The project is divided in two sections: the formeris focused on the study of the relationship between the NO system, mitochondrial structure/activity and skeletal muscle wasting, paying attention on the role of autophagy and using a mouse model in which NOS1 (nNOSμ) is absent. My data demonstrate that an altered NO signaling leads to mitochondrial dysfunction resulting in enhanced autophagy and reduced muscle growth, however not associated with atrophy induction. Furthermore autophagy is essential to maintain muscle mass, but its role on regenerating population and its impact on muscle growth and development has not been evaluated yet. Starting form conclusion in the second part of my PhD project i focalized my attention on the role of autophagy specifically on satellite cells population, generating a transgenic mice in which autophagy is selectively inhibited in satellite cells and studying their impact on muscle growth. My data suggest that autophagy is involved in the controlling of satellite cells functions. Autophagy loss of function in satellite cells impairs their proliferation rate as well as their capability to fuse and differentiate. The study of these two different transgenic mice reveals as in muscle, unbalanced autophagy from the early phase of growth affects satellite cells population causing muscle wasting and suggests how during skeletal muscle development is important to have appropriate levels of autophagy.