Final answer:
Pre-treatment with physostigmine increases force output upon ACh application to toad's rectus abdominus muscle by inhibiting the breakdown of ACh, enhancing its action and prolonging muscle contraction. Therefore, the statement is true and supports the explanation provided, which is also true.
Step-by-step explanation:
The application of acetylcholine (ACh) to the rectus abdominus muscle of a toad would produce higher force output after pre-treatment with physostigmine because physostigmine inhibits the enzyme acetylcholinesterase, which is responsible for breaking down ACh in the synaptic cleft. This means that ACh would remain in the synaptic cleft for a longer period, continuously stimulating the muscle and thus increasing the force of muscle contraction. The answer to the initial statement is a. TRUE AND TRUE. If a muscle contraction needs to be inhibited, one could interfere at several points: by inhibiting the action potential in the motor neuron, preventing the release of ACh, blocking the activity of ACh receptors, or disrupting the sliding filament process in the muscle fiber. For instance, blocking ACh receptors with a drug like d-tubocurarine leads to muscle relaxation and paralysis because the muscle cell becomes insensitive to motor nerve impulses and directly applied ACh. Similarly, Botulinum toxin (Botox) works by preventing the release of ACh from motor neurons, effectively causing muscle relaxation and paralysis. The disruption of ACh receptors, as seen in myasthenia gravis, results in muscle weakness, showing the vital role of ACh in the process of muscle contraction.