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1 Department of Physiology, St. George's Hospital Medical School, London, United Kingdom; Division of Physiology, Department of Medicine, University of California, San Diego, San Diego, CA, USA
2 Center for Exercise Science and Medicine, University of Glasgow, Glasgow, United Kingdom
3 Department of Biochemistry, St. George's Hospital Medical School, London, United Kingdom
4 Department of Pharmacology, St. George's Hospital Medical School, London, United Kingdom
5 Canadian Centre for Activity and Ageing, University of Western Ontario, London, Ontario, Canada
6 Department of Physiology, St. George's Hospital Medical School, London, United Kingdom; Center for Exercise Science and Medicine, University of Glasgow, Glasgow, United Kingdom
* To whom correspondence should be addressed. E-mail: bwhipp{at}rei.edu.
Traditional control theories of muscle O2 consumption are based upon an "inertial" feedback system operating through features of the ATP splitting (e.g. [ADP] feedback). More recently, however, it has been suggested that feedforward mechanisms (with respect to ATP utilisation) may play an important role by controlling the rate of substrate provision to the electron transport chain. This has been achieved by activation of the pyruvate dehydrogenase complex via dichloroacetate (DCA) infusion, prior to exercise. In order to investigate these suggestions six males performed repeated, high-intensity, constant-load quadriceps exercise in the bore of an MR spectrometer with each of prior DCA or saline (CON) intravenous infusions. VO2 was measured breath-by-breath (using a turbine and mass spectrometer) simultaneously with intramuscular [PCr], [Pi], [ATP] and pH (by 31P MRS), and arterialised-venous blood sampling. DCA had no effect on the time constant (
) of either VO2 increase or PCr breakdown (VO2 45.5±7.9s (SD) vs. 44.3±8.2s (SD; CON vs. DCA); PCr 44.8±6.6s vs. 46.4±7.5s; with 95% confidence intervals averaging < ± 2s). DCA, however, resulted in significant (P<0.05) reductions in: (i) end-exercise [lactate] (-1.0±0.9mM), intramuscular acidification (pH, +0.08±0.06 units) and [Pi] (-1.7±2.1mM); (ii) the amplitude of the fundamental components for [PCr] (-1.9±1.6mM) and VO2 (-0.1±0.07 l/min, or 8%); and (iii) the amplitude of the VO2 slow component. Thus, while the DCA infusion lessened the build-up of potential fatigue metabolites and reduced both the aerobic and anaerobic components of the energy transfer during exercise it did not enhance either VO2 or [PCr], suggesting that feedback, rather than feedforward, control mechanisms dominate during high-intensity exercise.
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