Hemoglobin P50 During a Simulated Ascent of Mt. Everest, Operation Everest II

The amount of O2 available to tissues is essentially the product of cardiac output, Hb, and O2 saturation. Saturation depends on PO2 and the O2Hb dissociation curve. With altitude, increased 2,3-DPG shifts the dissociation curve rightward, but hypocapnia and alkalosis move it leftward. We determined both standard and in vivo P50 in 5 fit subjects decompressed over 42 days in an altitude chamber to the equivalent of the Mt. Everest summit Operation Everest II. Arterial and venous blood was sampled at five altitudes PB 760, 429, 347, 282, 253 mmHg, and P02, Pco2, pH , O2 saturation, Hb and 2,3-DPG were measured. As reported previously, 2,3-DPG levels increased from 1.7 PB 760 to 3.8 mmolL PB 282. Standard P50 also increased from 28.2 mmHg at sea level to 33.1 on the summit, p 0.001. Alone, this would have lowered saturation by 12 percentage points at a summit arterial PO2 of approx. 30 mmHg. However, in vivo P50 remained between 26 and 27 mmHg throughout due to progressive hypocapnia and alkalosis. Calculations suggest that the increase in standard P50 did not affect summit VO2MAX, alveolar, arterial and venous PO2s, but reduced arterial and venous O2 saturations by 8.4 and 17.4 points, respectively, and increased O2 extraction by 7.9 percentage points. Reduced saturation was balanced by increased extraction, resulting in no significant overall O2 transport benefit, thus leaving unanswered the question of the purpose of increased 2,3- DPC concentrations at altitude.