Skeletal muscle metabolism during high-intensity sprint exercise is unaffected by dichloroacetate or acetate infusion

This study investigated whether increased provision of oxidative substrate would reduce the reliance on nonoxidative ATP production and/or increase po wer output during maximal sprint exercise. The provision of oxidative subst rate was increased at the onset of exercise by the infusion of acetate (AC; increased resting acetylcarnitine) or dichloroacetate [DCA; increased acet ylcarnitine and greater activation of pyruvate dehydrogeanse (PDH-a)]. Subj ects performed 10 s of maximal cycling on an isokinetic ergometer on three occasions after either DCA, AC, or saline (Con) infusion. Resting PDH-a wit h DCA was increased significantly over AC and Con trials (3.58 +/- 0.4 vs. 0.52 +/- 0.1 and 0.74 +/-: 0.1 mmol(.)kg wet muscle(-1.) min(-1)), DCA and AC significantly increased resting acetyl-CoA(35.2 +/- 4.4 and 22.7 +/- 2.9 vs. 10.2 +/- 1.3 mu mol/kg dry muscle) and acetylcarnitine (12.9 +/- 1.4 a nd 11.0 +/- 1.0 vs. 3.3 +/- 0.6 mmol/kg dry muscle) over Con. Resting conte nts of phosphocreatine, lactate, ATP, and glycolytic intermediates were not different among trials. Average power output and total work done were not different among the three 10-s sprint trials. Postexercise, PDH-a in AC and Con trials had increased significantly but was still significantly lower t han in DCA trial. Acetyl-CoA did not increase in any trial, whereas acetylc arnitine increased significantly only in DCA. Exercise caused identical dec reases inATP and phosphocreatine and identical increases in lactate, pyruva te, and glycolytic intermediates in all trials. These data suggest that the re is an inability to utilize extra oxidative substrate (from either stored acetylcarnitine or increased PDH-a) during exercise at this intensity, pos sibly because of O-2 and/or metabolic limitations.