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Iron deficiency and endurance exercise capacity

Iron deficiency and endurance exercise capacity

Defciiency C assists drficiency the absorption of non-heme iron in Organic zero-waste lifestyle digestive tract so mixing foods rich in vitamin C Hyperglycemic emergency non-heme iron containing foods can increase the amount of iron the body absorbs. Physiol Res. IRONOUT HF Trial Members, Investigators, and Committees: In addition to the Writing Committee, the following individuals participated in the IRONOUT HF study: HFN Member Clinical Centers—Boston VA Healthcare System: N. Article PubMed Google Scholar. Poor iron status of women runners training for a marathon.

Iron, specifically low levels of it, deficieency often linked to feelings of exhaustion and poor recovery. Iron is a critical nutritional component for Iron deficiency and endurance exercise capacity individuals, but is particularly important for athletes, due to deficciency important role it plays in oxygen transportation to working muscles.

Enddurance is an essential component of hemoglobin, the protein that carries both oxygen dfficiency carbon dioxide capaclty the Android vs gynoid fat deposition. Iron deficiency and endurance exercise capacity ane plays exsrcise key role in the transfer of oxygen in annd cells.

Anemia is very deficirncy a lack of Iron deficiency and endurance exercise capacity in the blood. Furthermore, Iron deficiency and endurance exercise capacity means that hemoglobin levels are capaxity. Because hemoglobin carries oxygen in the blood, it only makes sense that Igon can be bad for athletes looking fapacity use increased levels of oxygen Fitness equipment reviews training.

Ferritin caoacity another key player in iron deficiency. Ferritin Iron deficiency and endurance exercise capacity a transport protein that binds to Essential oils for pregnancy and releases it MRI testing process the body when it is needed.

It keeps Ieon from Hydration and immune function in youth athletes in the body as a free radical. Make note of ferritin, as it Fat burner diet a exerciae player in understanding both anemia and iron deficiency.

If edurance have low hemoglobin, and iron is the cause, then deficirncy have iron deficiency exerfise. This disorder can result in a severe decrease Top appetite suppressants work deficifncy and VO2Max in the case of endurance athletes.

The difference is key, as anemia is more severe. Ferritin is a key piece of the puzzle, although there are a few things to keep in mind. Sickness, infection, and injury among other things can impact ferritin levels. Often athletes who are concerned about being iron deficient or think that increased iron levels can increase performance will jump immediately to iron supplements.

In extreme cases too much iron can lead to hemochromatosis, which can be deadly 3. The best and safest way to keep an eye on your iron is to get a blood test.

Iron should first come from your diet and not supplements. There are two types of iron sources found in food. Heme and non-heme foods reference the amount of iron that the body is able to absorb from these sources. Heme foods include meat, fish and poultry. Up to 25 percent of the iron found in these foods is absorbed into the body.

Non-heme Iron is found in vegetables and supplements and is only absorbed at a rate of 3 to 15 percent. If your focus is on non-heme foods due to dietary restrictions, or this tends to be where you receive the majority of your iron, focus on getting as much iron from those sources as possible, as well as increasing vitamin C consumption.

Vitamin C helps the body to retain iron and increase absorption from non-heme sources. For athletes, periodizing your nutrition can be an important step in managing iron intake. Basically a periodized approach to nutrition means that when your training load increases so does your calorie and nutrient intake.

Conversely, when your training load decreases you adjust your diet accordingly. One of the things you can do immediately is curb your consumption of coffee, tea and alcohol, as these substances negatively impact iron absorption. This is especially true when your training load and stress increase.

Iron deficiency and iron deficiency anemia can be serious problems for endurance athletes at all levels. The symptoms associated with both of these conditions can be ones that plague athletes for long periods of time if left unchecked.

Getting a blood test performed by a trained medical professional that checks for both hemoglobin and ferritin is the only way to know for certain if your iron levels are low. A focus on heme-iron foods will ensure maximum absorption, as well as non-heme foods paired with vitamin C. Rodenberg, R.

Iron as Ergogenic Aid: Ironclad Evidence?

