Magnusson B, Hallberg L, Rossander L, Swolin B
Acta Med Scand. 1984;216(2):157-64.
A hematological comparison was performed between 43 middle and long distance male runners and 119 male controls. The hematocrit, serum iron, transferrin saturation and serum ferritin values were significantly lower in the athletes. The amount of bone marrow hemosiderin was also lower in the athletes than in a group of non-athletic men of the same age. Even if these values were clearly lower than in the controls, they were not low enough to indicate iron deficiency. The observations that sideroblast counts in bone marrow smears were normal and that both red cell indices and red cell protoporphyrin were normal strongly support the conclusion that lack of iron had not limitated erythropoiesis or the formation of an optimal red cell mass. Low serum haptoglobin values in most athletes indicated an increased intravascular hemolysis. As the hemoglobin-haptoglobin complex formed is taken up by hepatocytes, this implies that there is a shift in the red cell catabolism in these athletes from the reticuloendothelial system to the hepatocytes. This shift may explain the paradoxical findings of low serum ferritin concentrations and reduced contents of bone marrow hemosiderin. This is consistent with the observed normal erythropoiesis. It was concluded that runners "anemia" is no true anemia and not caused by iron deficiency. "Sports anemia" is thus no indication for routine iron supplementation.
对43名男性中长跑运动员和119名男性对照组进行了血液学比较。运动员的血细胞比容、血清铁、转铁蛋白饱和度和血清铁蛋白值显著较低。运动员骨髓含铁血黄素的量也低于同龄非运动员组。即使这些值明显低于对照组，但也未低到足以表明缺铁。骨髓涂片铁粒幼细胞计数正常、红细胞指数和红细胞原卟啉均正常的观察结果有力地支持了以下结论：铁缺乏并未限制红细胞生成或最佳红细胞量的形成。大多数运动员血清触珠蛋白值较低表明血管内溶血增加。由于形成的血红蛋白 - 触珠蛋白复合物被肝细胞摄取，这意味着这些运动员的红细胞分解代谢从网状内皮系统转移到了肝细胞。这种转移可能解释了血清铁蛋白浓度低和骨髓含铁血黄素含量降低这一矛盾的发现。这与观察到的正常红细胞生成一致。得出的结论是，跑步者“贫血”并非真正的贫血，也不是由缺铁引起的。因此，“运动性贫血”并非常规补充铁剂的指征。
