Contraction Stimulus

Contraction Stimulus

The neurotransmitter that stimulates skeletal muscle to contract is acetylcholine (ACh). Synthesized in the cytoplasm of motor neurons, ACh is released into the synaptic clefts between motor neuron axons and motor end plates. It rapidly diffuses, binding to certain protein receptors in the muscle fiber mem-brane, increasing permeability to sodium ions. These charged particles stimulate a muscle impulse that passes in many directions over the muscle fiber ­membrane. This impulse eventually reaches the sarcoplasmic reticulum (SR).

The SR has a high calcium ion concentration and responds by making the cisternae membranes more permeable, diffusing calcium into the sarcoplasm. Troponin and tropomyosin interact to form linkages between actin and myosin filaments. The muscular contraction also requires ATP and continues as long as ACh is released.

Muscle relaxation is caused by the decomposition of ACh via the enzyme acetylcholinesterase, which is always present. It prevents a single nerve impulse from stimulating the muscle fiber continuously. When the stimulus ceases, calcium ions are transported back to the SR. The actin and myosin linkages break, and the muscle relaxes. TABLE 9-2 describes the major com-ponents of muscular contraction and relaxation.

For muscle contraction, fibers must be activated (stimulated by nerve endings). This causes a change in membrane potential. The fiber must generate an ­electrical current (action potential) in its sarco-lemma, which occurs at the neuromuscular junction. This action potential is automatically moved along the sarcolemma. Intracellular calcium ion levels briefly rise, triggering the contraction. These parts of the process are called excitation­ contraction coupling. The contraction cycle involves molecular events that enable skeletal muscles to contract.