Like skeletal muscle cells, cardiac (heart) muscle cells, or myo-cardial cells, are striated; they contain actin and myosin filaments arranged in the form of sarcomeres, and they contract by means of the sliding filament mechanism. The long, fibrous skeletal muscle cells, however, are structurally and functionally separated from each other, whereas the myocardial cells are short, branched, and interconnected. Each myocardial cell is tubular in structure and joined to adjacent myocardial cells by electrical synapses, or gap junctions (see chapter 7, fig. 7.19).
The gap junctions are concentrated at the ends of each myocardial cell (fig. 12.31), which permits electrical impulses to be conducted primarily along the long axis from cell to cell. Gap junctions in cardiac muscle have an affinity for stain that makes them appear as dark lines between adjacent cells when viewed in the light microscope. These dark-staining lines are known as intercalated discs (fig. 12.32).
Electrical impulses that originate at any point in a mass of myocardial cells, called a myocardium, can spread to all cells in the mass that are joined by gap junctions. Because all cells in a myocardium are electrically joined, a myocardium behaves as a single functional unit. Thus, unlike skeletal muscles that produce contractions that are graded depending on the number of
■ Figure 12.32 Cardiac muscle. Notice that the cells are short, branched, and striated and that they are interconnected by intercalated discs.
cells stimulated, a myocardium contracts to its full extent each time because all of its cells contribute to the contraction. The ability of the myocardial cells to contract, however, can be increased by the hormone epinephrine and by stretching of the heart chambers. The heart contains two distinct myocardia (atria and ventricles), as will be described in chapter 13.
Cardiac muscle, like skeletal muscle, contains the tro-ponin complex of three proteins (see fig. 12.13). Troponin I helps inhibit the binding of the myosin crossbridges to actin; troponin T binds to tropomyosin in the thin filaments, and troponin C binds to Ca2+ for muscle contraction. Damage to myocardial cells, which occurs in myocardial infarction, causes troponins to be released into the blood. Fortunately for clinical diagnosis, troponins T and I are slightly different in cardiac muscle than in skeletal muscle. Thus, troponins T and I released by damaged myocardial cells can be distinguished and measured by laboratory tests using specific antibodies. Such tests are now an important tool in the diagnosis of myocardial infarction.
Fox: Human Physiology, I 12. Muscle: Mechanisms of I Text I © The McGraw-Hill
Eighth Edition Contraction and Neural Companies, 2003
Unlike skeletal muscles, which require external stimulation by somatic motor nerves before they can produce action potentials and contract, cardiac muscle is able to produce action potentials automatically. Cardiac action potentials normally originate in a specialized group of cells called the pacemaker. However, the rate of this spontaneous depolarization, and thus the rate of the heartbeat, are regulated by autonomic innervation. Regulation of the cardiac rate is described more fully in chapter 14.
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