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1 Physiology, The University of Melbourne, Parkville, Victoria, Australia
* To whom correspondence should be addressed. E-mail: gdwadley{at}unimelb.edu.au.
The purpose of this study was to determine if nitric oxide synthase (NOS) inhibition decreased basal and exercise-induced skeletal muscle mitochondrial biogenesis. Male Sprague-Dawley rats were assigned to one of four treatment groups: NOS inhibitor NG-nitro-L-arginine methyl ester (LNAME, ingested for 2 days in drinking water, 1mg/ml) followed by acute exercise, no LNAME ingestion and acute exercise, rest plus LNAME, and rest without LNAME. The exercised rats ran on a treadmill for 53 ± 2 min and were then killed four hr later. NOS inhibition significantly (p<0.05; main effect) decreased basal PGC1
mRNA levels and tended (p=0.08) to decrease mtTFA mRNA levels in the soleus, but not the EDL muscle. This coincided with significantly reduced basal levels of cytochrome oxidase (COX) I and COX IV mRNA, COX IV protein and COX enzyme activity following NOS inhibition in the soleus, but not the EDL muscle. NOS inhibition had no effect on citrate synthase or
HAD activity, or cytochrome c protein abundance in the soleus or EDL. NOS inhibition did not reduce the exercise-induced increase in PGC1
mRNA in the soleus or EDL. In conclusion, inhibition of NOS appears to decrease some aspects of the mitochondrial respiratory chain in the soleus under basal conditions, but does not attenuate exercise-induced mitochondrial biogenesis in the soleus or in the EDL.
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