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Influence of nitric oxide synthase inhibition on pulmonary O 2 uptake kinetics during supra‐maximal exercise in humans
Author(s) -
Wilkerson Daryl P.,
Campbell Iain T.,
Jones Andrew M.
Publication year - 2004
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2004.071894
Subject(s) - nitric oxide , nitric oxide synthase , kinetics , medicine , chemistry , ventilatory threshold , incremental exercise , endocrinology , saline , heart rate , vo2 max , cardiology , blood pressure , physics , quantum mechanics
We have recently reported that inhibition of nitric oxide synthase (NOS) with N G ‐nitro‐ l ‐arginine methyl ester ( l ‐NAME) accelerates the ‘phase II’ pulmonary O 2 uptake kinetics following the onset of moderate and heavy intensity submaximal exercise in humans. These data suggest that the influence of nitric oxide (NO) on mitochondrial function is an important factor in the inertia to aerobic respiration that is evident in the transition from a lower to a higher metabolic rate. The purpose of the present study was to investigate the influence of l ‐NAME on pulmonary kinetics following the onset of supra‐maximal exercise, where it has been suggested that O 2 availability represents an additional limitation to kinetics. Seven healthy young men volunteered to participate in this study. Following an incremental cycle ergometer test for the determination of , the subjects returned on two occasions to perform a ‘step’ exercise test from a baseline of unloaded cycling to a work rate calculated to require 105%, preceded either by systemic infusion of l ‐NAME (4 mg kg −1 in 50 ml saline) or 50 ml saline as a control (Con). Pulmonary gas exchange was measured on a breath‐by‐breath basis throughout the exercise tests. The duration of ‘phase I’ was greater with l ‐NAME (Con: 14.0 ± 2.1 versus l ‐NAME: 16.0 ± 1.6 s; P = 0.03 ), suggestive of a slower cardiovascular adaptation following the onset of exercise. However, the phase II time constant was reduced by 44% with l ‐NAME (Con: 36.3 ± 17.3 versus l ‐NAME: 20.4 ± 8.3 s; P = 0.01 ). The accumulation of blood lactate during exercise was also reduced with l ‐NAME (Con: 4.0 ± 1.1 versus l ‐NAME: 2.7 ± 2.1 m m ; P = 0.04 ). These data indicate that skeletal muscle NO production represents an important limitation to the acceleration of oxidative metabolism following the onset of supra‐maximal exercise in humans.