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Decreased hemoglobin-oxygen affinity is thought to be of adaptive value to humans and nonindigenous animals at high altitude. To test this, hemoglobin-oxygen affinity was modified by carbamoylation of hemoglobin in rats. Exposure of control (low oxygen affinity) and experimental (high oxygen affinity) animals to a pressure equivalent to high altitude revealed that increased, rather than decreased, hemoglobin-oxygen affinity will permit survival at greatly reduced environmental oxygen pressures.

Maternal exercise during pregnancy has been shown to improve the long‐term health of offspring in later life. Mitochondria are important organelles for maintaining adequate heart function, and mitochondrial dysfunction is linked to cardiovascular disease. However, the effects of maternal exercise during pregnancy on mitochondrial biogenesis in hearts are not well understood. Thus, the purpose of this study was to test the hypothesis that mitochondrial gene expression in fetal myocardium would be upregulated by maternal exercise. Twelve‐week‐old female C57BL/6 mice were divided into sedentary and exercise groups. Mice in the exercise group were exposed to a voluntary cage‐wheel from gestational day 1 through 17. Litter size and individual fetal weights were taken when pregnant dams were sacrificed at 17 days of gestation. Three to four hearts from the same group were pooled to study gene expression, protein expression, and enzyme activity. There were no significant differences in litter size, sex distribution, and average fetal body weight per litter between sedentary and exercised dams. Genes encoding mitochondrial biogenesis and dynamics, including nuclear respiratory factor‐1 (Nrf1), Nrf2, and dynamin‐related GTPase termed mitofusin‐2 (Mfn2) were significantly upregulated in the fetal hearts from exercised dams. Cytochrome c oxidase activity and ATP production were significantly increased, while the hydrogen peroxide level was significantly decreased in the fetal hearts by maternal exercise. Our results demonstrate that maternal exercise initiated at day 1 of gestation could transfer the positive mitochondrial phenotype to fetal hearts.

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Maternal exercise during pregnancy has been shown to improve long-term metabolic health on offspring in later life. Mitochondria are the critical site of metabolism, and are inherited by maternal origin. However, the effects of maternal exercise during pregnancy on fetal mitochondrial biogenesis are not well understood. PURPOSE: To test whether maternal exercise can activate genes associate with mitochondrial biogenesis in the fetal heart. METHODS: Female C57BL/6 mice were divided into sedentary and exercise groups. The mice in the exercise group were exposed to voluntary cage-wheel from gestational day 1 through 17, at which time they were sacrificed. Litter size and individual fetal weights (3 days before birth) were taken when pregnant dams were sacrificed. All fetuses were sexed and two to three hearts from same sex within the group were pooled to study gene expression: all data were presented by group since there was no sex difference within group. RESULTS: Exercise dams ran an average of 7.22 ± 0.41km/day until mid-pregnancy and gradually decreased to low levels (1.39 ± 0.43 km/day) through the remainder of gestation. Weight gain during pregnancy was not significantly different between exercise (14.45 ± 0.99g) and sedentary (15.99 ± 1.13g) pregnant dams. There were no significant differences in litter size, sex distribution, and average fetal body weight per litter between sedentary and exercise dams. Genes associated with mitochondrial biogenesis, including Ppargc1a (peroxisome proliferator-activated receptor gamma, coactivator 1 alpha), Nrf1 (nuclear respiratory factor-1), and Nrf2 (nuclear respiratory factor-2) were significantly upregulated in fetuses from exercise dams. CONCLUSION: Although total kilometers run per day (km/day) were significantly decreased in later stage of pregnancy, maternal exercise initiated at day 1 of gestation significantly increased genes associated with mitochondria biogenesis, indicating that maternal exercise enhances mitochondrial biogenesis and mitochondrial function.