Hemoglobin P 50 during A Simulated Ascent of Mt. Everest,Operation Everest II

Abstract

Wagner, Peter D., Harrieth E. Wagner, Bertron M. Groves, Allen Cymerman, and Charles S. Houston. Hemoglobin P₅₀ during a simulated ascent of Mt. Everest, Operation Everest II. High Alt. Med Biol. 8:32–42, 2007.—The amount of O₂ available to tissues is essentially the product of cardiac output, [Hb], and O₂ saturation. Saturation depends on P_O2 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 ” (P_B = 760, 429, 347, 282, 253 mmHg), and P_O2, P_CO2, pH, O₂ saturation, [Hb] and [2,3-DPG] were measured. As reported previously, 2,3-DPG levels increased from 1.7 (P_B = 760) to 3.8 mmol/L (P_B = 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 P_O2 of ∼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 V_O2MAX, alveolar, arterial and venous P_O2's, 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-DPG] concentrations at altitude.