RECOVERY METABOLISM OF TROUT WHITE MUSCLE - ROLE OF MITOCHONDRIA

Recovery from burst exercise in fish is very slow. Lactate conversion to glycogen occurs primarily within white muscle and must be fueled by mitochondrially produced ATP. In a parallel study we characterized the changes in tissue metabolites associated with burst exercise and recovery in rainbow trout (Oncorhynchus mykiss) white muscle. The present study examines whether the mitochondrial capacity to produce ATP may limit the rate of recovery of trout white muscle. The cost (ATP.min-1.g-1) of glycogen resynthesis (0.05-mu-mol lactate converted.min-1.g tissue-1) was compared with the mitochondrial capacity to produce ATP. The cost of recovery can be met by only 3.5% of the maximal mitochondrial capacity. In fact, during recovery trout white muscle mitochondria operate at a small fraction of their in vitro maximum. This capacity is suppressed in vivo by highly inhibitory ATP/ADP and limiting phosphate. The primary signal for increased ATP synthesis associated with recovery is not a change in ATP/ADP but probably phosphate, elevated because of phosphocreatine hydrolysis and adenylate catabolism in the purine nucleotide cycle. At low ADP availability and suboptimal phosphate (< 5 mM), acidosis enhances respiration. At high respiratory rates mitochondrial pyruvate oxidation is sensitive to pyruvate concentration over the physiological range (apparent Michaelis constant = 35-40-mu-M). This sensitivity is lost at the low rates that approximate in vivo respiration. Changes in lactate do not affect the kinetics of pyruvate oxidation. Fatty acid oxidation may spare pyruvate and lactate for use in glyconeogenesis, primarily through allosteric inhibition of pyruvate dehydrogenase rather than covalent modification.