Adult brown trout (300­600 g) were acclimated for 2 weeks to an artificial soft water (Ca2+, 50 µmol l-1) and maintained at either 5 °C (October to March) or 15 °C (May to August). Following insertion of a cannula into the dorsal aorta under MS-222 anaesthesia and a recovery period of 2 days, the fish were exposed to a 4 day episode of sub-lethal copper levels at pH 5 or kept at control conditions of pH 7 without copper. The copper concentrations had been predetermined by toxicity testing and were approximately 0.47 µmol l-1 at 5 °C and 0.08 µmol l-1 at 15 °C. At 5 °C, a group of fish was also exposed to approximately 0.08 µmol l-1 copper at pH 5. Plasma total ammonia (Tamm) concentration was significantly elevated by exposure to copper and pH 5. In resting trout exposed to the appropriate sub-lethal copper concentration at pH 5, Tamm was six and 7.5 times greater at 5 and 15 °C, respectively, than those of control trout at the respective temperatures. Although unconfirmed, an elevation of ammonia production alone seems unlikely to account for such substantial increases. From previous studies, there is little evidence of impairment of respiratory gas exchange in trout exposed to these copper concentrations and yet, in the acidic test waters, the gradient of NH3 partial pressure between fish and water was 5.5­6 times greater than that under control conditions. Swimming performance determined by the critical swimming speed (Ucrit) was reduced by copper and acid exposure, and a significant relationship existed between Ucrit and the plasma ammonia concentration of exercised trout. Ammonium ions influence several key enzymes involved in energy metabolism, and elevated ammonia levels might, therefore, reduce the capacity of muscle to exercise. Alternatively, ammonia may have affected the nervous coordination of exercise either centrally or by disrupting peripheral motor innervation.

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