The effects of deep and acute hypoxia (PwO2 = 25 Torr) on oxygen transport characteristics (Hill number (n) and P50) were investigated in trout at 15 degrees C. When a fish is submitted to such an acute and deep hypoxia, a metabolic acidosis develops as soon as the arterial oxygen tension drops to about 15 Torr. We first showed that the hemoglobin of blood sampled at the end of the acidification period has an increased oxygen affinity. This improved affinity could be explained by the internal alkalisation of erythrocytes due to the extrusion of protons via a beta-adrenergic stimulation of Na+/H+ exchanges occurring at the onset of hypoxia and responsible for extracellular acidosis. Secondly we observed a significant increase (about 20%) of the number of blood cells per volume of blood during the acidosis. This cell number stays constant afterwards. The dual effects of a higher hemoglobin oxygen affinity and a greater amount of available hemoglobin improving blood oxygen loading at the fish gills appear to be a fast adaptive response to acute hypoxia. Surprisingly, we found that the elevated affinity occurring during acidosis remained constant as long as the fish were maintained in hypoxia, in spite of possible large variations of extracellular pH (pHe). This result is difficult to reconcile with the idea that the increase in affinity is imposed by intracellular pH (pHi), since in red blood cells pHi depends on pHe, thus any modification of pHe would in this case modify oxygen affinity.