Both hypoxia and work are required to enhance expression of myoglobin in skeletal muscle. Focus on “Hypoxia reprograms calcium signaling and regulates myoglobin expression”

摘要

Myoglobin is expressed adaptively in muscle. In very young animals, and in the absence of muscle work, the myoglobin concentration in muscles remains very small. What factors lead to myoglobin genesis? Millikan (7) assembled a convincing body of observational and experimental evidence that sustained hard work is required for myoglobin expression. In 1962, Reynafarje (8) showed that life at high altitude favors high concentration of myoglobin in skeletal muscles of humans and small mammals. For a long time, the import of Reynafarjes findings was obscured by apparently contradictory studies showing that low oxygen pressure alone is not a sufficient stimulus for myoglobin expression. Now, Kanatous et al. (5), in the article under discussion, resolve this issue by showing that during hypoxia, myoglobin is elevated in the working heart, but not in the relatively idle skeletal musculature, of mice exposed to prolonged hypoxia. They conclude from their studies that hypoxia alone does not stimulate myoglobin expression, but that hypoxia in consort with repetitive contraction, exactly the conditions obtaining in the muscles of people residing at high altitude, does stimulate myoglobin genesis.