Muscle acetyl group availability is a major determinant of the
oxygen deficit in humans during submaximal exercise.
Timmons, James A., Thomas Gustafsson, Carl Johan Sundberg, Eva
Jansson, and Paul L. Greenhaff.
Department of Physiology and Pharmacology, University Medical
School, Queen's Medical Centre, Nottingham, United Kingdom; Section
of Environmental Physiology, Department of Physiology and
Pharmacology, Karolinska Institute, S-171 77 Stockholm, Sweden;
Department of Clinical Physiology, Huddinge University Hospital,
Karolinska Institute, S-141 86 Huddinge, Sweden
APStracts 4:0247E, 1997.
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, 9 male subjects performed 8 min of submaximal,
single leg, knee extension exercise following saline (Control) and
dichloroacetate (DCA) infusion on 2 separate occasions.
Administration of DCA increased resting skeletal muscle pyruvate
dehydrogenase complex activation status by three fold (Control = 0.4
+/- 0.1 vs DCA = 1.3 +/- 0.1 mmol acetyl-CoA/min/kg wet muscle at 37
degrees C, P< 0.01) and elevated acetylcarnitine concentration by
five fold (Control = 2.2 +/- 0.5 vs DCA = 10.9 +/- 1.2 mmol/kg dm,
P<0.01). During exercise, PCr degradation was reduced by 50%
following DCA (Control = 33.2 +/- 7.1 vs DCA = 18.4 +/- 7.1 mmol/kg
dm, 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.
Received 2 September 1997; accepted in final form 31 October
1997.
APS Manuscript Number E413-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 14 November 1997