Response

Dear Editor-in-Chief: We greatly appreciate the interest Drs. Morrison, Mekjavic, and Dolenc-Grošelj showed in our recent article (2). Below are our responses to their letter. THE TERM SLEEP QUALITY Krystal and Edinger (4) reviewed the clinical neurophysiological literature and stated that not only sleep latency, total sleep time, waking time after sleep onset, sleep efficiency, and awakenings but also the percentage or temporal amounts of sleep stages have also been used as indices of sleep quality. Furthermore, they showed that the delta power of non–rapid eye movement (NREM) sleep EEG is associated with the subjective sleep quality. NOCTURNAL ARTERIAL OXYGEN (SpO2) AND APNEA-HYPOPNEA INDEX (AHI) Morrison et al. cited a study by Block et al. (1) and stated that it showed an 11% decrease in the mean maximum SpO2 (under normoxia). However, this 11% decrease was calculated using data from 17 selected men who showed 4% desaturation. Eleven of the 17 men showed AHI above the clinical criterion (3), and respiratory events lasting more than 20 s. Four of the 17 men showed a minimum SpO2 of 68%, 70%, 72%, and 72%. These suggest that data from the men with AHI above the clinical criterion were strongly reflected in the 11% decrease in the mean maximum SpO2. Apnea-hypopnea index and SpO2 can be influenced by the characteristics of subjects, such as their age (1), obesity (1), and respiratory chemosensitivity (5). We examined well-trained young runners with a relatively low body mass index. Under normoxia, none of our subjects showed AHI above the clinical criterion. They initially showed low ventilatory chemosensitivities, and then the chemosensitivities increased but were still not high after five nights under hypoxia. They avoided intense exercise during the daytime. We are of the opinion that all these factors contributed to our results. ACCLIMATIZATION TO HYPOXIA Morrison et al. cited the studies by Rojc et al. (7) and Zieliński et al. (8). In contrast to claims by Morrison et al., Rojc et al. (7) reported that hypoxia-induced decreases in slow-wave sleep (SWS) and increased awakenings on the first night (at a 2990-m altitude) disappeared on the 10th night (at a 3881-m altitude). Zieliński et al. (8) did not detect hypoxia-induced deteriorated sleep at a 3200-m altitude. In both studies, AHI under hypoxia remained higher than under normoxia throughout the study period. Nussbaumer-Ochsner et al. (6) reported that the sleep quality under hypoxia is initially impaired but improves with acclimatization in association with improved SpO2, whereas periodic breathing persists. We think that the results of the studies by Rojc et al. (7) are in line with the study by Nussbaumer-Ochsner et al. (6). We also suggest that reduction of less than 90% SpO2 time during five nights under hypoxia contributed to improve the deteriorated SWS in our study. CONCLUSION At altitudes above 3000 m, many studies have evaluated the effect of acclimatization to hypoxia on sleep quality. However, under mild hypoxia (<2500-m altitude), ours is the first such study. We suggest that our study provides useful information for athletes and coaches who are planning a “living-high regimen.” Masako Hoshikawa Department of Sports Science Ryan McGinn Japan Institute of Sports Sciences Tokyo, JAPAN Sunao Uchida Faculty of Sport Sciences Waseda University Saitama, JAPAN