Artificial increase in mitochondrial contents by muscle-specific overexpression of PGC-1α without exercise plays a role in the initial development of glucose intolerance induced by high-fat diet feeding and in the activation of autophagy formation, but does not contribute to exercise adaptation, whereas the physical activity of voluntary wheel running increases wheel distance run and improves glucose tolerance induced by lipid overload, which is associated with a greater LCII/LC3I ratio of autophagosome regardless of PGC-1α content [94]. This evidence concerns the gene PPARGC1A and Glucose intolerance.