Muscle contractions



A muscle contraction (also known as a muscle twitch or simply twitch) occurs when a muscle cell (called a muscle fiber) lengthens or shortens. Locomotion in most higher animals is possible only through the repeated contraction of many muscles at the correct times. Contraction is controlled by the central nervous system comprised of brain and spinal cord. The brain controls voluntary muscle contractions, while the spine controls involuntary reflexes.

For voluntary muscles, contraction 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 the muscle fiber. 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, chewing have a reflex aspect to them; the brain will start the contractions, but continuation of the movements can become reflexive.

There are three general types of muscle contractions: skeletal muscle (voluntary and involuntary) contractions, heart muscle (involuntary) contractions, and smooth muscle (involuntary) contractions. Skeletal and cardiac muscle 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.

For skeletal muscles, the force exerted by the muscle is controlled by varying the frequency at which action potentials are sent to muscle fibers. Action potentials do not arrive at muscles synchronously, and during a contraction some fraction of the fibers in the muscle will be firing at any given time. Typically when a human is exerting a muscle as hard as they are consciously able, roughly one-third of the fibers in that muscle will be firing at once, but various physiological and psychological factors (including Golgi tendon organs and Renshaw cells) can affect that. This 'low' level of contraction is a protective mechanism to prevent avulsion of the tendon - the force generated by a 100% contraction of all fibres is sufficient to damage the body.

Skeletal muscle contractions


Skeletal muscles contract according to the sliding-filament model:


 * 1) An action potential originating in the CNS reaches an alpha motor neuron, which then transmits an action potential down its own axon.
 * 2) The action potential activates voltage-gated calcium channels on the axon, and calcium rushes in.
 * 3) Calcium causes vesicles containing the neurotransmitter acetylcholine to fuse with the plasma membrane, releasing acetylcholine into the synaptic cleft between the motor neuron terminal and the motor end plate of the skeletal muscle fiber.
 * 4) The acetylcholine diffuses across the synapse and binds to and activates nicotinic receptors on the motor end plate. Activation of the nicotinic receptor opens its intrinsic sodium/potassium channel, causing sodium to rush in and potassium to trickle out. Because the channel is more permeable to sodium, the muscle fiber membrane becomes more positively charged, triggering an action potential.
 * 5) The action potential spreads through the muscle fiber's network of T tubules, depolarizing the inner portion of the muscle fiber.
 * 6) The depolarization activates voltage-gated calcium channels in the T tubule membrane, which are in close proximity to calcium-release channels in the adjacent sarcoplasmic reticulum.
 * 7) Activated voltage-gated calcium channels physically interact with calcium-release channels to activate them, causing the sarcoplasmic reticulum to release calcium.
 * 8) The calcium binds to the troponin C present on the actin-containing thin filaments of the myofibrils. The troponin then allosterically modulates the tropomyosin. Normally the tropomyosin sterically obstructs binding sites for myosin on the thin filament; once calcium binds to the troponin C and causes an allosteric change in the troponin protein, troponin T allows tropomyosin to move, unblocking the binding sites.
 * 9) Myosin (which has ADP and inorganic phosphate bound to its nucleotide binding pocket and is in a ready state) binds to the newly uncovered binding sites on the thin filament. Myosin is now bound to actin in the strong binding state. The release of ADP and inorganic phosphate causes the myosin head to turn, causing a ratchet movement (actin acts as a cofactor in the release of inorganic phosphate, expediting the release). This will pull the Z-bands towards each other, thus shortening the sarcomere and the I-band.
 * 10) ATP binds myosin, allowing it to release actin and be in the weak binding state. (A lack of ATP makes this step impossible, resulting in the rigor state characteristic of rigor mortis.) The myosin then hydrolyzes the ATP and uses the energy to move into the "cocked back" state while releasing ADP and inorganic phosphate. In general, evidence (predicted and in vivo) indicates that each skeletal muscle myosin head moves 10-12 nm each power stroke, however there is also evidence (in vitro) of variations (smaller and larger) that appear specific to the myosin isoform.
 * 11) Steps 7 and 8 repeat as long as ATP is available and calcium is present on thin filament.
 * 12) While the above steps are occurring, calcium is actively pumped back into the sarcoplasmic reticulum. When calcium is no longer present on the thin filament, the tropomyosin changes conformation back to its previous state so as to block the binding sites again. The myosin ceases binding to the thin filament, and the contractions cease.

