Our results indicate that in aged mice with Fabry disease, VR (a) induced exercise training adaptations, (b) increased Akt/AMPK/eNOS signaling pathways in the aorta, (c) increased plasma NO levels, but (d) did not improve endothelial dysfunction and systemic markers of oxidative stress in the aorta. This evidence concerns the gene NOS3 and endothelial dysfunction.