Sarcolemma-localized nNOS is required to maintain activity after mild exercise

Yvonne M. Kobayashi, Erik P. Rader, Robert W. Crawford, Nikhil K. Iyengar, Daniel R. Thedens, John A. Faulkner, Swapnesh V. Parikh, Robert M. Weiss, Jeffrey S. Chamberlain, Steven A. Moore and Kevin P. Campbell ()
Additional contact information
Yvonne M. Kobayashi: Howard Hughes Medical Institute,
Erik P. Rader: Howard Hughes Medical Institute,
Robert W. Crawford: Howard Hughes Medical Institute,
Nikhil K. Iyengar: Department of Internal Medicine,
Daniel R. Thedens: Department of Radiology,
John A. Faulkner: University of Michigan, 2031 Biomedical Sciences Research Building, Ann Arbor, Michigan 48109-2200, USA
Swapnesh V. Parikh: Department of Internal Medicine,
Robert M. Weiss: Department of Internal Medicine,
Jeffrey S. Chamberlain: University of Washington School of Medicine, HSB, Room K243b, Seattle, Washington 98195-7720, USA
Steven A. Moore: University of Iowa, Roy J. and Lucille A. Carver College of Medicine, 4283 Carver Biomedical Research Building, 285 Newton Road, Iowa City, Iowa 52242-1101, USA
Kevin P. Campbell: Howard Hughes Medical Institute,

Nature, 2008, vol. 456, issue 7221, 511-515

Abstract: Signalling muscle fatigue Many neuromuscular conditions, such as Duchenne muscular dystrophy, involve an exaggerated exercise-induced fatigue response. Experiments in mice have identified a potential cause of this fatigue: when neuronal nitric oxide synthase (nNOS) is missing from its normal location on the muscle membrane, the blood vessels that supply the muscles fail to relax normally and the animals experience post-exercise fatigue. Sarcolemmal nNOS was found to be reduced in biopsies from patients with a range of distinct myopathies pointing towards a common mechanism of fatigue. These results suggest that patients with an exaggerated fatigue response to mild exercise may respond to treatment that improves exercise-induced signalling.

Date: 2008
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DOI: 10.1038/nature07414

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