In acclimatized humans at high altitude the reduction, compared to acute hypoxia, of the blood lactate concentration (la) at any absolute oxygen uptake (VO2), as well as the reduction of maximum la (lamax) after exhaustive exercise, compared to both acute hypoxia or normoxia, have been considered paradoxical, and these phenomena have therefore become known as the "lactate paradox". Since, at any given power output and VO2, mass oxygen transport to the contracting locomotor muscles is not altered by the process of acclimatization to high altitude, the gradual reduction in [la-]max in lowlanders exposed to chronic hypoxia seems not to be due to changes in oxygen availability at the tissue level. At present, it appears that the acclimatization-induced changes in [la-] during exercise are the result of at least two mechanisms: (1) a decrease in maximum substrate flux through aerobic glycolysis due to the reduced VO2max in hypoxia; and (2) alterations in the metabolic control of glycogenolysis and glycolysis at the cellular level, largely because of the changes in adrenergic drive of glycogenolysis that ensue during acclimatization, although effects of changes in peripheral oxygen transfer and the cellular redox state cannot be ruled out. With regard to the differences in lactate accumulation during exercise that have been reported to occur between lowlanders and highlanders, both groups either being acclimatized or not, these do not seem to be based upon fundamentally different metabolic features. Instead, they seem merely to reflect points along the same continuum of phenotypic adaptation of which the location depends on the time spent at high altitude.