Exercise protection in models of DM has been linked to normalization of nitro-oxidative stress and eNOS control [146], and improvements in PPARγ coactivator-1α and Akt signaling [521], both effects that may arise via restoration of sarcolemmal caveolae and caveolin control of eNOS [250, 275, 296–298] and Akt signaling [250–252, 299]. This evidence concerns the gene NOS3 and diabetes mellitus.