Muza Stephen R, Young Andrew J, Sawka Michael N, Forte Vincent A, Rock Paul B, Fulco Charles S, Cymerman Allen
US Army Research Institute of Environmental Medicine, Natick, MA 01760-5007, USA.
Wilderness Environ Med. 2004 Spring;15(1):18-24. doi: 10.1580/1080-6032(2004)015[0018:vasoaa]2.0.co;2.
The present study assessed the effects of acute hyperoxia on resting-minute ventilation (VE) during altitude acclimatization to 4300 m.
Resting-minute ventilation, end-tidal partial pressure carbon dioxide (PETCO2) and oxygen (P(ET)O2), and arterial oxygen saturation (SpO2) were measured during chronic poikilocapnic hypobaric hypoxia, supplemental oxygen breathing, and the subsequent return to hypobaric poikilocapnic hypoxia at altitude. Fifteen adult male lowlanders were studied at sea level and on the 3rd and 12th days at 4300 m. At sea level, subjects first breathed room air that was followed by 25-minute steady-state poikilocapnic hypoxia (FIO2 = 0.125). Ventilatory responses to acute poikilocapnic hypoxia (APH) were collected over the first 1-10 minutes, and responses to chronic poikilocapnic hypoxia (CPH) were collected over the last 3 minutes of the hypoxia exposure. At altitude, CPH was provided by ambient-air breathing (PIO2 = 86 mm Hg) that was interrupted by 10 minutes of oxygen breathing (FIO2 = 1.0, PIO2 = 460 mm Hg) and then a subsequent return to ambient air to measure APH ventilatory responses.
Between day 1 and day 12, during CPH, VE and SpO2 increased (P < .05) by 46% and 6%, respectively, whereas P(ET)CO2 decreased. On day 3 and day 12, breathing oxygen did not lower VE compared with CPH. However, the VE during APH immediately after oxygen breathing at high altitude was always greater (P < .05) than during CPH and did not change with duration of residence at altitude.
These results show that short-duration oxygen breathing increases the subsequent ventilatory response to poikilocapnic hypoxia in altitude-acclimatized lowlanders, resulting in a transient elevation of SpO2.
本研究评估了急性高氧对海拔4300米高原习服期间静息分钟通气量（VE）的影响。
在慢性变碳酸性低氧、补充氧气呼吸以及随后返回高原低碳酸性低氧状态期间，测量静息分钟通气量、呼气末二氧化碳分压（PETCO2）和氧分压（P(ET)O2）以及动脉血氧饱和度（SpO2）。对15名成年男性低地居民在海平面以及海拔4300米处的第3天和第12天进行了研究。在海平面时，受试者首先呼吸室内空气，随后进行25分钟的稳态变碳酸性低氧（FIO2 = 0.125）。在低氧暴露的前1 - 10分钟收集对急性变碳酸性低氧（APH）的通气反应，在低氧暴露的最后3分钟收集对慢性变碳酸性低氧（CPH）的反应。在高原时，CPH通过呼吸环境空气（PIO2 = 86 mmHg）提供，期间中断10分钟的氧气呼吸（FIO2 = 1.0，PIO2 = 460 mmHg），随后再返回环境空气以测量APH通气反应。
在第1天至第12天期间，在CPH期间，VE和SpO2分别增加（P < .05）46%和6%，而P(ET)CO2降低。在第3天和第12天，与CPH相比，吸氧并未降低VE。然而，在高原吸氧后立即进行APH期间的VE总是大于（P < .05）CPH期间，且不随在高原居住时间而变化。
这些结果表明，短时间吸氧会增加高原习服的低地居民随后对变碳酸性低氧的通气反应，导致SpO2短暂升高。
