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J Appl Physiol 96: 1033-1038, 2004. First published December 2, 2003; doi:10.1152/japplphysiol.00381.2003
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Influence of L-NAME on pulmonary O2 uptake kinetics during heavy-intensity cycle exercise

Andrew M. Jones,1 Daryl P. Wilkerson,1 Sally Wilmshurst,2 and Iain T. Campbell2

1Department of Exercise and Sport Science, Manchester Metropolitan University, Alsager ST7 2HL; and 2Department of Anaesthesia, Wythenshawe Hospital, Manchester M23 9LT, United Kingdom

Submitted 16 April 2003 ; accepted in final form 17 November 2003

We hypothesized that inhibition of nitric oxide synthase (NOS) by NG-nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial oxygen uptake (O2) by nitric oxide and result in a speeding of phase II pulmonary O2 kinetics at the onset of heavy-intensity exercise. Seven men performed square-wave transitions from unloaded cycling to a work rate requiring 40% of the difference between the gas exchange threshold and peak O2 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 O2 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 conditions (L) for baseline O2, the duration of phase I, or the amplitude of the primary O2 response. However, the time constant of the O2 response in phase II was significantly smaller (mean ± SE: C: 25.1 ± 3.0 s; L: 21.8 ± 3.3 s; P < 0.05), and the amplitude of the O2 slow component was significantly greater (C: 240 ± 47 ml/min; L: 363 ± 24 ml/min; P < 0.05) after L-NAME infusion. These data indicate that inhibition of NOS by L-NAME results in a significant (13%) speeding of O2 kinetics and a significant increase in the amplitude of the O2 slow component in the transition to heavy-intensity cycle exercise in men. The speeding of the primary component O2 kinetics after 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 O2 by nitric oxide. The cause of the larger O2 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.

respiratory; gas exchange



Address for reprint requests and other correspondence: A. M. Jones, Dept. of Exercise and Sport Science, Manchester Metropolitan Univ., Hassall Rd., Alsager, ST7 2HL, UK (E-mail: a.m.jones{at}mmu.ac.uk).




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