Neurocirculatory consequences of intermittent asphyxia in humans

We examined the neurocirculatory and ventilatory responses to intermittent asphyxia (arterial O-2 saturation = 79-85%, end-tidal Pco(2) = 3-5 Torr abo ve eupnea) in seven healthy humans during wakefulness. The intermittent asp hyxia intervention consisted of 20-s asphyxic exposures alternating with 40 -s periods of room-air breathing for a total of 20 min. Minute ventilation increased during the intermittent asphyxia period (14.2 +/-. 2.0 l/min in t he final 5 min of asphyxia vs. 7.5 +/- 0.4 l/min in baseline) but returned to the baseline level within 2 min after completion of the series of asphyx ic exposures. Muscle sympathetic nerve activity increased progressively, re aching 175 +/- 12% of baseline in the final 5 min of the intervention. Unli ke ventilation, sympathetic activity remained elevated for at least 20 min after removal of the chemical stimuli (150 +/- 10% of baseline in the last 5 min of the recovery period). Intermittent asphyxia caused a small, but st atistically significant, increase in heart rate (64 +/- 4 beats/min in the final 5 min of asphyxia vs. 61 +/- 4 beats/min in baseline); however, this increase was not sustained after the return to room-air breathing. These da ta demonstrate that relatively short-term exposure to intermittent asphyxia causes sympathetic activation that persists after removal of the chemical stimuli. This carryover effect provides a potential mechanism whereby inter mittent asphyxia during sleep could lead to chronic sympathetic activation in patients with sleep apnea syndrome.