While it is true that skeletal muscle cells and cardiac muscle cells share many common characteristics, they also have some important differences. Both types of muscle tissue show striations, the regular pattern of I bands and A bands with Z discs, but cardiac muscles have fewer T tubules. Both types of muscle tissue are surrounded by endomysium, yet skeletal muscle are able to function as single units while cardiac muscle functions only as a group in functional syncytium due to its intercalated discs studded with desmosomes and gap junctions. While both muscle tissues may be stimulated by the sympathetic nervous system, the cardiac muscle tissue is primarily controlled by the autorhythmic cells in the sinoatrial node, found in the right atrium. One of the most important differences between the two types of muscle is in the length of their refractory periods, and this is what we will focus on here.
Prior to discussing why refractory period lengths are important in cardiac muscle cells, we must define some terms and explain some processes that occur during cardiac muscle cell contraction. The first step in muscle cell contraction is depolarization. This occurs when there is a fluctuation of ions between the cell and the extracellular fluid such that the cytoplasm of the cell becomes less negatively charged that it is in a resting phase. After depolarization of the cell’s cytoplasm, the second stage, called excitation-contraction coupling, causes calcium ions to be released into the cytoplasm; various coupling stages then allow the actin and myosin myofilaments to slide along each other and contract the muscle cell. The final stage is repolarization. During repolarization, the ions that were transported between the cytoplasm and the extracellular fluid are returned to their original levels, causing calcium to exit the cytoplasm and the myosin and actin myofilaments to unhook their cross-bridges. This returns the cell to its resting, non-contracted, length. During the third stage, repolarization, there is a time period during which the muscle cell cannot respond to any stimulus. This time of non-responsiveness is called the refractory period.
In skeletal muscle cells, the contraction last from fifteen to one hundred milliseconds or more with a refractory period of one to two milliseconds. When a skeletal muscle is contracting, it may reach the end of its refractory period before it reaches the end of its contraction period. If this happens and another stimulus is applied to the skeletal muscle cell, the skeletal muscle cell will continue to contract without a period of total relaxation. If subsequent stimuli are applied at a steady rate, the cell will hold in a quivering incomplete tetanus. If subsequent stimuli occur quickly enough, the cell will hold a steady complete tetanus with no relaxation period at all but a continued sustained contraction. This can be very useful in skeletal muscles, as a father carries his child in one arm and a grocery bag in the other, or as a woman holds a plank position for her personal trainer at the gym.
In cardiac muscle cells, however, the refractory period is approximately two hundred fifty milliseconds, which is almost the same length of time as the cardiac muscle cell contraction period. If tetanus can be an advantage stemming from the shorter refractory period of skeletal muscle, we must ask why we would want longer refractory periods in cardiac muscle. First, longer refractory periods limit the probability that myocardial cells will experience tetany. The heart functions as a four-chambered pump, from atria to ventricle to either the pulmonary or the systemic circulation. If atrial myocardial cells were to be continuously contracted, there would be no time at which the ventricular pressure would be greater than atrial pressure. This would cause the atrioventricular valves to remain open at all times. If ventricular myocardial cells were to be continuously contracted, there would be no point at which the aortic pressure would be greater than ventricular pressure, causing the semilunar valves to remain open at all times. With either set of valves, or even just one of the four valves, always open, there would be a regurgitation of blood thereby decreasing the efficiency of the heart as a pump. As the heart would have to work harder to overcome this decreased stroke volume, it would ultimately hypertrophy and become weakened.
The second negative side effect of complete tetany of myocardial cells would be the actual lack of pumping. In order to function properly, the four chambers of the heart must first expand as they fill with blood during diastole, and then contract as they expel blood during systole. If a chamber is in a state of continual contraction, it will not contract further to expel its blood volume into the next chamber or artery in the circulatory system. Although the three other chambers may be able to provide some pressure to move the blood if only one chamber is non-functional, the heart would ultimately be compromised in its efficiency. Just as seen in the discussion of faulty valve operation, this inefficiency would lead to a harder-working and weakened heart.
A final consideration in myocardial refractory period lengths is the overall coordination of the contractile myocardial cells in the heart. Examination of a normal electrocardiogram shows that the electrical stimuli in the heart follow a regular pattern for optimal functioning. The sinoatrial node, known as the pacemaker, in the right atrium first generates an impulse at a rate of about seventy times per minute when moderated by the sympathetic and parasympathetic nervous systems, or about one hundred times per minute when not moderated. This impulse is spread to both the right and left atria causing atrial contraction, as well as to the atrioventricular node in the interatrial septum through the internodal pathway. After an intensely brief delay of only one-tenth of a second, the impulse is sent down the atrioventricular bundle and bundle branches in the interventricular septum toward the apex of the heart. The impulse then speeds down the Purkinje fibers and into the ventricular myocardial cells, leading to ventricular contraction that twists from the apex of the heart superiorly to the pulmonary trunk and aorta. If any of the cells become hyperexcitable due to a shortened refractory period, there will be an ectopic focus, or contraction-generating impulse starting at a point other than the sinoatrial node, resulting in extrasystole. An extrasystole, or premature contraction on one beat, creates a longer period for the chamber to fill before the next regular contraction; this second contraction is them felt more powerfully as the additional stretching of the heart causes a stronger contraction. Extrasystole in any of the heart chambers can be life-threatening. The Frank Starling law of the heart details the positive relationship between the degree of stretch from pre-contraction filling of the heart chamber and the force with which the chamber contracts.