Schoene R B, Roach R C, Hackett P H, Sutton J R, Cymerman A, Houston C S
Division of Pulmonary and Critical Care Medicine, Harborview Medical Center, University of Washington, Seattle 98104.
Med Sci Sports Exerc. 1990 Dec;22(6):804-10.
To assess the ventilatory adaptation during gradual ascent to extreme altitude, we studied seven healthy males as part of the 40 d simulated ascent of Mt. Everest in a hypobaric chamber. We measured resting ventilation (VE, l.min-1), arterial oxygen saturation (SaO2%), the ventilatory response to oxygen breathing, isocapnic hypoxic ventilatory response (HVR), and hypercapnic ventilatory response (HCVR) at sea level prior to the ascent (760 torr), 14,000 feet (428 torr), 24,000 feet (305 torr), and within 24 h of descent (765 torr). VE increased from 9.3 +/- 1.1 l.min-1 at 760 torr to 23.4 +/- 1.3 l.min-1 at 305 torr and remained elevated at 14.7 +/- 0.7 l.min-1 after descent. Oxygen breathing decreased VE by 9.6 +/- 1.3 l.min-1 at 305 torr. Isocapnic HVR (expressed as a positive slope of VE/SaO2, l.min-1.%SaO2(-1) increased from 0.18 +/- 0.07 at 760 torr to 0.34 +/- 0.11 and 0.38 +/- 0.5 at 428 torr and 305 torr (P less than 0.05) respectively. HVR was elevated further upon return to sea level (0.8 +/- 0.09, P less than 0.05). HCVR (S = VE/PETCO2, l.min-1.torr-1) increased from sea level (S = 4.4 +/- 0.09) to 305 torr (S = 18.7 +/- 3.5, P less than 0.01) and remained elevated upon return to sea level (S = 10.7 +/- 4.6, P less than 0.001). This study is the first to investigate the ventilatory response to such extreme altitude and so soon after descent and shows that hypoxic and hypercapnic responses increase during prolonged progressive hypoxic exposure and remain significantly elevated from pre-ascent levels immediately upon descent.
为评估在逐渐上升至极高海拔过程中的通气适应情况，我们对7名健康男性进行了研究，这是在低压舱内进行的为期40天的珠穆朗玛峰模拟攀登的一部分。我们在攀登前（760托）、14000英尺（428托）、24000英尺（305托）以及下降后24小时内（765托）的海平面测量了静息通气量（VE，升·分钟⁻¹）、动脉血氧饱和度（SaO₂%）、对吸氧的通气反应、等碳酸血症性低氧通气反应（HVR）和高碳酸血症性通气反应（HCVR）。VE从760托时的9.3±1.1升·分钟⁻¹增加到305托时的23.4±1.3升·分钟⁻¹，下降后仍维持在14.7±0.7升·分钟⁻¹。在305托时，吸氧使VE降低了9.6±1.3升·分钟⁻¹。等碳酸血症性HVR（以VE/SaO₂的正斜率表示，升·分钟⁻¹·%SaO₂⁻¹）从760托时的0.18±0.07分别增加到428托时的0.34±0.11和305托时的0.38±0.05（P<0.05）。返回海平面时HVR进一步升高（0.8±0.09，P<0.05）。HCVR（S = VE/PETCO₂，升·分钟⁻¹·托⁻¹）从海平面时（S = 4.4±0.09）增加到305托时（S = 18.7±3.5，P<0.01），返回海平面时仍维持升高（S = 10.7±4.6，P<0.001）。本研究首次调查了对如此极端海拔以及下降后如此短时间内的通气反应，结果表明，在长时间进行性低氧暴露期间，低氧和高碳酸血症反应增加，并且在下降后立即显著高于攀登前水平。
