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

This study investigated whether increased muscle acetylcarnitine provision (acetate infusion) or hyperoxia (100% O-2) would increase the rate of oxida tive phosphorylation and reduce the reliance on muscle substrate phosphoryl ation after the onset of moderate exercise. Eight subjects completed three randomized trials, each separated by 1 wk: 1) saline infusion for 1 h befor e exercise, while breathing room air for 20 min before exercise and during 120 s of cycling at 65% maximal exercise (V)over dotO(2) max) (CON), 2) sal ine infusion with 4 mmol/kg body wt sodium acetate, while breathing room ai r before and during exercise (ACE), and 3) saline infusion and breathing 10 0% O-2 before and during exercise (HYP). Muscle biopsies were sampled at re st 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 mu mol/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 dehydrog enase activity in the active form (PDHa) among CON, ACE, and HYP. During ex ercise, acetyl-CoA and acetylcarnitine were unchanged in ACE but increased over time in the CON and HYP trials, and PDHa increased similarly in all tr ials. Muscle phosphocreatine use, lactate accumulation, and substrate phosp horylation energy provision after 30 or 120 s of exercise were similar in a ll trials. In summary, increased acetylcarnitine availability did not accel erate the rate of oxidative phosphorylation at the onset of exercise, sugge sting that this is not a site of extra substrate. Hyperoxia had no effect o n substrate phosphorylation, suggesting that O-2 availability does not limi t oxidative phsophorylation at the onset of moderate exercise.