Abstract

T
Not surprisingly subjects in Limper's study showed much worse sleep quality at high altitude compared with sleep quality in their usual low-altitude sleep environment. Although hypoxia itself contributes to poor sleep at altitude (Khoo et al., 1996), other things besides oxygenation affect sleep quality, including the sleep environment and periodic breathing, which is a function of both “plant gain” and “controller gain” (Ainslie et al., 2013). This is also reflected in the 2018 update of the Lake Louise score that eliminated sleep as a questionnaire item (Roach et al., 2018). Positional saturation changes are real, but the response is highly variable among individuals, and it is unclear how consistent the response is from one time to the next in a given individual. Although we observed a mean positional SpO2 difference of 2.5%, nearly 11% of our subjects had a positional SpO2 change of >5%. At the same time, SpO2 during sleep is among the lowest values experienced while at high altitude (Anholm et al., 1992; Ainslie et al., 2013) and it is unknown whether the positional changes we observed carry over to more profound nocturnal desaturation. Whatever the mechanism(s) behind impaired sleep at high altitude, changes in body position are likely to be less effective at ameliorating acute mountain sickness than acetazolamide (Fischer et al., 2004; Limper et al., 2020). We agree with the comments of Limper that findings in healthy young individuals cannot be extrapolated to patients with heart or lung disease when they travel to altitude.
