Vascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico, Albuquerque, NM.
Department of Health, Exercise, and Sport Sciences, University of New Mexico, Albuquerque, NM.
Med Sci Sports Exerc. 2024 Oct 1;56(10):1867-1881. doi: 10.1249/MSS.0000000000003479. Epub 2024 May 15.
Chronic, high-altitude hypoxic exposure increases the risk of high-altitude pulmonary hypertension (PH). Emerging evidence shows maternal exercise may improve offspring resistance to disease throughout life. The purpose of this study is to determine if maternal exercise mitigates chronic hypoxic-induced changes in the offspring indicative of high-altitude PH development.
Female adult C57BL/6J mice were randomly allocated to nonexercise or exercise conditions. Exercise consisted of voluntary running wheel exercise for 4 wk during the perinatal period. Three days after birth, the pups remained at low altitude (normoxia) or were exposed to hypobaric hypoxia of 450 mm Hg to simulate ~4500 m of altitude exposure until 8 wk of age. The study consisted of four groups: hypoxia + nonexercise pregnancy, hypoxia + exercise, or the respective normoxia conditions (normoxia + nonexercise or normoxia + exercise). Offspring body size, motor function, right ventricular systolic pressure (RVSP), and cardiopulmonary morphology were assessed after 8 wk in normoxia or hypoxia.
Both hypoxic groups had smaller body sizes, reduced motor function, increased hematocrit, RVSP, muscularization in medium-sized pulmonary arteries, as well as right ventricular hypertrophy and contractility compared with the normoxic groups ( P < 0.05).
Chronic hypoxia simulating 4500 m attenuated growth, lowered motor function, and elicited PH development. Voluntary maternal exercise did not significantly decrease RVSP in the offspring, which aligned with a lack of effect to attenuate abnormal body size and cardiopulmonary development due to chronic hypoxia. These findings are preliminary in nature, and more powered studies through larger group sizes are required to generalize the results to the population.
慢性、高海拔缺氧暴露会增加高原性肺动脉高压（PH）的风险。新出现的证据表明，母体运动可能会提高后代终生对疾病的抵抗力。本研究的目的是确定母体运动是否减轻了慢性低氧诱导的后代变化，这些变化提示高原 PH 的发展。
将成年雌性 C57BL/6J 小鼠随机分配到不运动或运动条件下。运动包括在围产期进行 4 周的自愿跑步轮运动。出生后 3 天，幼仔仍留在低海拔（常氧）或暴露于 450 毫米汞柱的低压缺氧中，以模拟约 4500 米的海拔暴露，直到 8 周龄。研究包括四个组：缺氧+不运动妊娠、缺氧+运动，或相应的常氧条件（常氧+不运动或常氧+运动）。在常氧或缺氧 8 周后，评估后代的体型、运动功能、右心室收缩压（RVSP）和心肺形态。
与常氧组相比，两组缺氧组的体型较小，运动功能降低，血细胞比容增加，中等大小肺动脉的肌化，以及右心室肥厚和收缩力增加（P<0.05）。
模拟 4500 米的慢性缺氧会抑制生长、降低运动功能，并引发 PH 发展。自愿的母体运动并不能显著降低后代的 RVSP，这与由于慢性缺氧导致的异常体型和心肺发育的缺乏减弱作用一致。这些发现具有初步性质，需要通过更大的群体规模进行更多的有力研究，以将结果推广到人群中。
