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Acute exercise increases nitric oxide synthase activity in skeletal muscle
C K Roberts1, R J Barnard, A Jasman
1Department of Physiological Science, University of California, Los Angeles 90024, California, USA.
The American Journal of Physiology
|August 13, 1999
Summary
Acute exercise boosts skeletal muscle nitric oxide synthase (NOS) activity, with neuronal and endothelial NOS contributing. Glycogen depletion during exercise occurs independently of NOS activity.
Area of Science:
- Physiology
- Biochemistry
- Exercise Science
Background:
- Skeletal muscle nitric oxide synthase (NOS) plays a role in various physiological processes.
- Understanding the impact of acute exercise on NOS activity is crucial for exercise physiology.
Purpose of the Study:
- To investigate the effects of acute exercise on skeletal muscle NOS activity.
- To determine the contribution of neuronal NOS (nNOS) and endothelial NOS (eNOS) to total NOS activity in skeletal muscle.
- To examine the relationship between NOS activity and muscle glycogen depletion during exercise.
Main Methods:
- Rats were divided into control, exercise, and exercise + L-NAME groups.
- Exhaustive treadmill running was performed by exercise groups.
- NOS activity and muscle glycogen were measured, with selective and nonselective NOS inhibitors used in vitro.
Main Results:
- Acute exercise increased skeletal muscle NOS activity by 37% compared to controls.
- Both neuronal NOS (nNOS) and endothelial NOS (eNOS) contribute to basal and exercise-induced NOS activity.
- Muscle glycogen depletion occurred regardless of NOS activity levels.
Conclusions:
- Skeletal muscle possesses both basal neuronal NOS and endothelial NOS activity.
- An acute bout of exercise enhances skeletal muscle NOS activity.
- Glycogen depletion during exercise is independent of NOS activity.