Iron absorption in highly-trained runners: Does it matter when and where you eat your iron? Under Review.

Garvican, L. Intravenous iron supplementation in distance runners with low or suboptimal ferritin. Med Sci Sports Exerc, 46 2 , Baird-Gunning, J. Correcting iron deficiency. Aust Prescr, 39 6 , Woods, A. Four weeks of IV iron supplementation reduces perceived fatigue and mood disturbance in distance runners.

PLoS One, 9 9 , e Haemoglobin mass in an anaemic female endurance runner before and after iron supplementation. Int J Sports Physiol Perform, 6 1 , Examining the decay in serum ferritin following intravenous iron infusion: a retrospective cohort analysis of Olympic sport female athletes.

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Peter Peeling, Nikita Fensham, and Alannah McKay 5 min read. Iron deficiency. Restoring iron status. Consumption of iron in food or via oral supplements can be used to address low iron status.

Whereas in athletes with severe iron deficiency, parenteral iron provision may be a viable solution. Parenteral iron treatment infusion or injection. The impact of parenteral iron provision is greater in anaemic athletes with low pre-infusion serum ferritin concentrations i.

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com customercare cbspd. Iron is one of the most abundant elements, essential for the completion of numerous important biological functions, including electron transfer reactions, gene regulation, binding and transport of oxygen, regulation of cell growth and differentiation.

Only a minor quantity 0. Besides its essential character, excessive free iron could adversely affect the human body, by augmenting oxidative stress, mainly via the Fenton and Haber-Weiss reactions.

Ferritin, hemosiderin and transferrin, assist the system to maintain iron balance under tight control by keeping free iron levels low and hence restrain the conversion of hydrogen peroxide to the highly reactive hydroxyl radical [ 3 ] that disturbs cellular homeostasis when it is increased at toxic levels.

Iron absorption is the main mechanism through which iron balance is maintained. Nevertheless, iron losses may occur at multiple organs, such as the gastrointestinal tract [ 4 - 6 ], the skin [ 7 , 8 ], the urinary tract [ 4 ], and additionally due to several physiological conditions such as the menstrual cycle in women [ 9 , 10 ].

Thus, from a typical daily diet of kcal that contains adequate quantities of meat, 1. In general, daily iron turnover absorption and excretion is approximately mg per day [ 1 , 2 , 7 ]. There is a strong body of evidence suggesting that exercise affects iron status [ 14 - 17 ], although other studies do not support this association [ 18 - 20 ].

Iron plays a critical role in oxygen transport as it is necessary for the formation of Hb, the oxygen transport protein that is critical for aerobic capacity. Iron is also needed for the optimal function of many oxidative enzymes affecting the intracellular metabolism i.

Not only prolonged aerobic exercise but, to some extent, short duration activities i. sprints , may influence the above mechanisms [ 22 ]. Consequently, a compromised iron status would negatively affect physical performance. On the other hand, iron deficiency is frequently attributed to exercise [ 14 - 16 ].

Therefore, iron supplementation is commonly used to avoid exercise-induced perturbations of iron homeostasis and maintain the required iron stores that are necessary to address exercise needs or enhance physical performance. Numerous studies have attempted to clarify the effectiveness of enhanced iron intake, either through diet or through supplement consumption, to restore iron status or to enhance physical performance.

Yet, no valid conclusions have been drawn. The results of these studies are contradictory as some of them produced positive effects [ 23 , 24 ] whereas others dispute such effects [ 25 ]. An important factor in iron absorption seems to be the previous iron status of the individual. This means that, several iron parameters are seen to be ameliorated following iron supplementation in situations of iron deficiency, whereas this is not always the case for individuals with normal iron status.

In this chapter, an attempt will be made, to clarify the effect of exercise on iron status in athletes. Furthermore, an effort will be made to address the role of dietary or supplemented iron on several indices of physical performance.

Finally, the mechanisms through which exercise may alter iron homeostasis will also be discussed. Iron is an indispensable factor for the formation of Hb, the protein responsible for oxygen transport from the respiratory organs to the peripheral tissues.

