Abstract

During swimming activity Callinectes sapidus incurred a severe hemolymph acidosis due to elevated levels of P CO 2 and lactate. Although hemolymph lactate concentration rose steadily during 1 h of exercise, hemolymph pH was maximally depressed within the first 15 min. A discrepancy between the quantities of lactate and H + released from the tissues into the hemolymph is explained by a large apparent efflux of H + into the ambient seawater, presumably via a branchial ion exchange process. Ammonia excretion increased 6 fold during exercise, but it is not clear if this contributed to the excretion of H +. The total quantity of H + excreted into the environment during exercise and recovery far exceeded that which could be attributed to hemolymph lactic acid, indicating that some of the excreted H + must have originated from other sources, such lactic acid which dissociated intracellularly, with the lactate anions remaining in the cells. Because lactate anions increase hemocyanin O 2 affinity when unopposed by the Bohr shift, the excretion of a large portion of the metabolic H + load, leaving lactate behind in the hemolymph, has important consequences for the regulation of O 2 transport during swimming.

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