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1 Department of Human Biology & Nutritional Sciences, University of Guelph, Guelph, Ontario N1G 2W1; and 2 Department of Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5
This study investigated whether
hyperoxic breathing (100% O2) or increasing oxidative
substrate supply [dichloroacetate (DCA) infusion] would increase
oxidative phosphorylation and reduce the reliance on substrate
phosphorylation at the onset of high-intensity aerobic exercise. Eight
male subjects cycled at 90% maximal O2 uptake
(
O2 max) for 90 s in three
randomized conditions: 1) normoxic breathing and saline
infusion over 1 h immediately before exercise (CON), 2)
normoxic breathing and saline infusion with DCA (100 mg/kg body wt),
and 3) hyperoxic breathing for 20 min at rest and during
exercise and saline infusion (HYP). Muscle biopsies from the vastus
lateralis were sampled at rest and after 30 and 90 s of exercise.
DCA infusion increased pyruvate dehydrogenase (PDH) activation above
CON and HYP (3.10 ± 0.23, 0.56 ± 0.08, 0.69 ± 0.05 mmol · kg wet
muscle
1 · min1,
respectively) and significantly increased both acetyl-CoA and acetylcarnitine (11.0 ± 0.7, 2.0 ± 0.5, 2.2 ± 0.5 mmol/kg dry muscle, respectively) at rest. However, DCA and HYP did not
alter phosphocreatine degradation and lactate accumulation and,
therefore, the reliance on substrate phosphorylation during 30 s
(CON, 51.2 ± 5.4; DCA, 56.5 ± 7.1; HYP, 69.5 ± 6.3 mmol ATP/kg dry muscle) and 90 s of exercise (CON, 90.6 ± 9.5; DCA, 107.2 ± 13.0; HYP, 101.2 ± 15.2 mmol ATP/kg dry
muscle). These data suggest that the rate of oxidative phosphorylation
at the onset of exercise at 90% O2 max
is not limited by oxygen availability to the active muscle or by
substrate availability (metabolic inertia) at the level of PDH in
aerobically trained subjects.
pyruvate dehydrogenase activity; oxidative phosphorylation; substrate phosphorylation; 100% oxygen; dichloroacetate; acetylcarnitine
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