Abstract

Human populations have lived at high altitudes for lengths of time which are likely to be shortest in Colorado, intermediate in Peru, and longest in Tibet. We hypothesized that the longest-resident high-altitude populations have beccome better adapted than shorter-resident groups as a result of superior abilities to transport and/or utilize O2 . Because birth weights are reduced at high altitude and decreased birth weight is associated with increased infant mortality, our criterion for assessing adaptation was preservation of birth weights close to values associated with the lowest mortality risk. Colorado (3,100 m) and Peru (4,300 m) birth weights averaged 3,186±70 g and 2,920±90 g respectively. A sample of 15 births from Tibet (3,658 m) weighed 3,307±110 g which was more than their altitude counterparts and close to sea-level norms. Pregnancy increased maternal ventilation at all three study sites. In Peru, the resultant elevation in arterial O2 saturation offset the pregnancy-induced fall in hemoglobin concentration to preserve arterial O2 content at nonpregnant levels. Arterial O2 content decreased slightly in Colorado and more markedly in Tibet in the pregnant compared to the nonpregnant state. The Colorado and Peru women with the greatest rise in ventilation and ventilatory sensitivity to hypoxia produced the heaviest birthweight infants, suggesting that maternal arterial oxygenation was an important determinant of fetal growth. The pregnant women in Tibet did not have higher levels of arterial O2 content than the pregnant Colorado or Peru women nor did maternal arterial O2 content relate to birth weight in Tibet. Infant birth weight in Tibet tended to be correlated with the ratio of uterine artery to common iliac artery mean flow velocity, suggesting that redistribution of lower-extremity blood flow to favor the uterine circulation may have acted to augment uterine O2 delivery in the Tibet women. Thus, the limited data available suggested that the Tibetans may be better adapted as judged by less fetal growth retardation and may utilize maternal O2 transport mechanisms not reliant upon increased arterial O2 content.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.