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The effects of prelatent and latent iron deficiency on physical work capacity Newhouse, Ian Joseph


In order to examine the effects of prelatent/latent iron deficiency on physical work capacity and selected muscle enzyme activities, forty female subjects were studied before and after eight weeks of supplementation with either oral iron or a matching placebo. Initially, female volunteers engaged in regular endurance running were screened for iron deficiency by blood analysis (serum ferritin and hemoglobin). Forty non-anemic subjects with deficient iron stores underwent physiological and anthropometric tests to obtain a comprehensive profile. The specific physical work capacity tests were alactic and lactacid power on the Wingate cycle ergometer test, lactacid capacity on the anaerobic speed test, anaerobic (ventilatory) threshold using gas exchange variables, V0₂ max. and the max. treadmill velocity during the V0₂ max. test. Muscle biopsy samples pre-, and post- treatment were assayed for citrate synthase and alpha-glycerophosphate dehydrogenase activity. Treatment was oral iron supplementation (320 mg ferrous sulfate = 100 mg elemental iron taken as SLOW-Fe® twice a day) or a matching placebo. The subjects were randomly assigned to one of the treatment groups and a double-blind method of administration of the supplements was used. It was hypothesized that work capacity would be enhanced following oral iron supplementation, possibly due to the repletion of iron containing oxidative enzymes important in energy production. Results could not strongly support this hypothesis with the difference between the two groups on the work capacity and enzyme activity variables being statistically nonsignificant. Serum ferritin values rose from a mean of 12.4+4.5 to 37.7+19.7 ngml⁻¹ for the experimental group and 12.2±4.3 to 17.2±8.9 for the controls; (p=0.0025). Hemoglobin levels remained fairly constant for both treatment groups; 13.4±0.6 to 13.5±0.5 gdl⁻¹ (experimental), and 13.0±0.6 to 13.1+0.5 (control); (p=0.6). Pre to post values on the work capacity variables, experimental vs control respectively were: Alactic power, 8.8 to 8.4 watts-kg⁻¹ body wt. vs 8.4 to 8.2; lactacid capacity, 6.9 to 6.9 watts-kg⁻¹ body wt. vs 7.0 to 6.0; anaerobic speed test, 41.3 to 45.1 seconds vs 43.7 to 44.8; anaerobic threshold, 7.4 to 7.5 mileshour⁻¹ vs 7.2 to 7.2; V0₂ max, 51.3 to 52.7 ml-kg⁻¹ min⁻¹ vs 50.6 to 50.6; max velocity during V0₂ max, 9.8 to 9.8 mileshour⁻¹ vs 9.6 to 9.5. Except for alactic power, the change in work capacity favored the iron treated group. Noting this trend, further study may be warranted. Prelatent/latent iron deficiency appeared not to depress the activities of the two enzymes measured. Cytoplasmic alpha-glycerophosphate dehydrogenase activity rose from 0.066 to 0.085 units for the experimental group (p=.58) vs .058 to .066 for the control group and citrate synthase activity changed from 0.047 to 0.048 (experimental) vs 0.039 to 0.042 (control). It can be concluded that eight weeks of iron supplementation to prelatent/latent iron deficient, physically active females does not significantly enhance work capacity nor the activity of 2 oxidative muscle enzymes (citrate synthase and cytoplasmic alpha-glycerophosphate dehydrogenase). Within the limitations of this study the presence of a serum ferritin below 20 ng-ml⁻¹ does not pose a significant handicap to anaerobic or aerobic capacity.

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