spinal cord to the individual muscle cells. These axons can be up to three feet long, forming bundles called nerves similar to individual wires bundled in a cable. When the nerve cell is activated, it releases acetylcholine, its neurotransmitter, that crosses the synaptic cleft, which is the space between the nerve cell and the motor end plate of the muscle cell. It binds to the muscle cell receptors at the motor end plate, causing positively charged ions to pass through the cell membrane, raising the membrane potential so that it is less negative. This is called depolarization. This depolarization triggers the action potential that spreads to all parts of the muscle cell. In the meantime, there is an enzyme called acetylcholinesterase that degrades the acetylcholine so it can no longer act on the motor end plate. When the muscle cell is activated with an action potential, there are invaginations of the sarcolemma (cell membrane) called T-tubules or transverse tubules. They ensure that the activated membrane can get closer to the sarcoplasmic reticulum. This is where it can affect the calcium transport inside or outside the sarcoplasmic reticulum. The Ttubule with membranes of the sarcoplasmic reticulum on either side is called a triad. The triad surrounds the myofibril, which is what contains actin and myosin.
SEQUENCE OF MUSCLE CONTRACTION EVENTS In understanding the structure of the muscle fiber, you need to see that the shortening of these long, thin muscle cells involves two kinds of fiber in them, which are actin and myosin. The shortening relies on the presence of calcium ions in the cytoplasm of the muscle cell, which causes un-shielding of actin binding sites, which had been shielded by troponin and tropomyosin. Calcium also activates enzymes that will activate the myosin heads. Figure 3 shows actin and myosin in the muscle cell.
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