It has been known for may years that hypoxaemia in the fetus induces a number of biophysical, cardiovascular, endocrine and metabolic responses by the fetus, some of which are not sustained if the period of hypoxaemia is extended. For instance, fetal breathing and body movements and the circulating concentrations of many of the stress-related hormones return to control levels during prolonged periods of hypoxaemia. In particular, circulating fetal blood glucose concentrations gradually return to control levels, after an initial increase. The initial increase is primarily due to a catecholamine-mediated increase in glucose production from glycogen stores leading to a marked reduction in glycogen content. During prolonged periods of hypoxaemia, however, the decrease in fetal blood glucose concentrations is principally due to a decrease in the activity of the major enzymes responsible for glycogenolysis and not to a total depletion of glycogen stores. It is suggested that the decrease in enzyme activity could be due to a prostaglandin E2-mediated antagonism of catecholamine-activated glycogenolysis. In contrast, fetal blood lactate concentrations increase to a plateau after 4-5 h of hypoxaemia and remain at this elevated level for the duration of the hypoxaemia. Circulating lactate concentrations do not increase further, despite production by hypoxic tissues remaining high, due to an increase in lactate clearance by the placenta; under normal conditions the placenta releases lactate into the fetal circulation. It is considered that many of these changes are important adaptive responses which allow the fetus to survive in a sub-optimal intrauterine environment.