Changes in acetate availability : effect upon substrate utilisation at rest and during exercise
The aim of the present series of studies was to investigate the effect of sodium acetate ingestion on energy metabolism with particular emphasis upon changes in fat and carbohydrate utilisation at rest and during exercise. Ingestion of sodium acetate at rest reduced fat oxidation by 30% over a 90 min period post-ingestion assuming that 90% of the ingested organic acid was oxidised during this time. The decrease in fat utilisation was found to be almost entirely accounted for by oxidation of the exogenous acetate such that carbohydrate utilisation was unaffected. Plasma glycerol concentration was unchanged following ingestion of the sodium salt, suggesting that the suppression in fat metabolism following acetate ingestion was not due to reduced lipid availability and may have been located intracellularly. Through the use of stable isotope techniques it was subsequently shown that 80% of the ingested bolus was oxidised over 180 min post-ingestion when sodium acetate was ingested at a dose of 2 mmol.kg-1 body mass. Fat utilisation was found to be significantly lower over this period compared to ingestion of a similar dose of sodium bicarbonate (18.43 ± 7.12 vs. 13.85 ± 4.69 g in the bicarbonate and acetate trials, respectively; P < 0.05), with no difference in carbohydrate utilisation between trials. Despite acetate being shown to have no effect upon carbohydrate utilisation, it was observed in a separate study that acetate ingestion improved glucose tolerance during a 75 g oral glucose tolerance test. Blood glucose and plasma insulin concentration were significantly elevated 15 min after consumption of a glucose load compared with a trial matched on fluid volume, sodium ingested and changes in acid-base balance (bicarbonate ingestion). Glucose and insulin then decreased at a quicker rate between 30 and 120 min post-ingestion of the glucose load following sodium acetate ingestion. In a second series of studies the effect of perturbing substrate utilisation at rest on metabolism during subsequent prolonged exercise was examined. Ingestion of sodium acetate at a dose of 4 mmol.kg-1 body mass was shown to suppress fat oxidation at rest (0.11 ± 0.03 vs. 0.06 ± 0.02 g.min-1 in the bicarbonate and acetate trials, respectively; P < 0.05) with no effect upon carbohydrate utilisation thus supporting the previous findings.