Effects of long-term swimming exercise on cellular iron metabolism in rats

xvii, 329 leaves : ill. ; 30 cm.PolyU Library Call No.: [THS] LG51 .H577P ABCT 2000 XiaoBackground: Previous studies have shown controversial effects of exercise on iron metabolism. A general suggestion is that exercise may lead to a low iron status. To date, mechanisms of the exercise-induced low iron status are still unclear. Studies in this thesis were proposed to further determine the effects of long-term exercise on iron metabolism and their regulatory mechanisms in an animal model. Methods: Swimming exercise was performed on rats to investigate: (1) the effect of long-term (up to 12 months) swimming exercise on iron status; (2) the changes in cellular iron uptake in bone marrow; (3) the role of nitric oxide (NO) in exercise-induced changes in iron status. Results: The main findings are: (1) Long-term swimming led to a low iron status presented by decreased plasma iron (PI), transferrin (Tf) iron saturation (TS) and storage iron in the liver, spleen, heart, kidney, and bone marrow cells; (2) Exercise led to an increased expression of the surface Tf receptor (TfR) in erythroblast without any change in TfR affinity, and enhanced TfR-mediated iron uptake; (3) As compared with 3-month period of exercise, 6- and 12-month exercise periods did not induce a significant decrease in plasma hemoglobin and hematocrit. A true 'sport anemia' can not be developed. (4) The Vmax and Km of cellular Fe(II) uptake in bone barrow cells were significantly affected by 6-month periods of strenuous exercise; (5) Exercise decreased cytosolic aconitase activity in the liver, spleen, and bone marrow cells, indicating that exercise may genetically affect expression of iron binding protein; (6) Exercise increased plasma NO products, which correlated well with PI. However, such statistical correlation was not found in sedentary rats; (7) Exercise increased NO production in the liver, spleen and bone marrow cells, which could be completely blocked by NO synthase inhibitor, L-NAME, while low iron storage could just partly be blocked by L-NAME, indicating that NO may be partly associated with exercise-induced low iron status. (8) The decreased cytosolic aconitase activity in exercise could be intervened by L-ANME, in the liver, spleen and bone marrow cells. NO might lead to a low iron status, possibly through its genetically regulatory effect of iron metabolism with exercise. Conclusions: Results in this thesis support that exercise may lead to a low iron status. Such a low iron status is similar to, but in part different from, what is caused by a nutritional iron deficiency, since an exercise-induced low iron status does not progressively develop to the anemia stage. With respect to NO roles, such a low iron status during exercise is similar to that associated with chronic diseases, but the two mechanisms may be partly different since NO involves iron retention in RE cells in chronic diseases. Based on the current knowledge about regulation of iron metabolism, a new NO hypothesis has been presented that NO may be one of the factors in exercise-induced low iron status, and may not be due to iron deficiency.Department of Applied Biology and Chemical TechnologyPh.D., Dept. of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, 2000