Vegetarian athletes should be particularly vigilant to include iron-rich foods in their diet.
For all three groups, monitoring of dietary intake and good nutritional counseling may preclude a negative iron balance and should be the first line of action in the prevention of iron deficiency. Indiscriminant pharmacologic intervention should be viewed as an undesirable means of achieving adequate iron intake, since in the least, it marginalizes the importance of promoting good nutritional habits in the athletic population. From the above priorities it is apparent that the female runner who consumes a vegetarian diet would likely be at greatest risk for a negative iron balance.
The use of supplements, however, must be a judicious choice based not upon the likelihood of anemia, but ideally upon hematologic evaluation. Using complex preparations may provide less iron than suspected, and warrant a careful re-examination with regard to efficacy. Clinically utilized oral iron preparations contain ferrous sulfate, hydrated or gluconated, or ferrous gluconate or ferrous fumarate. These preparations contain from 37 to 106 mg elemental iron. Supplementation is not without consequence, however; the use of high doses of supplemental iron is often associated with gastrointestinal distress and constipation, with a subsequent decline in compliance. In those genetically predisposed, hemochromatosis may develop following iron supplementation. Iron toxicity may even develop in those not genetically predisposed when ingesting dosages of 75 mg or more of supplemental iron.
In summary, it is clear that a decreased HCT and Hb will impair delivery of oxygen to tissues and lead to a reduced maximal oxygen uptake. Supplementation of individuals to normal HCT verifies the effects of hemoglobin iron on VO2 max. However, the effects of iron supplementation upon the athletic performance of those with clinically low serum ferritin is less clear, although limited evidence seems to suggest improved endurance performance and a decreased reliance upon glucose as an oxidative substrate. Whether such adaptations are beneficial at a subclinically reduced serum ferritin has not been established.
References
1. International Nutritional Anemia Consultative Group. Measurements of iron status. Report of the Nutrition Foundation. Washington (DC), 1985.
2. Skikne BS, Flowers CH, Cook JD. Serum transferrin receptor: a quantitative measure of tissue iron deficiency. Blood 1990;75:1870.
3. Bothwell TH, Charlton RW, Cook JB, Finch CA. Iron metabolism in man. Oxford: Blackwell Scientific. Oxford, 1979, Chaps. 1 3.
4. Cook JD, Dassenko SA, Lynch SR. Assessment of the role of nonheme iron availability in iron balance. Am J Clin Nutr 1991;54:717.
Dallman PR. Biochemical basis for the manifestations of iron deficiency. Ann Rev Nutr 1986;6:13.
5.
6. Finch CA, Huebers MD. Perspectives in iron metabolism. N Engl J Med 1982;25:1520.
7. Dallman PR. Manifestations of iron deficiency. Semin Hematol 1982;19:19.
8. Edgerton VR, Ohira Y, Hettiarachi J, Senewiratne B, Gardner GW, Barnard RJ. Elevation of hemoglobin and work tolerance in iron deficient subjects. J Nutr Sci Vitaminol 1981;27:77.
9. Perkkio MV, Jansson LT, Brooks GA, Refino CJ, Dallman PR. Work performance in iron deficiency of increasing severity. J Appl Physiol 1985;58:1477.
10. Wijn JF, De Jongste JL, Mosterd W, Willebrand D. Hemoglobin, packed cell volume, and iron binding capacity of selected athletes during training. Nutr Metab 1971;13:129.