Changes of iron stores and duodenal transepithelial iron transfer during regular exercise in rats.

It is unclear whether regular exercise depletes body iron stores and how exercise regulates iron absorption. In this study, growing female Sprague-Dawley rats were fed a high-iron diet (300 mg iron/kg) and subjected to swimming for 1, 3, or 12 months. Their body weight, liver nonheme iron content (NHI), spleen NHI, blood hemoglobin (Hb) concentration, hematocrit (Hct), and kinetics of 59Fe transfer across isolated duodenal segments were then compared with sedentary controls. The main results were as follows: exercise for 1 month enhanced the transepithelial 59Fe transfer and increased liver NHI content and Hb concentration; exercise for 3 months inhibited transepithelial 59Fe transfer without affecting the liver and spleen NHI content, Hb concentration, and Hct; exercise for 12 months did not affect these parameters as compared with the corresponding sedentary controls; and the changes in transepithelial iron transfer were not associated with basolateral iron transfer. Our findings demonstrated that chronic, regular exercise in growing rats with a high dietary iron content does not deplete iron stores in the liver and spleen and may possibly enhance or inhibit duodenal iron absorption and even maintain duodenal iron absorption at the sedentary level, at least, in part depending on growth.

Nitric oxide and iron metabolism in exercised rat with L-arginine supplementation.

The present study was designed to investigate whether L-arginine (Arg) supplementation in exercise affects nitric oxide (NO) synthesis in tissues and thus iron metabolism. Rats were assigned to one of four groups: EG (Exercise), SG (Sedentary), EAG (Exercise + Arg), and SAG (Sedentary + Arg). Both EG and EAG swam 2 h/day for 3 months. Both SAG and EAG received 3% Arg supplementation in their drinking water. The results showed that Arg supplementation in exercise (EAG) significantly increased nitrite and nitrate (NOx) concentration in the kidney and BMC, rather than in the liver, spleen and heart. Arg supplementation significantly increased both nonheme iron (NHI) and catalytic iron (CI) content in the kidney, to the extent that the ratio of CI/NHI or storage iron (SI)/NHI was not significantly affected, and significantly decreased NHI content and increased CI content in BMC, to the extent that SI content or SI/NHI was significantly decreased. These findings suggest that Arg supplementation in exercise, possibly through increasing NO synthesis, may change CI formation in the kidney and BMC, and affect iron storage in BMC rather than in the kidney.

[Effects of long-term swimming exercise on iron status of rats].

AIM: To observe the effects of different periods of exercise on the iron status. METHODS: Female rats were randomly divided into 3-, 6-, 12-month swimming exercise groups and their corresponding sedentary groups. The hematological indices of iron status and the non-heme iron (NHI) and total NHI (TNHI) of the organs were determined at the end of the desired period. RESULTS: As compared with the corresponding sedentary groups, plasma iron and transferrin-iron saturation of three exercise groups were decreased without significant changes of blood hemoglobin and hematocrit. The NHI contents and TNHI of the liver, spleen and kidney were decreased. Although the NHI contents of the heart decreased, TNHI was not significantly changed. TNHI of the organs in both the exercised and sedentary rats were found to increase with age. CONCLUSION: The exercise-induced low iron status with depleted iron storage is similar to the iron-deficiency status, but it could not be explained using the hypothesis of iron deficiency. Both the NHI redistribution and the maintained iron storage suggests the adaptation of low iron status to exercise. Therefore, the so-called exercise-induced iron deficiency could not exist.