Certain neurotransmitters (i.e., acetylcholine, catecholamines, and serotonin) are formed from dietary constituents (i.e., choline, tyrosine and tryptophan). Changing the consumption of these precursors alters release of their respective neurotransmitter products. The neurotransmitter acetylcholine is released from the neuromuscular junction and from brain. It is formed from choline, a common constituent in fish, liver, and eggs. Choline is also incorporated into cell membranes; membranes may likewise serve as an alternative choline source for acetylcholine synthesis.
There are no direct connections between nerves that make muscles contract (motor neurons) and skeletal muscle fibers. When a motor neuron depolarizes, an electrical current (the action potential) is passed down the nerve fiber.
Upon reaching the end of the neuron, the impulse causes the release of the neurotransmitter, acetylcholine.
The acetylcholine binds with receptors on the muscle membrane which are in close proximity to the neuron (the motor end plate).
The binding of the acetylcholine to the muscle membrane allows for the initiation of an action potential (which promotes the passing of an electrical current) on the muscle membrane. A special enzyme, acetylcholinesterase, breaks down the released acetylcholine so that it cannot continue to bind to the muscle membrane. In this way, the nerve controls the action of the muscle such that the muscle can only generate a current when the nerve has first generated a current. Once the muscle membrane has been excited by the electrical current, the same current causes the release of calcium (Ca++) by specialized storage sites throughout the muscle (called the sarcoplasmic reticulum). The released Ca++ comes into contact with the contractile machinery of the muscle fiber and muscle contraction can begin.
Muscle contractions occur when calcium ions interact two binding proteins, actin and myosin. These proteins help initiate the muscle contraction. This sequence of events happens when ever the motor units are stimulated activating the release of ACH over the synaptic junction of the motor neuron. Overtraining the muscle will deplete the ACH release causing actin and myosin to misfire. The motor units will become dull and the synapse will be weak. When this occurs the protein and fat synthesis within the muscle cell ceases. The catacholamine responsible for inhibiting the muscle permeability is cortisol.
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