Lack of adequate amounts of iron for the formation of Hb due to iron deficiency, can strongly affect physical work capacity, by reducing oxygen conveyance to the exercising muscles [ 21 ]. Iron is also a vital component for the formation of myoglobin, the iron-storage protein within the muscle that regulates the diffusion of oxygen from the erythrocytes to the cytoplasm and on to the mitochondria where it is used as the final acceptor of electrons processed by the respiratory chains producing water and forming energy in the process [ 26 , 27 ].

Apart from oxygen transport and storage, iron is also needed for the optimal function of many oxidative enzymes and proteins regulating the intracellular metabolism [ 21 , 27 , 29 ]. Iron deficiency negatively affects mitochondrial respiration mainly through the decline in heme iron-containing respiratory chain proteins cytochrome c and cytochrome c oxidase, as well as non-heme iron-containing enzymes succinate dehydrogenase and NADH dehydrogenase, but also the non-heme iron-sulfur protein content [ 27 ].

Staying at high altitude causes an increase in erythropoiesis in the bone marrow, stimulated by hypoxia. This increase in erythropoiesis is followed by an elevation in red blood cells volume and Hb concentration [ 30 , 31 ]. Iron deficiency could negatively affect the above mechanism by limiting the rate of erythropoiesis and consequently aerobic performance.

It has been demonstrated that athletes with low ferritin levels do not increase total red blood cell volume after 4 weeks at altitude, despite an acute increase in erythropoietin [ 32 ]. In contrast, a significant increase in erythropoietin but also in reticulocytes occurred in non-iron-deficient athletes during training at moderate altitude [ 30 ].

Such data suggests that iron sufficiency is critical for the favorable response of the athletes training to altitude, in an attempt to enhance their performance.

The need for iron supplementation in cases of iron deficiency anemia in athletes is indisputable. Nevertheless, the need for iron supplementation in situations of iron deficiency without anemia for enhanced performance is still under debate, despite the systematic use of iron supplements.

The majority of studies do not report significant changes in physical capacity following iron supplementation [ 25 , 33 , 34 ]. Nevertheless, there are studies indicating an improvement of physical performance in iron depleted non anemic athletes following iron supplementation [ 23 , 24 ].

Athletes at risk of iron deficiency include female and male middle and long distance runners, as well as all female athletes in other disciplines in which running is an important part of training or competition [ 17 ]. Iron demands during consecutive periods of intense training or competition are high, and may compromise iron status.

In [ 15 ] is reported that a brief recovery following the in-season period may be insufficient to restore the reduced iron stores prior to the start of the subsequent high-intensity pre-season training. Additionally, even when the recommended dietary intake of iron is established through a controlled diet, iron status perturbations may be inevitable.

In reference [ 35 ] the mean dietary intake of These findings point out that non-anemic iron depletion may impair performance. Athletes with the homozygous form of hemochromatosis gene may be at risk of excessive iron storage due to excessive iron absorption [ 17 ].

According to the Department of Health and Human Services, Centers for Disease Control and Prevention CDC [ 37 ], hemochromatosis symptoms are non-specific, but the most commonly associated early hemochromatosis symptoms may include fatigue, weakness, weight loss, abdominal pain, and arthralgia.

The simplest tests that indirectly indicate iron overloading are transferrin saturation TS and serum Ferr [ 37 , 38 ].

Nevertheless, the confirmation of hemochromatosis can be achieved indirectly by quantitative phlebotomy and hereditary hemochromatosis genotyping, or indirectly by liver biopsy [ 37 , 38 ].

Due to the significant role of iron in optimal physical performance and health, the evaluation of iron status in athletes is of great importance in order to prevent iron deficiency. Iron status evaluation is not a single-parameter estimation.

Day-to-day or acute phase response variations occur in several indices of iron status. Therefore, in order to make a valuable and more accurate assessment, the estimation of iron status indices and several hematological parameters is needed.

These will be described in the following sections. Additionally, the reference range for the main indicators of iron status, as well as reported values in elite athletes is presented in Table 1. The most commonly used hematological index is haemoglobin which reflects the effects of mechanisms that control the red cell mass RCM and plasma volume PV.

