Final answer:
Impaired mitochondrial function in a cardiac muscle cell would disrupt aerobic metabolism and ATP production, essential for maintaining ionic gradients that dictate the cell's resting potential. The energy deficit can result in altered resting membrane potential, which impairs the cell's ability to undergo proper depolarization and repolarization, potentially affecting heart function.
Step-by-step explanation:
If mitochondrial function is impaired in a cardiac muscle cell, it would be unable to perform efficient aerobic metabolism, which is essential for synthesizing adenosine triphosphate (ATP). ATP is critical for maintaining the ionic gradients across the membrane that are required for the resting potential of the cell.
Consequently, an energy deficit would occur, leading to decreased ability to pump ions, primarily Na+, K+, and Ca2+, against their gradients, which could alter the resting membrane potential.
For contractile cells, with their normal resting potential of approximately -80 mV to -90 mV, this perturbation could affect the stability of their resting phase and hence their capacity for effective depolarisation and repolarisation during action potentials.
For conductive cells, the impaired mitochondrial function would affect their autorhythmicity, as their ability to cycle through the phases of slow depolarization and repolarization is directly dependent on the cell's energy status.