Lessons from chronic intermittent and sustained hypoxia at high altitudes.

Recurrent sleep apnea (RSA), mimicking chronic intermittent hypoxia (CIH), may trigger unique adaptations in oxygen sensing in the carotid body, and consequent cellular functions unlike the effects of sustained hypoxia (SH). As a mechanism, an augmented generation of reactive oxygen species (ROS) in CIH has been invoked at the exclusion of SH effects. The ROS might act at hypoxia inducible factors (HIF-1s), giving rise to various genes whose function is to restore the tissue P(O(2)) close to the original. In a spate, review articles on the CIH effects at sea level have appeared but little on high altitude (HA). Their views have been reexamined with the primary focus on the peripheral chemoreception. At HA, RSA is more common in the lowlanders because of a high ventilatory sensitivity to hypoxia (with the consequent effects) unlike the high altitude natives (HAN). Undoubtedly, the HIF-1s play a central role at HA, the mechanisms of which are unknown and explorable.