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.

Voluntary muscular contractions can be classified several ways; one of which categorizes them as either eccentric or concentric. In the case of eccentric contraction, the force generated is insufficient to overcome the resistance placed on the muscle and the muscle fibers lengthen as they contract. In the case of concentric contraction, the force generated is sufficient to overcome the resistance, and the muscle shortens as it contracts.

Alternatively, muscle contractions can be categorized as isometric or isotonic. An isometric contraction occurs when the muscle remains the same length despite building tension; an example of this is muscle contraction in the presence of an afterload. Isotonic contractions occur when tension in the muscle remains constant despite a change in muscle length. This can occur only when a muscle's maximal force of contraction exceeds the total load (preload and afterload) on the muscle.

Smooth muscle contraction
The interaction of sliding actin and myosin filaments is similar in smooth muscle. 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 troponin. 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, specifically on the 20 kilodalton (kd) myosin light chains on amino acid residue-serine 19 to initiate contraction and activate 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 kd 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 decrease, the 20 kd myosin light chains phosphorylation decreases, and energy utilization decreases, however there is a sustained maintenance of force in tonic smooth muscle. During contraction of muscle, rapidly cycling crossbridges form between activated actin and phosphorylated myosin generating force. The maintenance of force is hypothesized to result from dephosphorylated "latch-bridges" that slowly cycle and maintain force. A number of kinases such as ROCK, 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 called twitchin.

Concentric contraction
A concentric contraction is a type of muscle contraction in which the muscles generates enough force to overcome the resistance to joint movement so it shortens as it contracts.

During a concentric contraction, a muscle is stimulated to contract according to the sliding filament mechanism. This occurs throughout the length of the muscle, generating force at the musculo-tendinous junction, causing the muscle to shorten and changing the angle of the joint. In relation to the elbow and bicep, the contraction of the bicep would cause the hand to move from close to the leg, to close to the shoulder (a bicep curl). A concentric contraction of the tricep would change the angle of the joint in the opposite direction.

Eccentric contraction
An eccentric contraction is a type of muscle contraction in which the resistance (such as a weight carried in the hand) is greater than the force applied by the muscle so that the muscle lengthens as it contracts. Eccentric contractions also occur when the muscular force is used to brake or slow the opening of a joint.

Most individuals are familiar with concentric contractions, where the muscle shortens. In terms of a bicep curl, during a complete concentric contraction the biceps shorten and elbow goes from fully straight (hand at mid-thigh) to completely bent (hand at the shoulder). In contrast, during an eccentric contraction the muscle lengthens, the hand moving from shoulder to thigh and the elbow straightening. In essence, rather than the muscle producing an active force to move a weight, the muscle works to 'brake' or resist the motion, slowing down the opening of the joint. It is known that desmin, titin, and other z-line proteins are involved but the mechanism of eccentric contractions is poorly understood in comparison to cross-bridge cycling in concentric contractions.

Because the contraction works in the opposite direction the muscles are generally supposed to move (i.e. muscles can only shorten, never lengthen), 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 strength training and/or bodybuilding they are normally called "negatives." Normally muscle fibers move across each other pulling the Z-lines together, closing the joint. During an eccentric contraction, the myosin heads try to pull (controlling the movement), but the opening of the joint reacts to pull back, 'breaking' some of the myosin heads. This also occurs during regular contractions, but as a result of more of the individual heads being pulled in the wrong direction, more are broken. As a result, exercise featuring a heavy eccentric load can actually support a greater weight (muscles are approximately 10% 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 and toughness than concentric contractions alone.

Eccentric contractions in movement
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 rehab of weak or injured tendons. Achilles tendonitis has been shown to benefit from high load eccentric contractions.