In
vertebrate animals, there are three types of
muscle tissues: skeletal, smooth, and cardiac.
Skeletal muscle constitutes the majority of muscle mass in the body and is responsible for locomotor activity.
Smooth muscle forms
blood vessels, the
gastrointestinal tract, and other areas in the body that produce sustained contractions.
Cardiac muscle makes up the heart, which pumps blood. Skeletal and cardiac muscles are called
striated muscle because of their striped appearance under a microscope, which is due to the highly organized alternating pattern of A bands and I bands.
Skeletal muscle Excluding reflexes, all
skeletal muscle contractions occur as a result of signals originating in the brain. The brain sends electrochemical signals through the
nervous system to the
motor neuron that
innervates several muscle fibers. In the case of some
reflexes, the signal to contract can originate in the
spinal cord through a feedback loop with the grey matter. Other actions such as locomotion, breathing, and chewing have a reflex aspect to them: the contractions can be initiated either consciously or unconsciously.
Neuromuscular junction A
neuromuscular junction is a
chemical synapse formed by the contact between a
motor neuron and a
muscle fiber. It is the site in which a motor neuron transmits a signal to a muscle fiber to initiate muscle contraction. The sequence of events that results in the depolarization of the muscle fiber at the neuromuscular junction begins when an action potential is initiated in the cell body of a motor neuron, which is then propagated by
saltatory conduction along its axon toward the neuromuscular junction. Once it reaches the
terminal bouton, the action potential causes a
ion influx into the terminal by way of the
voltage-gated calcium channels. The
influx causes
synaptic vesicles containing the neurotransmitter
acetylcholine to fuse with the plasma membrane, releasing acetylcholine into the
synaptic cleft between the motor neuron terminal and the neuromuscular junction of the skeletal muscle fiber. Acetylcholine diffuses across the synapse and binds to and activates
nicotinic acetylcholine receptors on the neuromuscular junction. Activation of the nicotinic receptor opens its intrinsic
sodium/
potassium channel, causing sodium to rush in and potassium to trickle out. As a result, the
sarcolemma reverses polarity and its voltage quickly jumps from the resting membrane potential of −90mV to as high as +75mV as sodium enters. The membrane potential then becomes hyperpolarized when potassium exits and is then adjusted back to the resting membrane potential. This rapid fluctuation is called the end-plate potential. The voltage-gated ion channels of the sarcolemma next to the end plate open in response to the end plate potential. They are sodium and potassium specific and only allow one through. This wave of ion movements creates the action potential that spreads from the motor end plate in all directions. The action potential creates a near synchronous activation of thousands of
calcium sparks and causes a cell-wide increase in calcium giving rise to the upstroke of the
calcium transient. The Ca2+ released into the cytosol binds to
Troponin C by the
actin filaments. This bond allows the actin filaments to perform
cross-bridge cycling, producing force and, in some situations, motion. 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. 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. 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
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. Physiologically, this contraction is not uniform across the sarcomere; the central position of the thick filaments becomes unstable and can shift during contraction but this is countered by the actions of the elastic myofilament of
titin. This fine myofilament maintains uniform tension across the sarcomere by pulling the thick filament into a central position.
Cross-bridge cycle Cross-bridge cycling is a sequence of molecular events that underlies the sliding filament theory. A
cross-bridge is a myosin projection, consisting of two myosin heads, that extends from the thick filaments. With the ATP hydrolysed, the cocked myosin head now contains
adenosine diphosphate (ADP) +
Pi. Two ions bind to
troponin C on the actin filaments. The troponin- 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. The time between a stimulus to the motor nerve and the subsequent contraction of the innervated muscle is called the
latent period, which usually takes about 10 ms and 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. 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. Summation can be achieved in two ways:
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, 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. 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.
Smooth muscle Smooth muscles can be divided into two subgroups:
single-unit and
multiunit. Single-unit smooth muscle cells can be found in the gut and blood vessels. Because these cells are linked together by gap junctions, they are able to contract as a functional
syncytium. Single-unit smooth muscle cells contract myogenically, which can be modulated by the autonomic nervous system. 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 is influenced by multiple inputs such as spontaneous electrical activity, neural and hormonal inputs, local changes in chemical composition, and stretch. Unlike skeletal muscle, E-C coupling in cardiac muscle is thought to depend primarily on a mechanism called
calcium-induced calcium release, 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. Another protein,
receptor accessory protein 5 (REEP5), functions to keep the normal morphology of junctional SR. 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
sinoatrial node or
atrioventricular node and conducted to all cells in the heart via
gap junctions. The action potential travels along the surface membrane into
T-tubules (the latter are not seen in all cardiac cell types) and the depolarization causes extracellular 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 influx causes a small local increase in intracellular . The increase of intracellular is detected by RyR2 in the membrane of the sarcoplasmic reticulum, which releases in a
positive feedback physiological response. This positive feedback is known as
calcium-induced calcium release). The spatial and temporal summation of ~30,000 sparks gives a cell-wide increase in cytoplasmic calcium concentration. 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 . 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. 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 does not have to leave the cell entirely. At high heart rates, phospholamban is phosphorylated and deactivated thus taking most from the cytoplasm back into the sarcoplasmic reticulum. Once again,
calcium buffers moderate this fall in concentration, permitting a relatively small decrease in free concentration in response to a large change in total calcium. The falling 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==