Mechanism of Muscle Contraction
According to sliding filament theory of muscle contraction, the actin and myosin filaments slide pass to each other with the help of cross-bridges to reduce the length of the sarcomeres. As a muscle contracts, the Z lines come closer together, the width of the I bands decreases, the width of the H zones decrease, but there is no change in the width of the A band.
|Mechanism of muscle contraction|
During relaxation, myosin cross-bridges separate from actin and actin filaments slide back from A-bands. Calcium is an essential element for the contraction of muscles. During muscle contraction, chemical energy is changed into mechanical energy.
In a resting muscle fibre, the outside of sarcolemma is positively charged with respect to the inside. This potential difference across a membrane is called resting potential. A membrane with a resting potential is said to be polarized. It is maintained by sodium and potassium ions.
Sodium ions predominate on the outside of the sarcolemma and potassium ions predominate on the inside. Na+ ions are pumped out as quickly as they enter and K+ ions are sent in as soon as they leave, both by active transport. This process of moving ions against concentration is called sodium pump (= sodium-potassium exchange pump).
The portion of the sarcolemma that lies beneath the nerve endings (axon terminals) is called the motor–end plate. When the neural signal reaches the motor-end plate, it releases a neurotransmitter, acetylcholine, which generates an action potential by depolarizing the sarcolemma. This spreads through the muscle fibre and causes the release of calcium ions into the sarcoplasm.
The calcium ions bind to troponin causing a change in its shape and position. This is turn alters the shape and the position of tropomyosin, to which troponin binds. This shift exposes the active sites on the F – actin molecules. Myosin cross-bridges are then able to bind to these active sites.
In the presence of myosin ATPase, Ca++ and Mg++ ions, ATP breaks down into ADP and inorganic phosphate, releasing energy in the head of the myosin molecule. Energy from ATP causes energized myosin cross bridges to bind to actin and move, causing thin myofilaments to slide along the thick myofilaments. This leads to muscle contraction.
The myosin, releasing the ADP and Pi goes back to its relaxed state. A new ATP binds and the cross-bridge is broken. The ATP is again hydrolysed by the myosin head and the cycle of cross-bridge formation and breakage is repeated causing further sliding. The process continues till the Ca++ ions are pumped back to the sarcoplasmic cisternae resulting in the masking of actin filaments. This causes the return of ‘Z’ lines back to their original position, i.e., relaxation.
During strenuous exercise, the muscle does not get sufficient oxygen to meet its energy needs immediately. So it contracts anaerobically and accumulates lactic acid produced by anaerobic glycolysis. During recovery, the oxygen consumption of muscle exceeds.
The extra oxygen consumed during recovery is called oxygen debt of the muscle. It is used in oxidizing the accumulated lactic acid aerobically and in restoring the depleted creatine phosphate and ATP in the muscle fibre.