Mitochondria, main energy sources of the cells, are causes and targets of increased oxidative stress which plays a key role in peripheral artery disease and ischemia-reperfusion(IR)-induced muscular impairments. Here, we will synthetize data from several experiments. Rats were randomized to control, IR (clamping of the infra-renal aorta for 3 h followed by 2 h of reperfusion), and IR+ pre- or postconditioning groups. Complexes I, II, III and IV activities of the mitochondrial respiratory chain were measured using glutamate-malate (Vmax), succinate (Vsucc) and TMPD-ascorbate(VTMPD) in gastrocnemius permeabilized fibers. Superoxide anion production was assessed by dihydroethidium (DHE) staining. IR significantly reduced maximal oxydative capacity (Vmax, -26%, p<0.05), complexe II, III and IV activities (Vsucc, -28%, p<0.05) and complexe IV activity (VTMPD, -25%). IR increased dihydroethidium (DHE) staining (+200%, p<0.05). Pre- and post-conditioning similarly counteracted these deleterious effects, increasing mitochondrial complexes activities and restoring muscle DHE staining. Aortic cross clamping induces muscle mitochondrial dysfunction and reactive oxygen species overproduction. Both pre- and post-conditioning protect skeletal muscle mitochondria, likely by reducing oxidative stress and preserving antioxidant defence. Whether this approach targeted toward mitochondria might reduce patients morbidity during major vascular surgeries deserve further investigations.