Adult Atlantic salmon (Salmo salar) were exposed for 48 h to water from acidified (pH 5.2) Fossbekk River (Norway), with and without 94 µg aluminium (Al)/L added as AlCl3, and to water from circumneutral (pH 6.7) Ims River (Norway) (controls). Cardiac output, heart rate, and stroke volume were monitored throughout the exposure period with Doppler flow probes placed around the ventral aorta of the fish. Fish exposed to Fossbekk River water without added Al showed few physiological disturbances. When 94 µg Al/L was added to Fossbekk River water, most of the fish died before the end of the 48-h exposure period, and a large elevation in heart rate was observed together with a decrease in plasma chloride concentrations and an increase in haematocrit, plasma glucose and plasma cortisol levels. Cardiac output was maintained at basal levels during the first 24 h of exposure because the tachycardia was accompanied by a concomitant reduction of stroke volume. Signs of arrhythmia appeared after 32 h of exposure and were associated with a further decrease in stroke volume that caused cardiac output to decrease below basal levels. The incapacity of the tachycardia to elevate cardiac output and the subsequent death of the fish suggest that this response to low pH and Al is more of a maladaptation reaction than a compensatory or adaptative reaction.

Exposure of sexually mature pre‐spawning Atlantic salmon Salmo salar to Fossbekk water (pH 5·2) for 7 days led to a significant reduction in critical swimming speed (U‐crit) in females but not in males. Exposure to Fossbekk water +A1 (as AlCl3) for 24 h led to a significant reduction in U‐crit in both males and females. In contrast to fish exposed for 7 days to Fossbekk water, fish exposed to Fossbekk+A1 had accumulated much more aluminium and mucus on their gills. Losses of plasma ions were similar in both groups exposed to acid water. Blood glucose was twice as high in fish exposed to Fossbekk water for 7 days compared with fish exposed to Fossbekk+A1 for 24 h. Plasma cortisol was still elevated compared with controls after exposure to Fossbekk water for 7 days. Possible mechanisms for the observed decrease in U‐crit at the different exposures are discussed.

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