Iron Deficiency and Lactic Acid Production Dr. Kim Colter This treatise is an attempt to describe the various ways in which iron deficiency can impair distance running performance, with a focus on how iron deficiency without anemia impairs performance via increased production of lactic acid during racing and anaerobic training. Some hematologists are on record stating that iron deficiency in the absence of anemia does not impair athletic performance. Their reasoning is that if an athlete has a hemoglobin concentration in the normal range, they should have a normal ability to transport oxygen to exercising muscle during exercise. If you ask a hematologist what is the best measure of total body iron stores, they will give you two answers—the presence of stainable iron in a bone marrow aspiration (a painful, invasive procedure), and the serum ferritin level. Ferritin is a protein that transports iron in the blood stream. It is possible, and frequently occurs, that human beings are iron deficient as measured by serum ferritin, but not anemic as measured by hemoglobin level and hematocrit. Distance runners (and other endurance athletes) who have low ferritins (less than 30) with normal hemoglobin/hematocrit values often do not race well. I will cite a few examples that I am personally aware of regarding distance running and iron deficiency: A 16 year old female, high school junior, has difficulty finishing races at the end of the season, particularly on hilly courses leading up to her state championship race. She qualified for the state race her freshman and sophomore seasons, but doesn't qualify as a junior. Her ferritin is measured at 16. She is not anemic. She begins twice daily iron sulfate 324 mg and the next year has a ferritin of 40 throughout the cross country season. She earns all state recognition with her best time ever on a hilly state championship course her senior season. A 19 year old Division I scholarship female XC and track athlete is struggling during her junior year of college to run the times she ran in high school for 1600/1500 meters. Her ferritin is 19. She is not anemic. After iron therapy raises her ferritin to >30 she is again able to run times that earn her "all Big 12" honors in her senior year. A 15 year old female high school XC runner is having difficulty finishing races, and collapses in a hot early season XC race her sophomore year. Her ferritin is 10. She is not anemic. She now has a ferritin in the 40's and is running 5K's in the 20:30 range and is her team's number 4 runner. A 19 year-old female Grinnell distance runner is struggling during her sophomore year and unable to run the times she ran her freshman year. Her serum ferritin is 14. After correction of her total body iron deficit her race performance improves nicely during her junior and senior years. How do we explain the deterioration in race performance in these athletes when their total body iron stores are low, and the improvement in race performance when their total body iron deficit is restored, if it is not due to anemia? Research has shown that
irondeficient animals have low levels of alpha glycerol phosphatase, an enzyme found in the mitochondria of skeletal muscle. Iron deficient animals with low levels of alpha glycerol phosphatase produced higher levels of lactate during treadmill running, and were unable to sustain treadmill running as long as animals with normal levels of total body iron and normal levels of alpha glycerol phosphatase. For those wishing to see the experimental design that demonstrates that iron deficiency in the absence of anemia leads to increased lactate production and decreased ability to sustain exercise, the original paper written by Clement Finch et al is appended. I have a friend and medical school classmate who is a truly brilliant scientist at Washington University Medical School (our alma mater.) Tim is a hematologist. When I discussed this subject with Tim, he expressed the opinion that any difference in performance in iron deficient athletes was probably due to subtle differences in hemoglobin concentration—i.e. anemia was responsible. Tim brought up his experience with a few patients with polycythemia vera, a condition in which the bone marrow makes too many red blood cells. P. vera patients are treated by regularly withdrawing blood and deliberately creating iron deficiency to keep their hemoglobin from being too high. Tim told me about one of his P.vera patients, a doctor, who had a serum ferritin of 0. Tim's patient didn't complain of fatigue and jogged two miles at lunchtime regularly. I pointed out to Tim that the athletes I have seen who have low ferritins and poor race performances didn't complain of fatigue, either, and didn't have any difficulty running their weekly long runs of 6 to 11 miles at paces that constituted 55-65% of VO2 max, either. What they had difficulty doing was racing at paces above their anaerobic threshold, because they, like the animals in Clement Finch's study, were producing higher levels of lactate during running at race pace and were unable to sustain these paces as long as their competitors who were not iron deficient, or indeed as long as they were able to sustain the same pace when iron levels were restored to normal as reflected in serum ferritin. When Tim reviewed the study by Clement Finch that I have appended, he said, "It must be true, Clement Finch is a good scientist." How do we know what level of serum ferritin is enough to prevent excessive production of lactate when running at race pace? I do not think we can rely on the listed lower limit of normal that is given on laboratory reports for serum ferritin. I have asked Coach Joe Vigil, who coaches Olympic marathoner and medallist, Deena Kastor, about serum ferritin. Coach Vigil states that Deena Kastor has her serum ferritin tested four times a year and with serum ferritins between 28 and 36 is able to produce world class race results. I have seen the opinion of some sports physiologists that in order to obtain benefit from altitude training that serum ferritin needs to be 30 or above. For that reason, I have encouraged endurance athletes who are my patients to supplement iron in quantities sufficient to attain a serum ferritin of 30 or greater. I have encouraged athletes to take iron supplements that have 60mg of elemental iron per tablet, the level that is found in a 324 mg iron sulfate tablet, and to take one or two of these tablets per day. In my experience, those who are iron deficient can raise their serum ferritin to greater than 30 in about three months taking two tablets a day. Most female runners can maintain their serum ferritin at 30 or more taking one 324 mg iron sulfate tablet per day. Some
