Sliding Filament Theory Muscle contraction occurs by a sliding filament mechanism whereby the sarcomeres shorten (the Z-lines come closer together) by the action of the actin filaments sliding over the myosin filaments. Myosin filaments may look somewhat like a golf club but they are not inflexible. In fact, muscle contraction would be impossible if the myosin molecules did not have a "hinge" along the shaft that allows for a ratchet movement of the head. The force behind muscle contraction is the ratchet movement of these tiny myosin heads toward the center of their sarcomere. This ratchet movement occurs many times during a muscle contraction. Electron microscopy combined with chemical experiments show that muscle is composed of 2 contractile proteins: a) Thin filaments: actin, attached to Z line, found in both A and I bands b) Thick filaments: myosin, found in A band
When muscle contracts the actin filaments slide into the A band, overlapping with myosin. When muscle contracts: a) the Z lines move closer together b) the I band becomes shorter c) the A band stays at the same length This is called the "sliding filament" model of muscle contraction. <ul><li>The filaments slide together </li></ul><ul><li>because myosin attaches to actin and </li></ul><ul><li>pulls on it. </li></ul><ul><li>Myosin head (H) attaches to actin </li></ul><ul><li>filament (A), forming a crossbridge. </li></ul><ul><li>After the crossbridge is formed the </li></ul><ul><li>myosin head bends, pulling on the actin </li></ul><ul><li>filaments and causing them to slide: </li></ul><ul><li>Muscle contraction is a little like </li></ul><ul><li>climbing a rope. The crossbridge cycle </li></ul><ul><li>is: grab -> pull -> release, repeated over </li></ul><ul><li>and over </li></ul>
<ul><li>During muscle contraction the myofilaments myosin and actin slide </li></ul><ul><li>toward each other and overlap. This shortens the sacromere and the </li></ul><ul><li>entire muscle. Muscle cells are "shocked" by nerve impulses from </li></ul><ul><li>motor neurons. </li></ul><ul><li>The point of attachment of the nerve to the muscle is called a </li></ul><ul><li>neuromuscular junction. A motor neuron and its muscle cells are </li></ul><ul><li>referred to as a motor unit. The nerve impulse is carried from the </li></ul><ul><li>neuron across the gap to the membrane (sarcolemma) of the muscle cell </li></ul><ul><li>by a chemical called acetycholine. </li></ul>
<ul><li>After the impulse is passed an enzyme called cholinesterase "de-activates" acetylcholine, readying the muscle for the next nerve impulse. Stimulation of the muscle cell causes Ca++ ions to be released into the cell. This binds with the actin filaments causing them to expose active sites to the myosin cross bridges. The cross bridges bind to the active sites, forming a new molecular structure which causes the cross bridge to bend toward the center, pulling the actin filament with it. </li></ul><ul><li>Energy from ATP is used to break the bond, straighten the cross bridge, and allow the cross bridge to form a new bond with another active site further down the actin filament. This cycle continues until the muscle contraction is complete. Then ATP is used to cause active transport to move the calcium ions out of the muscle fiber causing relaxation of the muscle. </li></ul><ul><li> </li></ul><ul><li> </li></ul><ul><li> </li></ul>
Role of Calcium ions <ul><ul><ul><li>A sudden inflow of Ca is the trigger for muscle contraction. In the resting state the protein tropomyosin winds around actin and covers the myosin binding sites. The Ca binds to a second protein, troponin, and this action causes the tropomyosin to be pulled to the side, exposing the myosin binding sites. With the sites exposed muscle will contract if ATP is present. </li></ul></ul></ul><ul><ul><ul><li>Impulses conducted along the transverse tubules stimulate the release of Ca++ from the sarcoplasmic reticulum into the cytoplasm. Ca++ difuses toward the myofibrils and causes contraction. </li></ul></ul></ul><ul><ul><ul><li>Troponin and Tropoyosin are two regulatory proteins associated with the thin filaments. Tropomyosin lies against the thin filament and troponin is bound to tropomyosin. In a resting muscle fiber, the concentration of Ca++ in the cytoplasm is very low, and tropomyosin is located close to the myosin-binding sites on the thin filament. In this position, tropomyosin physically blocks the myosin heads from binding actin, thus preventing contraction. In a stimulated muscle fiber, the Ca++ released by the sarcoplasmic reticulum binds to troponin. The Ca++ troponin complex pulls the tropomyosin away from the myosin-binding sites on actin, allowing cross-bridges to form. </li></ul></ul></ul>
