Why do fish die after severe exercise?

Authors

  • C. M. Wood,

    1. Department of Biology, McMaster University, Hamilton, Ontario, Canada L8S 4K1
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  • J. D. Turner,

    1. Department of Biology, McMaster University, Hamilton, Ontario, Canada L8S 4K1
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    • *

      Department of Physiology and Biophysics, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, U.S.A.

  • M. S. Graham

    1. Department of Biology, McMaster University, Hamilton, Ontario, Canada L8S 4K1
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    • Marine Science Research Laboratory, Memorial University of Newfoundland, St John's, Newfoundland, Canada A1C 5S7.


Abstract

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.

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