physicians prefer the use of ferrous gluconate supplements, which are 11.6% elemental iron (240mg ferrous gluconate tablet contains 27mg elemental iron.) Iron sulfate tablets are 20% elemental iron (324 mg iron sulfate tablet contains 60 mg elemental iron.) Runners taking ferrous gluconate will have to take more tablets per day to get the same elemental iron dosage as runners taking iron sulfate tablets. Standard vitamin and mineral supplements with 18mg of elemental iron per tablet are not sufficient when trying to correct an iron deficient state. I would not encourage the use of "slow release" iron supplements. Iron is absorbed in the duodenum (in the upper GI tract.) Iron that makes it to the colon will contribute to constipation. Iron is best absorbed when taken with orange juice or Vitamin C. Absorption of iron is inhibited by taking it with tea. I have encouraged runners to have their serum ferritin tested at the end of the fall cross country season and at the end of spring track season. If iron deficiency is discovered at these times, there is time to allow correction of the iron deficiency before the next season of endurance activity begins. When iron deficiency is discovered half way through a cross country or track season, it is difficult to correct the iron deficiency with oral iron before the championship events that occur at the end of the season. Because female runners lose iron with menses, the issue of iron deficiency in female runners is addressed more often than in males. However, the serum ferritin data done on male Grinnell cross country runners at the end of the 2007 season make it clear that iron loss during running can make male runners iron deficient as well. We must remember that some members of the population will carry one or both alleles of the gene for hemochromatosis, a disease of excess iron storage. Runners who carry the hemochromatosis gene could potentially be harmed by indiscriminately using iron supplements. If runners have a family history of hemochromatosis, they should be tested by their physicians to see if they indeed carry the gene mutation responsible for hemachromatosis.. Runners whose serum ferritins are greater than 150 should probably consider having their serum iron tested, and if their serum iron is greater than the upper limits of normal, being tested for the hemochromatosis gene and reducing their level of supplementation. References: • Finch, Clement et al, "Lactic Acid Production as a Result of Iron Deficiency", J. Clinical Investigation, 1979 July, Volume 64 (1), pp 129-137 • A nice summary of an excellent high school coach's experience with iron issues in cross country runners is found at: www.trackandfieldnews.com/hs/coachscorner/20051215.htmlIron Deficiency and Lactic Acid Production Dr. Kim Colter • This treatise is an attempt to describe the various ways in which iron deficiency can impair distance running performance, with a focus on how iron deficiency without anemia impairs performance via increased production of lactic acid during racing and anaerobic training. • Some hematologists are on record stating that iron deficiency in the absence of anemia does not impair athletic performance. Their reasoning is that if an athlete has a hemoglobin concentration in the normal range, they should have a normal ability to transport oxygen to exercising muscle during exercise. If you ask a hematologist what is the best measure of total body iron stores, they will give you two answers—the presence of stainable iron in a bone marrow aspiration (a painful, invasive procedure), and the serum ferritin level. Ferritin is a protein that transports iron in the
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blood stream. It is possible, and frequently occurs, that human beings are iron deficient as measured by serum ferritin, but not anemic as measured by hemoglobin level and hematocrit. Distance runners (and other endurance athletes) who have low ferritins (less than 30) with normal hemoglobin/hematocrit values often do not race well. I will cite a few examples that I am personally aware of regarding distance running and iron deficiency: A 16 year old female, high school junior, has difficulty finishing races at the end of the season, particularly on hilly courses leading up to her state championship race. She qualified for the state race her freshman and sophomore seasons, but doesn't qualify as a junior. Her ferritin is measured at 16. She is not anemic. She begins twice daily iron sulfate 324 mg and the next year has a ferritin of 40 throughout the cross country season. She earns all state recognition with her best time ever on a hilly state championship course her senior season. A 19 year old Division I scholarship female XC and track athlete is struggling during her junior year of college to run the times she ran in high school for 1600/1500 meters. Her ferritin is 19. She is not anemic. After iron therapy raises her ferritin to >30 she is again able to run times that earn her "all Big 12" honors in her senior year. A 15 year old female high school XC runner is having difficulty finishing races, and collapses in a hot early season XC race her sophomore year. Her ferritin is 10. She is not anemic. She now has a ferritin in the 40's and is running 5K's in the 20:30 range and is her team's number 4 runner. A 19 year-old female Grinnell distance runner is struggling during her sophomore year and unable to run the times she ran her freshman year. Her serum ferritin is 14. After correction of her total body iron deficit her race performance improves nicely during her junior and senior years. How do we explain the deterioration in race performance in these athletes when their total body iron stores are low, and the improvement in race performance when their total body iron deficit is restored, if it is not due to anemia? Research has shown that irondeficient animals have low levels of alpha glycerol phosphatase, an enzyme found