To resolve the sources of amino nitrogen which is accumulated as intracellular solute during hyperosmotic volume regulation, components of protein metabolism were monitored during compensation for a change from 15 to 30% salinity in the blue mussel, Mytilus edulis L. Net solute gain stemmed primarily from a marked reduction in total output from the metabolic pool of free amino acids, most of this ‘saving’ resulting from slower whole-body protein synthesis, and the remainder from lower nitrogenous excretion. Indeed, total inputs to the metabolic pool of free amino acids actually decreased over the period of net solute gain at 30%. Associated contributions from dietary assimilation, de novo synthesis and the direct uptake of dissolved amino acids were each negligible, indicating that breakdown products from endogenous body protein were the only significant source of amino nitrogen accumulated during hyperosmotic regulation. This accumulation represented more than 3% of soft-tissue protein nitrogen within the whole animal. We therefore impress that the excretion, during hyposaline adjustment, of all nitrogen previously accumulated as solute in response to equivalent hypersaline change, represents a major component cost of cell volume regulation, and which helps to explain stress and even mortality consequent upon what may be small but frequent fluctuations of salinity.