Effects of moderate-intensity continuous training on cardiac mitochondrial bioenergetics, oxidative balance, and mitochondrial dynamic in juvenile overnourished rats

Early life overnutrition can promote lasting metabolic and cardiovascular dysfunction. This study evaluated the effects of post-weaning exercise training on cardiac mitochondrial function, oxidative status, and mitochondrial-related gene expression in rats. After overnutrition period, male Wistar rats were assigned to sedentary or trained groups. The exercise protocol consisted of moderate-intensity treadmill running for 4 weeks. Exercise capacity was assessed before and after the intervention through a progressive running test to determine maximal running velocity (Vmax). Body weight was monitored and after euthanasia, fresh mitochondrial fractions were isolated from the left ventricle by differential centrifugation. Mitochondrial respiration was measured using a Clark-type oxygen electrode. Citrate synthase activity, swelling, reactive oxygen species (ROS) production, lipid peroxidation (MDA), protein carbonyls, redox status (NAD/NADH and GSH/GSSG), total thiol content, and the expression of PGC-1α, TFAM, FIS1, OPA1, and UCP2 were evaluated. Data were analyzed using Student’s t-test and two-way ANOVA followed by Tukey’s post hoc test. Exercise training increased Vmax (p = 0.014), indicating improved exercise capacity. In left ventricular mitochondria, training enhanced respiratory efficiency and citrate synthase activity (p = 0.028), reduced ROS production (p = 0.035), and attenuated oxidative damage, as shown by lower MDA (p = 0.011) and protein carbonyl levels (p = 0.022). However, mitochondrial swelling analyses did not differ between groups. Antioxidant defenses were strengthened, with an increased GSH/GSSG ratio (p = 0.009) and preserved thiol content (p = 0.041). Exercise also upregulated PGC-1α, TFAM, and FIS1 expression. Post-weaning exercise improves cardiac mitochondrial function, reduces oxidative stress, and modulates mitochondrial dynamics in rats exposed to early life overnutrition.