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  There is increasing evidance that nitric oxide (NO) is an important hemodynamic and metabolic regulator during the performance of physical activity. Futhermore, there are adaptations in this system as a result of exercise training that likely contribute to increased functional capacity and the cardioprotective effects associated with higher fitness levels. Exercise has particular efficacy in restoring dysfunction of the vascular endotherial NO system, which is becoming established as a precursor to the atherosclerotic process.
  The production of NO from L-arginine is catalysed by the nitric oxide synthase (NOS), which involves NOS Ⅰ, NOS Ⅱ, and NOS Ⅲ, NO has been implicated in such diverse processes as vasodilation, inhibition of platelet aggregation, immune function, cell growth, neurotransmission, metabolic regulation and excitation-contraction coupling. The vast animal literature, together with more recent human studies, indicates that endurance exercise training for a period ranging from days to several weeks enhances basal release of NO from aorta, active and inactive muscle and coronary arteries. This adaptation may contribute to the reduction in resting blood pressure and increase in blood flow to skeletal muscle. Also, NO system is modified by training in the setting of cardiovascular disease in humans and that these effects may contribute to increased functional capacity. Recent animal study data also suggest that this benefit may extend to skeletal muscle NO, which appears, among other functions, to mediate glucose uptake during exercise. However, the role of NO in the coronary circulation and skeletal muscle, particularly with regard to glucose uptake, is yet to be elucidated.

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