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Oxygen uptake on-kinetics in dog gastrocnemius in situ following activation of pyruvate dehydrogenase by dichloroacetate

Bruno Grassi, Michael C. Hogan *, Paul L. Greenhaff †, Jason J. Hamann ‡, Kevin M. Kelley ‡, William G. Aschenbach ‡, Dumitru Constantin-Teodosiu † and L. Bruce Gladden ‡

The aim of the present study was to determine whether the activation of the pyruvate dehydrogenase complex (PDC) by dichloroacetate (DCA) is associated with faster O₂ uptake (_O2) on-kinetics. _O2 on-kinetics was determined in isolated canine gastrocnemius muscles in situ (n = 6) during the transition from rest to 4 min of electrically stimulated isometric tetanic contractions, corresponding to ~60-70 % of peak _O2. Two conditions were compared: (1) control (saline infusion, C); and (2) DCA infusion (300 mg (kg body mass)^-1, 45 min before contraction). Muscle blood flow (Q˙ ) was measured continuously in the popliteal vein; arterial and popliteal vein O₂ contents were measured at rest and at 5-7 s intervals during the transition. Muscle _O2 was calculated as Q˙ multiplied by the arteriovenous O₂ content difference. Muscle biopsies were taken before and at the end of contraction for determination of muscle metabolite concentrations. DCA activated PDC at rest, as shown by the 9-fold higher acetylcarnitine concentration in DCA (vs. C; P < 0.0001). Phosphocreatine degradation and muscle lactate accumulation were not significantly different between C and DCA. DCA was associated with significantly less muscle fatigue. Resting and steady-state _O2 values during contraction were not significantly different between C and DCA. The time to reach 63 % of the _O2 difference between the resting baseline and the steady-state _O2 values during contraction was 22.3 ± 0.5 s in C and 24.5 ± 1.4 s in DCA (n.s.). In this experimental model, activation of PDC by DCA resulted in a stockpiling of acetyl groups at rest and less muscle fatigue, but it did not affect 'anaerobic' energy provision and _O2 on-kinetics.

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