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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to examine the effects of mild iron deficiency on physical work capacity, 40 prelatent iron-deficient female endurance runners were studied before and after 8 wk of supplementation with either oral iron (320 mg ferrous sulfate) or a matching placebo. Subjects underwent the following physical work capacity tests: the Wingate cycle ergometer test, the anaerobic speed test, the ventilatory threshold, VO2max, and maximal treadmill velocity during the VO2max test. Muscle biopsy samples pre- and post-treatment were obtained from 17 of the subjects, and these were assayed for citrate synthase and cytoplasmic alpha-glycerophosphate dehydrogenase activity. Subjects were randomly assigned to one of the treatment groups, and a double-blind method of administration of the supplements was used. The differences in improvement scores between the two groups on the work capacity and enzyme activity variables were statistically nonsignificant (P greater than 0.05). Serum ferritin values rose from a mean of 12.4 +/- 4.5 to 37.7 +/- 19.7 ng.ml-1 for the experimental group and from 12.2 +/- 4.3 to 17.2 +/- 8.9 ng.ml-1 for the controls (P = 0.0025), whereas hemoglobin levels remained fairly constant for both groups (P = 0.6). Eight weeks of iron supplementation to prelatent/latent iron-deficient, physically active females did not significantly enhance work capacity. Within the limitations of this study, the presence of a serum ferritin below 20 ng.ml-1 does not pose a significant handicap to physical work capacity.
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PMID:The effects of prelatent/latent iron deficiency on physical work capacity. 273 74

Most of the previous studies on the effects of iron deficiency on skeletal muscle respiratory capacity and work performance have been investigated in severe or moderate iron-deficiency anemia. We report here that even in mild iron deficiency where the hemoglobin concentration was 10 g/dl and the iron stores in livers and spleen were not completely depleted, a marked reduction in succinate dehydrogenase was observed in skeletal muscles but not in heart. Similarly, cytochrome oxidase activities were reduced. Although no significant change in glycerophosphate dehydrogenase was detected in the iron-deficient rats, exposure to cold in this group greatly reduced this enzyme activity. As cold acclimatization accelerates marrow erythropoiesis (20) which in turn, demands more iron, it seems that in the iron-insufficient state, this iron demand for marrow activity may persist at the expense of the tissue iron pool, resulting in a marked reduction in glycerophosphate dehydrogenase activities. Since succinate dehydrogenase plays a significant role in the impairment of mitochondrial function and early fatigue of iron-deficient muscle (11), the present study shows that even in mild iron deficiency, some loss of muscle functions could result as succinate dehydrogenase activities were greatly reduced.
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PMID:Biochemical effects of mild iron deficiency and cold acclimatization on rat skeletal muscle. 300 73

Since information pertinent to the effect of prelatent or latent iron deficiency on tissue iron is scare, the present study was aimed at producing this stage of iron deficiency in rats by phlebotomy and to determine whether the mitochondrial iron-containing enzymes, succinate dehydrogenase (SDH) and glycerophosphate dehydrogenase (GPDH) were affected. These phlebotomized rats showed a subclinical aneamic picture in the blood together with reduced plasma iron and storage iron in the spleen and liver, but an elevated plasma total iron-binding capacity (TIBC). Under this latent iron deficient state, the SHD in the heart and the skeletal muscle with mixed-fibre types (gastrocnemius and plantaris) but not the red (soleus) and white fibres (vastus lateralis) showed reduced activities. No significant changes in GPDH activities were found in these organs. This finding is consistent with our early report (Quisumbing et al., 1985) that even in mild iron deficiency, some loss of mitochondrial functions could have occurred and this could affect the muscular endurance. SDH was more affected by latent iron deficiency than GPDH.
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PMID:Will latent iron deficiency affect the mitochondrial iron-containing enzymes? 402 19

Young rats were made iron deficient by feeding them a low-iron diet for 8 wk. Iron deficiency resulted in a 50% decrease in cytochrome c and cytochrome oxidase and a 26% decrease in mitochondrial glycerol-3-phosphate dehydrogenase activity in skeletal muscle. Respiratory capacity of muscle homogenates was reduced 55%. After 8 days of iron treatment, respiratory capacity, cytochrome c, cytochrome oxidase, and glycerol-3-phosphate dehydrogenase had returned 50% toward normal. Maximum O2 uptake of contracting hindlimb muscles averaged 8.5 mumol O2.min-1.g-1 in control, 4.3 mumol O2.min-1.g-1 in iron-deficient, and 6.2 mumol O2.min-1.g-1 in the 8-day-iron-repleted rats. Muscle fatigue during 10 min of stimulation was greater in the iron-deficient group. Lactate concentration in red muscle was higher in iron-deficient than in control rats after stimulation. The muscle fatigue and lactate responses returned 50% toward normal during 8 days of iron treatment. We conclude that iron deficiency results in a decrease in skeletal muscle capacity for aerobic metabolism and, by this mechanism, increases susceptibility to fatigue.
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PMID:Physiological and biochemical effects of iron deficiency on rat skeletal muscle. 626 4