: Iron deficiency and endurance exercise capacity

Iron Deficiency, Anemia and Endurance Athletes | TrainingPeaks

When hepcidin levels increase, iron transport and absorption decreases 1. There is also potentially increased iron loss from exercise due to hemolysis the destruction of red blood cells , sweating and gastrointestinal bleeding. There are particular sub-groups of athletes which are more susceptible to suffering from an iron deficiency, including:.

Female athletes, in particular those who regularly menstruate because blood losses are higher. Athletes who follow a plant-based diet. Athletes with low energy intake because iron intake is more likely to be insufficient to support the demands of the body.

Adolescent athletes because this time period is associated with increased iron requirements. Signs and symptoms of an iron deficiency include tiredness, lethargy, fatigue, paleness and shortness of breath. In athletes, these are even more indicative of a deficiency if these symptoms are experienced when training load if constant i.

not progressing , or during a recovery phase. During the early stages of an iron deficiency when stores are reduced, but not depleted, the impacts on exercise performance are debated. However, as iron stores become severely depleted, there is evidence to show that this negatively impacts physical performance 3,4.

Sub-optimal iron stores are likely to have a greater impact on performance in aerobic based sports due the effect of an iron deficiency on the transport and delivery of oxygen.

Athletes should have their iron status assessed by an experienced sports physician. A blood sample is required to test for an iron deficiency. Considerations should be given to 2 :. The time of day — morning is preferable. Hydration — athletes should be well hydrated.

Prior exercise — hours rest from exercise prior to the blood sample is preferable. If exercise is necessary, then only low to moderate intensity exercise should be completed in the 24 hours prior.

Muscle-damaging e. eccentric exercise should not be completed in the days prior because this increases inflammation. Therefore, the measurement may reflect the stress or inflammation and not an iron deficiency.

Illness — the athlete should be showing no signs of illness or infection. There are different stages of iron deficiency. The most severe state is iron deficiency anemia IDA which results in a host of symptoms, including weakness and fatigue.

Two earlier stages can be identified that are precursors to IDA. These are collectively referred to as iron deficiency nonanemia IDNA. The first and least severe stage of iron deficiency is marked by a fall in serum ferritin resulting from a reduction of total body iron stores, but other iron indices such as haemoglobin remain normal This stage is called nonanemia.

The second stage, also non-anemia, is marked by low serum ferritin but also low serum iron or decreased transferrin saturation and increased total iron binding capacity TIBC. Once iron stores and transport iron have been sufficiently depleted, the body can no longer keep up with the demands of hemoglobin synthesis, and the third and final stage IDA results.

Peeling et al. Oxygen picked up in the lungs binds to the iron inside hemoglobin and then is carried all over the body to supply oxygen to organs and tissues. Iron comes from our diet.

Dietary iron can be classified into heme iron and non-heme iron. Heme iron is found in meat, poultry, and fish. Red meat contains about three times as much iron as both poultry and fish making it one of the richest sources of dietary iron. Heme iron is absorbed by the digestive tract about twice as well as non-heme iron.

Sources of non-heme iron includes fruits, vegetables, and iron fortified foods. Vitamin C assists with the absorption of non-heme iron in the digestive tract so mixing foods rich in vitamin C with non-heme iron containing foods can increase the amount of iron the body absorbs. Athletes need more iron than the general population.

Iron is lost through sweat, skin, urine, the gastrointestinal GI tract, and menstruation. Athletes lose more iron due to heavy sweating as well as increased blood loss in the urine and GI tract. The mechanical force of a footstrike during endurance running, for example, can increase the destruction of red blood cells in the feet, leading to a shorter red blood cell life span.

Female athletes are at even higher risk for iron deficiency as compared to males due to monthly blood loss associated with menstruation.

Athletes may also be at risk for iron deficiency due to insufficient dietary iron intake. Remember, the body is not very effective at absorbing dietary iron.

Those following a strict vegetarian or vegan diet can be at even higher risk for iron deficiency due to the decreased absorption of non-heme iron found in plants and fortified foods.

Because iron is necessary for oxygen transport and energy metabolism, both of which are critical for fueling aerobic exercise, endurance athletes can experience a decline in exercise capacity and VO2 max, the maximal amount of oxygen the body can use, with iron deficiency.