Normal values lie between Alongside Hb, hematocrit Hct , the mean corpuscular haemoglobin concentration MCHC , as well as the size and volume of red blood cells RBC are also useful markers for anemia [ 16 , 29 ]. The classic Hb and Hct changes as a result of acute or chronic exercise should be kept in mind before a diagnosis is to be made.

Namely, acute strenuous and prolonged exercise typically leads to an increase of Hb and Hematocrit due to hemoconcentration [ 43 ]. On the other hand, a decrease in the concentration of these indices may be seen within the first days of a regular cardiovascular training program due to hemodilution.

This decrease is temporary and most athletes demonstrate normal Hb levels at the completion of training or the end of a competitive phase [ 43 , 44 ]. Serum Ferr concentration is one of the most frequently used indices in iron status examination.

Serum concentration of Ferr and, in conditions of iron overload hemosiderin [ 2 ], serve as an indicator for body iron stores, available for protein and heme synthesis. Such values indicate the onset of a first stage iron deficiency [ 40 ]. Ferritin seems to be age- and sex-dependent, since lower values are reported for children and pre-menopause women as compared to adults and men, respectively.

Nevertheless, the expression and appearance of Ferr in serum are influenced by other factors as well. Ferritin is an acute-phase reactant and its serum concentration may be increased by liver disease, infections and other inflammatory conditions, malignant diseases, renal failure, cardiovascular diseases, high alcohol consumption, and aging [ 44 - 46 ].

Some types of physical activity are accompanied by inflammation-like reactions that can induce an acute phase response and increased Ferr levels for several days. In summary, although serum Ferr concentration is commonly reported to be affected by training [ 4 , 16 , 35 ], there should be some caution before iron adequacy or inadequacy is diagnosed in athletes when ferritin is the only available evaluating index.

Iron concentration, together with Total Iron Binding Capacity TIBC and TS provide information about iron status in plasma or serum. Total Iron Binding Capacity TIBC reflects the total number of binding sites for iron atoms on transferrin per unit volume of plasma or serum [ 48 ].

TIBC does not change before iron stores are depleted [ 48 ]. In depleted iron stores a rise in TIBC levels occurs as more free binding sites on transferrin are available for iron.

Transferrin is the iron binding protein that delivers iron to cells [ 48 ]. Transferrin levels are not affected by inflammatory reactions or other diseases and can therefore be used for diagnosing iron deficiency even under such conditions [ 44 ].

This stage is characterized by iron deficient erythropoiesis, with a restricted iron supply in the absence of anemia [ 40 ]. Since TIBC is rather stable, any alteration in plasma TS will be the result of changes in iron concentration.

Consequently, anything that alters iron concentration will alter TS as well [ 48 ]. Transferrin saturation in conjunction with serum Ferr concentration and Hb are the three critical parameters for the determination of the severity of iron deficiency. Erythrocyte Protoporphyrin EP or Zinc Protoporphyrin ZPP , and the soluble Transferrin Receptor sTfR reflect the adequacy or inadequacy of iron for erythropoiesis into the bone marrow and tissues.

Protoporphyrin is a carrier molecule and together with ferrous iron forms the heme group of Hb, myoglobin and other heme-containing enzymes.

In cases of iron absence, instead of iron, zinc is incorporated to protoporphyrin and ZPP is formed. A rise in ZPP concentration is one of the first indicators of insufficient iron levels in bone marrow [ 50 , 51 ].

Additionally, the ratio of EP to Hb is an excellent indicator of iron failure to meet the normal demands of bone marrow [ 50 ]. Day-to-day variation of EP concentration is reported to fall around 6. The concentration of sTfR has also been used as an indicator of iron deficiency erythropoiesis [ 19 , 41 ].

Plasma sTfR is a truncated form of the cellular receptor TfR , which is responsible for binding and transferring iron into the cell. Transferrin receptor is upregulated when the cell needs more iron, and sTfR is proportional to the cellular TfR content. Normal concentration of sTfR ranges within 1.

