be broadly separated into twitch, summation, and tetanic contractions. In a twitch contraction, a single action potential, whether from a motor neuron or from within the muscle, causes the muscle fiber to produce a single contraction and relaxation cycle called a twitch. If another muscular action potential was produced before complete relaxation of the muscle fiber, then the next contraction will simply sum onto the previous twitch, thereby production summation response. If the frequency of muscular action potentials increases, the muscle reaches peak force and plateaus at this level, resulting in a tetanic contraction.
Length-tension relationship relates the strength of an isometric contraction to the length of the muscle at which the contraction occurs. Muscles operate with greatest active tension when close to an ideal length (often their resting length). When stretched or shortened beyond this (whether due to the action of the muscle itself or by an outside force), the maximum active tension generated decreases. This decrease is minimal for small deviations, but the tension drops off rapidly as the length deviates further from the ideal. Due to the presence of elastic proteins within a muscle cell (such as titin) and extracellular matrix, as the muscle is stretched beyond a given length, there is an entirely passive tension, which opposes lengthening. Combined together, there is a strong resistance to lengthening an active muscle far beyond the peak of active tension.
Force–velocity relationship: The speed at which a muscle changes length (usually regulated by external forces, such as load or other muscles) also affects the force it can generate. Force declines in a hyperbolic fashion relative to the isometric force as the shortening velocity increases, eventually reaching zero at some maximum velocity. The reverse holds true for when the muscle is stretched – force increases above isometric maximum, until finally reaching an absolute maximum. This has strong implications for the rate at which muscles can perform mechanical work (power). Since power is equal to force times velocity, the muscle generates no power at either isometric force (due to zero velocity) or maximal velocity (due to zero force). Instead, the optimal shortening velocity for power generation is approximately one-third of maximum shortening velocity.
These two fundamental properties of muscle have numerous biomechanical consequences, including limiting running speed, strength, and jumping distance and height.
It is important to note that contraction of smooth muscle need not require neural input—that is, it can function without an action potential. It does so by integrating a huge number of other stimuli such as humoral and paracrine (for instance epinephrine, angiotensin II, AVP, endothelin), metabolic (e.g. oxygen, carbon dioxide, adenosine, potassium ions, hydrogen ions), or physical stimuli (e.g. stretch receptors, shear stress). This integrative character of smooth muscle allows it to function in the tissues in which it exists, such as being the controller of local blood flow to tissues undergoing metabolic changes. In these excitation-free contractions, then, there of course is no excitation-contraction coupling.
Some stimuli for smooth muscle contraction, however, are neural. All neural input is autonomic (involuntary). In these the mechanism of excitation-contraction coupling is as follows: parasympathetic input uses the neurotransmitter acetylcholine. Acetylcholine receptors on smooth muscle are of the muscarinic receptor type; as such they are metabotropic, or G-protein / second messenger coupled. Sympathetic input uses different neurotransmitters; the primary one is norepinephrine. All adrenergic receptors are also metabotropic. The exact effects on the smooth muscle depend on the specific characteristics of the receptor activated—both parasympathetic input and sympathetic input can be either excitatory (contractile) or inhibitory (relaxing). The main mechanism for actual coupling involves varying the calcium-sensitivity of specific cellular machinery. However it occurs, increased intracellular calcium binds calmodulin, which activates myosin light chain kinase (MLCK). MLCK phosphorylates the regulatory light chains of the myosin heads. Phosphorylated myosin heads are able to cross bridge-cycle. Thus, the degree to and velocity of which a whole smooth muscle contracts depends on the level of phosphorylation of myosin heads. Myosin light chain phosphatase removes the phosphate groups from the myosin heads, thus ending cycling (and leaving the muscle in latch-state).
The interaction of sliding actin and myosin filaments in smooth muscle is similar to skeletal muscles. There are differences in the proteins involved in contraction in vertebrate smooth muscle compared to cardiac and skeletal muscle. Smooth muscle does not contain troponin, but does contain the thin filament protein tropomyosin and other notable proteins – caldesmon and calponin. Contractions are initiated by the calcium-activated phosphorylation of myosin rather than calcium binding to the troponin complex that regulates myosin binding sites on actin in skeletal and cardiac muscle. Contractions in vertebrate smooth muscle are initiated by agents that increase intracellular calcium. This is a process of depolarizing the sarcolemma and extracellular calcium entering through L-type calcium channels, and intracellular calcium release predominately from the sarcoplasmic reticulum. Calcium release from the sarcoplasmic reticulum is from Ryanodine receptor channels (calcium sparks) by a redox process and Inositol triphosphate receptor channels by the second messenger inositol triphosphate. The intracellular calcium binds with calmodulin, which then binds and activates myosin light-chain kinase. The calcium-calmodulin-myosin light-chain kinase complex phosphorylates myosin on the 20 kilodalton (kDa) myosin light chains on amino acid residue-serine 19, initiating contraction and activating the myosin ATPase. The phosphorylation of caldesmon and calponin by various kinases is suspected to play a role in smooth muscle contraction.
Phosphorylation of the 20 kDa myosin light chains correlates well with the shortening velocity of smooth muscle. During this period, there is a rapid burst of energy utilization as measured by oxygen consumption. Within a few minutes of initiation, the calcium level markedly decreases, the 20 kDa myosin light chains' phosphorylation decreases, and energy utilization decreases; however, force in tonic smooth muscle is maintained. During contraction of muscle, rapidly cycling crossbridges form between activated actin and phosphorylated myosin, generating force. It is hypothesized that the maintenance of force results from dephosphorylated "latch-bridges" that slowly cycle and maintain force. A number of kinases such as rho kinase, ZIP kinase, and protein kinase C are believed to participate in the sustained phase of contraction, and calcium flux may be significant.
In invertebrate smooth muscle, contraction is initiated with calcium directly binding to myosin and then rapidly cycling cross-bridges generating force. Similar to vertebrate tonic smooth muscle, there is a low calcium and low energy utilization catch phase. This sustained phase or catch phase has been attributed to a catch protein that is similar to myosin light-chain kinase and titin, also known as connectin.
Unlike skeletal muscle, excitation–contraction coupling in cardiac muscle is thought to depend primarily on a mechanism called calcium-induced calcium release. Though the proteins involved are similar, the DHPR and RyR (type 2) are not physically coupled. Instead, RyRs are activated by a calcium trigger, which is brought about by the activation of DHPRs. Further, cardiac muscle tend to exhibit diad (or dyad) structures, rather than triads.
Excitation–contraction coupling was a term coined in 1952 to describe the physiological process of converting an electrical stimulus to a mechanical response. This process is fundamental to muscle physiology, whereby the electrical stimulus is usually an action potential and the mechanical response is contraction. Excitation–contraction coupling can be dysregulated in many diseases.Though excitation–contraction coupling has been known for over half a century, it is still an active area of biomedical research. The general scheme is that an action potential arrives to depolarize the cell membrane. By mechanisms specific to the muscle type, this depolarization results in an increase in cytosolic calcium that is called a calcium transient. This increase in calcium activates calcium-sensitive contractile proteins that then use ATP to cause cell shortening.
The mechanism for muscle contraction evaded scientists for years and requires continued research and updating. The sliding filament theory describes a process used by muscles to contract. It is a cycle of repetitive events that cause a thin filament to slide over a thick filament and generate tension in the muscle. It was independently developed by Andrew F. Huxley and Rolf Niedergerke and by Hugh Huxley and Jean Hanson in 1954.
value (help). Philosophical Transactions: Biological Sciences 355 (1396): 539–543. doi:10.1098/rstb.2000.0595.