Exhaustive exercise induced a severe short-lived (0–1 h) respiratory, and longer-lived (0–4 h) metabolic, acidosis in the extracellular fluid of the rainbow trout. Blood ‘lactate’ load exceeded blood ‘metabolic acid’ load from 1–12 h after exercise. Over-compensation occurred, so that by 8–12 h, metabolic alkalosis prevailed, but by 24 h, resting acid-base status had been restored. Acid-base changes were similar, and lactate levels identical, in arterial and venous blood. However, at rest venous RBC pHi was significantly higher than arterial (7.42 versus 7.31). After exercise, arterial RBC pHi remained constant, whereas venous RBC pHi fell significantly (to 7.18) but was fully restored by 1 h. Resting mean whole-body pHi, measured by DMO distribution, averaged approx. 7.25 at a pHe of approx. 7.82 and fell after exercise to a low of 6.78 at a pHe of approx. 7.30. Whole-body pHi was slower to recover than pHe, requiring up to 12 h, with no subsequent alkalosis. Whole-body ECFV decreased by about 70 ml kg-1 due to a fluid shift into the ICF. Net H+ excretion to the water increased 1 h after exercise accompanied by an elevation in ammonia efflux. At 8–12 h, H+ excretion was reduced to resting levels and at 12–24 h, a net H+ uptake occurred. Lactate excretion amounted to approx. 1% of the net H+ excretion and only approx. 2% of the whole blood load. Only a small amount of the anaerobically produced H+ in the ICF appeared in the ECF and subsequently in the water. By 24 h, all the H+ excreted had been taken back up, thus correcting the extracellular alkalosis. The bulk of the H+ load remained intracellular, to be cleared by aerobic metabolism.

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