Juvenile red sea bream, Pagrus major, were exposed to hypoxia, a gentle decrease in partial pressure of oxygen (PO2) down to 26 mmHg, and subsequently maintained beneath this pressure, at 27.8oC. The increasing trend in respiratory frequency of the fish, caused by hypoxia, reached a maximum level at about 38 mmHg PO2 and thereafter decreased. The fish sank to the bottom around an hour after the PO2 fell below 26 mmHg, and after another half hour respiration was arrested. The hematocrit value and plasma glucose level were slowly increased by hypoxia up to the point at which the fish sank, although mean cellular hemoglobin content (MCHC) was decreased at the maximum level of respiratory frequency. Lactate dehydrogenase, creatine kinase activities, and lactic acid level in muscle, and hepatopancreas lactate concentration, were remark- ably enlarged at the time the fish sank. Cytochrome c oxidase (CCO) activity in the brain sig- nificantly increased with increasing hypoxia load, though not in the gills. On the other hand, CCO activity in the hepatopancreas, kidney, and muscle markedly decreased at the maximum level of respiratory frequency, although its activity in these organs and the heart increased after the time at which the fish sank. These results suggest that metabolic depression in red sea bream in response to hypoxia temporarily occurs from the maximum level of respiratory frequency, though the meta- bolic function abreacts at around the time the fish sink.