Laboratory of Human Nutrition, Institute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zürich, Zurich, Switzerland.
Swiss Federal Institute of Sports, Magglingen, Switzerland.
Am J Clin Nutr. 2018 Dec 1;108(6):1324-1333. doi: 10.1093/ajcn/nqy247.
Iron status is a determinant of physical performance, but training may induce both low-grade inflammation and erythropoiesis, exerting opposing influences on hepcidin and iron metabolism. To our knowledge, the combined effects on iron absorption and utilization during training have not been examined directly in humans.
We hypothesized that 3 wk of exercise training in recreational male runners would decrease oral iron bioavailability by increasing inflammation and hepcidin concentrations.
In a prospective intervention, nonanemic, iron-sufficient men (n = 10) completed a 34-d study consisting of a 16-d control phase and a 22-d exercise-training phase of 8 km running every second day. We measured oral iron absorption and erythroid iron utilization using oral 57Fe and intravenous 58Fe tracers administered before and during training. We measured hemoglobin mass (mHb) and total red blood cell volume (RCV) by carbon monoxide rebreathing. Iron status, interleukin-6 (IL-6), plasma hepcidin (PHep), erythropoietin (EPO), and erythroferrone were measured before, during, and after training.
Exercise training induced inflammation, as indicated by an increased mean ± SD IL-6 (0.87 ± 1.1 to 5.17 ± 2.2 pg/mL; P < 0.01), while also enhancing erythropoiesis, as indicated by an increase in mean EPO (0.66 ± 0.42 to 2.06 ± 1.6 IU/L), mHb (10.5 ± 1.6 to 10.8 ± 1.8 g/kg body weight), and mean RCV (30.7 ± 4.3 to 32.7 ± 4.6 mL/kg) (all P < 0.05). Training tended to increase geometric mean iron absorption by 24% (P = 0.083), consistent with a decreased mean ± SD PHep (7.25 ± 2.14 to 5.17 ± 2.24 nM; P < 0.05). The increase in mHb and erythroid iron utilization were associated with the decrease in PHep (P < 0.05). Compartmental modeling indicated that iron for the increase in mHb was obtained predominantly (>80%) from stores mobilization rather than from increased dietary absorption.
In iron-sufficient men, mild intensification of exercise intensity increases both inflammation and erythropoiesis. The net effect is to decrease hepcidin concentrations and to tend to increase oral iron absorption. This trial was registered at clinicaltrials.gov as NCT01730521.
铁状态是身体表现的决定因素，但训练可能会引起低度炎症和红细胞生成，对铁调素和铁代谢产生相反的影响。据我们所知，在人类中，尚未直接研究训练期间对铁吸收和利用的综合影响。
我们假设 3 周的运动训练会通过增加炎症和铁调素浓度来降低运动男性的口服铁生物利用度。
在一项前瞻性干预研究中，非贫血、铁充足的男性（n=10）完成了一项 34 天的研究，包括 16 天的对照阶段和 22 天的每天 8 公里跑步的运动训练阶段。我们使用口服 57Fe 和静脉内 58Fe 示踪剂在训练前后测量口服铁吸收和红细胞内铁利用情况。我们通过一氧化碳再呼吸测量血红蛋白质量（mHb）和总红细胞体积（RCV）。在训练前后测量铁状态、白细胞介素 6（IL-6）、血浆铁调素（PHep）、促红细胞生成素（EPO）和红细胞生成素。
运动训练诱导炎症，表现为平均 ± SD IL-6 增加（0.87 ± 1.1 至 5.17 ± 2.2 pg/mL；P<0.01），同时增强红细胞生成，表现为平均 EPO 增加（0.66 ± 0.42 至 2.06 ± 1.6 IU/L）、mHb（10.5 ± 1.6 至 10.8 ± 1.8 g/kg 体重）和平均 RCV（30.7 ± 4.3 至 32.7 ± 4.6 mL/kg）（均 P<0.05）。训练使铁吸收的几何平均增加了 24%（P=0.083），与 PHep 的平均 ± SD 降低一致（7.25 ± 2.14 至 5.17 ± 2.24 nM；P<0.05）。mHb 的增加与 PHep 的降低有关（P<0.05）。房室模型表明，mHb 增加所需的铁主要（>80%）来自储存动员，而不是增加饮食吸收。
在铁充足的男性中，运动强度的轻度增加会增加炎症和红细胞生成。其净效应是降低铁调素浓度，并倾向于增加口服铁吸收。该试验在 clinicaltrials.gov 上注册为 NCT01730521。
