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Acidosis inhibits oxidative phosphorylation in contracting human skeletal muscle in vivo
Author(s) -
Jubrias Sharon A.,
Crowther Gregory J.,
Shankland Eric G.,
Gronka Rodney K.,
Conley Kevin E.
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.045872
Subject(s) - oxidative phosphorylation , creatine , isometric exercise , acidosis , medicine , chemistry , skeletal muscle , endocrinology , phosphocreatine , adenosine triphosphate , creatine kinase , biochemistry , energy metabolism
This study tested the hypothesis that acidic pH inhibits oxidative ATP supply during exercise in hand (first dorsal interosseus, FDI) and lower limb (leg anterior compartment, LEG) muscles. We measured oxidative flux and estimated mitochondrial capacity using the changes in creatine phosphate concentration ([PCr]) and pH as detected by 31 P magnetic resonance (MR) spectroscopy during isometric exercise and recovery. The highest oxidative ATP flux in sustained exercise was about half the estimated mitochondrial capacity in the LEG (0.38 ± 0.06 vs . 0.90 ± 0.14 m m ATP s −1 , respectively), but at the estimated capacity in the FDI (0.61 ± 0.05 vs . 0.61 ± 0.09 m m ATP s −1 , respectively). During sustained exercise at a higher contraction rate, intracellular acidosis (pH < 6.88) prevented a rise in oxidative flux in the LEG and FDI despite significantly increased [ADP]. We tested whether oxidative flux could increase above that achieved in sustained exercise by raising [ADP] (> 0.24 m m ) and avoiding acidosis using burst exercise. This exercise raised oxidative flux (0.69 ± 0.05 m m ATP s −1 ) to nearly twice that found with sustained exercise in the LEG and matched (0.65 ± 0.11 m m ATP s −1 ) the near maximal flux seen during sustained exercise in the FDI. Thus both muscles reached their highest oxidative fluxes in the absence of acidosis. These results show that acidosis inhibits oxidative phosphorylation in vivo and can limit ATP supply in exercising muscle to below the mitochondrial capacity.