Nitric oxide is produced within skeletal muscle fibres and has various functions in skeletal muscle. There is evidence that NO may be essential for normal increases in skeletal muscle glucose uptake during contraction/exercise. Although there have been some discrepant results, it has been consistently demonstrated that inhibition of NO synthase (NOS) attenuates the increase in skeletal muscle glucose uptake during contraction in mouse and rat muscle ex vivo, during in situ contraction in rats and during exercise in humans. The NO-mediated increase in skeletal muscle glucose uptake during contraction/exercise is probably due to the modulation of intramuscular signalling that ultimately increases glucose transporter 4 (GLUT4) translocation and is, surprisingly, independent of blood flow. In this review, we discuss the evidence for and against a role of NO in regulating skeletal muscle glucose uptake during contraction/exercise and outline the possible mechanism(s) involved. Emerging findings regarding the role of neuronal NOS mu (nNOSμ) in this process are also discussed.
Epiglottic entrapment is a condition in racing horses, associated with abnormal respiratory noises and exercise intolerance. Epiglottic entrapment has been linked to both poor and superior athletic performance, leading to concerns regarding whether surgery is indicated, and whether surgical correction may have a deleterious effect on future race performance. The objective of the current study was to assess the race-day performance of horses racing with epiglottic entrapment and the effect of surgical correction on performance outcomes using an intra-oral technique in anaesthetised horses. A case-control study was conducted at the Singapore Turf Club from 2008 to 2011. Controls were selected 1:1 to cases, based on Malaysian Racing Authority number. The performance of horses racing with epiglottic entrapment was recorded and post-surgery race performance was described. Further, post-surgery race performance was compared between cases and with non-case controls. Twenty horses raced with epiglottic entrapment were retrospectively enrolled. There was a significant difference in racing performance in case horses racing with and without epiglottic entrapment (P
This study investigated effects of cessation of exercise and honey supplementation on bone properties in young female rats. Eighty-four 12-week-old Sprague-Dawley female rats were divided into 7 groups: 16S, 16J, 16H, 16JH, 8J8S, 8H8S, and 8JH8S (8 = 8 weeks, 16 = 16 weeks, S = sedentary without honey supplementation, H = honey supplementation, and J = jumping exercise). Jumping exercise consisted of 40 jumps/day for 5 days/week. Honey was given to the rats at a dosage of 1 g/kg body weight/rat/day via force feeding for 7 days/week. Jumping exercise and honey supplementation were terminated for 8 weeks in 8J8S, 8H8S, and 8JH8S groups. After 8 weeks of cessation of exercise and honey supplementation, tibial energy, proximal total bone density, midshaft cortical moment of inertia, and cortical area were significantly higher in 8JH8S as compared to 16S. Continuous sixteen weeks of combined jumping and honey resulted in significant greater tibial maximum force, energy, proximal total bone density, proximal trabecular bone density, midshaft cortical bone density, cortical area, and midshaft cortical moment of inertia in 16JH as compared to 16S. These findings showed that the beneficial effects of 8 weeks of combined exercise and honey supplementation still can be observed after 8 weeks of the cessation and exercise and supplementation.
Inhibition of nitric oxide synthase (NOS) significantly attenuates the increase in skeletal muscle glucose uptake during contraction/exercise, and a greater attenuation is observed in individuals with Type 2 diabetes compared with healthy individuals. Therefore, NO appears to play an important role in mediating muscle glucose uptake during contraction. In this study, we investigated the involvement of neuronal NOSμ (nNOSμ), the main NOS isoform activated during contraction, on skeletal muscle glucose uptake during ex vivo contraction. Extensor digitorum longus muscles were isolated from nNOSμ(-/-) and nNOSμ(+/+) mice. Muscles were contracted ex vivo in a temperature-controlled (30°C) organ bath with or without the presence of the NOS inhibitor N(G)-monomethyl-l-arginine (L-NMMA) and the NOS substrate L-arginine. Glucose uptake was determined by radioactive tracers. Skeletal muscle glucose uptake increased approximately fourfold during contraction in muscles from both nNOSμ(-/-) and nNOSμ(+/+) mice. L-NMMA significantly attenuated the increase in muscle glucose uptake during contraction in both genotypes. This attenuation was reversed by L-arginine, suggesting that L-NMMA attenuated the increase in muscle glucose uptake during contraction by inhibiting NOS and not via a nonspecific effect of the inhibitor. Low levels of NOS activity (~4%) were detected in muscles from nNOSμ(-/-) mice, and there was no evidence of compensation from other NOS isoform or AMP-activated protein kinase which is also involved in mediating muscle glucose uptake during contraction. These results indicate that NO regulates skeletal muscle glucose uptake during ex vivo contraction independently of nNOSμ.