ron-deficient rats have an impaired work performance,
even when their anemia is corrected. By exchange
transfusion. Muscle activity is associated with higher
blood lactate concentration than is observed in ironreplete
animals. The accumulation of lactate is a result of
excessive production as lactate clearance from the blood
was shown to be unaffected. By adjusting the workload to
a lower level, it was possible to divide iron-deficient
animals into two groups, one capable of continued
treadmill running and another in which animals stopped
before 20 min. In the former, blood lactate concentration
reached a plateau at moderate levels, whereas it
continued to increase in the latter until the animal
stopped running. Levels of alpha-glycerophosphate
oxidase in skeletal muscle mitochondria were found to be
much lower in the second group (p<0.001). Lactate
infusion into normal animals was shown to interfere with
work performance, and maintenance of a normal pH in
iron-deficient and iron-replete animals did not prevent the
impairment in work associated with high blood lactate
concentrations. Additional evidence was obtained that
energy substrate (blood glucose and free fatty acids,
muscle glycogen) was adequate in iron-deficient animals.
Oxygen tension in their vena caval blood was higher than
in controls. Furthermore, the in situ behaviour of
electrically stimulated gastroenemius and soleus muscles
appeared similar to that of control animals. Because the
stimulation of the single muscle in the iron-deficient
animal did not result in appreciable elevation of blood
lactate and did not show impaired contractility further
supported the hypothesis that the elevation of blood
lactate caused the decreased work performance. It is
concluded that iron deficiency by a depletion in the iron containing
mitochondrial enzyme, alpha-glycerophosphate
oxidase, impairs glycolysis, resulting in excess
lactate formation, which at high levels leads to cessation
of physical activity.
CA Finch, at al, J Clin Invest 1979;64:129-137
Copyright © 2003 Anamol Laboratories Ltd.
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