Muscle contraction

Top-down view of skeletal muscle

Muscle contraction is the activation of tension-generating sites within muscle fibers.[1][2] 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.[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]

Muscle contractions can be described based on two variables: length and tension.[1] A muscle contraction is described as isometric if the muscle tension changes but the muscle length remains the same.[1][3][4][5] In contrast, a muscle contraction is isotonic if muscle length changes but the muscle tension remains the same.[1][3][4][5] If the muscle length shortens, the contraction is concentric;[1][6] 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.[7] 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 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.

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 those in skeletal muscle tissues.

Types

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][3][4][5] If the muscle length changes while muscle tension remains the same, then the muscle contraction is isotonic.[1][3][4][5] In an isotonic contraction, the muscle length can either shorten to produce a concentric contraction or lengthen to produce an eccentric contraction.[1][6] Furthermore, if the muscle length shortens, the contraction is concentric.[1][6] 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.[7] Therefore, neither length nor tension is likely to remain constant when the muscle is active during locomotor activity.

Isometric contraction

Main article: Isometric exercise

An isometric contraction of a muscle generates tension without changing length.[1][3][4][5] 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.

Isotonic contraction

In isotonic contraction, the tension in the muscle remains constant despite a change in muscle length.[1][3][4][5] This occurs when a muscle's force of contraction matches the total load on the muscle.

Concentric contraction

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.

Eccentric contraction

In eccentric contraction, the tension generated 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). 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 (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.[10][12] While unaccustomed heavy eccentric contractions can easily lead to overtraining, moderate training may confer protection against injury.[10]

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 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.

Physiology

Muscle fibers in relaxed (above) and contracted (below) positions

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.[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. 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:[17] 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.[18] Temporal summation can occur if even a single presynaptic neuron stimulates a postsynaptic neuron at a fast enough rate.[19]

Skeletal muscle

Molecular mechanisms of skeletal muscular function

Excitation-contraction coupling in skeletal muscles

Excitation–contraction coupling is the process by which a muscular action potential in the muscle fiber causes the myofibrils to contract.[20] 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:

  1. The membrane potential of a skeletal muscle cell is depolarized by an action potential (e.g. from synaptic activation from an alpha motor neuron)
  2. This depolarisation activates non-gated voltage sensors, DHPRs (differing from the cardiac DHPR, which is a gated calcium channel)
  3. This activates RyR type 1 via foot processes (involving conformational changes that allosterically activates the RyRs)
  4. As the RyRs open, calcium is released from the SR into the local junctional space, which then diffuses into the bulk cytoplasm to cause a calcium spark. Note that the SR has a large calcium buffering capacity partially due to a calcium-binding protein called calsequestrin
  5. The near synchronous activation of thousands of calcium sparks by the action potential causes a cell-wide increase in calcium giving rise to the upstroke of the calcium transient.
  6. The calcium released into the cytosol binds to Troponin C by the actin filaments, to allow cross-bridge cycling, producing force and, in some situations, motion
  7. The sarco/endoplasmic reticulum calcium-ATPase (SERCA) actively pumps calcium back into the SR
  8. As calcium declines back to resting levels, the force declines and relaxation occurs

Sliding filament theory

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.[19] It was independently developed by Andrew Huxley and Rolf Niedergerke and by Hugh Huxley and Jean Hanson in 1954.[21][22]

