1103 Chapter 10. Muscle Tissue
10.7 Cardiac Muscle Tissue
Learning Objectives
By the end of this section, you will be able to:
- Describe the microscopic anatomy of cardiac muscle cells by outlining the structure and function of:
- Intercalated discs
- Sarcomeres
- T-tubules and the sarcoplasmic reticulum
- Describe the mechanism of contraction in cardiac muscle, including the triggers for calcium release, the roles of calcium during contraction, and the source of energy for cardiac muscle cells
- Describe the functional significance of self-excitatory cardiac muscle cells
Cardiac muscle tissue is only found in the heart. Highly coordinated contractions of cardiac muscle pump blood into the vessels of the circulatory system. Similar to skeletal muscle, cardiac muscle is striated and organized into sarcomeres, possessing the same banding organization as skeletal muscle (Figure 1). However, cardiac muscle fibers are shorter than skeletal muscle fibers and usually contain only one nucleus, which is located in the central region of the cell. Cardiac muscle fibers also possess many mitochondria and myoglobin, as ATP is produced primarily through aerobic metabolism. Cardiac muscle fibers cells also are extensively branched and are connected to one another at their ends by intercalated discs. An intercalated disc allows the cardiac muscle cells to contract in a wave-like pattern so that the heart can work as a pump.
Intercalated discs are part of the sarcolemma and contain two structures important in cardiac muscle contraction: gap junctions and desmosomes. A gap junction forms channels between adjacent cardiac muscle fibers that allow the depolarizing current produced by cations to flow from one cardiac muscle cell to the next. This joining is called electric coupling, and in cardiac muscle it allows the quick transmission of action potentials and the coordinated contraction of the entire heart. This network of electrically connected cardiac muscle cells creates a functional unit of contraction called a syncytium. The remainder of the intercalated disc is composed of desmosomes. A desmosome is a cell structure that anchors the ends of cardiac muscle fibers together so the cells do not pull apart during the stress of individual fibers contracting (Figure 2).
Contractions of the heart (heartbeats) are controlled by specialized cardiac muscle cells called pacemaker cells that directly control heart rate. Although cardiac muscle cannot be consciously controlled, the pacemaker cells respond to signals from the autonomic nervous system (ANS) to speed up or slow down the heart rate. The pacemaker cells can also respond to various hormones that modulate heart rate to control blood pressure.
The wave of contraction that allows the heart to work as a unit, called a functional syncytium, begins with the pacemaker cells. This group of cells is self-excitable and able to depolarize to threshold and fire action potentials on their own, a feature called autorhythmicity; they do this at set intervals which determine heart rate. Because they are connected with gap junctions to surrounding muscle fibers and the specialized fibers of the heart’s conduction system, the pacemaker cells are able to transfer the depolarization to the other cardiac muscle fibers in a manner that allows the heart to contract in a coordinated manner.
Unlike skeletal muscle, extracellular Ca2+ is required to initiate release from the sarcoplasmic reticulum (SR). The SR in cardiac muscle fibers is simpler than that of skeletal muscle fibers, lacking terminal cisterns, and there is no direct physical link between proteins in the T-tubule and proteins in the SR membrane, so depolarization of the T-tubule membrane cannot directly cause Ca2+ release from the SR. Instead, cardiac muscle cells have voltage-gated calcium channels in the sarcolemma and along the T-tubules that open when the membrane is depolarized, allowing Ca2+ to enter the cardiac muscle fiber from the extracellular fluid. This calcium then causes the opening of calcium-gated calcium channels in the SR membrane that release additional Ca2+ into the sarcoplasm. This mechanism allows cardiac muscle to have a relatively long-lasting depolarization “plateau” in its fibers. This sustained depolarization (and Ca2+ entry) provides for a longer contraction than is produced by an action potential in skeletal muscle.