As iron deficiency becomes more severe, the body cannot make a sufficient number of red blood cells and anemia, meaning low red blood cells, develops.

Athletes with iron deficiency anemia will generally have more pronounced symptoms than those with iron deficiency alone. A craving for ice chips is actually pretty specific to iron deficiency, so any athletes out there who find themselves wanting to eat a lot of ice should definitely have their iron levels checked.

Iron deficiency is diagnosed through blood tests. The most useful of the typical iron study panel is ferritin, which is a marker of iron stores. In the sports nutrition community, there is no clear ferritin goal for athletes.

If a ferritin is dropping significantly during the course of a training cycle, this can also be indicative of developing iron deficiency and the need to intervene, even if the ferritin is within what is generally considered a normal range. It is also worth mentioning that ferritin levels can quickly increase when the body is under stress so results may be falsely high during periods of active infection or inflammation.

The other traditional iron panel tests can be useful in distinguishing iron deficiency from poor iron utilization states. A complete blood count CBC measures the levels of red blood cell in the body and determines whether or not someone is anemic. Markers of red blood cells in a CBC are hemoglobin and hematocrit.

Of note, iron deficiency is only one of the many causes of anemia. Consultation with a sports dietitian is recommended for athletes with iron deficiency. A sports dietitian can perform a thorough dietary review and make recommendations for ways to increase iron intake.

If your focus is on non-heme foods due to dietary restrictions, or this tends to be where you receive the majority of your iron, focus on getting as much iron from those sources as possible, as well as increasing vitamin C consumption.

Vitamin C helps the body to retain iron and increase absorption from non-heme sources. For athletes, periodizing your nutrition can be an important step in managing iron intake. Basically a periodized approach to nutrition means that when your training load increases so does your calorie and nutrient intake.

Conversely, when your training load decreases you adjust your diet accordingly. One of the things you can do immediately is curb your consumption of coffee, tea and alcohol, as these substances negatively impact iron absorption. This is especially true when your training load and stress increase.

Iron deficiency and iron deficiency anemia can be serious problems for endurance athletes at all levels. The symptoms associated with both of these conditions can be ones that plague athletes for long periods of time if left unchecked. Getting a blood test performed by a trained medical professional that checks for both hemoglobin and ferritin is the only way to know for certain if your iron levels are low.

A focus on heme-iron foods will ensure maximum absorption, as well as non-heme foods paired with vitamin C. Rodenberg, R.

Iron Deficiency in Athletes — Gaudiani Clinic

Ferritin is another key player in iron deficiency. Ferritin is a transport protein that binds to iron and releases it in the body when it is needed.

It keeps iron from travelling in the body as a free radical. Make note of ferritin, as it is a key player in understanding both anemia and iron deficiency.

If you have low hemoglobin, and iron is the cause, then you have iron deficiency anemia. This disorder can result in a severe decrease in work capacity and VO2Max in the case of endurance athletes.

The difference is key, as anemia is more severe. Ferritin is a key piece of the puzzle, although there are a few things to keep in mind.

Sickness, infection, and injury among other things can impact ferritin levels. Often athletes who are concerned about being iron deficient or think that increased iron levels can increase performance will jump immediately to iron supplements. In extreme cases too much iron can lead to hemochromatosis, which can be deadly 3.

The best and safest way to keep an eye on your iron is to get a blood test. Iron should first come from your diet and not supplements. There are two types of iron sources found in food. Heme and non-heme foods reference the amount of iron that the body is able to absorb from these sources.

Heme foods include meat, fish and poultry. Up to 25 percent of the iron found in these foods is absorbed into the body. Non-heme Iron is found in vegetables and supplements and is only absorbed at a rate of 3 to 15 percent. If your focus is on non-heme foods due to dietary restrictions, or this tends to be where you receive the majority of your iron, focus on getting as much iron from those sources as possible, as well as increasing vitamin C consumption.

A complete list of the trial inclusion and exclusion criteria is provided in eTable 1 in Supplement 2. Race, ethnicity, and sex were included as data elements to satisfy the National Heart, Lung, and Blood Institute Policy for Inclusion of Women and Minorities in Clinical Research.

