The British freshwater crayfish Austropotamobius pallipes

lives in streams or pools that are liable to dry up or become stagnant, and these animals are known to leave water voluntarily to forage or to invade neighbouring habitats (Huxley, 1896; Taylor and Wheatly, 1980). When placed in air, the gills collapse and the crayfish suffer continuously from systemic hypoxia and hypercapnia. Associated with an initial virtual anoxia and a switch to anaerobic metabolism, lactate levels in the haemolymph increase to 13 times their submerged level within 1 h of aerial exposure, and the animals experience an uncompensated metabolic and respiratory acidosis (Taylor and Wheatly, 1981). Despite the apparent impairment of gas exchange, the animals survived prolonged periods of aerial exposure, at least in part because of a mechanism first described for the shore crab Carcinus maenas (Truchot, 1975). This entails progressive mobilization of HCO3−, compensating for the initial acidosis on entry into air. This recovery in acid–base status compensates a rightward Bohr shift, restoring oxygen delivery to the tissues (Taylor and Wheatly, 1981). Although this description of the respiratory adaptations enabling crayfish to survive in air seemed sufficient as that paper went to press, we were encouraged to return to the problem by another novel contribution from Truchot (1980) that described how haemocyanin oxygen-affinity was increased by the accumulation of lactate. We were able to identify this effect in the crayfish, where it combined with an equally potent effect of Ca2+ on oxygen affinity. Levels of Ca2+ in the haemolymph increased progressively when crayfish were placed in air, an effect we interpreted as arising from mobilisation of HCO3− from internal stores of calcium carbonate (Taylor et al., 1987; Truchot, 1987; Whiteley, 1999). Together, these compensatory mechanisms increase the oxygen affinity to a point where submerged rates of oxygen uptake are restored (Taylor and Wheatly, 1981; Taylor and Innes, 1988; Taylor et al., 1991) so that survival in air is ultimately limited by the inability of crayfish to maintain water balance (Tyler-Jones and Taylor, 1986). On recovery of oxygen transport capacity, it was noted that lactate levels in the haemolymph, after having been elevated for the first 5 h in air, fell progressively to submerged levels, while the crayfish remained in air (Taylor and Wheatly, 1981; Morris et al., 1986). This could be interpreted as biochemical recycling of lactate, possibly to reform glycogen stores, via gluconeogenesis from pyruvate. However, on replacement in water after 24 h in air, crayfish experienced an apparent lactate washout, with haemolymph lactate levels rising to those measured on initial exposure to air. This implies that lactate was sequestered somewhere in a body compartment while the animals were in air (Taylor and Wheatly, 1981). The site of this sequestration has not been determined. Lactate levels in abdominal muscle were elevated after 3 h in air but fell in line with changes in the haemolymph during prolonged aerial exposure (Tyler-Jones 941 The Journal of Experimental Biology 204, 941–946 (2001) Printed in Great Britain © The Company of Biologists Limited 2001 JEB2958