In healthy near-term women, blood flow to the uteroplacental circulation is estimated as 841 mL/min, which is greater than in other mammalian species. We argue that as uterine venous Po₂ sets the upper limit for O₂ diffusion to the fetus, high uterine artery blood flow serves to narrow the maternal arterial-to-uterine venous Po₂ gradient and thereby raise uterine vein Po₂. In support, we show that the reported levels for uterine artery blood flow agree with what is required to maintain normal fetal growth. Although residence at high altitudes (>2,500 m) depresses fetal growth, not all populations are equally affected; Tibetans and Andeans have higher levels of uterine artery blood flow than newcomers and exhibit normal fetal growth. Estimates of uterine venous Po₂ from the umbilical blood-gas data available from healthy Andean pregnancies indicate that their high levels of uterine artery blood flow are consistent with their reported, normal birth weights. Unknown, however, are the effects on placental gas exchange of the lower levels of uterine artery blood flow seen in high-altitude newcomers or hypoxia-associated pregnancy complications. We speculate that, by widening the maternal artery to uterine vein Po₂ gradient, lower levels of uterine artery blood flow prompt metabolic changes that slow fetal growth to match O₂ supply.