Muscle fatigue may be defined as any exercise-induced reduction in the ability of a muscle to generate force or power. Fatigue during a sustained maximal contraction, when all the motor units are used and the rate of neural firing is maximal—as when lifting an extremely heavy weight—appears to be due to an accumulation of extracellular K+. (Remember that K+ leaves axons and muscle fibers during the repolarization phase of action potentials.) This reduces the membrane potential of muscle fibers and interferes with their ability to produce action potentials. Fatigue under these circumstances lasts only a short time, and maximal tension can again be produced after less than a minute's rest.
Muscle fatigue during moderate exercise occurs as the slow-twitch fibers deplete their reserve glycogen and fast-twitch fibers are increasingly recruited. Fast-twitch fibers obtain their energy through anaerobic respiration, converting glucose to lactic acid, and this results in a rise in intracellular H+ and a fall in pH. The decrease in muscle pH, in turn, promotes muscle fatigue, but the exact physiological mechanisms by which this occurs are not well understood. The increased concentration of H+ may interfere with cross-bridge formation, but other factors may also be involved. Depletion of glycogen, production of lactic acid, and other metabolic changes have been shown to somehow interfere with the ability of the sarcoplasmic reticulum to release Ca2+ when a muscle fiber is stimulated by a nerve. This interference with excitation-contraction coupling, rather than a depletion of muscle ATP, appears to underlie muscle fatigue.
The foregoing is a description of the reasons that muscle tissue can fatigue during exercise. When humans exercise, however, we often experience fatigue before our muscles themselves have fatigued sufficiently to limit exercise. Put another way, our maximum voluntary muscle force is often less than the maximum force the our muscle is itself capable of producing. This demonstrates central fatigue—muscle fatigue caused by changes in the CNS rather than by fatigue of the muscles themselves. During exercise, a progressive reduction in the voluntary activation of muscles demonstrates central fatigue.
Evidence suggests that central fatigue is complex. In part, it involves a reduced ability of the "upper motoneurons" (in the brain) to drive the "lower motoneurons" (in the spinal cord). Muscle fatigue thus has two major components: a peripheral component (fatigue in the muscles themselves) and a central component (fatigue in the activation of muscles by motoneurons).
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This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.