We have investigated the metabolic fate of blood lactate in resting rainbow trout and in fish recovering from a bout of exhaustive exercise. At rest and during recovery from exercise, the majority of blood lactate was oxidized, the proportion increasing with increasing oxygen consumption. It is estimated that, during recovery from exhaustive exercise, lactate released from the muscle has the potential to fuel a significant portion of oxidative metabolism. The bulk of the remaining blood lactate reappeared in the muscle lactate pool, probably via direct uptake by the muscle. There was a significant incorporation of blood lactate into the muscle glycogen pool, providing strong evidence for in situ glycogenesis as the mode for muscle glycogen replenishment. To investigate the role of the liver in blood lactate clearance, trout were functionally hepatectomized by ligation of the hepatic portal circulation. The exercise performance of hepatectomized fish was equal to that of sham- operated fish and controls, indicating that muscle relies primarily on endogenous fuel stores. Furthermore, blood lactate levels immediately after exercise were greater and muscle metabolic recovery was faster in hepatectomized fish than in sham-operated fish and controls. These observations suggest that glycogen resynthesis in trout muscle may be retarded because of a non- recoverable loss of substrate (i.e. lactate) from the muscle, because the lactate released is utilized by the liver. These results are discussed in view of what is known about these processes in other ectothermic vertebrates.

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