ABSTRACT
Two of the best-known aspects of altitude acclimatization are the increase in red cell numbers per unit volume and the increase in hemoglobin concentration. These are achieved, initially, by a reduction in plasma volume (PV) and later by an increase in red cell mass (RCM). The mechanism for PV reduction on ascent to altitude is probably via carotid body stimulation by hypoxia, which reduces the reabsorption of sodium by the kidney via neural pathways. Hypoxia causes an increase in erythropoietin (EPO), which stimulates the bone marrow to increase red cell output. The EPO gene is induced by hypoxia through a nuclear factor, the hypoxia-inducible factor-1 alpha (HIF-1α). Although EPO levels rise within a few hours, the increase in RCM takes weeks and only reaches a steady state after some 6 months. Plasma volume is restored to near sea level values after a few weeks. The rise in hemoglobin concentration is roughly linear with altitude up to about 5500 m and is similar in acclimatized lowlanders and residents of high altitude throughout most of the world, though with wide individual variation. However, Tibetan and, possibly, Ethiopian
highlanders have lower hemoglobin levels than other high altitude residents at similar altitudes. Extreme polycythemia among residents or lowlanders staying at altitude for many years is considered pathological and termed chronic mountain sickness (Chapter 22).
