Without intervention following spinal cord injury (SCI), paralyzed skeletal muscles undergo myofiber atrophy and slow-to-fast myofiber type transformations. We hypothesized that chronic spasticity-associated neuromuscular activity post-SCI would promote recovery from such deleterious changes. We examined segmental tail muscles of (1) chronic spinal rats with long-standing tail spasticity (7 months post-sacral spinal cord transection; older chronic spinals), (2) chronic spinal rats that experienced less spasticity early post-injury (young chronic spinals), and (3) rats without spasticity post-transection with bilateral deafferentation (spinal isolated). These were compared to tail muscles of age-matched normal rats. Using immunohistochemistry, we observed myofiber distributions of 15.9±3.5% type I, 18.7±10.7% type IIA, 60.8±12.6% type IID(X), and 2.3±1.3% type IIB in young normals, which were not different in older normals. Young chronic spinals demonstrated transformations toward faster myofibers with decreased type I and increased type IID(X), paralleled by substantial myofiber atrophy compared to young normals. Spinal isolated rats also demonstrated decreased type I myofiber proportions, increased type II myofiber proportions, and severe myofiber atrophy. Following 4 months of complete spasticity (older chronic spinals), myofiber transformations were reversed, with no significant differences in type I, IIA, IID(X), or IIB proportions compared to age-matched normals. Moreover, following this prolonged spasticity, type I, IIA, and IIB myofibers recovered from atrophy, and type IID(X) myofibers partially recovered. Our results indicate that, early post-transection or after long-term spinal isolation, relatively inactive myofibers atrophy and transform toward faster myofibers. However, long-term spasticity apparently produces neuromuscular activity that promotes recovery of myofiber types and myofiber sizes.