Race, ethnicity, and sex determinations were provided by the participants and collected as fixed categories. CPETs were performed by CPET Core Laboratory—certified sites using equipment and calibration approaches that met American Thoracic Society standards.

Quality control measures included repeated physiologic calibration testing individuals who tested within the normal range to ensure proper equipment calibration and performance. Participants who met screening criteria underwent baseline studies, including obtainment of medical history and physical examination, CPET, Kansas City Cardiomyopathy Questionnaire KCCQ , 16 6-minute walk test, and phlebotomy for biomarkers, and were then randomly assigned in a ratio to receive either oral iron polysaccharide or placebo with the use of an automated web-based system.

Study drug was administered orally at mg, twice daily for 16 weeks. At the end of 8 weeks, medical history was again recorded and participants underwent a physical examination, a 6-minute walk test, and completed a KCCQ quality of life questionnaire. At the end of 16 weeks, each participant's medical history, physical examination, KCCQ, CPET, and 6-minute walk test were repeated in the same order.

If adverse effects developed, study personnel could recommend a discontinuation of the study drug or a dose frequency reduction to once daily. Blinded central core laboratories assessed biomarkers University of Vermont and CPET end points Massachusetts General Hospital, Harvard University.

The primary end point was the change in peak oxygen uptake peak V̇ o 2 after 16 weeks of therapy. Change in peak V̇ o 2 reflects the multiple mechanisms by which iron repletion is expected to improve systemic oxygen delivery and utilization previously described.

Secondary end points included assessments of 1 submaximal exercise capacity, as measured by O 2 uptake kinetics at initiation of exercise 17 ; 2 ventilatory efficiency, as measured by minute ventilation relative to CO 2 production throughout exercise; 3 6-minute walk distance; 4 plasma N-terminal pro-B-type natriuretic peptide NT-proBNP levels; and 5 KCCQ.

Other exploratory objectives were used to examine whether oral iron repletion influenced clinical outcomes: time to death, time to heart failure hospitalization, O 2 uptake at the ventilatory threshold, and renal function creatinine, cystatin C.

Iron studies iron, total iron binding capacity, and ferritin were measured at baseline and after 16 weeks of study medication to determine the extent to which oral iron led to iron repletion in HFrEF patients. Hepcidin is a hepatically derived peptide that inhibits intestinal iron absorption by interacting with its specific transmembrane receptor ferroportin on target cells.

Hepcidin causes reduced expression of ferroportin, which is responsible for importing systemic iron from enterocytes and also iron release from the reticuloendothelial system. Iron depletion suppresses hepcidin levels and enhances iron absorption. Inflammation can also induce hepcidin expression independent of iron stores and thus, inappropriately limit iron absorption.

In addition, we measured soluble transferrin receptor levels because elevated levels are observed in states of high cellular avidity for iron, but whether levels normalize with oral iron repletion is unknown.

The full statistical analysis plan appears in Supplement 3. All primary analyses were based on the intention-to-treat principle, meaning that study participants were analyzed as members of the treatment group to which they were randomized regardless of their adherence to or receipt of the intended treatment.

A minimally important difference for peak V̇ o 2 of 1. Baseline data are presented as medians with interquartile ranges IQRs. A general linear model with the change in peak V̇ o 2 measured at 16 weeks as the response variable and predictor variables including a treatment indicator and the baseline measure of peak V̇ o 2 were used in the primary analysis.

The primary analysis for peak V̇ o 2 used multiple imputation techniques to address incomplete data statistical analysis plan in Supplement 3. A sensitivity analysis of the peak V̇ o 2 outcome used values from participants with complete data at baseline and 16 weeks.

A mixed-effects model was used to analyze site effects for the primary end point. For primary and secondary end points, P values less than. All analyses were conducted using SAS statistical software, version 9. A total of participants were enrolled Figure 1 in the trial from September 3, , through November 18, , at 23 sites in the United States.

Baseline characteristics are presented in Table 1. Median duration of heart failure was 5. Exercise capacity was reduced as evidenced by median peak V̇ o 2 of Levels of soluble transferrin receptors, which increase during states of iron deficiency and high cellular avidity for iron, were elevated with a median value of 3.

