Abstract
Exposure to 0.05 mm 2,4-dinitrophenol (DNP), 1 mm NaN3, and 1 mm KCN reveals the following differences between normal and dystrophic excised, curarized gastrocnemius muscles of mice of strain 129. DNP briefly enhances twitch but not tetanus tension in rested dystrophic mice before depressing both tensions. In rested normal mice these tensions decline immediately. NaN3 reduces tensions in rested normal mice for 30 min; slow recovery follows. Half-relaxation rate is also reduced. In rested dystrophic mice tension does not recover from depression in NaN3, and the relaxation rate increases. During fatigue, tension output in dystrophic declines less rapidly than in normal mice, regardless of inhibitors. NaN3 accentuates fatigue-associated increases of contraction rate in dystrophic mice, but accelerates the usual reduction of this rate in normal ones. The two muscle groups also show quantitative differences in their responses to the inhibitors. Except for some DNP effects, all changes are reversible. Known actions of the inhibitors account only inadequately for these observations, and no clearly identifiable metabolic lesions of dystrophic muscles emerge.