A suboptimal prenatal environment can affect organogenesis and the natural development of an individual by epigenetic modifications of the genome. While these changes are permanent, it is common not to see any pathological effects until adulthood. The impact of nutritional insults during development has been well-studied in a wide variation of physiological systems. Less studied however, are the effects of hypoxic developmental insults. To this end, our aim is to investigate the long-term effects of prenatal hypoxia on cardiovascular metabolism of adult offspring. We have utilised spectrophotometry to investigate mitochondrial enzyme activity combined with high resolution respirometry to investigate in vivo mitochondrial efficiency and production of reactive oxygen species. With these methods we aim to identify changes in myocardial mitochondrial energy production, taking a step towards understanding the effect of intrauterine hypoxia on cardiac energetics. Pregnant mice were placed in hypoxic chambers with 14% O2 from gestational day 3-19 and reared in normoxia until six months of age. Heart tissue was harvested and enzymatic activity of citrate synthase and mitochondrial Electron Transport Chain Complexes I-IV was measured using spectrophotometry. High resolution respirometry lets us further investigate the status of the mitochondria, with emphasis on oxygen consumption and ROS production. Preliminary data show promising differences between treatment and control groups, as well as sexual dimorphism regarding response and effect. We hope to be able to identify possible mechanistic changes, on a cellular level, that underlie the pathological cardiovascular phenotype associated with intrauterine hypoxia.