Intrauterine growth restriction (IUGR) represents a rate of fetal growth that is less than average for the population and the growth potential of a specific infant. IUGR produces infants who are small for gestational age (SGA) but also appropriate for gestational age (AGA). It refers to growth less than expected for gestational age and is most often under 10th percentiles for age. It develops during the late second and third trimesters of gestation. The etiology of IUGR is multifactorial. One of the most important factors which leads to IUGR is a decrease of nutrients and oxygen delivered to the fetus by the placenta. The growth of adipose tissue and skeletal muscle is limited by the declined fetal nutrient supply later in gestation. IUGR affects about 24% of babies born in developing countries. Worldwide, IUGR is the second cause of perinatal morbidity and mortality behind the premature birth and a major predisposing factor to metabolic disorders throughout postnatal life, even at adult age. Skeletal muscle represents about 35-40% of the body mass and plays an essential role in metabolic homeostasis, being responsible for 65% of fetal glucose consumption. A reduction in skeletal muscle growth characterizes IUGR fetuses compared to normal weight neonates. The decrease in muscle mass is not compensated after birth and persists until adulthood. This is a review of the literature, a neonatological, clinical point of view on the effects of IUGR on striated muscles. The available studies on this subject are currently the results of experimental research on animals, and information about the human fetus and newborn are scarce.
Keywords: Fetus; Glucose; Intrauterine growth restriction; Muscle; Newborn.