Involvement of nitric oxide synthase in skeletal muscle adaptation to chronic overload
The purpose of this study was to determine the necessity of nitric oxide (NO) for hypertrophy and fiber-type transition in overloaded (OL) skeletal muscle. Endogenous NO production was blocked by administering N G-nitro-l-arginine methyl ester (l-NAME; 0.75 mg/ml; ∼100 mg · kg−1 · day−1) in drinking water. Thirty-eight female Sprague-Dawley rats (∼250 g) were randomly divided into four groups: control-nonoverloaded (Non-OL), control-OL, l-NAME-Non-OL, andl-NAME-OL. Chronic overload of the plantaris was induced bilaterally by surgical removal of the gastrocnemius and soleus. Rats in the Non-OL groups received sham surgeries. l-NAME treatment began 24 h before surgery and continued until the rats were killed 14 days postsurgery. Although OL induced hypertrophy in both control (+76%) and l-NAME (+39%) conditions ( P < 0.05), mean plantaris-to-body mass ratio in thel-NAME-OL group was significantly lower ( P< 0.05) than that in the control-OL group. Microphotometric analysis of histochemically determined fiber types revealed increases in cross-sectional area ( P < 0.05) for all fiber types (types I, IIA, and IIB/X) in the OL plantaris from control rats, whereas l-NAME-OL rats exhibited increases only in type I and IIB/X fibers. SDS-PAGE analysis of myosin heavy chain (MHC) composition in the plantaris indicated a significant ( P< 0.05) OL effect in the control rats. Specifically, the mean proportion of type I MHC increased 6% ( P < 0.05), whereas the proportion of type IIb MHC decreased ∼9% ( P < 0.05). No significant OL effects on MHC profile were observed in the l-NAME rats. These data support a role of NO in overload-induced skeletal muscle hypertrophy and fiber-type transition.