Muscle contraction
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]
For the contractions to happen, the muscle cells must rely on the interaction of two types of filaments: thin and thick filaments.
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.
In
Unlike skeletal muscle, the contractions of
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.
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][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.
Isometric contraction
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.
Isotonic contraction
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.
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
Eccentric contraction
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.
During an eccentric contraction of the
Though the muscle is doing a negative amount of
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 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.
Vertebrate
In
Skeletal muscle
Excluding reflexes, all
Neuromuscular junction
A
Excitation–contraction coupling
Excitation–contraction coupling (ECC) is the process by which a
Excitation–contraction coupling (ECC) occurs when depolarization of skeletal muscles (usually through neural innervation) results in a muscle action potential. This action potential spreads across the muscle's surface and into the muscle fiber's network of
When the desired motion is accomplished, relaxation can be achieved quickly through numerous pathways. Relaxation is quickly achieved through a Ca2+ buffer with various cytoplasmic proteins binding to Ca2+ with very high affinity.[20] These cytoplasmic proteins allow for quick relaxation in fast twitch muscles. Although slower, the sarco/endoplasmic reticulum calcium-ATPase (SERCA) actively pumps Ca2+ back into the sarcoplasmic reticulum, resulting in a permanent relaxation until the next action potential arrives.[19]
Mitochondria also participate in Ca2+ reuptake, ultimately delivering their gathered Ca2+ to SERCA for storage in the sarcoplasmic reticulum. A few of the relaxation mechanisms (NCX, Ca2+ pumps and Ca2+ leak channels) move Ca2+ completely out of the cells as well.[21] As Ca2+ concentration declines to resting levels, Ca2+ releases from Troponin C, disallowing cross bridge-cycling, causing the force to decline and relaxation to occur. Once relaxation has fully occurred, the muscle is able to contract again, thus fully resetting the cycle.
Sliding filament theory
The
Cross-bridge cycle
Cross-bridge cycling is a sequence of molecular events that underlies the sliding filament theory. A
ions bind to troponin C on the actin filaments. The troponin-Ca2+
complex causes tropomyosin to slide over and unblock the remainder of the actin binding site. Unblocking the rest of the actin binding sites allows the two myosin heads to close and myosin to bind strongly to actin.[26] The myosin head then releases the inorganic phosphate and initiates a power stroke, which generates a force of 2 pN. The power stroke moves the actin filament inwards, thereby shortening the sarcomere. Myosin then releases ADP but still remains tightly bound to actin. At the end of the power stroke, ADP is released from the myosin head, leaving myosin attached to actin in a rigor state until another ATP binds to myosin. A lack of ATP would result in the rigor state characteristic of rigor mortis
Cross-bridge cycling is able to continue as long as there are sufficient amounts of ATP and Ca2+
in the cytoplasm.[26] Termination of cross-bridge cycling can occur when Ca2+
is actively pumped back into the sarcoplasmic reticulum. When Ca2+
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 Ca2+
ions leave the troponin molecule to maintain the Ca2+
ion concentration in the sarcoplasm. The active pumping of Ca2+
ions into the sarcoplasmic reticulum creates a deficiency in the fluid around the myofibrils. This causes the removal of Ca2+
ions from the troponin. Thus, the tropomyosin-troponin complex again covers the binding sites on the actin filaments and contraction ceases.
Gradation of skeletal muscle contractions
The strength of skeletal muscle contractions can be broadly separated into twitch, summation, and
If another muscle action potential were to be produced before the complete relaxation of a muscle twitch, then the next twitch will simply sum onto the previous twitch, thereby producing a summation.[29] Summation can be achieved in two ways:[30] frequency summation and multiple fiber summation. In frequency summation, the force exerted by the skeletal 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. In a typical circumstance, when humans are exerting their muscles as hard as they are consciously able, roughly one-third of the fibers in each of those muscles will fire at once[citation needed], though this ratio can be affected by various physiological and psychological factors (including Golgi tendon organs and Renshaw cells). This 'low' level of contraction is a protective mechanism to prevent avulsion of the tendon—the force generated by a 95% contraction of all fibers is sufficient to damage the body. In multiple fiber summation, if the central nervous system sends a weak signal to contract a muscle, the smaller motor units, being more excitable than the larger ones, are stimulated first. As the strength of the signal increases, more motor units are excited in addition to larger ones, with the largest motor units having as much as 50 times the contractile strength as the smaller ones. As more and larger motor units are activated, the force of muscle contraction becomes progressively stronger. A concept known as the size principle, allows for a gradation of muscle force during weak contraction to occur in small steps, which then become progressively larger when greater amounts of force are required.
Finally, if the frequency of muscle action potentials increases such that the muscle contraction reaches its peak force and plateaus at this level, then the contraction is a tetanus.
Length-tension relationship
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.[31] 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, there is a strong resistance to lengthening an active muscle far beyond the peak of active tension.
