This study examined the mechanisms by which Na+ and Clare regulated in freshwater rainbow trout during exercise and stress. Aerobic exercise (at approximately 2 body lengths s−1) caused a brief increase in diffusive Na+ efflux and a brief decline in plasma Na+ and Clconcentrations. This disturbance was rapidly compensated by a threefold increase in Na+ and Clinflux (over the first 10–12 h of exercise) and by a reduction in Na+ efflux to 40 % of the control value by 7 h of exercise. The compensation produced a significant increase in whole− body [Na+], whereas whole−body [Cl] remained unchanged. In contrast, confinement stress (for 4 or 8 h) caused an eightfold increase in Na+ and Clefflux which was sustained for at least the first 5 h of stress and resulted in large decreases in whole−body [Na+] and [Cl]. Compensation of the losses was not complete until 24 h post−stress and was achieved by increases in Na+ and Cl influx (of similar magnitude and timing to those observed during exercise) as well as reductions in Na+ and Cl efflux to nearly zero. We conclude that ion influx increased because of an activation of inactive transport sites in the gills, whereas efflux was reduced by a reduction in branchial ionic permeability; both responses are mediated hormonally. Although the hormonal control mechanisms are as yet poorly defined, we argue that growth hormone and prolactin are responsible for the regulation of influx and efflux, respectively, and rule out either cortisol or epinephrine as having any role, at least with respect to the rapid [NaCl] regulation evident during exercise.

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