Exposure to hypoxia produces long-lasting sympathetic activation in humans.
Xie, Ailiang, James B. Skatrud, Dominic S. Puleo, and Barbara J. Morgan.
Departments of 1Medicine and 2Surgery, University of Wisconsin, and Middleton Memorial Veterans Hospital, Madison, Wisconsin 53705
APStracts 8:0329A, 2001.
The relative contributions of hypoxia and hypercapnia in causing persistent sympathoexcitation after exposure to the combined stimuli were assessed in nine healthy human subjects during wakefulness. Subjects were exposed to 20 min of isocapnic hypoxia (arterial O2 saturation, 77-87%) and 20 min of normoxic hypercapnia (end-tidal "pco2", +5.3-8.6 Torr above eupnea) in random order on 2 separate days. The intensities of the chemical stimuli were manipulated in such a way that the two exposures increased sympathetic burst frequency by the same amount (hypoxia: 167 ± 29% of baseline; hypercapnia: 171 ± 23% of baseline). Minute ventilation increased to the same extent during the first 5 min of the exposures (hypoxia: +4.4 ± 1.5 l/min; hypercapnia: +5.8 ± 1.7 l/min) but declined with continued exposure to hypoxia and increased progressively during exposure to hypercapnia. Sympathetic activity returned to baseline soon after cessation of the hypercapnic stimulus. In contrast, sympathetic activity remained above baseline after withdrawal of the hypoxic stimulus, even though blood gases had normalized and ventilation returned to baseline levels. Consequently, during the recovery period, sympathetic burst frequency was higher in the hypoxia vs. the hypercapnia trial (166 ± 21 vs. 104 ± 15% of baseline in the last 5 min of a 20-min recovery period). We conclude that both hypoxia and hypercapnia cause substantial increases in sympathetic outflow to skeletal muscle. Hypercapnia-evoked sympathetic activation is short-lived, whereas hypoxia-induced sympathetic activation outlasts the chemical stimulus.
Received 13 March 2001; accepted in final form 21 May 2001
APS Manuscript Number A234-1.
Article publication pending J Appl Physiol
ISSN 1080-4757 Copyright 2001 The American Physiological Society.
Published in APStracts on 29 June 2001