SLAPNEA

Humans sleeping at high altitude (HA) commonly experience periodic breathing (PB), characterized by apneas alternating with periods of hyperventilation. PB is a consequence of the increased pulmonary ventilation at HA, which reduces arterial CO2 tension (PaCO2) towards the apneic threshold. During sleep, a small further PaCO2 reduction triggers an apnea, followed by an exaggerated hyperventilation that reverts PaCO2 below the apneic threshold and initiates the next apnea.
We aim to investigate whether PB contributes to maladaptive responses to HA that are currently incompletely understood, namely activation of the sympathetic nervous system, acute mountain sickness, and deterioration of sleep quality.
Sixteen healthy volunteers will spend a familiarization night in a hypoxic chamber at a simulated altitude of 4,000 m. Four weeks later, they will complete two three-night sojourns at the same altitude, again separated by at least four weeks. In one, nocturnal PB will be prevented by slightly increasing the CO2 fraction in the inspired air and thus preventing PaCO2 from decreasing below the apneic threshold, whereas in the other inspiratory CO2 will remain unchanged. The order of the sojourns will be randomized, and subjects blinded. Before the familiarization and in the end of the sojourns we will measure muscle sympathetic nerve activity by microneurography both in normoxia and hypoxia and after inhibition of the chemoreflex by pure O2. Baroreflex sensitivity will be assessed at the same time points by the burst incidence method. Throughout the sojourns symptoms of acute mountain sickness will be monitored, reactive O2 species measured in venous blood, and sleep quality recorded by polysomnography.