AJP - Cell Physiology, Vol 253, Issue 2 C263-C268, Copyright © 1987 by American Physiological Society
Hyperoxia, mitochondrial redox state, and lactate metabolism of in situ canine muscle
B. R. Wolfe, T. E. Graham and J. K. Barclay
The effect of hyperoxia on lactate production and release and the
mitochondrial NAD+-to-NADH ratio was studied in the in situ canine
gastrocnemius to determine whether elevated PO2 altered metabolic
regulation. Dogs breathed either air (21% O2) [arterial O2 partial pressure
(PaO2) 90 mmHg; n = 8] or hyperoxia (100% O2) (PaO2 546 mmHg; n = 8). The
left muscle was stimulated for 10 min at 3 Hz and then both right and left
muscles were quick frozen in N2. Hyperoxia did not affect O2 uptake, blood
flow, and developed tension. Activity increased glucose 6-phosphate
(G-6-P), D-fructose 6-phosphate (F-6-P), NH3, lactate, and F-6-P/F-1,6-P in
both treatment groups. No significant differences in arterial or venous
lactate, muscle lactate, glucose uptake, or glycogen depletion were noted
in hyperoxia. Cytoplasmic NAD+/NADH was in a more oxidized state in
hyperoxia at rest but not during activity. The increase in NH3 with
stimulation was significantly larger in hyperoxia. Activity decreased
alpha-ketoglutarate in hyperoxia but not in air. At stimulation, the
estimated mitochondrial NAD+/NADH increased in both groups suggesting that
hypoxia was not present. Thus hyperoxia did not affect mitochondrial redox
state or lactate production and release in active muscle.
