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Influence of swimming activity on sodium and water balance in the rainbow trout (Salmo gairdneri). Wood, Christopher Michael

Abstract

The permeability of the teleost branchial exchanger to oxygen and carbon dioxide is apparently enhanced during exercise by increased blood perfusion of thin walled high surface area pathways in the gills, the secondary lamellae. However this augmented permeability to respiratory gases may well be accompanied by unfavourable elevations of water and electrolyte fluxes between internal and external environments. The object of the present study was to investigate the effect of imposed swimming activity on sodium and water regulation in the fresh water adapted rainbow trout, Salmo gairdneri. Radiotracer methods were used to measure unidirectional components of branchial sodium exchange in fish at rest, during one hour of swimming, and during one hour of recovery from this exercise condition. Sodium fluxes during extended exercise (up to 8 hours) were quantified by similar techniques in a second series of experiments. These long term swimming trials provided flux rate data.at a wide range of external sodium concentrations; analysis of these results helped to elucidate the relative importance of different mechanisms of branchial sodium transfer in the rainbow trout. Finally, determinations of urine flows and body weight changes under controlled exercise conditions in a swimming respirometer permitted an analysis of water regulation and direct measurement of renal electrolyte losses during activity. The sodium uptake system of Salmo gairdneri in the present study had an extremely high affinity for the ion (half saturation concentration = .014 mEq Na+/L). Both unidirectional flux rates at the gills of rainbow trout were greater than those reported for any other fresh water teleost of comparable size, despite external sodium levels much lower than those used by other workers. The presence of an exchange diffusion mechanism for sodium in the trout gill was strongly indicated but not confirmed.. Branchial transport of the electrolyte was tentatively divided into a large exchange diffusion component, and smaller active influx and simple diffusional efflux elements. In resting animals, branchial sodium influx and efflux rates were equal. However short term activity (1 hour) was associated with a 70% increase in efflux of sodium across the gills, creating a net sodium deficit. This effect was quickly reversed (within 5 minutes) upon the termination of swimming. As influx did not vary, these phenomena probably represented changes in the simple diffusional efflux component without disturbance of carrier mediated sodium transport mechanisms. Branchial water entry was also greatly elevated at the start of exercise. These results were interpreted in terms of augmented passive movements of sodium and water caused by increased blood perfusion of the high permeability respiratory pathways of the gills during swimming. The extended exercise experiments revealed that the high sodium efflux rate of the first hour of activity diminished, during the second hour, and had returned to resting levels by the third and subsequent hours of swimming; influx again remained unchanged. The initial high branchial water entry was also apparently curtailed, but over a shorter time interval (15 - 60 minutes after the onset of activity). These reductions in branchial permeability to water and sodium were interpreted as compensations to decrease the osmotic penalty of exercise. As water entry through the gills declined, urinary output was augmented; an elevated renal sodium loss accompanied the diuresis. However sodium efflux through the kidney remained small relative to the efflux of this electrolyte through the gills. A final equilibrium between branchial entry and renal excretion of water was attained, but at a higher turnover rate than during rest. Before this balance, however, urinary elimination had over-compensated for the initial water gain. The resulting net water deficit reduced the blood space below resting volume, causing a slight increase in plasma sodium levels despite enhanced branchial and renal losses of the ion. An ischemia of "white" muscle may also have accompanied the haemoconcentration. In summary, the results indicated that an initial osmoregulatory disturbance was associated with a redistribution of blood flow through the gills during swimming, but that both branchial hydromineral permeability and the functioning of other systems could be modified by compensations necessary to maintain sodium and water balance during extended exercise.

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