Heat stress (HS) is a key limiting factor to efficient animal production and negatively impacts health and development during postnatal life. In addition, hyperthermia during in utero development can permanently alter postnatal phenotypes and negatively impact future animal performance. While the teratogenic effects of prenatal HS have been extensively evaluated, the impact of in utero HS exposure on future mammalian thermoregulation, nutrient partitioning, and bioenergetics is undefined. To determine the postnatal consequences of in utero HS, pregnant first parity sows and rats were exposed to either thermal neutral (TN) or HS conditions for the entire gestation, the first half, or second half of gestation. To account for differences in maternal nutrient intake, we utilized an ad libitum TN control group and a pair-fed TN control group of rats. Progeny were evaluated for differences in production performance, nutrient partitioning, thermoregulation, and post-absorptive metabolism. In a series of experiments, it was determined that prenatal HS exposure increased postnatal adipose deposition at the expense of skeletal muscle mass and permanently increased core body temperature during future development. When compared with in utero HS-exposed rats, pair-fed TN exposed progeny had increased adipose tissue and reduced lean tissue mass. In opposition to some previously published reports, postnatal HS exposure seems to reduce maintenance costs, which may have implications toward energy efficiency during times of thermal stress. In summary, HS modifies animal metabolism and physiology during both pre- and postnatal development and reduces livestock production efficiency.