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- W2024995767 abstract "Human muscle typically cannot sustain exercise at maximum VO2. Neither insufficient O2 nor muscle fatigue explain this limit. One important factor may be an inhibition of oxidative phosphorylation (oxphos) that prevents raising ATP supply to the mitochondrial capacity. PURPOSE This study tested whether acidic intracellular pH inhibits oxphos during exercise in human muscle. METHODS We evaluated oxidative energetics during both sustained and brief maximal (MAX) exercise in hand (first dorsal interosseus, FDI) and leg (anterior compartment, LEG) muscles. We evaluated the kinetics of changes in [PCr] and pH as measured by 31P magnetic resonance spectroscopy during isometric exercise and recovery. RESULTS The LEG sustained exercise without acidosis at an ox flux of half its estimated mitochondrial oxidative capacity (0.70 ±0.07 mM ATP sec−1). The FDI reached its oxidative capacity (0.47 ±0.04 mM ATP sec−1) under the same conditions. Increasing the exercise rate resulted in lower pH, higher [ADP] but no increase in ox flux in the LEG; the FDI showed lower pH, no change in [ADP], and decreased ox flux. No acidification occurred during MAX exercise, and both muscles achieved high [ADP] and an ox flux equal to their oxidative capacities. CONCLUSION These results suggest that acidosis uncouples ox flux from the signal for oxphos, [ADP]. In addition, intense exercise without acidosis results in an ox flux near the muscle oxidative capacity. Thus, pH has an inhibitory effect on ox flux that suggests a direct effect of pH on mitochondrial function. Supported by NIH Grants AR-41928 and AR-45184." @default.
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- W2024995767 date "2003-05-01" @default.
- W2024995767 modified "2023-09-27" @default.
- W2024995767 title "ACIDOSIS LIMITS OXIDATIVE FLUX IN CONTRACTING HUMAN MUSCLE" @default.
- W2024995767 doi "https://doi.org/10.1097/00005768-200305001-00504" @default.
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