Abstract
Exhaustive activity in starry flounder resulted in an acidosis in the whole-body extracellular fluid (ECF) and intracellular fluid (ICF) compartments. In the ECF, the acidosis consisted of a short-lived respiratory component (increase in CO₂ tension [Pco₂]) followed by a longer-lived metabolic component (decrease in [ ]). The acid-base disturbance was corrected by 8-12 h. There was little lactate accumulation in the blood, with levels rarely greater than 1-2 mmol/liter, and at all times the blood metabolic acid load (ΔH⁺m) was in excess of the blood lactate load (ΔLa⁻). Blood [glucose] increased by 50%. Whole-body extracellular fluid volume (ECFV) fell by 17% owing to a shift of fluid into the intercellular fluid volume (ICFV), causing a general hemoconcentration. Exercise also caused an acidosis in the whole-body intracellular compartment, with intracellular pH dropping from a rest value of 7.58 to a low of 7.24. The whole-body intracellular acidosis was corrected ~4 h sooner than the extracellular disturbance and became alkalotic at 8 h, returning to normal at 12 h. Associated with this acid-base disturbance was an increased efflux of acidic equivalents (H⁺) to the environmental water, coincident with a large increase in the titratable-acidity flux. Ammonia excretion increased only slightly. Analysis of the distribution of metabolic acid between the ECF, ICF, and environmental water revealed that until 4 h postexercise, the bulk of the acid load remained in the intracellular compartment. Approximately 20% passed through the extracellular fluid and was transiently stored in the environmental water at 4-12 h. This flux of H⁺ to the water was associated with an intracellular alkalosis and thus appeared to hasten correction of intracellular acid-base status, perhaps as a means of aiding metabolic recovery.

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