Final answer:
Ingesting a chemical that irreversibly binds to acetylcholine receptors prevents normal neurotransmitter binding, leading to the inability of skeletal muscle to contract, which would likely result in muscle paralysis.
Step-by-step explanation:
An individual who has ingested a chemical that irreversibly binds to the acetylcholine receptors in the sarcolemma, rendering them useless, would experience a notable impact on skeletal muscle function. Acetylcholine (ACh) is essential for the excitation-contraction coupling in skeletal muscle. When ACh is released into the synaptic cleft at the neuromuscular junction (NMJ), it normally binds to nicotinic receptors on the sarcolemma, causing a transient increase in membrane permeability to sodium ions (Na+), leading to depolarization. This depolarization initiates a cascade of events that result in muscle fiber contraction.
If acetylcholine receptors are inactivated, ACh cannot bind to them, which means that sodium ions would not enter the muscle fiber, and depolarization would not occur. Without depolarization, there would be no subsequent excitation-contraction coupling, resulting in the inability of the muscle to contract. This effect would be immediate and could potentially lead to muscle paralysis. This scenario is similar to what happens with the effect of Botulinum toxin (BONT) or with diseases such as myasthenia gravis, which impair ACh receptors' function causing muscle weakness or paralysis.