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Why do fish die after severe exercise?
Author(s) -
Wood C. M.,
Turner J. D.,
Graham M. S.
Publication year - 1983
Publication title -
journal of fish biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.672
H-Index - 115
eISSN - 1095-8649
pISSN - 0022-1112
DOI - 10.1111/j.1095-8649.1983.tb04739.x
Subject(s) - metabolic acidosis , biology , acidosis , lactic acid , medicine , lactic acidosis , respiratory acidosis , endocrinology , respiratory system , anion gap , trout , fish <actinopterygii> , anatomy , fishery , genetics , bacteria
Trout fitted with dorsal aortic cannulae were subjected to 6 min of intensive exercise and monitored over the following 12 h recovery period. Delayed mortality was 40%; the majority of deaths occurred 4–8 h post‐exercise. Surviving fish exhibited a short‐lived haemoconcentration reflected in increased haematocrit, haemoglobin, plasma protein, Na + and Ch ‐ levels; an extended rise in plasma [K + ]; a quickly corrected respiratory acidosis; and a more prolonged metabolic acidosis in concert with a rise in blood lactate. Dying fish exhibited very similar trends except for a significantly greater metabolic acidosis, lower plasma [Cl ‐ ], and the apparent accumulation of an unknown anion in the blood prior to death. Cardiac failure did not occur. Blood metabolic acid levels, while elevated, were only ∼ 50% of peak lactate anion levels and well within the normal range of tolerance, as were all other changes observed in the blood of non‐survivors. The hypothesis that post‐exercise mortality is due to excessive ‘lactic acid’ accumulation in the blood is discounted. It is suggested that intracellular acidosis may be the proximate cause of death.