Angus calves born and raised at high altitude adapt to hypobaric hypoxia by increasing alveolar ventilation rate but not hematocrit.

Journal of animal science

PubMedID: 27898867

Gulick AK, Garry FB, Holt TN, Retallick-Trennepohl K, Enns RM, Thomas MG, Neary JM. Angus calves born and raised at high altitude adapt to hypobaric hypoxia by increasing alveolar ventilation rate but not hematocrit. J Anim Sci. 2016;94(10):4167-4171.
The objective of this study was to evaluate the effect of altitude on arterial blood-gases and hematocrit in Angus-based calves. It was hypothesized that alveolar ventilation rate, as indicated by arterial pCO, would increase with altitude but hematocrit would not. Five Angus-based herds ( = 30 to 80 per cohort) located at 105 m, 1,470 m, 2,010 m, 2,170 m, and 2,730 m above sea level were enrolled in this prospective cohort study. A portable analyzer measured blood-gas tensions in coccygeal arterial blood. Calves at 1,470 m, 2,170 m, and 2,730 m were sampled twice, at approximately 4 mo and 7 mo of age. Calves at 105 m and 2,010 m were sampled once, at 7 or 4 mo of age, respectively. Linear regression analyses were used to determine the fixed effect of herd (a proxy for altitude) on the 4 outcome variables pCO, pO, pH, and hematocrit, while controlling for age and sex. As hypothesized, alveolar ventilation rate increased with altitude ( < 0. 001). Hematocrit, however, did not show a clear association with altitude except for an increase from 105 m to = 1,470 m ( < 0. 001). Arterial pO decreased significantly with increasing altitude in calves at 4 mo and 7 mo of age ( < 0. 001). The adjusted mean values of the 4 variables studied were similar at 4 and 7 mo of age for all of the herds studied. This indicates that suckling calves show minimal respiratory or erythrocytic adaptation to hypoxemia and hypocapnia with increasing age, regardless of altitude. We propose that the lack of an erythrocytic response in hypoxemic calves born and raised at high altitude prevents a deleterious increase in viscous resistance and, consequently, pulmonary arterial pressure. This physiological response, or lack thereof, may be a survival adaptation in a species predisposed to hypoxia-induced pulmonary hypertension.