Crustaceans are often tolerant of hypoxic exposure and many regulate O(2) consumption at low ambient O(2). In acute hypoxia, most increase branchial water flow, and many also increase branchial haemolymph flow, both by an increase in cardiac output and by shunting flow away from the viscera. The O(2)-binding affinity of crustacean O(2) carriers increases in hypoxic conditions, as a result of hyperventilation induced alkalosis. In chronic hypoxic exposure some crustaceans do not sustain high ventilatory pumping levels but increased effectiveness of O(2)-uptake across the gills is maintained as a result of the build up of metabolites such as lactate and urate which also function to increase the haemocyanin O(2)-binding affinity. Chronic exposure to hypoxia also may increase O(2)-binding capacity and promote the synthesis of new high O(2)-affinity carrier molecules. Exposure to untenable rates or levels of O(2) depletion causes many decapodan crustaceans to surface and ventilate the gills with air. Burrowing crayfish provide an example of animals, which excel in all these mechanisms. Control mechanisms involved in compensatory responses to hypoxia are discussed.