Final answer:
Decreased acetylcholinesterase is not a mechanism of enhanced neuromuscular function in response to exercise training; exercise generally leads to increased end-plate size and acetylcholine receptor density.
Step-by-step explanation:
The mechanism of enhanced neuromuscular junction function that is not a response to exercise training is B. decreased acetylcholinesterase (AChE). During exercise, improvements in neuromuscular junction function involve an increase in end-plate size and an increase in acetylcholine receptor density, which allow for more effective transmission of nerve impulses to muscle fibers, leading to stronger and more efficient muscle contractions.
However, decreasing acetylcholinesterase would not be beneficial as this enzyme's role is to breakdown acetylcholine in the synaptic cleft, preventing prolonged muscle contraction. If AChE were decreased, acetylcholine would remain bound to receptors longer, potentially leading to unwanted extended muscle contraction instead of enhancing function.