Force-velocity relationships
Force–velocity relationship relates the speed at which a muscle changes its length (usually regulated by external forces, such as load or other muscles) to the amount of force that it generates. 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 intrinsic property of active muscle tissue plays a role in the active damping of joints that are actuated by simultaneously active opposing muscles. In such cases, the force-velocity profile enhances the force produced by the lengthening muscle at the expense of the shortening muscle. This favoring of whichever muscle returns the joint to equilibrium effectively increases the damping of the joint. Moreover, the strength of the damping increases with muscle force. The motor system can thus actively control joint damping via the simultaneous contraction (co-contraction) of opposing muscle groups.[32]
Smooth muscle
Unlike single-unit smooth muscle cells, multiunit smooth muscle cells are found in the muscle of the eye and in the base of hair follicles. Multiunit smooth muscle cells contract by being separately stimulated by nerves of the autonomic nervous system. As such, they allow for fine control and gradual responses, much like motor unit recruitment in skeletal muscle.
Mechanisms of smooth muscle contraction
The contractile activity of smooth muscle cells can be tonic (sustained) or phasic (transient)
, and not Na+
. Like skeletal muscles, cytosolic Ca2+
ions are also required for crossbridge cycling in smooth muscle cells.
The two sources for cytosolic Ca2+
in smooth muscle cells are the extracellular Ca2+
entering through calcium channels and the Ca2+
ions that are released from the sarcoplasmic reticulum. The elevation of cytosolic Ca2+
results in more Ca2+
binding to
-activated phosphorylation of myosin rather than Ca2+
binding to the troponin complex that regulates myosin binding sites on actin like in skeletal and cardiac muscles.
Termination of crossbridge cycling (and leaving the muscle in latch-state) occurs when myosin light chain phosphatase removes the phosphate groups from the myosin heads. 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 use 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 use 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
flux may be significant.
Neuromodulation
Although smooth muscle contractions are myogenic, the rate and strength of their contractions can be modulated by the
Cardiac muscle
There are two types of cardiac muscle cells: autorhythmic and contractile. Autorhythmic cells do not contract, but instead set the pace of contraction for other cardiac muscle cells, which can be modulated by the autonomic nervous system. In contrast, contractile muscle cells (cardiomyocytes) constitute the majority of the heart muscle and are able to contract.
Excitation-contraction coupling
In both skeletal and cardiac muscle excitation-contraction (E-C) coupling, depolarization conduction and Ca2+ release processes occur. However, though the proteins involved are similar, they are distinct in structure and regulation. The dihydropyridine receptors (DHPRs) are encoded by different genes, and the
Unlike skeletal muscle, E-C coupling in cardiac muscle is thought to depend primarily on a mechanism called calcium-induced calcium release,[35] which is based on the junctional structure between T-tubule and sarcoplasmic reticulum. Junctophilin-2 (JPH2) is essential to maintain this structure, as well as the integrity of T-tubule.[36][37][38] Another protein, receptor accessory protein 5 (REEP5), functions to keep the normal morphology of junctional SR.[39] Defects of junctional coupling can result from deficiencies of either of the two proteins. During the process of calcium-induced calcium release, RyR2s are activated by a calcium trigger, which is brought about by the flow of Ca2+ through the L-type calcium channels. After this, cardiac muscle tends to exhibit diad structures, rather than triads.
Excitation-contraction coupling in cardiac muscle cells occurs when an action potential is initiated by pacemaker cells in the
to enter the cell via L-type calcium channels and possibly sodium-calcium exchanger (NCX) during the early part of the plateau phase. Although this Ca2+ influx only count for about 10% of the Ca2+ needed for activation, it is relatively larger than that of skeletal muscle. This Ca2+
influx causes a small local increase in intracellular Ca2+
. The increase of intracellular Ca2+
is detected by RyR2 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[35] and gives rise to calcium sparks (Ca2+
sparks[40]). The spatial and temporal summation of ~30,000 Ca2+
sparks gives a cell-wide increase in cytoplasmic calcium concentration.[41] The increase in cytosolic calcium following the flow of calcium through the cell membrane and sarcoplasmic reticulum is moderated by calcium buffers, which bind a large proportion of intracellular calcium. As a result, a large increase in total calcium leads to a relatively small rise in free Ca2+
.[42]
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, using ATP hydrolysis, the myosin head pulls the actin filament toward the centre of the sarcomere.
Following systole, intracellular calcium is taken up by the sarco/endoplasmic reticulum ATPase (SERCA) 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 (NCX) and, to a lesser extent, a plasma membrane calcium ATPase. Some calcium is also taken up by the mitochondria.[43] An enzyme, phospholamban, serves as a brake for SERCA. At low heart rates, phospholamban is active and slows down the activity of the ATPase so that Ca2+
does not have to leave the cell entirely. At high heart rates, phospholamban is phosphorylated and deactivated thus taking most Ca2+
from the cytoplasm back into the sarcoplasmic reticulum. Once again, calcium buffers moderate this fall in Ca2+
concentration, permitting a relatively small decrease in free Ca2+
concentration in response to a large change in total calcium. The falling Ca2+
concentration allows the troponin complex to dissociate from the actin filament thereby ending contraction. The heart relaxes, allowing the ventricles to fill with blood and begin the cardiac cycle again.
