Abstract
Background/objectives: Perinatal hypoxia–ischemia (HI) is a major cause of brain injury and is associated with long-term neurological impairments, including white matter injury, astrogliosis, microgliosis, and hypomyelination. Maternal exercise has emerged as a potential non-pharmacological strategy to improve fetal development and increase resilience to prenatal insults. This study investigated whether maternal exercise during pregnancy protects against neuroglial alterations in the corpus callosum of offspring subjected to prenatal HI. Methods: Adult female Wistar rats were assigned to sedentary or exercise groups. The exercise protocol consisted of daily swimming sessions with progressive durations (3–30 min/day) over 10 days. Blood glucose levels and oxidative stress markers (GSH, TBARS, and DPPH) were evaluated to characterize the physiological effects of the protocol. Prenatal HI was induced on gestational day 18 by transient occlusion of the uterine arteries for 45 min, whereas sham-operated dams underwent identical surgical procedures without arterial occlusion. Offspring were euthanized on postnatal days (P) 16 and 23, and brain sections were processed for immunohistochemistry using antibodies against glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP). Images were quantitatively analyzed using Image-Pro Plus, and statistical analyses were performed using SPSS software. Results: The exercise protocol did not show oxidative stress, hypoglycemia, or exhaustion. Female offspring from HI group exhibited astrogliosis at P16, which persisted until P23; however, maternal exercise prevented this response at P23. No changes in MBP immunoreactivity were detected in females. Male offspring did not develop astrogliosis but displayed hypomyelination at P23, which was prevented by maternal exercise. Conclusion: These findings demonstrate that maternal exercise during pregnancy attenuates sex-dependent neuroglial alterations induced by prenatal HI, supporting its potential as a preventive strategy to reduce white matter injury and improve neurodevelopmental outcomes.