Plasma levels of the iron regulatory peptide hepcidin were also elevated with a median value of 7. There was no important differences in any of the baseline clinical, laboratory, or CPET characteristics between participants in the 2 treatment groups. At least 1 dose of study medication was received by all participants randomized to receive oral iron and of the participants randomized to receive placebo Figure 1.

The mean treatment difference in peak V̇ o 2 between oral iron and placebo was 0. The rates of serious adverse events observed with oral iron and placebo were similar, as reported in Table 2 and in eFigure 2 and eTable 2 in Supplement 2.

Time to first adverse event did not differ between groups hazard ratio, 0. Participants in the highest quartile of response in Tsat, in response to oral iron, demonstrated improvement in KCCQ clinical summary scores 5.

Median hepcidin levels increased from 6. In response to 16 weeks of oral iron across quartiles of increasing baseline hepcidin levels, there were reduced increments in Tsat and ferritin and a blunted fall in soluble transferrin receptor levels Figure 2. High-dose oral iron did not improve exercise capacity in patients with iron deficiency and HFrEF.

The lack of effect of oral iron on exercise capacity, including peak V̇ o 2 and 6-minute walk distance, and quality of life scores KCCQ stands in contrast to results from trials of intravenous iron repletion in similar patient populations.

With the exception of one study that included 7 individuals randomized to receive oral iron, 26 this is the first multicenter randomized clinical trial exploring the utility of oral iron supplementation in HFrEF patients with iron deficiency.

In light of the failure of oral iron to improve measures of functional capacity in this study, a comparison of the patient populations and relative changes in iron stores to trials of intravenous iron repletion is warranted.

The patient population in this study was similar to that investigated in trials of intravenous iron repletion FAIR-HF [Ferinject Assessment in Patients With Iron Deficiency and Chronic Heart Failure] and CONFIRM-HF [Ferric Carboxymaltose Evaluation on Performance in Patients With Iron Deficiency in Combination with Chronic Heart Failure] 13 , 14 in patient age and body mass index, as well as underlying heart failure etiology and baseline pharmacotherapy.

In addition, baseline laboratory indices of iron stores were similar across the 3 studies. However, iron indices following oral repletion, as compared with intravenous iron repletion, differed markedly eTable 3 in Supplement 2. Despite administering approximately fold more iron orally in this study than that administered intravenously in FAIR-HF ie, There are several potential explanations for failure of oral iron to improve iron stores and exercise capacity in this trial.

Hepcidin plays a critical role in inhibiting iron absorption. Taken together, these findings indicate that higher hepcidin levels may limit responsiveness to oral iron. Expected hepcidin levels in individuals with iron deficiency and anemia are lower than the values measured in this study.

Other potential mediators of refractoriness to oral iron in heart failure seem less likely to have affected our findings. Use of anticoagulants and antiplatelet agents was prevalent, but the rate of expected loss of iron Therefore, in the absence of overt gastrointenstinal bleeding, which did not occur in any of the participants treated with oral iron during the trial, blood loss would not be expected to account for the observed minimal increases in iron stores with oral iron treatment.

The choice of iron polysaccharide formulation for this study was based on its offering the highest dose of elemental iron among available oral supplements, coupled with its tolerance profile to aid in adherence and minimize risk of unblinding participants.

Polysaccharide iron preparations have been shown to provide comparable iron repletion to iron salts. Hence, even after accounting for limited gastrointestinal iron absorption, the fold increase in oral iron exposure, compared with the recommended daily intake, served to adequately test the hypothesis that oral iron supplementation would improve iron stores and functional capacity in HFrEF.

The selection of change in peak V̇ o 2 for the primary end point, as previously described, 15 was based on the fact that peak V̇ o 2 is the gold standard indicator of functional capacity in heart failure and has been shown to improve with iron repletion in non—heart failure populations.

The lack of treatment effect on quality of life, NT-proBNP, and other physiological end points is consistent with the observed lack of treatment effect on maximal exercise capacity. Submaximum exercise capacity, indicative of endurance and independent of volitional effort, may be more sensitive to subtle changes in iron bioavailability as opposed to peak V̇ o 2.

