Maternal Exercise And Its Impact On Cardiac Mitochondrial Function In Neonatal Mice

The role of intrauterine and perinatal environments in shaping the cardiometabolic health of offspring is increasingly evident. Mitochondrial dysfunction is a known contributor to cardiovascular diseases. Our previous research highlighted the positive impact of maternal exercise during pregnancy on mitochondrial enzyme activities and ATP production in fetal hearts. PURPOSE: To investigate if maternal exercise training during pregnancy and lactation impacts cardiac mitochondrial function of her neonates. METHODS: Female C57BL/6 J mice were randomly assigned to sedentary and exercise groups three weeks prior to mating. The exercise group was provided access to a voluntary wheel in their cages until the end of lactation. At postnatal days 8-10, their offspring were evaluated. To control for maternal effects and reduce litter bias, one male and one female mouse from each litter were selected for analysis. RESULTS: No sex-based differences were noted, allowing pooled data analysis. Offspring body weight, ventricular weight, and blood glucose levels showed no significant group differences. Electron transport chain subunits across Complexes I-V were similar in both groups. However, offspring from exercising mothers exhibited a notable decrease in mitochondrial LEAK state under saturating concentrations of fatty acid substrates (Octanoylcarnitine+Malate). CONCLUSION: Maternal exercise during pregnancy does not substantially alter cardiac mitochondrial respiratory function in neonatal hearts, but may improve the efficiency of fatty acid oxidation with potential long-term benefits. With cardiac metabolism and fuel usage evolving with age, further longitudinal studies are warranted to assess the long-term implications of maternal exercise on cardiac health. NIH, NIGMS, grant GM125603