Résumé
This study examined the aerobic running performance of myostatin-deficient aged mice (Mstn-/-), a hypermuscular genetic model. Next, the effects of activating AMP-activated protein kinase on aerobic exercise performance was analysed by 4-weeks treatment of 5-aminoimidazole-4-carboxamide (AICAR), a known inducer of mitochondrial biogenesis. The results showed reduced aerobic running performance in mstn-deficient aged mice, especially in endurance. AICAR treatment induced no significant improvement in aerobic exercise parameters in mice, but reduced differences in endurance capacity between Mstn-/-and Mstn +/+. Biological analysis are currently in process to identify the mitochondria mechanisms involved.