Hypoxic depression of circadian rhythms in adult rats

Because the circadian rhythms of oxygen consumption ((V) over dotO(2)) and body temperature (T-b) could be contributed to by differences in thermogene sis and because hypoxia depresses thermogenesis in its various forms, we te sted the hypothesis that hypoxia blunts the normal daily oscillations in (V ) over dotO(2) and T-b. Adult rats were instrumented for measurements of T- b and activity by telemetry; (V) over dotO(2) was measured by an open-flow method. Animals were exposed to normoxia (21% O-2), hypoxia (10.5% O-2), an d normoxia again, each 1 wk in duration, in either a 12:12-h light-dark cyc le ("synchronized") or constant light ("free running"). In this latter case , the period of the cycle was similar to 25 h. In synchronized conditions, hypoxia almost eliminated the T-b circadian oscillation, because of the blu nting of the T-b rise during the dark phase. On return to normoxia, T-b rap idly increased toward the maximum normoxic values, and the normal cycle was then reestablished. In hypoxia, the amplitude of the activity and (V) over dotO(2) oscillations averaged, respectively, 37 and 56% of normoxia. In fr ee-running conditions, on return to normoxia the rhythm was reestablished a t the expected phase of the cycle. Hence, the action of hypoxia was not on the clock itself but probably at the hypothalamic centers of thermoregulati on. Hyperoxia (40% O-2) or hypercapnia (3% CO2) had no significant effects on circadian oscillations, indicating that the effects of hypoxia did not r eflect an undifferentiated response to changes in environmental gases. Modi fications of the metabolism and T-b rhythms during hypoxia could be at the origin of sleep disturbances in cardiorespiratory patients and at high alti tude.