AJP - Cell Physiology, Vol 259, Issue 1 C26-C28, Copyright © 1990 by American Physiological Society
Failure of glutamate dehydrogenase system to predict oxygenation state of human skeletal muscle
A. Katz, M. K. Spencer and K. Sahlin
Department of Kinesiology, University of Illinois, Urbana 61801.
In a recent study, the total tissue contents of glutamate (Glu), ammonium
(NH+4), and 2-oxoglutarate (2-OG) were used to estimate changes in the
mitochondrial redox state ([NAD+]/[NADH]) of contracting skeletal muscle
with intact circulation [Am. J. Physiol. 253 (Cell Physiol. 22): C263-C268,
1987]. These metabolites participate in the glutamate dehydrogenase (GDH)
reaction, which, based on a number of assumptions, theoretically enables
calculation of the mitochondrial redox state as follows (brackets indicate
concentrations): [NAD+]/[NADH] = ([NH+4] [2-OG])/[( Glu]Kapp), where Kapp
is the apparent equilibrium constant for GDH. The purpose of this study was
to determine whether changes in the total tissue contents of Glu, NH+4, and
2-OG could be used to predict a reduction of the mitochondrial redox state
in anoxic skeletal muscle. Anoxia was induced in the quadriceps femoris
muscle by 10 min of circulatory occlusion (low metabolic rate) and
isometric contraction to fatigue (high metabolic rate). The mean (+/- SE)
value for the metabolite ratio ([NH+4][2-OG]/[Glu]) at rest was 6 +/- 3
mmol/kg dry wt (x 10(-4]. No significant change occurred after circulatory
occlusion (4 +/- 2 x 10(-4); P greater than 0.05), whereas an almost
60-fold increase was observed after isometric contraction (P less than
0.05). Because the muscle was anoxic under both conditions, a significant
decrease in the metabolite ratio should have occurred. These data
demonstrate that changes in total tissue contents of Glu, NH+4, and 2-OG
cannot be used to estimate changes in the redox and oxygenation state of
mitochondria in intact human skeletal muscle.
