Blanco, Cesar E.

Motor units in cat diaphragm and tibialis posterior muscles were classified physiologically as slow-twitch, fast-twitch, fatigue-resistant, fast-twitch fatigue-intermediate, or fast-twitch fatigable. Motor unit fibers were then identified by glycogen depletion and classified as type I, IIa, IIb, or IIx on the basis of myofibrillar adenosinetriphosphatase-staining profiles and immunoreactivity for myosin heavy-chain (MHC) isoforms. In both muscles, slow-twitch and fast-twitch fatigue-resistant units comprised type I and IIa fibers expressing MHC-slow and MHC-2A isoforms, respectively. Fast-twitch fatigue-intermediate and fast-twitch fatigable units comprised type IIx fibers expressing the MHC-2X isoform. Some fast-twitch fatigue-intermediate units had a mixed composition with a few fibers (approximately 10%) expressing the MHC-2A isoform. Motor unit fiber succinate dehydrogenase (SDH) activity was quantified, and variability was estimated by the interquartile range, which was lower among motor unit fibers than in adjacent fibers of the same histochemical type but comparable to that along the length of individual fibers. We conclude that, despite the mixed-MHC phenotype of some diaphragm and tibialis posterior motor units, SDH activity is relatively uniform. This supports the hypothesis that motoneurons exert a predominant influence on muscle fiber SDH activity.

The effect of chronic exogenous testosterone (T) treatment on neuromuscular transmission in the diaphragm (Dia) muscle of adult male rats was determined. The contribution of neuromuscular transmission failure (NTF) to Dia fatigue was evaluated by superimposing intermittent direct muscle stimulation on repetitive nerve stimulation of isometric contraction in vitro. T treatment significantly reduced the contribution of NTF to Dia fatigue by ∼20% ( P < 0.001). Fiber type-specific effects on NTF were determined by measuring Dia fiber glycogen levels subsequent to repetitive nerve or muscle stimulation. T treatment had no effect on glycogen depletion in Dia type I and IIa fibers regardless of stimulation route. In the control group, type IIx fibers demonstrated significantly less glycogen depletion after nerve stimulation compared with direct muscle stimulation ( P < 0.05), suggesting the presence of NTF. In contrast, T treatment increased glycogen depletion of type IIx fibers during nerve stimulation to levels similar to those after direct muscle stimulation. These data indicate that testosterone treatment substantially improves neuromuscular transmission in the Dia.

postnatal development. Both twitch contraction time and half-relaxation time decreased progressively with age. Correspondingly, the force-frequency curve was shifted to the left early in development compared with adults. The ratio of peak twitch force to maximum tetanic force decreased with age. Fatigue resistance of the diaphragm was highest at birth and then progressively decreased with age. At birth, most diaphragm muscle fibers stained darkly for myofibrillar adenosinetriphosphatase after alkaline preincubation and thus would be classified histochemically as type II. During subsequent postnatal development, the proportion of type I fibers (lightly stained for adenosinetriphosphatase) increased while the number of type II fibers declined. At birth, type I fibers were larger than type II fibers. The size of both fiber types increased with age, but the increase in cross-sectional area was greater for type II fibers. On the basis of fiber type proportions and mean cross-sectional areas, type I fibers contributed 15% of total muscle mass at birth and 25% in adults. Thus postnatal changes in diaphragm contractile and fatigue properties cannot be attributed to changes in the relative contribution of histochemically classified type I and II fibers. However, the possibility that these developmental changes in diaphragm contractile and fatigue properties correlated with the varying contractile protein composition of muscle fibers was discussed.