Energy in the form of ATP is used to conduct many functions of striated muscle cells. In addition to the energy required for synthesis of structural components of the cell, large amounts are needed to support the events associated with contraction—crossbridge cycling, calcium translocations, and membrane electrical activity.
A large amount of ATP is used during contraction because each cycle of each crossbridge involves the hydrolysis of one ATP molecule; the higher the rate of crossbridge cycling, the higher the rate of ATP use. As discussed earlier, crossbridge cycling rate determines the velocity of shortening, which is determined by the afterload placed on the muscle. Thus, more ATP is consumed by a muscle cell that is shortening rapidly against a light afterload than is consumed during an isometric contraction. Also, muscle cells that have myosin isoforms with high ATPase activity (fast-twitch skeletal) will use more ATP during contraction than will muscle cells that have myosin isoforms with lower ATPase activity (slow-twitch skeletal and cardiac).
Adenosine triphosphate is also used during cycling of the cytoplasmic calcium that couples cell excitation to crossbridge cycling. In this case, ATP hydrolysis is not needed directly to effect the rise in intracellular calcium. This rise is due to the rapid release of calcium from the SR and, in the case of cardiac muscle, to the influx of calcium from the extracellular fluid. Both release and influx occur down large concentration gradients for calcium. ATP hydrolysis is required to lower cytosolic calcium levels to allow the cell to relax. This requires moving calcium against a large electrochemical gradient to maintain the calcium gradients between the extracellular fluid and sarcoplasmic reticulum, on the one hand, and the cytoplasm, on the other. In skeletal muscle, cytosolic calcium is reduced by the uptake of calcium into the lateral SR. This involves a calcium pump, with each cycle requiring hydrolysis of one ATP molecule. In cardiac muscle, most of the calcium is handled just as in skeletal muscle. However, some calcium must be removed from the cell to balance, over the long term, that which enters during the action potential. This calcium is removed through the activity of a sodium-calcium countertransport. Sodium-calcium countertransport does not use ATP directly. It is driven by the gradient in sodium that exists across the membrane as a result of the sodium pump. This pump uses ATP to remove sodium from the cell while bringing in potassium.
As with the events responsible for the rise in intracellular calcium, the events associated with muscle cell membrane resting and action potentials also do not use ATP directly; rather, the ionic fluxes responsible for these potentials are due to the opening and closing of channels to allow ions to move down their electrochemical gradients. Resting potential is due mostly to gradients in potassium, whereas action potentials are due mostly to gradients in sodium and potassium in skeletal muscle and to gradients in sodium, potassium, and calcium in cardiac muscle cells. As in other cells, gradients of sodium and potassium are maintained by the sodium pump; as discussed previously, this pump also helps maintain the calcium gradient in cardiac muscle cells.
Resting ATP levels in muscle cells are enough to sustain contraction only for brief periods. ATP must be replenished as rapidly as it is hydrolyzed so that ATP levels fall minimally during periods of contraction. Like most other cells, muscle can derive ATP from both glycolysis and oxidative phosphorylation; however, muscle cells also have a more immediate precursor for the generation of ATP. Creatine phosphate is a high-energy molecule that can rephosphorylate ADP to ATP. Creatine phosphate concentrations do fall early during a period of contraction and, if not replenished, can supply enough energy for only a few contractions; however, it does supply energy early on until the required increases in glycolysis and/or oxidative phosphorylation take place.
The proportions of ATP generated by glycolysis and oxidative phosphorylation vary from cell to cell. Human skeletal muscle cells are divided mainly into two types, based on both the myosin isoform present and on metabolic pathways (see Table 1). One type, fast-twitch glycolytic, possesses a myosin isoform with high ATPase activity. As expected, this muscle exhibits a large Vmax and derives most of its ATP from glycolysis. The other type, slow-twitch oxidative, possesses a myosin isoform with a lower ATPase activity and a concomitant lower Vmax. It generates most of its ATP via oxidative phosphorylation. Cardiac muscle cells have their own myosin isoform, which also has low ATPase activity. Thus, it more closely resembles that found in slow oxidative skeletal muscle cells. These cells also derive most of their ATP from oxidative phosphorylation.
The slow-twitch oxidative skeletal muscles and cardiac muscle contain myoglobin. This heme-containing protein aids in the transfer of oxygen from the hemoglobin of blood to the mitochondria of the muscle cells, thus facilitating ATP generation through oxidative metabolism. Myoglobin also imparts a red color to the muscle. On the other hand, fast-twitch glycolytic skeletal muscles do not contain myoglobin and, thus, lack the red color. This difference accounts for the latter being referred to as white muscles.
Individual skeletal muscles vary in the proportion of the slow oxidative and fast glycolytic cells they contain; however, most muscles will contain both. Within each muscle, motor units are organized such that an individual a-motor neuron will innervate only one type of cell. In general, motor units composed of fast glycolytic cells will be smaller than those composed of slow oxidative cells. When the muscle is called on to do work, the type of motor unit activated will vary depending on the type of work. Short, rapid movements use mainly fast glycolytic units, whereas slower, more sustained, movements use slow oxidative units.
Berne RM, Levy MN. Physiology, 4th ed. St. Louis: Mosby, 1998 Berne RM, Sperelakis N, Eds. Handbook of physiology, Section 2: The cardiovascular system, Vol. 1: The heart. Bethesda, MD: American Physiological Society, 1979 Engel AG, Franzini-Armstrong C, Eds. Myology, basic and clinical,
2nd ed. New York: McGraw-Hill, 1994 Gordon AM, Homsher E, Regnier M. Regulation of contraction in striated muscle. Physiol Rev 2000; 80:853-924 Swynghedauw B. Developmental and functional adaptation of contractile proteins in cardiac and skeletal muscles. Physiol Rev 1986; 66:710-771
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