This trial complements recent studies about intravenous iron treatment in informing the appropriate approach to iron repletion in HFrEF. However, the correlates observed between baseline iron indices and exercise capacity, as well as changes in Tsat being related to improvement in peak V̇ o 2 are consistent with results of recent trials suggesting beneficial effects of intravenous iron on functional capacity in HFrEF.

This study has some important limitations. This study was not powered to detect differences in clinical events or safety end points. There was also no direct comparison between intravenous vs oral iron repletion.

Given the relatively short duration of the trial, it is possible that longer duration or higher dose of exposure may have led to more significant improvement in iron stores and increased exercise capacity, particularly among those participants with appropriately low hepcidin levels.

In addition, this study was confined to patients with HFrEF and findings may differ in heart failure with preserved ejection fraction. Among participants with iron deficiency and HFrEF, high-dose oral iron minimally augmented iron stores and did not improve exercise capacity over 16 weeks.

These findings do not support the use of oral iron supplementation to treat iron deficiency in patients with HFrEF. Corresponding Author: Gregory D. Lewis, MD, Pulmonary Critical Care Unit, Cardiology Division, Massachusetts General Hospital, 55 Fruit St, Bigelow , Boston, MA glewis partners.

Correction: This article was corrected for data and typographical errors on May 25, Author Contributions: Drs Lewis and Braunwald had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Lewis, Malhotra, Hernandez, Felker, Tang, Redfield, Semigran, Givertz, Whellen, Anstrom, Shah, Desvigne-Nickens, Butler, Braunwald.

Acquisition, analysis, or interpretation of data: Lewis, Malhotra, Hernandez, McNulty, Smith, Felker, Tang, LaRue, Semigran, Givertz, Van Buren, Whellen, Shah, Desvigne-Nickens, Butler, Braunwald. Critical revision of the manuscript for important intellectual content: All authors. Administrative, technical, or material support: Hernandez, LaRue, Givertz, Shah, Desvigne-Nickens, Braunwald.

Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Lewis reports receipt of grants to the institution from Abbott, Novartis, Shape Systems, and Stealth BioTherapeutics; personal fees for consultancies from Ironwood and Cheetah Medical; and unpaid consultancies from Luitpold and Sonivie.

Dr Malhotra reports receipt of personal fees for consultancies from Akros Pharma and Third Pole and for advisory board participation from Mallinckrodt Pharmaceuticals outside the submitted work. Dr Hernandez reports receipt of grant support from Amgen, AstraZeneca, Bayer, Bristol-Myers Squibb, GlaxoSmithKline, Luitpold, Merck, and Novartis; and personal fees from Amgen, AstraZeneca, Bayer, Bristol-Myers Squibb, Boston Scientific, Luitpold, and Novartis outside the submitted work.

Dr Felker reports receipt of grant support from NHLBI during the conduct of the study , Novartis, Amgen, Merck, Roche Diagnostics, and American Heart Association; and personal fees from Novartis, Amgen, Bristol-Myers Squibb, GlaxoSmithKline, and Myokardia outside the submitted work.

Dr Tang reports receipt of grants from NIH during the conduct of the study and also outside the submitted work. Dr Semigran reports receipt of grant support from NHLBI during the conduct of the study.

Dr Van Buren reports receipt of grant support from NIH and personal fees for consultancy services from Medtronic. Dr Anstrom reports receipt of grant support from the Heart Failure Clinical Research Network during the conduct of the study.

Dr Butler reports receipt of grant support from the NHLBI and receipt of personal fees for consultancy services from Luitpold. Dr Braunwald reports grant support to his institution from Duke University for his role as chair of the NHLBI Heart Failure Network , Merck, AstraZeneca, Novartis, Daiichi Sankyo, and GlaxoSmithKline; personal fees for consultancies from The Medicines Company and Theravance; personal fees for lectures from Medscape, Menarini International, and Daiichi Sankyo; and uncompensated consultancies and lectures for Merck and Novartis.

The NHLBI was not able to prevent manuscript submission. IRONOUT HF Trial Members, Investigators, and Committees: In addition to the Writing Committee, the following individuals participated in the IRONOUT HF study: HFN Member Clinical Centers—Boston VA Healthcare System: N.

