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Objective: To determine the effect of iron supplementation on iron status and endurance capacity. Design: Randomized, double-blind iron supplementation. Setting: University of Missouri-Columbia and surrounding community. Subjects: Twenty iron-deficient (serum ferritin, sFero16 mg/l; serum transferrin receptor, sTfR48.0 mg/l; or sTfR/log sFer index 44.5), nonanemic (hemoglobin, Hb4120 g/l, women; 4130 g/l, men) men and women (18-41 years) were recruited via fliers and newspaper advertisements; 20 of 31 eligible subjects participated. Interventions: A 30 mg measure of elemental iron as ferrous sulfate or placebo daily for 6 weeks. Results: Dietary iron intake and physical activity did not differ between groups before or after supplementation. Iron supplementation significantly increased sFer compared to placebo (P ¼ 0.01), but did not affect Hb or hematocrit. Iron supplementation prevented the decline in ventilatory threshold (VT) observed in the placebo group from pre-to postsupplementation (P ¼ 0.01); this effect was greater in individuals with lower sFer before intervention (Po0.05). Changes in sFer from pre-to post-treatment were positively correlated with changes in VT (P ¼ 0.03), independent of supplementation. The iron group significantly increased gross energetic efficiency during the submaximal test (P ¼ 0.04). Changes in sFer were negatively correlated with changes in average respiratory exchange ratio during the submaximal test (Po0.05). Conclusions: Iron supplementation significantly improves iron status and endurance capacity in iron-deficient, nonanemic trained male and female subjects.

This study was designed to characterize left ventricular (LV) function and mass in a modified cardiomyopathy model in the dog in which right ventricular pacing rates are gradually increased throughout 38 days. On the last day of the pacing protocol, ejection fraction was reduced (25 +/- 3 vs. 60 +/- 1%) and LV end-diastolic diameter index (a ratio of LV end-diastolic diameter to body weight, 2.09 +/- 0.02 vs. 1.79 +/- 0.08 mm/kg) and LV mass index (a ratio of LV mass to body weight, 5.2 +/- 0.3 vs. 4.3 +/- 0.2 g/kg) were greater than in the normal dogs (P < 0.05, respectively). Cardiac filling pressures increased, and LV diastolic function and coronary blood flow were impaired. After 4 wk of recovery from the progressive pacing protocol, LV end-diastolic diameter index (2.12 +/- 0.06 mm/kg) and LV mass index (5.6 +/- 0.2 g/kg) remained increased. Ejection fraction was improved (38 +/- 4%) but still depressed. LV diastolic function, coronary blood flow, and cardiac filling pressures returned to levels seen in the normal dogs. This modified cardiomyopathy model associated with LV hypertrophy complements the conventional tachycardia-induced cardiomyopathy model without LV hypertrophy.

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