Does NO/NOS play a role in mitochondrial biogenesis after exercise?
It has been shown that NO donors and analogues of the downstream messenger of NO, cGMP, increase mitochondrial biogenesis in muscle cells.53 Although nNOS is the major NOS isoform in skeletal muscle, both eNOS and nNOS isoforms are expressed within skeletal muscle fibers, with eNOS more abundant in oxidative, and nNOS more abundant in glycolytic skeletal muscles in rodents.12,54-56 NO production, total NOS activity and cGMP, increase during contraction in rodent skeletal muscle9,10,12 and may therefore be involved in the upregulation of mitochondrial biogenesis after exercise. We found that ingestion of the non-specific NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) for 2 days reduced basal skeletal muscle mitochondrial biogenesis but had no effect on the increase in mitochondrial biogenesis after an acute bout of exercise.57 Similarly, the increase in mitochondrial biogenesis markers in response to acute exercise and exercise training is intact in nNOS knock-out and eNOS knoc
