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Limits of human lung function at high altitude

Robert B. Schoene^*

Department of Medicine, Division of Respiratory and Critical Care Medicine, University of Washington, Seattle, WA 98122, USA

View larger version (24K): [in a new window]   Fig. 1. Data from the 1981 American Medical Research Expedition to Everest showing that maximal exercise ventilation in liters per minute (BTPS) (dashed line) increased as the inspired partial pressure of oxygen decreased from sea-level values (150mmHg) to approximately 60mmHg (at an altitude of approximately 6300m), but decreased as climbers approach the extreme altitude of the summit of Mount Everest, where the inspired partial pressure of oxygen was 42mmHg. The increase in ventilation is secondary to the hypoxic stimulation of exercise hyperpnea and the level of exercise, which was approximately 200W of work at 6300m, while the hypoxic stimulus was greater at 8848m, but the work capacity was greatly reduced (West et al., 1983) (with permission). 1mmHg=0.133kPa.

View larger version (13K): [in a new window]   Fig. 2. Data from the 1981 American Medical Research Expedition to Everest showing that individuals with higher hypoxic ventilatory responses (HVR) performed better at higher altitudes that those with lower HVRs (redrawn from data) (Schoene et al., 1984).

View larger version (24K): [in a new window]   Fig. 3. Data from four subjects (A–D) exercising at sea level (filled circles) and 5050m altitude (open squares) showing that the work of breathing, expressed as respiratory power (calmin-1), was substantially greater at high altitude (Cibella et al., 1999, with permission). 1cal=4.19J.

View larger version (14K): [in a new window]   Fig. 4. (A) Data from subjects exercising at sea level (filled circles) and 5050m altitude (open squares) demonstrating the maximal oxygen cost of breathing (O2rm,max) during maximal ventilation at physiological levels of mechanical efficiency (range 5–20%). (B) Similar data except that O2rm,max is expressed as a percentage of the total maximal rate of O2 uptake (O2tot,max). These data show that the work of breathing is substantially higher at this altitude than at sea level (from Cibella et al., 1999, with permission). Values are means + S.E.M.

View larger version (19K): [in a new window]   Fig. 5. Data from highly trained cyclists showing that, at maximum exercise, as the work of breathing increases, both the blood flow to the legs (legs) and the rate of oxygen consumption of the legs (O2legs) decrease. These studies were performed at resting ventilation and maximal ventilation both in a control state and with inspiratory loading (from Harms et al., 1997, with permission).

View larger version (17K): [in a new window]   Fig. 6. Plots of the partial pressure of oxygen (mmHg) at sea level (A) and the summit of Mount Everest (B) versus the transit time of blood across the pulmonary capillary. These schematic representations demonstrate that, as one ascends, the driving pressure for oxygen from the air to the blood is lower, such that there is not time for equilibration for oxygen across the pulmonary capillary. This phenomen results in arterial oxygen desaturation, which is accentuated with higher levels of exercise (from West and Wagner, 1980, with permission). 1mmHg=0.133kPa.

View larger version (22K): [in a new window]   Fig. 7. Arterial oxygen saturation, as measured by ear oximetry, plotted against work rate at sea level and 6300m altitude in humans exercising to maximal effort. The lower two lines were obtained with subjects breathing 16 and 14% oxygen at 6300m (from West et al., 1983, with permission).

View larger version (19K): [in a new window]   Fig. 8. Relationship between alveolar–arterial PO2 difference and the rate of oxygen uptake in Operation Everest II, a high-altitude chamber study designed to simulate an ascent by humans over 40 days to the summit of Mount Everest (8828m). These data were obtained from a multiple inert gas elimination technique that measures ventilation/perfusion relationships and show that the predicted alveolar–arterial PO2 difference (mmHg) could be accounted for only in part by ventilation/perfusion inequality. The remaining difference was attributed to a diffusion limitation of oxygen from the air to the blood (from Wagner et al., 1987, with permission). 1mmHg=0.133kPa. Values are means + S.E.M.

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