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Nonmetabolic fatigue in exercising human muscle

Departments of Neurology, Children's Hospital of San Francisco, University of California
Magnetic Resonance Unit, Veterans Administration Medical Center, San Francisco, CA

Human muscle fatigue, assessed by declining maximum voluntary contraction (MVC), may be caused by impairment of excitation-contraction coupling as well as by metabolic alterations within the muscle. To distinguish between these 2 possibilities, we assessed changes in excitation-contraction coupling by measuring twitch tension (TT) and twitch potentiation (P-TT) of the human adductor pollicis and tibialis anterior, while we analyzed metabolic changes using ³¹P magnetic resonance spectroscopy. Low-intensity exercise produced a much greater fall of TT and P-TT than MVC, high energy phosphates, or intracellular pH (pHi). In addition, the recovery of TT and P-TT was much slower than recovery of MVC, high energy phosphates, or pHi. These results suggest that the greater fall of TT and the delayed recovery following low-intensity exercise are caused by impaired excitation-contraction coupling.

Address correspondence and reprint requests to Dr. Miller, 3700 California Street (OPR 613), San Francisco, CA 94118.

Supported by a grant from the Muscular Dystrophy Association (to Dr. Miller), a grant from the National Institutes of Health (DK33923), and a Veterans Administration Medical Research Service Merit Review grant (to Dr. Weiner).

Presented in part³⁹ at the fortieth annual meeting of the American Academy of Neurology, Cincinnati, OH, April 1988.

Received August 16, 1988. Accepted for publication in final form April 5, 1989.

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