Exhaustive ‘burst-type’ exercise in the rainbow trout resulted in a severe acidosis in the white muscle, with pHi dropping from 7.21 to a low of 6.62, as measured by DMO distribution. An accumulation of lactate and pyruvate, depletions of glycogen, ATP and CP stores, and a fluid shift from the extracellular fluid to the intracellular fluid of white muscle were associated with the acidosis. The proton load was in excess of the lactate load by an amount equivalent to the drop in ATP, suggesting that there was an uncoupling of ATP hydrolysis and glycolysis. Initially, lactate was cleared more quickly than protons from the muscle, a difference that was reflected in the blood. It is suggested that during the early period of recovery (0–4 h), the bulk of the lactate was oxidized in situ, restoring pHi to a point compatible with glyconeogenesis. At that time, lactate and H+ were used as substrates for in situ glyconeogenesis, which was complete by 24 h. During this time, lactate and H+ disappearance could account for about 75% of the glycogen resynthesized. The liver and heart showed an accumulation of lactate, and it is postulated that this occurred as a result of uptake from the blood. Associated with the lactate load in these tissues was a metabolic alkalosis. Except for an apparent acidosis immediately after exercise, the acid-base status of the brain was not appreciably affected. Despite the extracellular acidosis, red cell pHi remained nearly constant.

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