Abstract
Breathing hyperoxic air decreases muscle glycogenolysis, which leads to decreased lactate contents and increases in exercise performance in humans. These findings suggest alterations in skeletal muscle carbohydrate metabolism. PURPOSE: The study had two aims 1) to determine if the decreased muscle and blood lactate found during steady state exercise with hyperoxic vs. normoxic breathing is due to decreased muscle glycogenolysis, leading to decreased pyruvate and lactate accumulations and efflux and 2) to elucidate the mechanisms behind the decreased glycogenolysis. We hypothesized that 60% O2 would decrease muscle glycogenolysis, from decreases in free ADP and AMP, resulting in decreased pyruvate and lactate contents and efflux with no change in pyruvate dehydrogenase (PDH) activity (pyruvate oxidation). METHODS: Seven active male subjects cycled for 40 min at 70% VO2peak, on two occasions while breathing 21 or 60% O2. Arterial and venous blood and blood flow measurements were obtained throughout each trial, and muscle biopsies were taken at rest and following 10, 20 and 40 min of exercise. RESULTS: During exercise, muscle glycogenolysis was reduced by 16% with hyperoxia (267 ± 19 vs. 317 ± 21 mmol glycosyl units · kg−1 dw), but pyruvate accumulation and pyruvate oxidation via PDH activity were unaffected (60%: 3.02 ±0.50 vs. 21%: 3.03 ± 0.39 mmol · kg−1·min−1). However, the reduced glycogenolysis with hyperoxia did result in a 22% reduction (p<0.05) in muscle lactate accumulation (60%: 22.6 ± 6.4 vs. 21%: 31.3 ± 8.7 mmol · kg−1 dw) and decreased blood lactate efflux and total lactate production over 40 min of cycling. We also found that hyperoxia significantly decreased PCr degradation (60%: 36.4 ± 4.0 vs. 21 %: 29.9 ± 5.1 mmol · kg−1 dw), attenuated (p<0.05) the accumulations of Cr and calculated ADPf and AMPf (AMPf: 60%: 3.55 ± 1.14 vs. 21%: 5.67 ± 1.60 umol · kg−1 dw) and reduced (p<0.05) blood epinephrine concentration by ∼44% throughout 40 min of cycling. CONCLUSION: Hyperoxia decreased muscle glycogenolysis, with no change in pyruvate oxidation via PDH, resulting in significantly less muscle and blood lactate accumulation during 40 min of cycling - a tighter metabolic match between pyruvate production and oxidation. The decreased glycogenolysis during exercise with hyperoxia appeared to be the result of attenuated accumulations of the potent allosteric effectors of glycogen phosphorylase, specfically free ADP and AMP and a decreased epinephrine concentration during exercise. Lastly, the significantly diminished rate of PCr utilization during hyperoxia suggests an increase energy provision via oxidative phosphorylation during aerobic exercise.
Published Version
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