Oxygen consumption (VO2) was measured in normoxia as ambient temperature (Ta) was lowered from 40 to 15 degrees C, at the rate of 0.5 degrees C/min (thermoneutrality approximately 33 degrees C). In 2-day-old rats born in hypoxia after hypoxic gestation, the Ta-VO2 relationship was as in controls; their interscapular brown adipose tissue (IBAT) was hypoplastic (less proteins and DNA), with lower concentration of the mitochondrial uncoupling protein thermogenin. In 8-day-old rats exposed to hypoxia postnatally (day 2 to day 8), at any Ta below thermoneutrality VO2 was higher than in controls; also, in this group IBAT was hypoplastic with decreased thermogenin. Additional measurements under various experimental conditions indicated that the increased thermogenic capacity was not explained by the smaller body mass and increased blood oxygen content or by the eventuality of intermittent cold stimuli during the chronic hypoxia. On the other hand, chronic hypercapnia (3% CO2 in normoxia, from day 2 to day 8) also resulted in increased normoxic thermogenesis. We conclude that chronic hypoxia in the perinatal period 1) reduces IBAT mass and thermogenin concentration and 2) can increase the newborn's thermogenic capacity because of stress-related mechanisms not specific to hypoxia.