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Journal of Experimental Biology, Vol 194, Issue 1 225-253, Copyright © 1994 by Company of Biologists
JOURNAL ARTICLES |
C Wood and R Munger
This study tests the hypothesis that the increase in blood PCO2 and associated respiratory acidosis after exhaustive exercise play an important role in stimulating ventilation during post-exercise recovery in fish. Injection of bovine carbonic anhydrase (10 mg kg-1) into the bloodstream of rainbow trout caused a persistent 40 % increase in the HCO3- dehydration capacity of the blood. The treatment was designed to increase CO2 excretion and therefore to reduce PCO2 build-up and acidosis after exercise. Aerobic and anaerobic swimming performance were not affected by carbonic anhydrase, and there were only very minor effects on arterial blood acid­base status in resting fish. However, carbonic anhydrase attenuated post-exercise increases in PaCO2 and decreases in pHa by about 50 % without altering arterial O2 variables, red cell swelling or the intracellular pH of the brain or muscle tissues. The effects on arterial pH (pHa) resulted largely from alleviation of the increase in PaCO2. In accordance with the original hypothesis, normal post-exercise hyperventilation was greatly attenuated, through reductions in both ventilatory stroke volume and frequency, and excess post-exercise O2 consumption was reduced. Post-exercise increases in plasma levels of adrenaline and noradrenaline were also reduced by the carbonic anhydrase treatment. Overall, there was a strong correlation between increases in relative ventilation and decreases in pHa after exhaustive exercise. The results provide functional significance for the phenomenon of PaCO2 elevation and associated respiratory acidosis after exercise and are consistent with other recent studies indicating an important secondary drive to ventilation in fish based on arterial acid­base status, in addition to the primary drive based on arterial O2 levels.
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