1NMR Laboratory, Institute of Myology, F-75651 Paris, France; 2CEA, IBM, MIRCen, IdM NMR Laboratory, F-75651 Paris, France; 3Unite de Diabetologie et Nutrition, Universite Catholique de louvain, B-1200 Brussels, Belgium
Inhibiting myostatin (mstn) causes spectacular increase in muscle mass, and has opened the path to therapeutic approaches. Yet possible compromised force production have been reported in isolated muscle. We investigated vascular and metabolic response to exercise in vivo in mstn-/- and wild-type mice using interleaved arterial spin labeling NMR imaging and 31P spectroscopy. Specific force and maximum perfusion were identical. Mitochondrial oxidative capacities were reduced in mstn-/-, while hyperemia was prolonged. These integrated results formed coherent evidence of a non-pathologic shift towards a more glycolytic metabolism in this model as was confirmed by histology.