Effects of Mild Hypobaric Hypoxia on Oxygen Saturation During Sleep

Overview

Ascent to altitude lowers oxygen saturation. In addition, sleep lowers oxygen saturation at any altitude. In a prior study, we observed that sleep at 8000 feet resulted in pronounced reduction in oxygen saturation, but did not result in reduced post sleep neurobehavioral performance or impaired sleep quality or quantity. We plan to do a more sophisticated physiological evaluation of the respiratory mechanisms responsible for the reduced oxygen saturation and determine if there are any adverse consequences to this level of intermittent hypoxia. We anticipate that central respiratory apnea is the physiologic mechanism, and that there will not be persistent changes in autonomic nervous activity measured by heart rate variability.

This study has 6 primary objectives/hypotheses: 1. Replicate findings of earlier study in which no effects of altitude were observed on post sleep neurobehavioral performance, sleep quantity or quality. 2. Determine if sleep at 6000 feet has effects similar to sleep at 8000 feet. 3. Identify if central or obstructive apnea is responsible for the reduction in oxygen saturation observed during sleep at 8000 feet. 4. Determine if respiratory abnormalities observed at 6000 feet are similar but less severe than at 8000 feet. 5. Determine if there are individual differences in respiratory physiology at sea level that enable prediction of pronounced respiratory disturbances during sleep at altitude. 6. Determine if changes in autonomic nervous activity, measured by heart rate variability, occur, and if so, do they persist for 8 hours. Twenty healthy males between 30 and 60 years of age whose baseline apnea-hypopnea index is less than 15/hour will be recruited from the general population surrounding Burnaby, British Columbia, Canada. Women are excluded because of the changes in sleep structure associated with the menstrual cycle. Participants will be involved in the blinded crossover study for a 14 day period during which time they will monitor their sleep by actigraphy and sleep diaries, will spend 2 nights an altitude chamber at Simon Fraser University at ambient barometric pressure to become adapted to sleeping in that environment, then spend 3 study nights, each followed by 2 rest nights, sleeping at barometric pressures equivalent to sea level, 6000 feet, and 8000 feet. The order of exposures will be randomly balanced. Pre study physiologic measures will include hypoxic ventilatory response, hypercapnic ventilatory response, and during one of the adaptation nights, apnea hypoxia index. Study sessions will consist of a 4 hour presleep period, a 6 hour sleep period, and a 1 hour post sleep period at the study barometric pressure. During the study sessions, heart rate, SpO2, polysomnographic measures, nasal air flow rates, and chest motion will be monitored and recorded. Psychomotor Vigilance Task response time will be measured before and after the sleep period. Heart rate will be recorded by ambulatory recording equipment for 8 hours following return to ambient barometric pressure conditions. This will be analyzed to determine if changes in heart rate variability are persistent. Outcomes of primary interest will include total sleep time, duration of sleep stages, oxygen saturation, heart rate and heart rate variability, respiratory rates, air flow, and chest motion to assess if central or obstructive apnea is temporally related to reductions in oxygen saturation.