Cardiac muscles are the muscles of the heart. Their arrangement of actin and myosin is similar to that of striated skeletal muscles. Unlike other types of muscles, cardiac muscles never get tired. Cardiac muscles have special features.
They are shorter and thicker than skeletal muscle cells. They branch out like the letter Y and they are linked by intercalated discs, which have gap junctions providing a source of communication between cells through these channels as shown in Figure 1(b). The T-tubules are larger in cardiac muscles than skeletal muscles, allowing greater influx of Ca2+ ions from the extracellular fluid into myocytes. Unlike skeletal muscles, the cardiac muscles are autorhythmic because they contract independently of the nervous system and has an intrinsic rhythm. They can contract without nervous stimulation. They are predominantly mono-nucleated. Depolarisation of cardiac muscles is different from skeletal muscles. Also, the repolarisation takes much longer in cardiac muscles than skeletal and thus they cannot be stimulated at high frequency.
Figure 1. (a) Light micrograph of a cardiac muscle; (b) Cardiac myocytes and intercalated discs.
Action potential in cardiac muscles
The action potential in cardiac muscles is significantly different from that of neurons and skeletal muscles. They have a stable resting membrane potential of -90 mV. It has a prolonged action potential. Graph 2 shows that these muscles depolarise very quickly. It also shows an overshoot and a long plateau phase. Once stimulated, the voltage gated Na+ channels open causing Na+ ions inflow and depolarizing the cardiac muscle cell to the threshold level. A positive feedback cycle is triggered by opening additional Na+ gates bringing the action potential to nearly +30mV. Soon after this, the Na+ gates close quickly. This process allows the spread of action potential over the sarcolemma leads to an opening of voltage-gated slow Ca2+ channels. This allows a small amount of Ca2+ ions to enter the cytosol of cardiac muscle cells from extracellular fluids, binding to the ligand binding calcium channels on the sarcoplasmic reticulum (SR). This releases a greater quantity of Ca2+ from sarcloplasmic stores into the sarcoplasm.
This second wave of Ca2+ ions causes a prolonged myocardial contraction for 200-250 msec with a long plateau in action potential. This sustained contraction is necessary for expulsion of blood from the heart chambers. The plateau slowly falls because some K+ leaks out but most of the K+ channels remain closed until the end of plateau. Ca2+ ions are then transported back to the SR and extracellular fluid at the end of plateau phase and Ca2+ channels close. At the same time, the K+ channels open, causing rapid diffusion of K+ from the cells. Membrane voltage rapidly returns to the resting membrane potential, causing the muscles to relax.
An action potential in skeletal muscles falls back to resting potential within 2 msec, while in cardiac muscles its depolarization is prolonged for 200-250 msec. This may be due to the slow removal of cytosolic Ca2+ ions by the SR or the Ca2+ channels in the SR closes very slowly.
Graph 2. The graph shows the action potential of a ventricular myocyte. The red curve represents rising and falling muscle tension as the myocardium contracts and relaxes.
- Figure 1 adapted from Saladin (2003, p. 726)
- Graph 2 adapted from Saladin (2003, p. 730)