When oxygenation is compromised the fetus is capable of a number of adaptive responses, both protective and potentially pathologic, which can be categorized as those affecting fetal metabolism and those affecting fetal oxygen transport. However, both the extent and the duration of the impairment in oxygenation will bear on these adaptive responses. While fetal O2 extraction is increased when oxygenation is acutely compromised thus maintaining O2 consumption, with chronic hypoxemia there is a decrease in O2 consumption paralleling that in O2 delivery and contributed to by the resultant fall-off in growth and alterations in behavioural activity. While a redistribution of blood flow to vital organs continues to be evident, this will be less pronounced than that seen with acute hypoxemia reflecting diminished hormonal changes, underlying metabolic alterations, and the extent to which fetal blood gases are normalized. Much of this information is based on experimental data using unanesthetized fetal sheep with chronic catheterization; however, clinical outcome data and the use of investigative techniques including ultrasound scanning and cordocentesis have supported the relevance of this experimental data to the human situation.