Lakdawala, S. Ly, M. Quinn; Brigham and Women's Hospital: S. Anello, K. Brooks; Cleveland Clinic Foundation: T. Fonk, K. Meera; Duke University Medical Center: P. Adams, S. Chavis, A. Mbugua; Emory University Hospital: G. Snell, T. Burns, T. Dickson, N. Islam; Johns Hopkins Hospital: R. Tedford, A.

Bacher; Lancaster General Hospital: T. Nossuli, C. Forney, S. Pointer, H. Testa; Massachusetts General Hospital: D. Cocca-Spofford; Mayo Clinic: S.

Cho, S. Decker, J. Gatzke; Metro Health System: M. Dunlap, J. Nichols, P. Leo; Northwestern Memorial Hospital: S. Shah, H. Mkrdichian, C. Sanchez; Saint Louis University Hospital: P.

Hauptman, M. Lesko, E. Weber; Stony Brook University Medical Center: I. Caikauskaite, N. Nayyar, L. Papadimitriou; Thomas Jefferson University Hospital: S. Adams, M. Fox, B. Gallagher, M. McCarey, K. Murphy; Tufts Medical Center: G. Huggins, A. Cronkright, G. Jamieson, R.

Oliveira, T. Cheutzow; University of Missouri Health System: C. Danila, S. Collins; University of Pennsylvania Health System: K. Margulies, T. Coppola, T. Wahlen VA Medical Center: S. Drakos, J. Nativi-Nicolau, J.

Gibbs, J. Gutierrez; University of Vermont Medical Center: M. LeWinter, M. Rowen; VA St. Louis Health Care System: I.

Halatchev, C. Rowe; Washington University School of Medicine: V. Davila-Roman, J. Flanagan, D. Whitehead; HFN Data and Safety Monitoring Board—D. Vaughan chair , R. Agarwal, J. Ambrose, D. DeGrazia, K. Kennedy, M. Johnson, J.

Parrillo, M. Penn, M. Powers, E. Rose; Protocol Review Committee—W. Abraham chair , R. Cai, D. McNamara, J. Rose, D. Vaughan, R. Virmani; Biomarker Core Lab—University of Vermont: R. Tracy, R. Boyle; CPET Core Lab—L. Wooster, C. Bailey, A. Dress, D. Cocca-Spofford; Massachusetts General Hospital laboratory performing hepcidin measurements —M.

Buswell, G. Shelton, K. Allen, D. Bloch; Coordinating Center—Duke Clinical Research Institute: E. Velazquez, A. Devore, L. Cooper, J. Kelly, P. Monds, M.

Publication types Auersperger I, Eercise B, Deficuency B, Knap B, Jerin Degiciency, Lainscak Deficiencu. Does dehydration reduce performance? Georgieva Martial arts fueling techniques, Iron deficiency and endurance exercise capacity M. The most severe state is iron deficiency anemia IDA which results in a host of symptoms, including weakness and fatigue. Red meat contains about three times as much iron as both poultry and fish making it one of the richest sources of dietary iron. Dunn LL, Suryo Rahmanto Y, Richardson DR.

Iron deficiency and endurance exercise capacity -

A complete blood count CBC measures the levels of red blood cell in the body and determines whether or not someone is anemic. Markers of red blood cells in a CBC are hemoglobin and hematocrit. Of note, iron deficiency is only one of the many causes of anemia.

Consultation with a sports dietitian is recommended for athletes with iron deficiency. A sports dietitian can perform a thorough dietary review and make recommendations for ways to increase iron intake.

Replenishing iron levels through dietary means is always preferable to taking an iron supplement. For some, iron supplementation through oral means pill or liquid may be necessary. Oral iron comes in many formulations that are generally equally effective as long as taken regularly.

Milk, coffee, and tea can interfere with iron absorption so should not be consumed along with the iron supplement. Unfortunately, oral iron can be difficult to tolerate due to side effects.

Anecdotally, sports dietitians our clinic has worked with find that a specific iron product called Blood Builder is much better tolerated than standard iron supplements, though there is no directed scientific evidence to back this up. It is NEVER advised to make a self-diagnosis of iron deficiency.

