We tested the hypothesis that acute hypoxia may alter the circadian pattern of body temperature in adult humans. Six healthy subjects were studied in normoxia, hypoxia (approximately 13% inspired O(2)), and again normoxia, each session lasting >24 h and spaced a few days apart, with a constant routine protocol of sustained wakefulness and minimal activity. Some parameters (e.g., tympanic and abdominal temperatures, heart rate) were recorded continuously; others (e.g., oxygen consumption and pulmonary ventilation) were monitored for approximately 10 min every 2 h. The amplitudes of the circadian oscillation of tympanic, abdominal, and calf skin temperatures were reduced in hypoxia, averaging, respectively, 61%, 80% and 50% of the normoxic amplitude. Oxygen consumption and pulmonary ventilation, which presented a circadian pattern in normoxia, had no longer significant oscillations during hypoxia, whereas the opposite was the case for heart rate and diastolic pressure. Therefore, acute hypoxia can disturb the normal circadian patterns and, specifically, depress those of body temperature. These effects, qualitatively similar to those observed in chronically hypoxic animals and humans, could contribute to sleep disturbances at high altitude.

The aim of the present study was to determine whether or not voluntary breath-holding time (BHT) changes with the time of the day. BHT with airways closed at end-expiration was measured in six male subjects in the sitting position during the morning (08.00-12.00 hours, on days 1, 6, 7 and 8) and evening (20.00-24.00 hours, on days 2 and 4). BHT increased with the number of days of testing and, at day 8, the morning values averaged 160% of those on day 1. Also, Delta P ACO2 [the difference between end-tidal partial pressure of CO2 ( P CO2) and alveolar P CO2 ( P ACO2) at the breaking point] increased in proportion to BHT. Hence the BHT/Delta P ACO2 ratio remained nearly constant. Voluntary hyperventilation prolonged BHT and increased Delta P ACO2. Conversely, in hypoxia (13% O2 for 1-2 h), BHT and Delta P ACO2 were reduced proportionally. During the evening sessions, most of the BHT/Delta P ACO2 ratios in normoxia, hypoxia or after hyperventilation were higher than the corresponding morning values, with the group difference reaching statistical significance for the measurements in normoxia and hypoxia. In conclusion, voluntary BHT varies in both duration and its relationship with Delta P ACO2 between the morning and evening hours. The results should also imply that, with an interruption of breathing, changes in alveolar and arterial gases are not the same at different times of the day.