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Iron And Endurance Athletes

Nutrition Research Courtesy of First Endurance www.FirstEndurance.com

Iron and Endurance Athletes
By Shawn Dolan PhD, Kris Walker MD & Robert Kunz MS


Iron is one of the most abundant minerals on earth and is essential to normal human physiology. About 2/3 of the body's iron is found in hemoglobin, the protein in red blood cells that carries oxygen to cells. An adequate supply of iron is necessary for the body to produce hemoglobin and red blood cells (RBC). If too little iron is available, fewer and/or smaller RBC's are produced, leading to decreased oxygen carrying capacity of the blood. This is called iron deficiency anemia and can cause fatigue, poor work capacity, and decreased immunity. It is important to understand there are different levels of iron deficiency. The least severe is when someone has low iron stores (low serum ferritin levels), the next is depleted iron stores (using cut-off values), while the most severe category is iron deficiency anemia.

Endurance athletes depend on efficient oxygen delivery to working muscles, so even mild anemia can have deleterious effects on performance. Some hypothesize that iron deficiency, even without anemia, can impair endurance. However, one review of iron supplementation showed that in seven of 8 studies iron stores increased with supplementation as measured by serum ferritin levels, while no increase in performance was found unless hemoglobin also increased. In the eighth study, there was an unexplainable drop in endurance performance in the control group which confounded the results (Garza et al.,1997).

Dietary iron comes in two forms: heme and non-heme. Heme iron is found in animal foods that originally contained hemoglobin, such as meat, fish, and poultry. Non-heme iron comes in foods such as beans, spinach, raisins, and fortified cereals and breads. Heme iron is better absorbed than non-hem iron, but most dietary iron sources are non-heme. The recommended daily value for iron intake is 18 milligrams of elemental iron for women (19-50 yr) and 8 milligrams for men and women over the age of 50.. Three ounces of beef contains 3.2 mg of heme iron and one cup of lima beans contains 4.5 mg of non-heme iron. Absorption of non-heme iron can be increased by consuming it with heme iron or with ascorbic acid (vitamin C). Some substances that decrease iron absorption are the tannins and polyphenols found in tea and coffee, calcium, and phytates found in whole grains and legumes. One study showed that taking 30-50 mg of ascorbic acid can overcome the inhibitory effects of tannins and phytate on iron absorption (Siegenberg et al., 1991).

There is contradictory evidence regarding the prevalence of iron deficiency anemia in athletes. Most studies show an increased prevalence of iron deficiency anemia in athletes. One study showed that iron deficiency developed over an 11 week cross country season, with 17% of males and 45% of females becoming iron deficient(Rowland et al., 1987). Dietary choices may explain most of this, but evidence exists for increased iron and red blood cell turnover (Beard & Tobin, 2000). Intense exercise may increase the need for iron by 30%. This may be due to increased red blood cell turnover, effects of increased nitric oxide or other unknown mechanisms. In sports, especially in endurance sports where low body weight can be an advantage, caloric restriction can result in inadequate dietary iron intake. Females, especially those with heavy menstrual periods or with eating disorders, are especially prone to iron deficiency. However, the most common cause of a low hematocrit (a ratio of red blood cells to whole blood) in athletes is pseudo-anemia, which is a dilution of the blood caused by plasma expansion. This is not true anemia, as the actual number of red blood cells is not decreased (Portal & Dubnov, 2003). Another study showed that endurance athletes were less likely than the general population to have iron deficiency. Out of 52 controls, 50% were iron deficient, and out of 126 atheletes, 26% were iron deficient (Malczewska et al., 2000).

Iron supplementation is indicated when an athlete has iron deficiency anemia and dietary sources are not sufficient to replace the necessary iron. A low iron level with a low to normal hemoglobin may be a relative indication for iron supplementation in order to increase performance. Iron supplementation is available in ferrous and ferric forms, with ferrous forms being the best absorbed. Ferrous fumarate contains 33% elemental iron, ferrous sulfate contains 20%, ferrous gluconate contains 12%, iron amino acid chelate 2.5%. Therapeutic doses of iron supplements may cause side effects such as nausea, vomiting, constipation, diarrhea, dark colored stools and/or abdominal distress. Taking the supplement in two or three divided doses and with food (titrating up to the recommended dose) may help limit these symptoms. Since Iron amino acid chelate is metabolized differently than other ferrous sources, it can also improve these symptoms. Rarely, iron injections are needed, but require close medical supervision.

Dietary constituents that are known to decrease the absorption of inorganic iron appear to have little or no effect on the absorption of heme iron. This is because inorganic iron must be ionized in order to be absorbed. Heme-iron contains iron bound to protein. Iron amino acid chelate is a type of iron that does not ionize in the gut, and therefore, like heme iron, is not affected by the dietary factors that inhibit inorganic iron salts. Because of this and other factors Iron amino acid chelate is absorbed at an average rate 59% greater than that of ferrous sulfate. (Monson et al., 1988). Thirty one scientific reports published on Iron amino acid chelate prove superior absorption characteristics, greater tolerance, lower toxicity, less dietary interaction, higher stability and much lower pro-oxidant activity. (Albion Research Notes, 1997).

