Fetal growth restriction (FGR) caused by placental insufficiency (PI) leads to poor skeletal muscle growth and performance. This study aims to understand the mechanisms that limit muscle growth in FGR and explore the potential for reversing FGR-related deficiencies through oxygen and glucose supplementation. In FGR fetal sheep created with maternal heat stress, we have identified mitochondrial defects that lower oxidative metabolism and muscle growth. We plan to test the hypothesis that correcting oxygen and glucose concentrations in FGR fetuses will promote protein accretion, restore mitochondrial activity, and stimulate muscle growth. The proposed objectives will test the combined effect of sustained oxygen and glucose correction on net fetal protein accretion rates, mitochondrial metabolism, and the plasticity of skeletal muscle growth. The findings will provide fundamental knowledge on the mechanisms that obstruct skeletal muscle metabolism and growth in FGR. Understanding how nutrient replacement approaches, combined with oxygen supplementation, can improve the health of FGR fetuses will inform future studies and help establish effective strategies for managing FGR and promoting health.