Abstract

A quantitative analysis of O 2 and CO 2 transport was conducted in resting and exercising rainbow trout, and these data were used to quantify the magnitude of coupling between O 2 and CO 2 exchange, in vivo. The release of Bohr protons during haemoglobin-oxygenation was non-linear over the Hb–O 2 equilibrium curve used in trout subjected to different levels of sustained exercise. At low swimming speeds, when venous blood O 2 content (Cv O 2 ) was high, there was a small acidosis as blood passed through the gills, indicating more protons were released during oxygenation of Hb than were consumed during HCO 3 − dehydration. At higher swimming speeds, when Cv O 2 was low, there was a significant alkalosis in arterial relative to venous blood, indicating that fewer protons were released upon oxygenation than HCO 3 − ions were dehydrated to CO 2. Haldane coefficients (moles of protons released per mole of O 2 which binds to Hb), calculated from steady state arterial and mixed-venous parameters, revealed that under resting conditions all blood CO 2 removed from the blood during gill transit was stoichiometrically related to O 2 uptake through the release of Bohr protons during Hb oxygenation. The magnitude of coupling between CO 2 excretion and O 2 uptake decreased from 100% to less than 40% at the maximal swimming velocity when the largest region of the Hb–O 2 equilibrium curve was used for gas exchange. The non-linear release of Bohr protons over the range of Hb–O 2 saturation in the blood reduces HCO 3 − dehydration at the gills during greater work loads elevating arterial P CO 2 levels, leading to an increase in HCO 3 − buffer capacity of the blood and tissues.

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