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1 Department of Kinesiology, Texas Woman's University, Denton, Texas 76201; and 2 Center for Exercise Science, University of Florida, Gainesville, Florida 32611
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
NG-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, and
L-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 the L-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.
rat; plantaris; compensatory hypertrophy; NG-nitro-L-arginine methyl ester; fiber type
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