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Blockade of myostatin/ActRIIB signaling has been proposed as a therapeutic strategy for Duchenne muscular dystrophy (DMD) because of its supposed stimulating effect on skeletal muscle size and function. Here we show that constitutive lack of myostatin in Mstn−/− mice resulted in increased muscle fatigability, decreased exercise performance, exercise-induced abnormal lactic acidemia and decreased mitochondrial...
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