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1 Department of Physiology and
Pharmacology, University Medical School, Queen's Medical Centre,
Nottingham N97 2UH, United Kingdom;
2 Section of Environmental
Physiology,
The delay in skeletal muscle mitochondrial ATP
production at the onset of exercise is thought to be a function of a
limited oxygen supply. The delay, termed the oxygen deficit, can be
quantified by assessing the above baseline oxygen consumption during
the first few minutes of recovery from exercise. During submaximal exercise, the oxygen deficit is reflected by the extent of muscle phosphocreatine (PCr) breakdown. In the present study, nine male subjects performed 8 min of submaximal, single leg knee extension exercise after saline (Control) and dichloroacetate (DCA) infusion on
two separate occasions. Administration of DCA increased resting skeletal muscle pyruvate dehydrogenase complex activation status threefold (Control = 0.4 ± 0.1 vs. DCA = 1.3 ± 0.1 mmol
acetyl-CoA · min
1 · kg
wet muscle1 at 37°C,
P < 0.01) and elevated
acetylcarnitine concentration fivefold (Control = 2.2 ± 0.5 vs. DCA = 10.9 ± 1.2 mmol/kg dry mass,
P < 0.01). During exercise, PCr
degradation was reduced by ~50% after DCA (Control = 33.2 ± 7.1 vs. DCA = 18.4 ± 7.1 mmol/kg dry mass,
P < 0.05). It would appear,
therefore, that in humans acetyl group availability is a major
determinant of the rate of increase in mitochondrial respiration at the
onset of exercise and hence the oxygen deficit.
acetylcarnitine; pyruvate dehydrogenase complex; phosphocreatine
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