This paper reviews recent evidence from epidemiological, follow-up and experimental studies that sub-optimal conditions during gestation can cause alterations in respiratory function that persist during postnatal life. Several studies indicate that placental insufficiency, which can be associated with fetal substrate deprivation, hypoxia and low birthweight, may be followed by evidence of respiratory compromise in later life. Similarly, it is becoming evident that maternal smoking affects fetal lung development and that the effects can persist into postnatal life. A reduced period of fetal development, due to preterm birth, may be associated with prolonged postnatal respiratory consequences which are independent of factors operating during the early postnatal period. Disorders of pregnancy that compress the fetal lungs, or that cause the abolition of fetal breathing movements, commonly lead to lung hypoplasia. We have been interested in the prenatal causes and postnatal effects of fetal lung hypoplasia and have used an ovine model of lung hypoplasia induced by prolonged removal of amniotic fluid. This leads to a reduction in the expansion of the fetal lungs which appears to be a common underlying cause of fetal lung hypoplasia. Studies of lung function in lambs chronically exposed as fetuses to a lack of amniotic fluid showed that, although lung hypoplasia was apparently present throughout the 28-day postnatal study period, major alterations in respiratory function were attributable to changes in chest wall compliance. Thus, it is apparent that sub-optimal intrauterine conditions can have lasting effects on the structure and function of respiratory organs. Available evidence indicates that the degree to which these organs can recover postnatally may be restricted.