Role of Nitric Oxide in Contraction Induced Glucose Transport

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Abstract
Nitric oxide (NO) is a vasoactive substance, which was first described as endothelium derived relaxing factor (EDRF). Subsequently, NO has been found to be a messenger molecule abundantly present in the nervous system. Functioning as a neurotransmitter in the peripheral nervous system, NO mediates an array of physiological functions such as gastrointestinal motility, regional blood flow, smooth muscle contraction, neuroendocrine activity and immune function. Recently NO biosynthesis has been found in skeletal muscle, where NO exerts an effect on both the metabolic and contractile processes. This review will focus on the actions of NO in skeletal muscle metabolism. NO donors have been shown to increase glucose transport in skeletal muscle. Inhibition of NOS activity blunts contraction-stimulated glucose transport but has no effect on insulin-stimulated glucose transport. NOS protein expression is enhanced by chronic exercise suggesting that NO may play a role in the improved glucose tolerance and increased insulin sensitivity characteristic of the trained state.