The term “excitation-contraction coupling” refers to the mechanism by which the action potential causes the myofibrils of muscle to contract. There are differences in this mechanism in cardiac muscle that have important effects on the characteristics of heart muscle contraction.

As is true for skeletal muscle, when an action potential passes over the cardiac muscle membrane, the action potential spreads to the interior of the cardiac muscle fiber along the membranes of the transverse (T) tubules. The T tubule action potentials in turn act on the mem branes of the longitudinal sarcoplasmic tubules to cause release of calcium ions into the muscle sarcoplasm from the sarcoplasmic reticulum. In another few thousandths of a second, these calcium ions diffuse into the myofibrils and catalyze the chemical reactions that promote sliding of the actin and myosin filaments along one another, which produces the muscle contraction.

Thus far, this mechanism of excitation-contraction coupling is the same as that for skeletal muscle, but there is a second effect that is quite different. In addition to the calcium ions that are released into the sarcoplasm from the cisternae of the sarcoplasmic reticulum, calcium ions also diffuse into the sarcoplasm from the T tubules themselves at the time of the action potential, which opens voltage-dependent calcium channels in the membrane of the T tubule (Figure 1). Calcium entering the cell then activates calcium release channels, also called ryanodine receptor channels, in the sarcoplasmic reticulum mem brane, triggering the release of calcium into the sarcoplasm.

FIG1. Mechanisms of excitation-contraction coupling and relaxation in cardiac muscle. ATP, adenosine triphosphate. 

Without the calcium from the T tubules, the strength of cardiac muscle contraction would be reduced considerably because the sarcoplasmic reticulum of cardiac muscle is less well developed than that of skeletal muscle and does not store enough calcium to provide full contraction. The T tubules of cardiac muscle, however, have a diameter five times as great as that of the skeletal muscle tubules, which means a volume 25 times as great. Also, inside the T tubules is a large quantity of mucopolysaccharides that are electronegatively charged and bind an abundant store of calcium ions, keeping them available for diffusion to the interior of the cardiac muscle fiber when a T tubule action potential appears.

The strength of contraction of cardiac muscle depends to a great extent on the concentration of calcium ions in the extracellular fluids. In fact, a heart placed in a calcium-free solution will quickly stop beating. The reason for this response is that the openings of the T tubules pass directly through the cardiac muscle cell membrane into the extracellular spaces surrounding the cells, allowing the same extracellular fluid that is in the cardiac muscle interstitium to percolate through the T tubules. Consequently, the quantity of calcium ions in the T tubule system (i.e., the availability of calcium ions to cause cardiac muscle contraction) depends to a great extent on the extracellular fluid calcium ion concentration.

In contrast, the strength of skeletal muscle contraction is hardly affected by moderate changes in extracellular fluid calcium concentration because skeletal muscle contraction is caused almost entirely by calcium ions released from the sarcoplasmic reticulum inside the skeletal muscle fiber.

At the end of the plateau of the cardiac action potential, the influx of calcium ions to the interior of the muscle fiber is suddenly cut off, and calcium ions in the sarcoplasm are rapidly pumped back out of the muscle fibers into both the sarcoplasmic reticulum and the T tubule extracellular fluid space. Transport of calcium back into the sarcoplasmic reticulum is achieved with the help of a calcium–adenosine triphosphatase (ATPase) pump (see Figure 1). Calcium ions are also removed from the cell by a sodium-calcium exchanger. The sodium that enters the cell during this exchange is then transported out of the cell by the sodium-potassium ATPase pump. As a result, the contraction ceases until a new action potential comes along.

Duration of Contraction. Cardiac muscle begins to contract a few milliseconds after the action potential begins and continues to contract until a few milliseconds after the action potential ends. Therefore, the duration of contraction of cardiac muscle is mainly a function of the duration of the action potential, including the plateau— about 0.2 second in atrial muscle and 0.3 second in ventricular muscle.