Final answer:
Injecting a drug that disables acetylcholinesterase in a leg muscle would increase acetylcholine levels, causing ongoing muscle contraction and potentially leading to spastic paralysis.
Step-by-step explanation:
If a leg muscle were injected with a drug that binds to and disables acetylcholinesterase, it would result in increased levels of the neurotransmitter acetylcholine in the neuromuscular junction. The lack of acetylcholinesterase activity would prevent the breakdown of acetylcholine, leading to prolonged stimulation of the muscle fibers. This would cause continuous muscle contraction, which could lead to a state called spastic paralysis due to constant activation.
Drugs such as physostigmine, neostigmine, and pyridostigmine that target acetylcholinesterase are used to treat diseases like myasthenia gravis and Alzheimer's, where enhanced neural transmission is beneficial. However, in the case of exposure to nerve agents like Sarin, the effects are harmful. Sarin irreversibly inhibits acetylcholinesterase, leading to overstimulation and potentially life-threatening outcomes.
Therefore, the absence of acetylcholinesterase activity at the neuromuscular junction leads to the accumulation of acetylcholine, initiating constant nerve impulses resulting in non-stop muscle contractions.