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Departments of Neurology, Medicine, and Radiology, California Pacific Medical Center; the Magnetic Resonance Unit, Veterans Administration Medical Center; and the University of California, San Francisco, San Francisco, CA.
Normal subjects (n = 7) performed rapid voluntary isometric contractions of the adductor pollicis and the tibialis anterior. Within the first minute of this low-intensity exercise, the speed of tension development slowed, accompanied by a prolongation in EMG burst duration. In contrast, electrically evoked contractions either became more rapid (twitch) or did not change (tetanus), suggesting a fatigue of central origin. 31P NMR measurements of high-energy phosphates showed that the relationship between the fall of maximum force and changes of phosphates and pH was similar to that produced by other high-intensity fatiguing exercise protocols. Thus, rapid movements produce fatigue through two major mechanisms. First, there is slowing of the speed of tension development which appears secondary to central fatigue. Second, the decline of muscle force is primarily attributable to changes in muscle pH or inorganic phosphate, which usually occurs only after high-intensity (but non-rapid) exercise.
Address correspondence and reprint requests to Dr. Robert G. Miller, California Pacific Medical Center, 3698 California Street, #545, San Francisco, CA 94118.
Supported in part by a grant from The Muscular Dystrophy Association (to Robert G. Miller), by The National Institutes of Health grant AM-DK 33923004 (to Michael W. Weiner), and by the Veterans Administration Medical Center (to Michael W. Weiner).
Received April 6, 1992. Accepted for publication in final form August 28, 1992.
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