Abstract

Evidence suggests elevated [Hb] at high altitude is a non‐advantageous, possibly misguided, response to high‐altitude hypoxia. In support of that, lower [Hb] is often observed in native high‐altitude resident Tibetans. To determine whether [Hb] in Tibetans is associated with peak VO2 and/or changes in particular step(s) of the O2 transport chain, we compared ventilation, lung diffusional conductance, cardiac output and systemic O2 delivery, and muscle O2 diffusional conductance in 21 Tibetan males with [Hb] ranging from 15.2 g/gl to 22.9 g/dl [Hb] by measuring their ventilation, VO2 and VCO2, heart rate, cardiac output, and arterial PO2, PCO2, pH, P50, and O2 saturation at peak exercise on a cycle ergometer. [Hb] showed a significant negative relationship with VO2/kg (r= −0.45, p< 0.05), cardiac output/kg (r= −0.54, p < 0.01), and diffusion capacity in muscle (DM/kg: r= −0.44, p<0.05) but not lung. Furthermore, VO2/kg was highly positively correlated with DM/kg (r=0.84, p< 2×10‐6), QT/kg (r=0.76, p < 7.5×10‐5), and arterial [H+] (r= 0.52, p < 0.02), and DM/kg was related to QT/kg (r=0.43, p < 0.051). These trends suggest that genetic mutations resulting in reduced [Hb] may convey an advantage in exercise capacity, possibly via higher cardiac function, ventilation, and diffusion capacity in the muscle and support the emerging hypothesis that the polycythemia of altitude is a misguided response to low cellular PO2.

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