Date of Award

12-1981

Degree Type

Thesis

Degree Name

Master of Science (MS)

Department

Biology

Supervisor

Professor C.M. Wood

Abstract

Strenuous exercise in both rainbow trout (Salmo gairdneri) and flathead sole (Hippoglossoides elassodon) caused substantial blood acidosis of combined respiratory (protons due to CO2 accumulation) and metabolic (protons due to metabolic acid accumulation) origin. The contribution of the respiratory component was maximal immediately following the cessation of exercise and was fully corrected within 1 h. The metabolic acid load in the blood reached a maximum at 0.5 - 1 h after exercise and required 8 - 12 h to recover fully.

Although lactic acid production by glycolysis generates stoichiometrically equivalent amounts of lactate and protons in muscle during exercise, their blood concentrations during recovery were quite different. Recovery in rainbow trout displayed a pattern in which lactate accumulated in the blood in excess of metabolic protons. The flathead sole exhibited the exactly opposite discrepancy where proton accumulation in the blood exceeded that of lactate. L(+)-lactic acid infusion experiments in both fish illustrated that preferential removal of either protons or lactate from the blood could not account for the observed lactate/proton discrepancies.

Experimentation using an isolated, perfused rainbow trout trunk showed that the myotome can differentially release lactate and protons into the extracellular space in response to the appropriate extracellular signals. Through the manipulation of extracellular pH and PCO2 it was possible to regulate the rate of proton efflux from the myotome. This and other evidence indicates that a differential release of protons and lactate from the muscle causes the observed discrepancies during in vivo recovery.

Simultaneous muscle and blood sampling in vivo suggests that most (≈90%) of the lactate and protons produced during exercise are retained within the myotome. This causes a water shift into the intracellular space which contracts the extracellular space, resulting in haemoconcentration and disturbance in plasma ion balance. The eventual fate of the lactate and proton load retained within the muscle would seem to be metabolic removal in situ, probably glyconeogenesis or oxidation.

A model is presented which can explain the complex events occurring during recovery from strenuous exercise. This model integrates the results from in vivo and in vitro experimentation and hypothesizes on the mechanism and control of lactate and proton utilization within the muscle cell and their movements between body compartments.

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