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Electrical Properties of muscle

المؤلف:  Kim E. Barrett, Susan M. Barman, Heddwen L. Brooks, Jason X.-J. Yuan

المصدر:  Ganongs Review of Medical Physiology

الجزء والصفحة:  25th E, P113

2026-09-10

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 The resting membrane potential of individual mammalian cardiac muscle cells is about –90 mV. Stimulation produces a propagated action potential that is responsible for initiating contraction. Although action potentials vary among the cardiomyocytes in different regions of the heart, the action potential of a typical ventricular cardiomyocyte can be used as an example (Figure 1). Depolarization proceeds rapidly and an overshoot of the zero potential is present, as in skeletal muscle and nerve, but this is followed by a plateau before the membrane potential returns to the baseline. In mammalian hearts, depolarization lasts about 2 ms, but the plateau phase and repolarization last 200 ms or more. Repolarization is therefore not complete until the contraction is half over.

Fig1. Comparison of action potentials and contractile response of a mammalian cardiac muscle fiber in a typical ventricular cell. In the top trace, the intracellular recording of the action potential shows the quick depolarization and extended recovery. In the bottom trace, the mechanical response is matched to the extracellular and intracellular electrical activities. Note that in the absolute refractory period (ARP), the cardiac myocyte cannot be excited, whereas in the relative refractory period (RRP) minimal excitation can occur.

As in other excitable tissues, changes in the external K+ concentration affect the resting membrane potential of cardiac muscle, whereas changes in the external Na+ concentration affect the magnitude of the action potential. The initial rapid depolarization and the overshoot (phase 0) are due to opening of voltage-gated Na+ channels similar to that occurring in nerve and skeletal muscle (Figure 2). The initial rapid repolarization (phase 1) is due to closure of Na+ channels and opening of one type of K+ channel. The subsequent prolonged plateau (phase 2) is due to a slower but prolonged opening of voltage-gated Ca2+ channels. Final repolarization (phase 3) to the resting membrane potential (phase 4) is due to closure of the Ca2+ channels and a slow, delayed increase of K+ efflux through various types of K+ channels. Cardiac myocytes contain at least two types of Ca2+ channels (T- and L-types), but the Ca2+ current is mostly due to opening of the slower L-type Ca2+ channels. Mutations or dysfunction in any of these channels lead to serious pathologies of the heart (eg, Clinical Box 1).

CLINICAL BOX 1.