  1. An action potential originating in the central nervous system reaches an alpha motor neuron, which then transmits an action potential down its own axon.
  2. The action potential propagates by saltatory conduction along the axon toward the neuromuscular junction. When it reaches the terminal bouton at the end of the axon, the action potential causes a calcium ion influx into the terminal by way of the voltage-gated calcium channels.
  3. 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.
  4. The 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 [23]
  5. The voltage-gated ion channels of the sarcolemma next to the end plate open in response to the end plate potential. These voltage gated channels 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.[23]
  6. The action potential spreads across the cell surface and into the muscle fiber's network of T-tubules, depolarizing the inner portion of the muscle fiber.
  7. The depolarization activates L-type voltage-dependent calcium channels (dihydropyridine receptors) in the terminal cisternae, which are in close proximity to calcium-release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum.
  8. The activated voltage-gated calcium channels physically interact with calcium-release channels to activate them, causing the sarcoplasmic reticulum to release calcium.
  9. The calcium binds to the troponin C present on the actin-containing thin filaments of the myofibrils. The troponin then allosterically modulates the tropomyosin. Under normal circumstances, 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.
  10. 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 (binding to the thin filament is very tightly coupled to the release of inorganic phosphate). Myosin is now bound to actin in the strong binding state forming a cross bridge between the myosin and actin. The release of ADP and inorganic phosphate are tightly coupled to the power stroke (actin acts as a cofactor in the release of inorganic phosphate, expediting the release). This is a bent, low-energy position. This will pull the Z-lines towards each other, thereby shortening the sarcomere and the I-band.
  11. ATP binds to myosin, allowing it to release actin and break the cross bridge (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" conformation. The cocked myosin head now contains ADP + Pi. If the tropomyosin has unblocked the myosin binding site on actin, then the myosin head can attach to the actin filament. After attachment to the actin filament, the release of the inorganic phosphate (Pi) initiates the power stroke as the myosin head pushes the actin filament past. At the end of the power stroke, ADP is released from the myosin head, and it is maintained in the rigor state until ATP binds again. 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.
  12. Steps 9 and 10 repeat as long as ATP is available and calcium is freely bound within the thin filaments.
  13. The last phase is relaxation which returns the muscle to resting length. Acetylcholine ceases being released across the neuromuscular junction because nerve signals stop arriving. 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. Like the ions in the neuromuscular junction, calcium is continually reabsorbed by the sarcoplasmic reticulum, but when the terminal cisternae no longer receive an action potential propagation they will no longer release calcium. Finally, the calcium dissociates from troponin and there is none the replace it. Thus, the troponin-tropomyosin complex goes through a conformational change and blocks the myosin binding active site on actin. Tension can no longer be upheld.
  14. 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 muscle relaxes.

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.[24]

Latent period

For Latent period for viruses, see Virus#Effects on the host cell.

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.[25]

Gradation of skeletal muscle contractions

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.[26] 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

For more details on this topic, see Hill's muscle model.
Muscle length versus isometric force

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.[27] 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 relationships

Force–velocity relationship: right of the vertical axis concentric contractions (the muscle is shortening), left of the axis eccentric contractions (the muscle is lengthened under load); power developed by the muscle in red.

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.

Smooth muscle

Further information: Smooth muscle

Excitation-contraction coupling in smooth muscle fibers

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).

Sliding filaments in smooth muscle fibers

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.

Invertebrate smooth muscles

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.

Cardiac muscle

Further information: Cardiac muscle

Excitation-contraction coupling in cardiac muscle fibers

Unlike skeletal muscle, excitation–contraction coupling in cardiac muscle is thought to depend primarily on a mechanism called calcium-induced calcium release.[28] 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.

  1. An action potential is initiated by pacemaker cells in the Sinoatrial node or Atrioventricular node and conducted to all cells in the heart via gap junctions.
  2. The action potential travels along the surface membrane into T-tubules (the latter are not seen in all cardiac cell types) and the depolarisation causes extracellular Ca2+
     to enter the cell via L-type calcium channels and possibly sodium-calcium exchanger during the early part of the plateau phase. This Ca2+
     influx causes a small local increase in intracellular Ca2+
    .
  3. The increase in Ca2+
     is detected by ryanodine receptors in the membrane of the sarcoplasmic reticulum which releases Ca2+
     in a positive feedback physiological response. This positive feedback is known as calcium-induced calcium release [28] and gives rise to calcium sparks (Ca2+
     sparks[29]).
  4. The spatial and temporal summation of ~30,000 Ca2+
     sparks gives a cell-wide increase in cytoplasmic calcium concentration.[30]
  5. The cytoplasmic calcium binds to Troponin C, moving the tropomyosin complex off the actin binding site allowing the myosin head to bind to the actin filament. From this point on the contractile mechanism is essentially the same as for skeletal muscle (above). Briefly:
  6. Using ATP hydrolysis the myosin head pulls the actin filament toward the centre of the sarcomere.
  7. Intracellular calcium is taken up by the sarco/endoplasmic reticulum ATPase pump back into the sarcoplasmic reticulum ready for the next cycle to begin. Calcium is also ejected from the cell mainly by the sodium-calcium exchanger and, to a lesser extent, a plasma membrane calcium ATPase and/or taken up by the mitochondria.[31]
  8. An enzyme, phospholamban, serves as a brake for the ATPase. At low heart rates, phospholamban is active and slows down the activity of the ATPase so that Ca does not have to leave the cell entirely. At high heart rates, phospholamban is phosphorylated and deactivated thus removing most Ca from the cell back into the sarcoplasmic reticulum. This allows the heart muscles to relax to allow for ventricular filling.
  9. Intracellular calcium concentration drops and troponin complex returns over the active site of the actin filament, ending contraction.

