Many marine invertebrates and fish are oxyconforming animals, many of them lack oxygen transport proteins, and several are known anaerobic experts, surviving hours and days at very low oxygen. These guys often display mitochondrial oxyconformity, accelerating respiratory performance even when oxygen in the medium becomes supersaturated. As various forms of stress, and especially exposure to critically high and low temperatures, are discussed to cause functional hypoxia in marine ectotherms, we were interested to see, if they induce a hypoxic response under thermal stress. In North Sea fish (Zoarces viviparus) HIF-1a is expressed under normoxic conditions and HIF DNA binding is enhanced during cold exposure and cold acclimation of the fish. HIF-1 DNA binding to the human Epo enhancer was dependent on cellular redox state, with lower HIF-binding at more oxidized redox potential. Redox state, in turn, was more reduced in the cold (-275mV) and more oxidized (-245mV) on severe warming of the fish. Although production of H2O2 by isolated fish mitochondria was below detection limit at control and stress temperatures, we detected a mild increase of some oxidative stress parameters on critical warming (2h). So warming induced free radical formation and oxidized tissue redox potential may be responsible for the inability of the fishes to induce a hypoxic response during warming. Longer survival at critically high temperatures is possible only through anaerobic metabolism.