Fetal programming under maternal heat stress: a focus on skeletal muscle growth and nutrition in livestock.

Abstract

An adverse in utero experience negatively impacts perinatal growth in livestock. Maternal heat stress (HS) during gestation reduces placental growth and function. This progressive placental insufficiency ultimately leads to fetal growth restriction (FGR). Studies in chronically catheterized fetal sheep have shown that FGR fetuses exhibit hypoxemia, hypoglycemia, and lower anabolic hormone concentrations. Under hypoxic stress and nutrient deficiency, fetuses prioritize basal metabolic requirements over tissue accretion to support survival. Skeletal muscle is particularly vulnerable to HS-induced placental insufficiency due to its high energy demands and large contribution to total body mass. In FGR fetuses, skeletal muscle growth is reduced, evidenced by smaller myofiber size and mass, reduced satellite cell proliferation, and slower rate of protein synthesis. Disruptions in skeletal muscle growth are associated with mitochondrial dysfunction, including reduced pyruvate flux into the mitochondrial matrix and lower complex I activity in the mitochondrial electron transport chain. This review summarizes current research on the mechanisms by which HS-induced placental insufficiency affects skeletal muscle growth in the fetus, with an emphasis on myogenesis, hypertrophy, protein synthesis, and energy metabolism. The evidence presented is primarily drawn from experiments using chronically catheterized fetal sheep exposed to maternal HS during mid-gestation. Additionally, we explore emerging nutritional strategies aimed at enhancing skeletal muscle growth in animals with FGR. These strategies hold promise not only for improving reproductive efficiency in livestock affected by prenatal stress but also for their translational relevance to human pregnancies complicated by placental insufficiency.