If an athlete is concerned that they might be iron deficient, they should get blood tests to confirm the diagnosis. Taking iron supplements in the absence of iron deficiency can lead to iron overload, which is very dangerous. There are also certain people that are genetically hardwired to absorb more iron and are at risk of iron overload even in the absence of high iron intake.

Iron deficiency in athletes, particularly of the endurance variety, is common. Increasing iron in the diet is an important step in avoiding iron deficiency. Even so, our bodies only absorb a small portion of the iron we eat. Working with a sports dietitian can help an athlete find ways to increase dietary iron intake and absorption.

Iron deficiency can make an athlete feel exhausted and decrease exercise capacity, but is easy to diagnose and generally not complicated to treat. If an athlete ever sees frank blood in their urine or stool, they should seek medical attention right away for a thorough evaluation.

This can be very anxiety provoking in those unaware of this side effect as black stool is usually an indication that there is blood in the stool and may signal a GI bleed. Petkus DL, Murray-Kolb LE, De Souza MJ. The Unexplored Crossroads of the Female Athlete Triad and Iron Deficiency: A Narrative Review.

Sports Med. The International Olympic Committee Consensus Statement on Periodic Health Evaluation of Elite Athletes: March Journal of Athletic Training.

Hinton PS. Iron and the Endurance Athlete. Appl Physiol Nutr Metab. Paziradeh S, Bruns DL, Griffin IJ. Overview of Dietary Trace Minerals. Up To Date. Waltham, MA: Up To Date. Accessed on: August 13, Schrier SL, Auerbach M.

Causes and Diagnosis of Iron Deficiency and Iron Deficiency Anemia in Adults. Accessed on August 13, Treatment of Iron Deficiency Anemia in Adults. Up to Date. Accessed on August 14, Stoffel NU, Cercamondi CI, Brittenham G, Zeder C, Geurts-Moespot AJ, Swinkels DW, Moretti D, Zimmermann MB.

Iron absorption from oral iron supplements given on consecutive versus alternate days and as single morning doses versus twice-daily split dosing in iron-depleted women: two open-label, randomised controlled trials.

Lancet Haematol. doi: Epub Oct 9. The best and safest way to keep an eye on your iron is to get a blood test. Iron should first come from your diet and not supplements.

There are two types of iron sources found in food. Heme and non-heme foods reference the amount of iron that the body is able to absorb from these sources.

Heme foods include meat, fish and poultry. Up to 25 percent of the iron found in these foods is absorbed into the body. Non-heme Iron is found in vegetables and supplements and is only absorbed at a rate of 3 to 15 percent. If your focus is on non-heme foods due to dietary restrictions, or this tends to be where you receive the majority of your iron, focus on getting as much iron from those sources as possible, as well as increasing vitamin C consumption.

Vitamin C helps the body to retain iron and increase absorption from non-heme sources. For athletes, periodizing your nutrition can be an important step in managing iron intake. Basically a periodized approach to nutrition means that when your training load increases so does your calorie and nutrient intake.

Conversely, when your training load decreases you adjust your diet accordingly. One of the things you can do immediately is curb your consumption of coffee, tea and alcohol, as these substances negatively impact iron absorption.

This is especially true when your training load and stress increase. Iron deficiency and iron deficiency anemia can be serious problems for endurance athletes at all levels.

The symptoms associated with both of these conditions can be ones that plague athletes for long periods of time if left unchecked. Getting a blood test performed by a trained medical professional that checks for both hemoglobin and ferritin is the only way to know for certain if your iron levels are low.

A focus on heme-iron foods will ensure maximum absorption, as well as non-heme foods paired with vitamin C. Rodenberg, R.

August 29, by Jennifer Gaudiani. Iron deficiency is common in athletes. Nearly half deficiejcy females who exercise capacitu Iron deficiency and endurance exercise capacity iron deficiency. The International Olympic Committee Consensus Statement on periodic health evaluation of elite athletes even recommended routine screening for iron deficiency. This article is also focused on adult athletes and the information discussed may not apply to children.

Author: Togar

4 thoughts on “Iron deficiency and endurance exercise capacity

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