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1 Dept Exercise and Sport Science, Manchester Metropolitan University, Alsager, Cheshire, United Kingdom
2 Dept Anaesthesia, Wythenshawe Hospital, Manchester, Cheshire, United Kingdom
* To whom correspondence should be addressed. E-mail: a.m.jones{at}mmu.ac.uk.
We hypothesised that inhibition of nitric oxide synthase (NOS) by nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial VO2 by nitric oxide and result in a speeding of phase II pulmonary VO2 kinetics at the onset of heavy intensity exercise. Seven males performed square-wave transitions from unloaded cycling to a work rate requiring 40% of the difference between the gas exchange threshold and VO2 peak with and without prior intravenous infusion of L-NAME (4 mg/kg in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath-by-breath and VO2 kinetics were determined from the averaged response to two exercise bouts performed in each condition. There were no significant differences between the control (C) and L-NAME (L) conditions for baseline VO2, the duration of phase I, or the amplitude of the primary VO2 response. However, the time constant of the VO2 response in phase II was significantly smaller (mean ± SEM C: 25.1 ± 3.0 vs. L: 21.8 ± 3.3 s; P<0.05) and the amplitude of the VO2 slow component was significantly greater (C: 240 ± 47 vs. L: 363 ± 24 ml.min-1; P < 0.05) following L-NAME infusion. These data indicate that inhibition of NOS by L-NAME results in a significant (13 %) speeding of phase II VO2 kinetics and a significant increase in the amplitude of the VO2 slow component in the transition to heavy intensity cycle exercise in man. The speeding of the phase II VO2 kinetics following L-NAME infusion indicates that at least part of the intrinsic inertia to oxidative metabolism at the onset of heavy intensity exercise may result from inhibition of mitochondrial VO2 by nitric oxide. The cause of the larger VO2 slow component amplitude with L-NAME requires further investigation but may be related to differences in muscle blood flow early in the rest-to-exercise transition.
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