In Northern Europe, small shallow lakes and ponds often becomes anoxic for several months every winter due ice blocking both photosynthesis and oxygen diffusion from air. The only fish that survives in these waters is the crucian carp (Carassius carassius) — the wild cousin of the goldfish (C. auratus). The crucian carp is arguably the most anoxia-tolerant fish species. Among vertebrates, its anoxia tolerance is only matched by that of some North American freshwater turtles (genera Trachemys and Chrysemys). However, unlike other anoxia-tolerant vertebrates, the crucian carp remains active during anoxia, although at a reduced level. The key adaptation allowing continued activity is probably its exotic ability to convert lactate to ethanol. However, producing ethanol and releasing it to the water is a wasteful strategy as an energy-rich hydrocarbon is forever lost. Indeed, when faced with falling oxygen levels, the crucian carp strives to take up the little oxygen there is in water, thereby avoiding to turn on ethanol production as long as possible when faced with falling oxygen levels. Thus, the crucian carp has a record high hemoglobin oxygen affinity, and when exposed to hypoxia, it has the remarkable ability to remodel it gills, resulting in a 7-8 fold increase in the respiratory surface area. In sharp contrast to anoxia tolerant turtles, which strongly suppresses cardiac work in anoxia, the crucian carp maintain cardiac output and ventilation at normal levels even after several days in anoxia. This suggests that being active in anoxia demands an active circulatory system for shuttling glycolytic substrates and removing ethanol. To maintain activity, also the brain has to continue to function in anoxia. Brain ATP levels and ion homeostasis are protected, and there is little evidence for reduced neuronal ion permeability in crucian carp, possibly with the exception for reduced expression of glutamate receptors of the NMDA type. Elevated levels of the inhibitory neurotransmitter GABA are likely to play a major role in reducing the energy use by both the brain and body. Molecular mechanisms involved in the anoxic defense involves AMP activated protein kinase (AMPK), while there is an apparent suppression of HIF induced pathways. Experiments followed current national guidelines for animal experimentation.