Exposure to hypoxia produces long-lasting sympathetic activation in humans

The relative contributions of hypoxia and hypercapnia. in causing persisten t sympathoexcitation after exposure to the combined stimuli were assessed i n nine healthy human subjects during wakefulness. Subjects were exposed to 20 min of isocapnic hypoxia (arterial O-2 saturation, 77-87%) and 20 min of normoxic hypercapnia (end-tidal PCO2, +5.3-8.6 Torr above eupnea) in rando m order on 2 separate days. The intensities of the chemical stimuli were ma nipulated 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; hype rcapnia: +5.8 +/- 1.7 l/min) but declined with continued exposure to hypoxi a and increased progressively during exposure to hypercapnia. Sympathetic a ctivity returned to baseline soon after cessation of the hypercapnic stimul us. In contrast, sympathetic activity remained above baseline after withdra wal of the hypoxic stimulus, even though blood gases had normalized and ven tilation returned to baseline levels. Consequently, during the recovery per iod, sympathetic burst frequency was higher in the hypoxia vs. the hypercap nia 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. Hypercapni a-evoked sympathetic activation is short-lived, whereas hypoxia-induced sym pathetic activation outlasts the chemical stimulus.