When iron stores become depleted and the functional pool of iron diminishes, the levels of sTfR increase [ 41 , 53 ]. In contrast to Ferr, sTfR is not an acute phase protein, and its concentration is not affected by infections or other inflammatory conditions [ 16 , 54 ]. Haptoglobin Hp is used as an index of hemolysis.

The destruction of the red blood cells membrane due to hemolysis allows Hb and its associated iron held within the cell to be released into the surrounding plasma.

Haptoglobin binds free Hb released from erythrocytes, inhibiting its pro-oxidative activity [ 44 ]. The binding of Hb to Hp causes a decline in Hp levels, and the formed haemoglobin-haptoglobin complex is taken up exclusively by hepatocytes, thus preventing the excretion of free Hb in the urine [ 20 ].

As a result, the regular return of catabolized red blood cells to the reticuloendothelial system RES is diminished. Therefore, the observed lower Hb concentration often seen in long distance runners may not always reflect iron deficiency.

The shift of iron turnover from hepatocytes rather than the RES may represent an alternative explanation of the observed compromised iron status [ 20 ]. The estimation of Hp levels could be of great importance in the verification of true iron deficiency even when other parameters such as Hb, serum Ferr, or bone marrow hemosiderin appear to be lower than normal values.

Additionally, day-to-day variations of the estimated indices, as well as exercise-induced changes in blood volume, acute phase reactions, infections, or other inflammatory conditions, should also be considered. The main iron status indicators: reference values for non-athletes and reported values in elite athletes.

Hb: Haemoglobin, Hct: Hematocrit, RBC: Red blood cells, MCV: Mean corpuscular volume, MCH: Mean corpuscular Hemoglobin concentration; RTC: Reticulocytes count, Ferr: Ferritin, TIBC: Total iron binding capacity, TS: Transferrin saturation, sTfR: soluble transferrin receptor, Hp: Haptoglobin, EP: Erythrocyte protoporphyrin.

N: normal iron status, D: iron deficiency, CS: Competitive season, R: Recovery, P: Preparation, EA: Endurance trained athletes, PA: Power trained athletes. There is a great body of evidence indicating that several hematological and iron status parameters often appear altered as a result of chronic exercise Table 2 giving the impression that athletes may be iron-deficient [ 14 - 17 , 22 , 43 ].

Several hematological variables in strength-trained athletes have been reported to be similarly low or even lower than that of endurance athletes [ 14 , 56 ]. Nevertheless, it is mostly the endurance type of training that has been linked to lower values of several hematological indices [ 35 , 43 ].

These lower levels in endurance athletes have been attributed to reticulocytosis and expansion of plasma volume associated with chronic aerobic training [ 35 , 43 , 56 ]. Although within normal range, athletes demonstrated lower values of serum Ferr but similar transferrin and Hp values compared with sedentary controls [ 43 ].

In some cases, the allowed recovery period before the next training phase may not be sufficient for the replenishment of the depleted iron stores [ 15 ], and this point definitely needs closer attention.

Based on data of several investigations, iron status disturbances are more frequent in female than in male athletes. In reference [ 14 ], female athletes were about twice as likely to exhibit reduced Ferr levels.

In that study, Similarly, the prevalence of iron deficiency was greater in female athletes of several events, as compared to male athletes. The cause of reduced levels in Ferr or serum iron in athletes is not fully understood.

Exercise-induced hemolysis, as documented by the reduced Hp values, may offer a plausible explanation. In reference [ 20 ], although no differences were observed in Hb concentration, the levels of iron concentration, Hct, Ferr, TS, and bone marrow hemosiderin were lower in athletes compared to controls.

However, no true iron deficiency was established based on the normal mean cell volume MCV and EP values, as well as on the normal sideroblast count in bone marrow smears of all athletes, confirming an adequate supply of iron to normoblasts.

The lower Hct and Ferr values in athletes could be explained by the simultaneous marked decline of Hp levels, indicating a shift of iron to the hepatocytes as a result of increased intravascular hemolysis. Not only chronic exercise, but also acute strenuous physical activity may alter several indices of iron status.

