[Neuronal NO-synthase as the molecular guard of myofiber stability. NO-dependent signaling pathways in the active and unloaded muscle].

The review is dedicated to the signaling pathways triggered by the nitric oxide II in skeletal muscle. Analysis of the current literature shows that during physical exercise of various intensity and regimen the nitric oxide is an essential trigger of the signaling pathways, leading to the alteration of the structural and metabolic myofiber profile and enhancement of its functional capacity. At the same time during the elevated muscle contractile activity (for instance, eccentric activity), NO serves as a protective and stabilizing agent, preventing from the intensification of the proteolytic processes. Data obtained from the experiments with the modulation of the NO at the background of the functional (gravitational) unloading give evidence that neuronal NO synthase activation in this experimental conditions allows to stabilize the degradation pathways and prevent from disuse atrophy development.