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Department of Anatomy & Physiology, University of Dundee, Dundee DD1 4HN, Scotland, UK;
*
Department of Sports Science, South Bank University, London, UK; and
Human Muscle Metabolism Research Group, Loughborough University, Loughborough, UK
3To whom correspondence should be addressed. E-mail: m.j.rennie{at}dundee.ac.uk.
After exhaustive exercise, intravenous or oral glutamine promoted
skeletal muscle glycogen storage. However, when glutamine was ingested
with glucose polymer, whole-body carbohydrate storage was elevated,
the most likely site being liver and not muscle, possibly due to
increased glucosamine formation. The rate of tricarboxylic acid (TCA)
cycle flux and hence oxidative metabolism may be limited by the
availability of TCA intermediates. There is some evidence that
intramuscular glutamate normally provides
-ketoglutarate to the
mitochondrion. We hypothesized that glutamine might be a more efficient
anaplerotic precursor than endogenous glutamate alone. Indeed, a
greater expansion of the sum of muscle citrate, malate, fumarate and
succinate concentrations was observed at the start of exercise (70%
VO2max) after oral glutamine than when placebo or ornithine
-ketoglutarate was given. However, neither endurance time nor the
extent of phosphocreatine depletion or lactate accumulation during the
exercise was altered, suggesting either that TCA intermediates were not
limiting for energy production or that the severity of exercise was
insufficient for the limitation to be operational. We have also shown
that in the perfused working rat heart, there is a substantial fall in
intramuscular glutamine and
-ketoglutarate, especially after
ischemia. Glutamine (but not glutamate,
-ketoglutarate or aspartate)
was able to rescue the performance of the postischemic heart. This
ability appears to be connected to the ability to sustain intracardiac
ATP, phosphocreatine and glutathione.
KEY WORDS: glutamine glycogen storage glutathione glucosamine tricarboxylic acid cycle
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