Abstract
In addition to an extracellular acidosis in which blood metabolic acid load greatly exceeded lactate load, exhaustive activity in starry flounder resulted in an intracellular acidosis of largely metabolic origin in the white muscle, with intracellular pH dropping from 7.56 to 7.27, as measured by DMO distribution. An accumulation of lactate and depletion of glycogen in addition to a shift of fluid from the extracellular to intracellular space were associated with the postexercise acidosis. Pyruvate levels increased in blood and later in muscle; the relative rise in pyruvate was greater than that in lactate so the lactate:pyruvate ratio declined. The muscle intracellular acidosis was corrected sooner than the extracellular acidosis (4-8 h vs. 8-12 h). The restoration of muscle pHi was associated with an increase in pyruvate, a restoration of glycogen stores, and clearance of the lactate load. It is suggested that both lactate and acidic equivalents (H⁺) were cleared from the muscle via in situ oxidation and/or glyconeogenesis and that the rapid correction of the intracellular acidosis through efflux of part of the H⁺ load facilitated metabolic recovery. The liver showed a progressive alkalinization after exercise. This alkalinization was of metabolic origin and not associated with lactate accumulation. Except for a short-lived depression 0.5 h after exercise, red cell intracellular pH remained virtually constant.

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