Muscle is a plastic tissue that responds and adapts to en- tor of mitochondrial biogenesis [8], seems to control Skeletal Muscle

Full list of author information is available at the end of the articlevironmental changes [1]. Energy balance is one of the checkpoints between muscle growth/hypertrophy and protein breakdown [2], and>10 % of atrophy-related genes are directly involved in energy production [3-5]. Mitochondrial dysfunction activates various proteolytic systems [2] and is associated with muscle atrophy in sev-eral myopathies [6,7]. Peroxisome proliferator-activated muscle wasting [3]. PGC-1α overexpression increases mitochondrial content [9] and resistance to fatigue [9] and reduces the rapid muscle atrophy associated with denervation, fasting, and FoXO 3 activation [3]. Re-cently, mice overexpressing PGC-1α have been shown to have an increased lifespan and to be protected from sar-copenia [10]. Therefore, targeting mitochondrial biogen-esis and metabolism up-regulation may have beneficial effects in muscle diseases. Evidence for the beneficial effects of submaximal aer-obic activities in DMD patients is slowly emerging. A re