Pregnancy swimming prevents early brain mitochondrial dysfunction and causes sex-related long-term neuroprotection following neonatal hypoxia-ischemia in rats

Neonatal hypoxia-ischemia (HI) is a major cause of cognitive impairments in infants. Antenatal strategies improving the intrauterine environment can have high impact decreasing pregnancy-derived intercurrences. Physical exercise alters mother-fetus unity and has been shown to prevent energetic challenge imposed by HI. This study aimed reveal neuroprotective mechanisms afforded pregnancy swimming on early metabolic failure late damage, considering animals' sex as variable. Pregnant Wistar rats were submitted daily (20′ tank filled with 32 °C water) during pregnancy. HI was performed male female pups at postnatal day 7. Electron chain transport, mitochondrial mass function ROS formation assessed right brain hemisphere 24 h after From PND45, reference working spatial memory tested Morris water maze. MicroPET-FDG images acquired injury (PND8) PND60, following behavioral analysis. induced failure, decreased enzymatic activity electron transport chain, increased production cortex hippocampus well caused glucose metabolism dysfunction impairments. Maternal able improve memory. The intergenerational effects sex-specific, since benefited most. In conclusion, maternal affect response offspring's brains, preserving its preventing damage sex-dependent manner, adding relevant information neuroprotection highlighting importance mitochondria therapeutic target for neuropathology.