A significant reduction in serum iron levels of The authors proposed that heavy sweating or a prelatent iron deficiency may explain the observed severe reduction of serum iron. However, sweat iron concentration does not correlate with the increased whole body sweat rates [ 8 ].

A slight increase in sTfr, although within the normal range, has also been recorded after incremental running to exhaustion, but not after 45 min of submaximal exercise or after 3 consecutive days of aerobic training in highly trained endurance cyclists [ 55 ].

After the incremental running, an increase in Ferr, as well as in Hb and Packed Cell Volume PCV was also observed. This increase was mainly attributed to the concurrent hemoconcentration, as evidenced by the pronounced fall in plasma volume. Regardless the acute or chronic character of exercise where most studies report variable responses in iron status, there are also studies that do not support significant differences in iron status between trained and untrained individuals.

Indeed, similar incidence of iron deficiency between male endurance young athletes and non-athletes involved in several sport disciplines has been reported [ 18 ].

High physical activity of athletes did not affect iron stores, as it was found to be higher than in control subjects. In a more recent study of the same institute [ 19 ] that involved female endurance athletes, lower incidence of iron deficiency was reported in athletes as compared to controls. These studies may lead to the assumption that the increased iron dietary intake and dietary factors involved in iron metabolism compensated for the augmented, exercise-induced losses of iron in young athletes.

Regarding iron deficiency in athletes whose iron intake was sufficient, the authors attributed its prevalence in its diminished absorption for the male, and its leak to the blood due to menstrual cycle for the female athletes.

Taken together, these studies that attempted to evaluate the effects of exercise on iron status of athletes suggest that high volume training during a competitive season may compromise iron homeostasis.

One determining factor that could help explain the reported discrepancies in iron status due to acute or chronic exercise is diet.

VO 2max : Maximum Oxygen Consumption, TT: Time Trial, CK: Creatine Kinase, Ferr: Ferritin, Fe: Iron, Tf: Transferrin, TS: Transferrin Saturation, sTfR: Soluble Transferrin Receptor, TIBC: Total Iron Binding Capacity, Hb: Haemoglobin, Hct: Hematocrit, PCV: Packed Cell Volume, Ret: Reticulocytes, WCC: White Cells Count, RBC: Red Blood Cells, RCV: Red Cells Volume, WBC: White Blood Cells, MCH: Mean corpuscular Haemoglobin, MCHC: Mean Corpuscular Haemoglobin Concentration, MCV: Mean Corpuscular Volume, BMHem: Bone Marrow Hemosiderin, EP: Erythrocyte Protoporphyrin, Hp: Haptoglobin, PV: Plasma Volume, BV: Blood Volume, GOT: Glutamic Oxaloacetic Transaminase, CRP: C Reactive Protein.

Iron absorption mainly, and to a lesser extent iron nutrition, are the two critical mechanisms by which iron balance is maintained since there is no other physiological process for iron excretion. Consequently, a low dietary iron intake, could lead to compromised iron status [ 9 ].

Usually, male, but not female athletes achieve the RDI for iron [ 14 , 17 , 63 ]. Iron bioavailability has been found to be affected by the type of the diet and by the type of dietary iron [ 11 ].

Hence, mixed diet and heme iron provide greater bioavailability and absorption as compared to a vegetarian diet and nonheme iron, [ 11 - 13 ]. Furthermore, iron deficiency augments iron absorption. Besides iron absorption and intake, several other mechanisms have been proposed to account for iron loss and iron balance disturbances, and ultimately the prevalence of iron deficiency in athletes.

These mechanisms include increased gastrointestinal blood loss, hematuria, hemolysis [ 5 , 6 , 17 , 64 - 67 ], increased iron loss in sweat [ 7 , 8 ], as well as menstruation in women [ 9 , 10 , 68 ]. In athletes, gastrointestinal bleeding usually accompanied by occult blood, is a well-established phenomenon, mostly seen in distance runners [ 6 , 60 ].

Running a marathon was associated with a gastrointestinal blood loss [ 67 ], and positive occult heme stools were found in runners after intensive training or competitive running [ 4 , 5 , 60 , 67 ].

