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As already presented in Chapter 10, the function of the heart is to pumpblood from the venous system into the arterial system from where it can be distributed to the capillaries of the tissues. The heart is made up of cardiac muscle which is striated due to the orderly arrangement of actin and myosin within the cell. As is true in other excitable cells, the action potential spreads over the entire cardiac muscle fiber cell membrane, including the T tubules. The T tubules are indentations of the cell membrane penetrating deeply into the cardiac muscle cell. The T tubules of cardiac muscle cells are about five times larger in diameter but fewer in number than the T tubules of skeletal muscle cells. Adjacent to the T tubules are the cisternae, which are modified portions of the sarcoplasmic reticulum (SR). The cisternae contain highly concentrated calcium, which is released when an action potential spreads over the cell membrane. Calcium entering the cell through the voltage-gated calcium channels during the plateau phase of the action potential elicits calcium release from the SR cisternae through the ryanodine receptor—calcium-induced calcium release or CICR. The calcium binds to troponin, which abolishes the inhibitory effect of troponin and tropomyosin on the interaction between actin and myosin. In the presence of ATP, the actin and myosin filaments bind and slide along each other, causing muscular contraction. Additionally, the calcium that enters the myocardial cells via slow calcium channels is essential in determining the strength of the contraction. Thus, extracellular calcium concentration directly affects cardiac muscle contraction while having little effect on the contraction of skeletal muscle (which relies almost entirely on the calcium ions released from the cisternae). When the slow calcium channels close, calcium pumps return the calcium to the inside of the SR or else pump it out of the cell to terminate contraction. The duration of contraction is mainly a function of the duration of the action potential—approximately 0.15 s in atrial muscle and 0.3 s in ventricular muscle.

Understanding the contractile properties of cardiac muscle is important to know in order to understand how the heart functions effectively as a pump that can alter its output four- to sixfold from the resting state. Muscle contraction can be either isometric (only tension is developed during the contraction and there is no change in muscle length, i.e., no shortening) or isotonic (muscle develops tension and then shortens). The two primary contractile properties of muscle that relate to myocardial performance, as studied using isometric and isotonic contractions, are the length-tension relationship and the force-velocity relationship.


A strip of cardiac muscle, such as a papillary muscle, can be studied in an isometric configuration, that is, in such a manner that the muscle’s resting length is set prior to stimulation and the muscle is not allowed to shorten during contraction; thus only tension is ...

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