History

Excitation-contraction coupling

Excitation–contraction coupling was a term coined in 1952 to describe the physiological process of converting an electrical stimulus to a mechanical response.[32] 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.

Sliding filament theory

The mechanism for muscle contraction evaded scientists for years and requires continued research and updating.[33] 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.[19] It was independently developed by Andrew F. Huxley and Rolf Niedergerke and by Hugh Huxley and Jean Hanson in 1954.[34][35]

See also

References

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  15. ↑ annell LJ, Taunton JE, Clement DB, Smith C, Khan KM (2001). "A randomised clinical trial of the efficacy of drop squats or leg extension/leg curl exercises to treat clinically diagnosed jumper's knee in athletes: pilot study.". Br J Sports Med 35 (1): 60–4. doi:10.1136/bjsm.35.1.60. PMID 11157465.
  16. ↑ Tassinary; Cacioppo (2000). "The Skeletomotor system: surface electromyography". In Cacioppo, John T.; Tassinary, Luois G.; Berntson, Gary G. Handbook of Psychophysiology (Second ed.). Cambridge: Cambridge University Press. ISBN 0-521-62634-X.
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  23. 1 2 Saladin, Kenneth S., Stephen J. Sullivan, and Christina A. Gan. Anatomy & Physiology: The Unity of Form and Function. 7th ed. New York: McGraw-Hill Education, 2015. Print.
  24. ↑ Horowits R, Podolsky RJ (November 1987). "The positional stability of thick filaments in activated skeletal muscle depends on sarcomere length: evidence for the role of titin filaments.". J Cell Biol. 105 (5): 2217–23. doi:10.1083/jcb.105.5.2217. PMC 2114850. PMID 3680378.
  25. ↑ Khurana, Indu (2006). "Characteristics of muscle excitability and contractility". Textbook Of Medical Physiology (1st ed.). Elsevier. pp. 101–2.
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  32. ↑ Sandow A (1952). "Excitation-Contraction Coupling in Muscular Response". Yale J Biol Med 25 (3): 176–201. PMC 2599245. PMID 13015950.
  33. ↑ Huxley, H. E. (April 2000). . "Past, Present and Future Experiments on Muscle" Check |url= value (help). Philosophical Transactions: Biological Sciences 355 (1396): 539–543. doi:10.1098/rstb.2000.0595.
  34. ↑ Huxley AF, Niedergerke R (1954). "Structural Changes in Muscle During Contraction: Interference Microscopy of Living Muscle Fibres". Nature 173 (4412): 971–973. doi:10.1038/173971a0. PMID 13165697.
  35. ↑ Huxley H, Hanson J (1954). "Changes in the cross-striations of muscle during contraction and stretch and their structural interpretation". Nature 173 (4412): 973–976. doi:10.1038/173973a0. PMID 13165698.

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External links

  1. ↑ 35. Saladin, Kenneth S., Stephen J. Sullivan, and Christina A. Gan. Anatomy & Physiology: The Unity of Form and Function. 7th ed. New York: McGraw-Hill Education, 2015. Print
  2. ↑ 36. Krans, J. L. (2010) The Sliding Filament Theory of Muscle Contraction. Nature Education 3(9):66
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