Invertebrate
Circular and longitudinal muscles
In
Obliquely striated muscles
Invertebrates such as annelids, mollusks, and nematodes, possess obliquely striated muscles, which contain bands of thick and thin filaments that are arranged helically rather than transversely, like in vertebrate skeletal or cardiac muscles.[46] In bivalves, the obliquely striated muscles can maintain tension over long periods without using too much energy. Bivalves use these muscles to keep their shells closed.
Asynchronous muscles
Advanced insects such as wasps, flies, bees, and beetles possess asynchronous muscles that constitute the flight muscles in these animals.[46] These flight muscles are often called fibrillar muscles because they contain myofibrils that are thick and conspicuous.[47] A remarkable feature of these muscles is that they do not require stimulation for each muscle contraction. Hence, they are called asynchronous muscles because the number of contractions in these muscles do not correspond (or synchronize) with the number of action potentials. For example, a wing muscle of a tethered fly may receive action potentials at a frequency of 3 Hz but it is able to beat at a frequency of 120 Hz.[46] The high frequency beating is made possible because the muscles are connected to a resonant system, which is driven to a natural frequency of vibration.
History
In 1780,
In 1952, the term excitation–contraction coupling was coined to describe the physiological process of converting an electrical stimulus to a mechanical response.[50] 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.
See also
- Anatomical terms of motion
- calcium-induced calcium release
- Cardiac action potential
- Cramp
- Dystonia
- Exercise physiology
- Fasciculation
- Hill's muscle model
- Hypnic jerk
- In vitro muscle testing
- Lombard's paradox
- Myoclonus
- Rigor mortis
- Spasm
- Uterine contraction
References
- ^ ISBN 978-0-321-98122-6.
- ISBN 978-0-321-98122-6.
- ^ ISBN 978-0-198-50022-3.
- ^ ISBN 978-0-521-57421-1.
- ^ ISBN 978-1-588-90572-7.
- ^ a b c d e f Bullock, John; Boyle, Joseph; Wang, Michael B. (2001). "Muscle contraction". NMS Physiology. Vol. 578 (4th ed.). Baltimore, Maryland: Lippincott Williams and Wilkins. pp. 37–56.
- ^ ISBN 978-0-415-36953-4.
- S2CID 28649208.
- ^ a b "Types of contractions". 31 May 2006. Retrieved 2 October 2007.
- ^ PMID 2275403.
- PMID 22539728.
- ^ Brooks, G.A; Fahey, T.D.; White, T.P. (1996). Exercise Physiology: Human Bioenergetics and Its Applications. Mayfield Publishing Co.
- S2CID 30259362.
- doi:10.3233/IES-2006-0223. Archived from the originalon 9 July 2012.
- PMID 11157465.
- ISBN 978-0-521-62634-7.
- ISBN 978-0199773893.
- ^ a b 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.
- ^ PMID 20961976.
- PMID 28509964.
- ISSN 1043-4046.
- ISBN 978-0-07-337825-1.
- ^ S2CID 4275495.
- ^ S2CID 4180166.
- PMID 3680378.
- ^ ISBN 978-0-071-39011-8.
- ISBN 978-0-123-82163-8.
- ^ Khurana, Indu (2006). "Characteristics of muscle excitability and contractility". Textbook Of Medical Physiology (1st ed.). Elsevier. pp. 101–2.
- S2CID 211100581. Retrieved 5 April 2022.
- S2CID 1770255.
- PMID 5921536.
- PMID 22275897.
- PMID 24058600.
- PMID 12673344.
- ^ PMID 6346892.
- PMID 25092313.
- PMID 20576937.
- PMID 10949023.
- PMID 29431104.
- PMID 8235594.
- PMID 7858131.
- OCLC 47659382.
- S2CID 4348240.
- ^ ISBN 978-1-464-10947-8.
- ^ S2CID 9983649.
- ^ ISBN 978-0-691-12634-0.
- PMID 10952872.
- ^ Wells, David Ames (1859). "How galvanic electricity was discovered". The Science of Common Things: A Familiar Explanation of the First Principles of Physical Science. New York: Ivison & Phinney. p. 290.
- ^ Whittaker, E. T. (1951), A History of the Theories of Aether and Electricity. Vol 1, Nelson, London
- PMID 13015950.
- PMID 10836507.
Further reading
- Krans, J. L. (2010) The Sliding Filament Theory of Muscle Contraction. Nature Education 3(9):66
- Saladin, Kenneth S., Stephen J. Sullivan, and Christina A. Gan. (2015). Anatomy & Physiology: The Unity of Form and Function. 7th ed. New York: McGraw-Hill Education.