Acute Exercise Increases Nitric Oxide Synthase Activity in Skeletal Muscle

Acute exercise increases nitric oxide synthase activity in skeletal muscle. Am.—This study examined the effects of acute exercise on skeletal muscle nitric oxide synthase (NOS) activity. Female Sprague-Dawley rats were divided into three groups: control, exercise, and exercise ϩ N G-nitro-L-arginine methyl ester (L-NAME). In the exercise ϩ L-NAME group, L-NAME was administered in the drinking water (1 mg/ml) for 2 days and subsequently the exercise and exercise ϩ L-NAME groups underwent a 45-min bout of exhaustive treadmill running after which NOS activity and muscle glycogen were measured. In the control and exercise groups, 1-amino-S-methylisothiourea (AMITU), a selective neuronal NOS inhibitor, with and without additional nonse-lective NOS blockade [with N G-monomethyl-L-arginine (L-NMMA)], was used in vitro to assess the contribution of nNOS to total NOS activity. The exercise bout increased NOS activity by 37% in exercise compared with control groups, and both groups had significantly greater NOS activity compared with exercise ϩ L-NAME. AMITU decreased total NOS activity in the control and exercise groups by 31.8 and 30.2%, respectively, and these activities were significantly greater than AMITU ϩ L-NMMA in both control and exercise groups. We conclude that 1) there is basal neuronal NOS and endothelial NOS activity in skeletal muscle, 2) an acute exercise bout increases NOS activity in skeletal muscle, and 3) glycogen depletion during exercise occurs irrespective of NOS activity. 1-amino-S-methylisothiourea; glycogen; muscle contraction NITRIC OXIDE (NO) is a signaling molecule formed from L-arginine by a number of different isoforms of nitric oxide synthase (NOS; Ref. 19). Both the neuronal NOS (nNOS) and the endothelial NOS (eNOS) isoforms are expressed in skeletal muscle (12, 13). nNOS is thought to be localized in the subsarcolemmal region of skeletal muscle and at the neuromuscular junction (12, 14), whereas eNOS is uniformly distributed in muscle fibers (13) as well as being located in the vessel wall. In addition, it has been demonstrated that both fast-and slow-twitch skeletal muscle can express both nNOS and eNOS protein (12, 13, 26). The quantity of the nNOS isoform appears to be related to the fiber-type distribution of a particular muscle, i.e., higher nNOS levels are associated with fast-twitch-glycolytic muscles (12). On the other hand, eNOS levels are associated with more oxidative muscles (13). Balon and Nadler (3) were the first to demonstrate an increase in NO release from muscles exposed to prior electrical stimulation. Prior exercise increases NO me-tabolite production (11), and NO concentrations …