The muscle activity and specific training protocols can modulate the neuromuscular plasticity, but in general and in aged people in particular, doesn't ? produce only positive effects but also, and in particular the aerobic ones? a massive quantity of Reactive Oxygen Species (ROS) which interact with biologic macromolecules and therefore potentially able to cause metabolic-functional changes in muscle. There is increasing evidence and recognition that ROS are not merely damaging agents inflicting random destruction to the cell structure and function, but useful signalling molecules to regulate growth, differentiation, proliferation, and apoptosis, at least within the physiological concentration. Recent evidence indicate that apart from their well known harmful action, ROS could play a positive role as second messengers via stimulation a number of transcriptional programs as the activation of myogenic responses. This could be most important for satellite cells to regenerate the muscle successfully following damage. Changes in nitric oxide (NO) concentration facilitates not only the fusion of myoblasts in myotubes but it works also as a retrograde message in nerve-myotube co-cultures. Our previous papers revealed that in the human aged muscle, the oxidative damage to macromolecules as DNA and lipids increases but also the anti-oxidant properties of some enzymes as catalase and glutathione transferase decrease, determining an impaired redox balance, conditioning also the functional capacity of myofibres and changing the control of Ca2+ homeostasis. These findings have been found not only in mature muscle fibres, but also in satellite cells, although their quiescent state, and the stress oxidative status could contribute to the alteration of regenerative capacity of skeletal muscle in which these cells are resident.