The origin of running-related intestinal bleeding has still to be clarified, but endoscopic examination has revealed bleeding lesions in the stomach and colon [ 65 , 66 ]. Exercise intensity, seems to play a significant role in the development of gastric ischemia [ 70 ], which increases mucosa permeability and enhances occult blood loss [ 6 ].

Increased iron loss through sweat has also been proposed as a mechanism related to the compromise of iron status as a result of increased sweat rates during exercise in athletes, or increased temperature in individuals living and exercising in hot climates.

The daily loss of iron from the skin has been reported to be 0. The reported 0. It has to be mentioned that although the sweat rate increases during the 1 st hour of exercise and remains constant thereafter, and males have higher sweat rates than females, the iron loss in males and females remains comparable.

Additionally, the sweat iron loss declines in both genders during the 2 nd hour of exercise [ 8 ], or after the first 30 min in a hot environment [ 7 ]. This reduction could be attributed to the initial sweat containing iron present in cellular debris [ 7 ], to the increased sweat rates while the total iron loss remains constant, or to a conservation mechanism that may prevent excessive iron loss during exercise [ 8 ].

Still, iron loss in sweat remains insignificant compared to that of the gastrointestinal tract. Another explanation for compromised iron status in athletes is the shift of iron return to hepatocytes, rather than the RES, as a consequence of the increased intravascular hemolysis occurring mostly in weight-bearing activities, such as running.

In these activities, hemolysis is due to the impact forces generated by the foot strike [ 73 , 74 ]. Increased intravascular hemolysis has been reported in runners [ 20 ] and female artistic gymnasts [ 73 ]. However, foot strike cannot totally explain the exercise-induced hemolysis since hypohaptoglobinemia, a situation that reveals the presence of hemolysis, has also been observed in swimmers [ 75 ].

In non-weight-bearing activities hemolysis may result from the compression of the blood vessels caused by the vigorous contraction of the involved muscles [ 75 ].

Female athletes seem to be more prone to the development of iron deficiency [ 14 , 16 ] and blood loss during menstruation may further explain this greater prevalence. Although menstrual blood loss in a single woman is very constant during menarche and throughout the fertile life, there is a large variation in blood loss among women [ 68 ].

Thus, in a mean cycle length of 28 days, menstrual blood loss may vary by as much as 26 - 44 ml, with a corresponding daily iron loss of about 0. This great variation in blood and iron loss reported by these two studies could be associated with an extensive use of oral contraceptives which are known to reduce the amount of blood loss during menstruation [ 77 ].

Finally, menstrual iron loss in women has been shown to negatively correlate with serum Ferr, and iron status to significantly correlate with the duration and intensity of the menses in endurance athletes [ 19 ]. Taking into consideration the iron loss during menstruation along with the relative failure to achieve the daily RDI for iron the greater frequency of iron deficiency in female athletes can be justified.

Whether the increased uptake of iron through diet or supplements improves iron status in athletes is still under debate. This is mainly due to the great divergence of iron doses, intervention period, population, and exercise regimens used between studies.

Table 3 summarizes the effects of iron supplementation on several indices of iron status. These eight athletes showed up-regulated 59 Fe absorption and a decreased liver iron concentration as compared to a control group.

The results of the eight athletes confirm that in cases of true iron deficiency, iron absorption is greater. Absence of iron supplementation resulted in decreased Hb levels despite mean dietary iron intakes of Taken together the aforementioned results suggest that the initial stage of either iron sufficiency or iron deficiency, combined with the amount of iron ingested, plays a critical role in the absorption of iron from diet or supplementation.

Supplementation of iron is commonly used, not only in iron-deficient athletes, but also in athletes with normal iron status. The rationale behind this practice dictates that supplementation will preserve or enhance their performance.

This concept is probably based on the catalytic role of iron on the oxygen transport and optimal function of oxidative enzymes and proteins during exercise. The hypothesis could be that with increased consumption of iron, the above mechanisms would be reinforced and exercise performance would be improved.

