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Am J Physiol Endocrinol Metab 281: E1144-E1150, 2001;
0193-1849/01 $5.00
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Vol. 281, Issue 6, E1144-E1150, December 2001

Effects of acetate infusion and hyperoxia on muscle substrate phosphorylation after onset of moderate exercise

Melissa K. Evans1, Ingrid Savasi1, George J. F. Heigenhauser2, and Lawrence L. Spriet1

1 Department of Human Biology and 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 increased muscle acetylcarnitine provision (acetate infusion) or hyperoxia (100% O2) would increase the rate of oxidative phosphorylation and reduce the reliance on muscle substrate phosphorylation after the onset of moderate exercise. Eight subjects completed three randomized trials, each separated by 1 wk: 1) saline infusion for 1 h before exercise, while breathing room air for 20 min before exercise and during 120 s of cycling at 65% maximal exercise (VO2 max) (CON), 2) saline infusion with 4 mmol/kg body wt sodium acetate, while breathing room air before and during exercise (ACE), and 3) saline infusion and breathing 100% O2 before and during exercise (HYP). Muscle biopsies were sampled at rest and after 30 and 120 s of exercise. ACE increased muscle acetyl-CoA and acetylcarnitine contents at rest vs. CON and HYP [22.9 ± 2.8 vs. 8.9 ± 2.4 and 10.5 ± 1.8 µmol/kg dry muscle (dm); 11.0 ± 1.2 vs. 3.5 ± 1.3 and 4.0 ± 1.2 mmol/kg dm]. Acetate had no effect on resting pyruvate dehydrogenase activity in the active form (PDHa) among CON, ACE, and HYP. During exercise, acetyl-CoA and acetylcarnitine were unchanged in ACE but increased over time in the CON and HYP trials, and PDHa increased similarly in all trials. Muscle phosphocreatine use, lactate accumulation, and substrate phosphorylation energy provision after 30 or 120 s of exercise were similar in all trials. In summary, increased acetylcarnitine availability did not accelerate the rate of oxidative phosphorylation at the onset of exercise, suggesting that this is not a site of extra substrate. Hyperoxia had no effect on substrate phosphorylation, suggesting that O2 availability does not limit oxidative phsophorylation at the onset of moderate exercise.

acetylcarnitine; acetyl-coenzyme A; oxidative phosphorylation; pyruvate dehydrogenase activity; lactate; phosphocreatine; oxygen


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