in the mitochondria of skeletal muscle. Iron deficient animals with low levels of alpha glycerol phosphatase produced higher levels of lactate during treadmill running, and were unable to sustain treadmill running as long as animals with normal levels of total body iron and normal levels of alpha glycerol phosphatase. For those wishing to see the experimental design that demonstrates that iron deficiency in the absence of anemia leads to increased lactate production and decreased ability to sustain exercise, the original paper written by Clement Finch et al is appended. I have a friend and medical school classmate who is a truly brilliant scientist at Washington University Medical School (our alma mater.) Tim is a hematologist. When I discussed this subject with Tim, he expressed the opinion that any difference in performance in iron deficient athletes was probably due to subtle differences in hemoglobin concentration—i.e. anemia was responsible. Tim brought up his experience with a few patients with polycythemia vera, a condition in which the bone marrow makes too many red blood cells. P. vera patients are treated by regularly withdrawing blood and deliberately creating iron deficiency to keep their hemoglobin from being too high. Tim told me about one of his P.vera patients, a doctor, who had a serum ferritin of 0. Tim's patient didn't complain of fatigue and jogged two miles at lunchtime regularly. I pointed out to Tim that the athletes I have seen who have low ferritins and poor race performances didn't complain of fatigue, either, and didn't have any difficulty running their weekly long runs of 6 to 11 miles at paces that constituted 55-65% of VO2 max, either. What they had difficulty doing was racing at paces above their anaerobic threshold, because they, like the animals in Clement Finch's study, were producing higher levels of lactate during running at race pace and were unable to sustain these paces as long as their competitors who were not iron deficient, or indeed as long as they were able to sustain the same pace when iron levels were restored to normal as reflected in serum ferritin. When Tim reviewed the study by Clement Finch that I have appended, he said, "It must be true, Clement Finch is a good scientist." How do we know what level of serum ferritin is enough to prevent excessive production of lactate when running at race pace? I do not think we can rely on the listed lower limit of normal that is given on laboratory reports for serum ferritin. I have asked Coach Joe Vigil, who coaches Olympic marathoner and medallist, Deena Kastor, about serum ferritin. Coach Vigil states that Deena Kastor has her serum ferritin tested four times a year and with serum ferritins between 28 and 36 is able to produce world class race results. I have seen the opinion of some sports physiologists
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that in order to obtain benefit from altitude training that serum ferritin needs to be 30 or above. For that reason, I have encouraged endurance athletes who are my patients to supplement iron in quantities sufficient to attain a serum ferritin of 30 or greater. I have encouraged athletes to take iron supplements that have 60mg of elemental iron per tablet, the level that is found in a 324 mg iron sulfate tablet, and to take one or two of these tablets per day. In my experience, those who are iron deficient can raise their serum ferritin to greater than 30 in about three months taking two tablets a day. Most female runners can maintain their serum ferritin at 30 or more taking one 324 mg iron sulfate tablet per day. Some physicians prefer the use of ferrous gluconate supplements, which are 11.6% elemental iron (240mg ferrous gluconate tablet contains 27mg elemental iron.) Iron sulfate tablets are 20% elemental iron (324 mg iron sulfate tablet contains 60 mg elemental iron.) Runners taking ferrous gluconate will have to take more tablets per day to get the same elemental iron dosage as runners taking iron sulfate tablets. Standard vitamin and mineral supplements with 18mg of elemental iron per tablet are not sufficient when trying to correct an iron deficient state. I would not encourage the use of "slow release" iron supplements. Iron is absorbed in the duodenum (in the upper GI tract.) Iron that makes it to the colon will contribute to constipation. Iron is best absorbed when taken with orange juice or Vitamin C. Absorption of iron is inhibited by taking it with tea. I have encouraged runners to have their serum ferritin tested at the end of the fall cross country season and at the end of spring track season. If iron deficiency is discovered at these times, there is time to allow correction of the iron deficiency before the next season of endurance activity begins. When iron deficiency is discovered half way through a cross country or track season, it is difficult to correct the iron deficiency with oral iron before the championship events that occur at the end of the season. Because female runners lose iron with menses, the issue of iron deficiency in female runners is addressed more often than in males. However, the serum ferritin data done on male Grinnell cross country runners at the end of the 2007 season make it clear that iron loss during running can make male runners iron deficient as well. We must remember that some members of the population will carry one or both alleles of the gene for hemochromatosis, a disease of excess iron storage. Runners who carry the hemochromatosis gene could potentially be harmed by indiscriminately using iron supplements. If runners have a family history of hemochromatosis, they should be tested by their physicians to see if they indeed carry the gene mutation responsible for hemachromatosis.. Runners whose serum ferritins are greater than 150 should probably consider having their serum iron tested, and if their serum iron is greater than the upper limits of normal, being tested for the hemochromatosis gene and reducing their level of supplementation. References: Finch, Clement et al, "Lactic Acid Production as a Result of Iron Deficiency", J. Clinical Investigation, 1979 July, Volume 64 (1), pp 129-137 A nice summary of an excellent high school coach's experience with iron issues in cross country runners is found at: www.trackandfieldnews.com/hs/coachscorner/20051215.html