Impact of placental insufficiency on fetal skeletal muscle growth

• Placental insufficiency results in redistribution of fetal cardiac output to vital organs at the expense of muscle.
• Fetal myoblast proliferation and myotube hypertrophy are reduced in the IUGR fetus.
• Birthweight is positively correlated with lean mass and grip strength.
• Reduced fetal muscle mass in IUGR may set the trajectory for catch-up growth that favors adiposity.
• Nutritional strategies are needed to improve muscle growth and body composition in the IUGR fetus and neonate.

Intrauterine growth restriction (IUGR) caused by placental insufficiency is one of the most common and complex problems in perinatology, with no known cure. In pregnancies affected by placental insufficiency, a poorly functioning placenta restricts nutrient supply to the fetus and prevents normal fetal growth. Among other significant deficits in organ development, the IUGR fetus characteristically has less lean body and skeletal muscle mass than their appropriately-grown counterparts. Reduced skeletal muscle growth is not fully compensated after birth, as individuals who were born small for gestational age (SGA) from IUGR have persistent reductions in muscle mass and strength into adulthood. The consequences of restricted muscle growth and accelerated postnatal “catch-up” growth in the form of adiposity may contribute to the increased later life risk for visceral adiposity, peripheral insulin resistance, diabetes, and cardiovascular disease in individuals who were formerly IUGR. This review will discuss how an insufficient placenta results in impaired fetal skeletal muscle growth and how lifelong reductions in muscle mass might contribute to increased metabolic disease risk in this vulnerable population.