Nevertheless, unlike the numerous studies addressing iron-deficient individuals, only few [ 25 , 57 , 63 ] have focused in iron-sufficient athletes. The response of iron stores during a sports season was assessed in professional football players with normal iron stores at the beginning of the season [ 57 ].

Supplementation took part for 15 days prior to the beginning of the season and 15 days during the middle season. Blood was collected three times during the season, one following the first supplementation period, another following the second supplementation period and a third time at the end of the season, where no iron supplementation had occurred.

Ferritin, as well as calculated iron stores, showed a significant reduction at the end of the season which coincided with the absence of iron supplementation. In contrast, Ferr and iron store levels remained stable following supplementation regardless of the intensive training.

In another study, non-anemic, non-iron-deficient adolescent male and female swimmers aged years old were either supplemented with 47 mg of elemental iron daily or consumed a diet rich in iron [ 25 ].

In that study, despite the significant fluctuations during the six months of training, iron levels, TS and Ferr levels were similar at the end of the study as compared to baseline values. The authors attributed the failure of high iron intake to affect iron status to homeostatic mechanisms such as iron absorption.

It could also be suggested that the quantity of elemental iron was not enough to improve iron status and that higher doses of iron are needed to achieve a favorable change in iron status.

The younger age and the possible higher demands in reference [ 25 ] compared with that of reference [ 57 ], may have influenced the absorption of iron that resulted in different responses in these two studies. The effect of dietary or supplemented iron on exercise-induced changes of iron status and physical performance.

VO 2max : Maximal Oxygen Consumption, VCO 2 : Exhaled Carbon Dioxide, VE: Ventilation, MAOD: Maximal Accumulated Oxygen Deficit, TTE: Time to Exhaustion, HR: Heart Rate, CK: Creatine Kinase, LA: Lactate, Ferr: Ferritin, Fe: Iron, Tf: Transferrin, TS: Transferrin Saturation, sTfR: Soluble Transferrin Receptor, TIBC: Total Iron Binding Capacity, Hb: Haemoglobin, Hct: Hematocrit, PCV: Packed Cell Volume, MCHC: Mean Corpuscular Haemoglobin Concentration, BV: Blood volume, PV: Plasma Volume, MCV: Mean Corpuscular Volumes, RBC: Red Blood Cells Count, RBCDW: Red Blood Cell Distribution Width, WCC: White Cells Count, MAOD: Maximal Accumulated Oxygen Deficit.

There is no doubt that iron-deficiency anemia, which amongst other indicators e. However, the need for iron supplementation in cases of depleted iron stores without observed anemia for optimal physical performance is still under debate Table 3. Some studies have shown that iron supplementation improved physical performance [ 23 , 24 ], whereas others report no alterations following iron supplementation [ 25 , 34 , 63 ].

The improvement of iron status due to iron supplementation has been accompanied by an improvement in endurance capacity [ 23 , 24 ]. Iron supplementation also prevented the decline in performance that was associated with the progressive reduction of serum Ferr levels [ 24 ]. Iron supplementation resulted in an increase in ferritin levels which was accompanied by an improvement of physical performance.

Subjects not receiving iron therapy exhibited a decline in their performance [ 24 ]. Besides the aforementioned positive results in exercise performance there are studies reporting no beneficial effects due to iron supplementation [ 25 , 34 , 63 ].

In reference [ 63 ], no significant improvement of iron status or metabolic parameters related to running performance was found after 2 weeks of mg elemental iron supplementation in non-anemic, iron-deficient female cross-country runners. Likewise, in [ 34 ], 8 weeks of iron supplementation in iron-depleted, non-anemic female distance runners, resulted in similar improvement of the endurance capacity in the supplemented and the placebo group, despite the improved iron status in the iron-supplemented group.

In another study, the injection of 2 mL of Ferrum H mg of elemental iron five times daily for 10 days did not result in any beneficial outcomes on submaximal economy, VO 2max and time to fatigue in non-anemic, iron-deficient female runners [ 33 ].

In one of the very few studies that used healthy, non-iron-depleted and non-anemic adolescent swimmers, the enhanced iron intake either through supplement or diet ranging from one to five times the RDA, did not change iron status or result in favorable changes of physical performance [ 25 ].

