Oxidative stress in the respiratory response to intermittent hypoxia in athletes and sleep apnea patients: similar mechanisms but opposite outcomes

The overproduction of reactive oxygen species (ROS) observed in response to intermittent hypoxia may either trigger adaptive physiological processes or play a role in mechanisms leading pathological situation such as respiratory disturbance. In a series of articles, we report that this ROS increase is likely involved in beneficial or detrimental adaptations depending to the intensity of the hypoxic stimulus and on the health state of the subject. In this context, oxidative stress appears to play a role in the signalling process that controls the hypoxia inducible factor 1 (HIF‐1). Although ROS is needed for stabilization of HIF‐1α, we demonstrated in humans submitted to moderate hypoxia, that ROS may also be involved in the increase of HIF‐1α transcription. Then, we observed in athletes that the ventilatory acclimatization to hypoxia after intermittent altitude training was improved by elevated oxidative stress through a stimulation of HIF‐1α pathway. Conversely, by exposing healthy subjects to chronic intermittent hypoxia simulating obstructive sleep apnoea (OSA), we reported that oxidative stress increased hypoxic ventilatory responses to hypoxia. This increase could promote unstable breathing and thereby might perpetuate OSA as it was previously suggested. Founded by International Olympic Committee, Alberta Heritage Foundation for Medical Research and Canadian Institutes of Health Research