Should all athletes supplement with iron? This can only be answered through a comprehensive blood analysis through your Doctor. Anemia has many causes. It can be due to decreased production of red blood cells, blood loss, or increased destruction, such as heel-strike hemolysis in runners. Decreased production can be due to bone marrow abnormalities, kidney problems, or more commonly, nutritional deficiencies. Vitamin B12 and folate deficiencies can also cause anemia. A physician can determine the presence or absence of anemia and do testing to determine the cause and direct appropriate treatment. Iron overload can occur with excessive supplementation or in people with genetic diseases such as hereditary hemochromatosis. Hemachromatosis affects one in 250 individuals of northern European descent and causes extremely efficient absorption and storage of iron. The iron is stored in body organs, resulting in cirrhosis of the liver, heart failure, possibly cancer (Fauci et al., 1998). Indiscriminate iron supplementation may induce hemochromatosis in susceptible individuals (Zoller et al., 2004). High iron stores have also been linked to ischemic heart disease. Some have suggested a protective effect of iron depletion on cardiovascular disease (Sullivan & Mascitelli, 2007).

Of particular concern is athletes taking iron in the hopes of increasing their performance and developing iron overload, eventually experiencing the above complications. In 1999, the Union Cycliste Internationale (UCI) began systematically testing athletes in the wake of the doping scandals uncovered in the 1998 Tour de France. Four times a year, all professional cyclists were required to submit to a battery of blood tests. The most glaring abnormality found in these tests was a high ferritin level, indicating high iron stores. The upper normal limit of ferritin is 300 mg/ml, and the average ferritin value in the 1000-plus athletes tested was 342 ng/ml. Almost half the cyclists had ferritin levels over 300 ng/ml, and one fourth had levels over 500 ng/ml. Iron supplementation has long been practiced by cyclists in the belief that iron enhances performance by increasing red blood cells. This actually is true only in iron deficiency anemia. Two concerns were raised: First, high levels of iron storage cause organ damage and the high levels persisted even after supplementation ceased. Second, excessive iron supplementation is linked with blood doping. The use of EPO to boost red blood cell production increases the body's need for iron. The good news is that average ferritin values have decreased by 33% between 1999 and 2002 (Deugnier et al., 2002; Zotter et al., 2004).

In summary, iron deficiency anemia decreases endurance performance and intense exercise may increase dietary iron requirements. Some groups of athletes, particularly menstruating female and vegetarian athletes, distance runners, and those on caloric restricted diets, are more prone to iron deficiency anemia. Iron supplementation is common in endurance sports, and will help endurance performance in anemia caused by iron deficiency. However, because anemia can have many different causes, low hemoglobin, especially if not responsive to iron supplementation, needs a complete medical workup. When iron supplementation is indicated, hemoglobin and serum ferritin levels should be checked regularly, to prevent complications from iron overload.


References:

Albion Research notes: Vol 6, No.4, 1997.

Beard J, Tobin B. Iron status and exercise. Am J Clin Nutr. 2000; 72(2 Suppl):594S-7S.

Deugnier Y, Loreal O, Carre F, Zoulim F, Vinel JP, Paris JC, Blaison D, Moirand R, Turlin B, Gandon Y, David V, Megret A, Guinot M. Increased body iron stores in elite road cyclists. Med Sci Sports Exerc. 2002 May; 34(5):876-80.

Fallon KE. Utility of hematological and iron-related screening in elite athletes. Clin J Sport Med. 2004 May;14(3):145-52.

Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, Hauser SL, Longo DL. Harrison's Principles of Internal Medicine Companion Handbook. 1998:980-1.

Garza D, Shrier I, Kohl HW 3rd, Ford P, Brown M, Matheson GO. The clinical value of serum ferritin tests in endurance athletes. Clin J Sport Med.

1997 Jan;7(1):46-53.

Malczewska J, Raczynski G, Stupnicki R. Iron status in femal endurance athletes and in non-athletes. Int J Sport Nutr Exerc Metab. 2000 Sep; 10(3):260-276.

Monson, ER. Iron nutrition and absorption: Dietary factors which impact bioabailability. J of Am Diet Assoc. 1988; 88, 786-790

Office of Dietary Supplements. National Institutes of Health. Dietary Supplement Fact Sheet: Iron. 2004. http://ods.od.nih.gov/factsheets/iron.asp.

Portal S, Epstein M Dubnov G. Iron deficiency and anemia in female athletes--causes and risks. Harefuah. 2003; 142(10):698-703, 717.

Rodenberg RE, Gustafson S. Iron as an ergogenic aid: ironclad evidence? Curr Sports Med Rep. 2007 Jul;6(4):258-64.

Rowland TW, Black SA, Kelleher JF. Iron deficiency in adolescent endurance athletes. J Adolesc Health Care. 1987 Jul;8(4):322-6.

Siegenberg D, Baynes RD, Bothwell TH, Macfarlane BJ, Lamparelli RD, Car Ng, MacPhail P, Schmidt U, Tal A, Mayet F. Ascorbic acid prevents the dose-dependent inhibitory effects of polyphenols and phytates on nonheme-iron absorption. Am J Clin Nutr. 1991 Feb;53(2):537-41.

Suedekum NA, Dimeff RJ. Iron and the athlete. Curr Sports Med Rep. 2005; 4(4):199-202.

Sullivan JL, Mascitelli L. Current status of the iron hypothesis of cardiovascular diseases. Recenti Prog Med. 2007 Jul-Aug;98(7-8):373-7.

The Merck Manual of Health & Aging. Anemia. http://www.merck.com/pubs/mmanual_ha/sec3/ch49/ch49b.html.

Zoller H, Vogel W. Iron supplementation in athletes--first do no harm. Nutrition. 2004 Jul-Aug;20(7-8):615-9.

Zotter H, Robinson N, Zorzoli M, Schattenberg L, Saugy M, Mangin P. Abnormally high ferritin levels among professional road cyclists. Br J Sports Med. 2004 Dec: 38(6):704-8.

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