DataSheet1_Acute high altitude exposure, acclimatization and re-exposure on nocturnal breathing.PDF

Background: Effects of prolonged and repeated high-altitude exposure on oxygenation and control of breathing remain uncertain. We hypothesized that prolonged and repeated high-altitude exposure will improve altitude-induced deoxygenation and breathing instability.
Methods: 21 healthy lowlanders, aged 18-30y, underwent two 7-day sojourns at a high-altitude station in Chile (4–8 hrs/day at 5,050 m, nights at 2,900 m), separated by a 1-week recovery period at 520 m. Respiratory sleep studies recording mean nocturnal pulse oximetry (SpO2), oxygen desaturation index (ODI, >3% dips in SpO2), breathing patterns and subjective sleep quality by visual analog scale (SQ-VAS, 0–100% with increasing quality), were evaluated at 520 m and during nights 1 and 6 at 2,900 m in the 1st and 2nd altitude sojourn.
Results: At 520 m, mean ± SD nocturnal SpO2 was 94 ± 1%, ODI 2.2 ± 1.2/h, SQ-VAS 59 ± 20%. Corresponding values at 2,900 m, 1st sojourn, night 1 were: SpO2 86 ± 2%, ODI 23.4 ± 22.8/h, SQ-VAS 39 ± 23%; 1st sojourn, night 6: SpO2 90 ± 1%, ODI 7.3 ± 4.4/h, SQ-VAS 55 ± 20% (p < 0.05, all differences within corresponding variables). Mean differences (Δ, 95%CI) in acute effects (2,900 m, night 1, vs 520 m) between 2nd vs 1st altitude sojourn were: ΔSpO2 0% (-1 to 1), ΔODI -9.2/h (-18.0 to -0.5), ΔSQ-VAS 10% (-6 to 27); differences in acclimatization (changes night 6 vs 1), between 2nd vs 1st sojourn at 2,900 m were: ΔSpO2 -1% (-2 to 0), ΔODI 11.1/h (2.5 to 19.7), ΔSQ-VAS -15% (-31 to 1).
Conclusion: Acute high-altitude exposure induced nocturnal hypoxemia, cyclic deoxygenations and impaired sleep quality. Acclimatization mitigated these effects. After recovery at 520 m, repeated exposure diminished high-altitude-induced deoxygenation and breathing instability, suggesting some retention of adaptation induced by the first altitude sojourn while subjective sleep quality remained similarly impaired.

背景：长期反复高原暴露对血氧合状态与呼吸调控的影响尚不明确。本研究假设，长期反复的高原暴露可改善高原诱导的低氧血症与呼吸不稳定状态。
方法：本研究纳入21名年龄18~30岁的健康平原居住者，先后两次前往智利某高原站点进行为期7天的旅居（每日于海拔5050米处停留4~8小时，夜间宿营于海拔2900米处），两次旅居之间安排为期1周的海拔520米处恢复期。分别于海拔520米处，以及两次高原旅居期间的海拔2900米处第1、6个夜间，开展呼吸睡眠相关检测，记录夜间平均脉搏血氧饱和度（SpO2）、氧减饱和度指数（ODI，定义为每小时SpO2下降超过3%的次数）、呼吸模式，并采用视觉模拟评分法（SQ-VAS，评分范围0~100分，分数越高睡眠质量越好）评估主观睡眠质量。
结果：在海拔520米处，夜间平均脉搏血氧饱和度（SpO2）为94±1%，氧减饱和度指数（ODI）为2.2±1.2次/小时，主观睡眠质量SQ-VAS评分为59±20分。首次旅居期间，海拔2900米处第1个夜间的对应指标为：SpO2 86±2%，ODI 23.4±22.8次/小时，SQ-VAS评分39±23分；第6个夜间的对应指标为：SpO2 90±1%，ODI 7.3±4.4次/小时，SQ-VAS评分55±20分（各指标组间差异均具有统计学意义，p<0.05）。对比两次高原旅居，急性暴露效应（海拔2900米第1夜间与520米处的差值）的平均差值（Δ，95%置信区间）分别为：ΔSpO2 0%（-1~1），ΔODI -9.2次/小时（-18.0~-0.5），ΔSQ-VAS评分10分（-6~27）；而在海拔2900米处，两次旅居的习服适应效应（第6夜间与第1夜间的差值）差异为：ΔSpO2 -1%（-2~0），ΔODI 11.1次/小时（2.5~19.7），ΔSQ-VAS评分-15分（-31~1）。
结论：急性高原暴露可引发夜间低氧血症、周期性低氧事件与睡眠质量受损，而高原习服可缓解上述不良效应。在海拔520米处完成恢复期后，再次高原暴露可减轻高原诱导的低氧血症与呼吸不稳定状态，提示首次高原旅居所诱导的适应效应存在一定留存，但主观睡眠质量仍维持在受损状态。