Aging normal and dystrophic mouse muscle: analysis of myogenicity in cultures of living single fibers.

In the early stages of Duchenne muscular dystrophy, chronic muscle degeneration is counterbalanced by regeneration whose progressive failure beyond the fifth year is attributed to an accelerated senescence associated with excessive myogenic cell division. This idea was tested by counting the numbers of myogenic cells accumulating over 90 h around individual living fibers isolated from muscles of dystrophic (mdx) and normal mice, 14-550 days of age. In cultures of normal muscle fibers, the number of myogenic cells per fiber decreased with increasing age of the animal. Cultures from young mdx mice exhibited an age-related increase in myogenic cell number, attaining at 50 days three times the number in control cultures. Thereafter, myogenic cell number progressively declined with animal age to control values. Thus, there is no evidence that extensive myoblast proliferation in young dystrophic mice-and, by association, in Duchenne muscular dystrophy patients-depletes their myogenic responsiveness in later life when they become weak and wasted.