Fetoplacental microcirculation abnormalities are reversed by aerobic exercise in mice with preeclampsia.

Preeclampsia (PE) is a hypertensive disorder of pregnancy characterized by hypertension and organ dysfunction, and is associated with impaired placental perfusion and systemic endothelial dysfunction. Aerobic exercise has been proposed as a potential nonpharmacological strategy to improve vascular function during pregnancy; however, its effects on fetoplacental microcirculation in PE remain poorly understood. Therefore, the objective of this study was to investigate whether maternal aerobic exercise during gestation could influence fetoplacental perfusion and maternal pathological features in an experimental model of PE induced by nitric oxide synthase inhibition. Fetoplacental and fetal regional perfusion were quantified using laser speckle contrast imaging across placental, umbilical, and multiple fetal vascular beds. In parallel, maternal cardiovascular parameters, including systolic blood pressure and heart weight, and renal parameters, including kidney weight and urinary protein excretion, were assessed, along with fetal and placental biometric measurements and placental angiogenic factors. PE was associated with impaired fetoplacental perfusion and maternal cardiovascular alterations, whereas maternal aerobic exercise was associated with improved fetoplacental microvascular perfusion and attenuation of maternal pathological features. These findings support maternal exercise as a potential nonpharmacological strategy to modulate fetoplacental vascular dysfunction in hypertensive pregnancy.NEW & NOTEWORTHY This study provides an in vivo, integrative assessment of fetoplacental microcirculation across multiple fetal-placental vascular beds using laser speckle contrast imaging in a preeclampsia model. We demonstrate that maternal aerobic exercise restores microvascular blood flow in key fetoplacental and fetal regions, counteracting endothelial dysfunction induced by nitric oxide synthase inhibition. These findings establish a methodological framework for studying fetoplacental microvascular physiology and identify exercise as a potent nonpharmacological modulator of microcirculatory impairment in hypertensive pregnancy.