The role of malate in exercise-induced enhancement of mitochondrial respiration.

Liver mitochondria isolated from rats immediately after exercise oxidize substrates more rapidly than do mitochondria from resting animals. In both fed and fasted rats, a 1-h period of exercise resulted in increased concentrations of malate in their livers and in the mitochondria isolated therefrom. This increase occurred in both untrained and exercise-trained rats. Because mitochondrial malate is known to facilitate mitochondrial uptake of other carboxylic substrates, it seems likely that the increased mitochondrial malate is responsible for the increased rate of oxidation. Rats injected with small amounts of malate (4.6 mumol/100 g body wt) yielded liver mitochondria with increased malate concentration and increased rates of oxidation of citrate, alpha-ketoglutarate, and succinate. The beta adrenergic antagonist propranolol (0.25 mg/100 g body wt) and the alpha 1 antagonist prazosin (same dose) did not abolish the effect of exercise on mitochondrial malate concentration or substrate oxidation.