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J. Biol. Chem., Vol. 262, Issue 19, 9109-9114, Jul, 1987
GA Dudley, PC Tullson and RL Terjung
This study evaluated the sensitivity of mitochondrial respiratory control
as a function of tissue oxidative capacity. The mitochondrial content of
rat skeletal muscle was increased by exercise training or decreased by
hypothyroidism. Muscles of the lower hindlimb were stimulated to
tetanically contract in situ for 3 min at one of four frequencies to elicit
a 30-fold range of oxygen consumption rates. Freeze-clamped sections of
fast-twitch red gastrocnemius muscle were extracted and analyzed for
metabolite levels. The sensitivity of respiratory control was examined for
three models of cytosolic respiratory control (ADPf, ATP/ADPf, and
ATP/(ADPf X Pi]; for each proposed model, sensitivity went up as
mitochondrial content increased. Thus, a smaller change in cytosolic
modulator (e.g., ADPf) is required as oxidative capacity increases.
Increases in the sensitivity of cytosolic respiratory control resulted in
lower flux through the near- equilibrium energy exchange reactions of
creatine kinase and myokinase such that calculated free concentrations of
ADP and AMP were less. Other energetically important reactions/pathways
were also affected. Accumulation of lactate and the deamination of AMP to
IMP were lower in tissues with higher mitochondrial content. In summary,
changes in oxidative capacity directly influence the sensitivity of
cytosolic respiratory control and this, in turn, has important consequences
for maintenance of cellular energy balance.
Influence of mitochondrial content on the sensitivity of respiratory control
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