The sarcolemma (plasma membrane) of an unstimulated muscle cell is polarized—that is, the inside of the sarcolemma is negatively charged with respect to the outside. The unstimulated state of the muscle cell, called the resting potential, is created by the presence of large, negatively charged proteins and nucleic acids inside the cell. A balance between K +
inside the cell and Na +
outside the cell contributes to the polarization. During an action potential, the balance of Na +
and K +
is upset so that the cell becomes depolarized. The series of events that occurs during and following an action potential in contractile muscle fibers of the heart is similar to that in skeletal muscle. Here is a description of these events:
Rapid depolarization occurs when fast‐opening Na + channels in the sarcolemma open and allow an influx of Na + ions into the cardiac muscle cell. The Na + channels rapidly close.
A plateau phase occurs during which Ca 2+ enters the cytosol of the muscle cell. Ca 2+ enters from the sarcoplasmic reticulum (endoplasmic reticulum) within the cell and also from outside the cell through slow‐opening Ca 2+channels in the sarcolemma. Within the cell, Ca 2+ binds to troponin, which in turn triggers the cross‐bridge binding that leads to the sliding of actin filaments past myosin filaments. The sliding of the filaments produces cell contraction. At the same time that the Ca 2+ channels open, K + channels, which normally leak small amounts of K + out of the cell, become more impermeable to K + leakage. The combined effects of the prolonged release of Ca 2+ and the restricted leakage of K + lead to an extended depolarization that appears as a plateau when membrane potential is plotted against time.
Repolarization occurs as K + channels open and K + diffuses out of the cell. At the same time, Ca 2+ channels close. These events restore the membrane to its original polarization, except that the positions of K + and Na + on each side of the sarcolemma are reversed.
A refractory period follows, during which concentration of K + and Na + are actively restored to their appropriate sides of the sarcolemma by Na +/K + pumps. The muscle cell cannot contract again until Na + and K + are restored to their resting potential states. The refractory period of cardiac muscle is dramatically longer than that of skeletal muscle. This prevents tetanus from occurring and ensures that each contraction is followed by enough time to allow the heart chamber to refill with blood before the next contraction.