<ul><li>Cross-bridges cycles continue as long as Ca++ remains attached to troponin. When nerve activity ceases, impulses in the muscle fiber also cease, and Ca++ is actively transported from the cytoplasm back into the sarcoplasmic reticulum. As Ca++ is released from troponin, tropomyosin returns to its inhibitory position on the thin filament, again preventing the myosin heads from binding to actin. The muscle fiber relaxes. </li></ul><ul><li>Muscle contraction stops when Ca++ is removed from the immediate environment of the myofilaments. The sarcoplasmic reticulum actively pumps Ca++ back into itself and this requires utilization of ATP. Troponin-tropomyosin reassume their inhibitory position between the actin and myosin molecules once Ca++ is removed. </li></ul>
Role of the energy source (ATP) <ul><li>ATP is the chief energy currency of all cells.The bulk of the energy that plants harvest during photosynthesis is channeled into production of ATP, and so is most of the energy stored in fat and starch. Cells use their supply of ATP to power almost very energy-requiring process they carry out, from supplying activation energy for chemical reactions and actively transporting substances across membranes, to moving through their environment and growing. ATP as a small unstable energy carrier that shuttles back and forth within the cell, picking up energy in one place and releasing it in another. ATP is so important in all organisms. </li></ul><ul><li>When a skeletal muscle is at rest, the myosin heads function as enzymes, cleaving ATP into ADP and P. The hydrolysis of ATP activates the myosin heads, putting them in an orientation that allows them to bind to specific sites on the actin of the thin filaments when the muscle is stimulated to contract. </li></ul><ul><li>ATP is active transport, the movement of substances across a membrane against their concentration gradients. In this case, the splitting of ATP activates a carrier protein in the membrane, perhaps by changing its shape so that it can transport a particular molecule or ion across the membrane. Once </li></ul>
<ul><li>the substance has been released on the other side, the carrier protein returns to its nonactived shape, ready to become energized by another. ATP molecule and shuttle another molecule or ion across the membrane. </li></ul><ul><li>ATP is the energy supply for contraction. It is required for the sliding of the filaments which is accomplished by a bending movement of the myosin heads. It is also required for the separation of actin and myosin which relaxes the muscle. When ATP runs down after death muscle goes into a state of rigor mortis. </li></ul>
Role of motor units <ul><li>The motor nerve and all the fibers it innervates is called the motor unit . The number of fibers is dependent on the necessity for fine control. In general, small muscles that react rapidly with fine control have one nerve and only a few muscle fibers. Those muscles that do not require fine control, such as the gastrocnemius (calf muscle), may have several hundred muscle fibers per motor unit. </li></ul><ul><li>The contraction of individual muscle fibers is all-or-none. Therefore, any graded response must come from the number of motor units stimulated at any one time. Summation is the adding together of individual muscle twitches to make a whole muscle contraction. This can be accomplished by increasing the number of motor units contracting at one time (spatial summation) or by increasing the frequency of contraction of individual muscle contractions (temporal summation). These processes almost always occur simultaneously within normal muscle contraction. Usually, individual motor units fire asynchronously. </li></ul><ul><li>All motor units are not created equal. Therefore one motor unit within a particular muscle may be as much as 50 times as strong as another. Smaller </li></ul>
<ul><li>motor units are much more easily excited than larger ones because they are innervated by smaller nerve fibers that have a naturally lower threshold for excitation. In spatial summation motor units are recruited by increasing the strength of the stimulus thereby increasing the strength of the contraction. </li></ul><ul><li>Motor unit is the smallest functional element of a skeletal muscle. The division of the muscle into motor units allows the muscle’s strength of contraction to be finely graded, a requirement for coordinated movements of the skeleton. Muscles that require a finer degree of control have smaller motor units than muscles that require less precise control but must exert more force. </li></ul><ul><li>The weakest contractions of a muscle are accomplished by the activation of a few small motor units. If a slightly stronger contraction is necessary. Additional small motor units are also activated. The initial increments to the total force generated by the muscle are therefore relatively small. If ever greater forces are required, more and larger motor units are brought into action, and the force increments become larger. The use of increased numbers and sizes of motor units in a contraction is termed recruitment, and it is another way in which the strength of muscle contraction is governed by the nervous system. </li></ul>
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