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We examined the magnitude of the hypoxic metabolic response in golden-mantled ground squirrels to determine whether the shift in thermoregulatory set point (T(set)) and subsequent fall in body temperature (T(b)) and metabolic rate observed in small mammals were greater in a species that routinely experiences hypoxic burrows and hibernates. We measured the effects of changing ambient temperature (T(a); 6--29 degrees C) on metabolism (O(2) consumption and CO(2) production), T(b), ventilation, and heart rate in normoxia and hypoxia (7% O(2)). The magnitude of the hypoxia-induced falls in T(b) and metabolism of the squirrels was larger than that of other rodents. Metabolic rate was not simply suppressed but was regulated to assist the initial fall in T(b) and then acted to slow this fall and stabilize T(b) at a new, lower level. When T(a) was reduced during 7% O(2), animals were able to maintain or elevate their metabolic rates, suggesting that O(2) was not limiting. The slope of the relationship between temperature-corrected O(2) consumption and T(a) extrapolated to a T(set) in hypoxia equals the actual T(b). The data suggest that T(set) was proportionately related to T(a) in hypoxia and that there was a shift from increasing ventilation to increasing O(2) extraction as the primary strategy employed to meet increasing metabolic demands under hypoxia. The animals were neither hypothermic nor hypometabolic, as T(b) and metabolic rate appeared to be tightly regulated at new but lower levels as a result of a coordinated hypoxic metabolic response.

No reports are available about the role of central adenosine in the respiratory and thermoregulatory responses to hypoxia in conscious rats. We therefore measured ventilation (VE) and body temperature (Tb) before and after intracerebroventricular injection of saline or aminophylline (adenosine antagonist), followed by a 30-min period of hypoxia exposure. Aminophylline did not change VE or Tb during normoxia; however, during hypoxia, it caused a significant increase in VE, and significantly attenuated hypoxic hypothermia. The present data indicate that central adenosine has an inhibitory effect on hypoxic hyperventilation and partially causes hypoxic hypothermia, suggesting that the ventilatory and metabolic interaction during hypoxia does not involve opposing mechanisms.