Final answer:
In HyPP and PC, mutations in sodium ion channels lead to prolonged depolarization, causing inactivation of these channels and preventing muscle contraction. This results in paralysis because not enough sodium ion channels can open in response to a stimulus.
Step-by-step explanation:
In conditions like hyperkalemic periodic paralysis (HyPP) and paramyotonia congenita (PC), mutations in sodium ion channels result in a small, prolonged membrane depolarization, which in turn causes normal sodium channels to become inactivated. This disruption in the normal function of sodium channels affects muscular function because during an action potential, the influx of sodium is critical for the depolarization phase. When sufficient sodium channels are inactivated due to prolonged depolarization, there are not enough responsive channels to propagate a normal action potential. This leads to an inability of muscles to contract in response to stimuli, resulting in muscle weakness or paralysis.
The correct answer to the question is: D. The muscle experiences paralysis because a stimulus cannot cause the opening of enough sodium ion channels. This is because normal muscular function is dependent on the rapid opening of voltage-gated sodium channels which initiate the action potential and lead to muscle contraction through excitation-contraction coupling. Inactivation of these channels thus prevents the necessary depolarization for muscle contraction, causing paralysis of the muscle.