The authors attributed the observed fluctuations over the training period of six months to the different demands of each training phase irrespective of iron treatment. These observations strengthen the notion that the initial levels of iron status are of critical importance in the improvement of physical performance as a result of iron supplementation.

In [ 35 ], the mean dietary intake of Consequently, the reductions in Hb and Ferr levels were lower in the athletes that were under iron supplementation. Although the favorable effects of iron supplementation on physical capacity in iron-deficient anemic athletes has been well established, relatively little research has been conducted addressing iron-deficient non-anemic athletes.

Therefore, further research is needed to clarify the necessity of iron supplementation in athletes with depleted iron stores, yet, normal Hb concentrations for improvement of their performance. Despite the great importance of iron balance in athletes, no normative data for athletes exist and hence it is essential such norms are established.

Such data would be more critical if appropriate discriminations were made, e. regarding the type of training endurance or power-training athletes , sex, age, or seasonal demands and so on.

The commonly used parameters for the estimation of iron status in the general population Hb, Hct, Ferr, iron concentration, TIBC, TS , may not always be adequately representative for athletes. Therefore, it would be useful if future studies incorporated additional parameters such as erythrocyte protoporphyrin, soluble transferrin receptor or haptoglobin, in order to get more accurate and complete estimation of iron status.

Iron is one of the most important elements for health and exercise performance. It is unclear whether iron intake by an athlete through diet is adequate in order to prevent iron balance disturbances and further research is needed to clarify dietary methods to prevent iron deficiency.

It seems that exercise, acute or chronic, results in significant disturbances in iron balance due to different reasons. Changes in iron absorption and iron intake due to exercise, iron losses through the gastrointestinal tract, intravascular hemolysis, and to a lesser extent iron losses through sweat, are probable mechanisms for iron balance disturbances during exercise.

Alterations in iron status balance are reported as a result of exercise, especially in endurance trained, and women athletes. Iron-deficiency without anemia is a very commonly reported phenomenon among athletes, and occasionally iron deficiency anemia is also reported.

Iron balance is of great importance for optimal work capacity, and a compromise of iron status would have detrimental effects on physical performance in iron-depleted anemic athletes. However, similar effects have not been well documented for athletes that are iron-deficient without the presence of anemia.

Nevertheless, iron supplementation among athletes is a very common practice, despite the discrepancy regarding its beneficial effects in non-anemic, iron-depleted, or even normal iron status athletes. This discrepancy is attributed to the divergence in iron doses, athletic population, and the great variance in the intervention period, and exercise regimens that are used between studies.

Because of the different demands in iron through the several phases of training or competitive periods, evaluation of iron status of the athletes should be performed at the beginning, at the midpoint, and finally at the end of the season.

Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Edited by Michael Hamlin. Open access Iron Supplementation and Physical Performance Written By Chariklia K. Deli, Ioannis G. Fatouros, Yiannis Koutedakis and Athanasios Z.

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Chapter metrics overview 3, Chapter Downloads View Full Metrics. Impact of this chapter. Chariklia K. Deli Department of Physical Education and Sport Science, University of Thessaly, Trikala, Greece Institute of Human Performance and Rehabilitation, Center for Research and Technology - Thessaly, Trikala, Greece Ioannis G.

Fatouros Institute of Human Performance and Rehabilitation, Center for Research and Technology - Thessaly, Trikala, Greece Department of Physical Education and Sport Science, University of Thrace, Komotini, Greece Yiannis Koutedakis Department of Physical Education and Sport Science, University of Thessaly, Trikala, Greece Institute of Human Performance and Rehabilitation, Center for Research and Technology - Thessaly, Trikala, Greece School of Sports, Performing Arts and Leisure, University of Wolverhampton, United Kingdom Athanasios Z.

Introduction Iron is one of the most abundant elements, essential for the completion of numerous important biological functions, including electron transfer reactions, gene regulation, binding and transport of oxygen, regulation of cell growth and differentiation. Estimation of red blood cell parameters The most commonly used hematological index is haemoglobin which reflects the effects of mechanisms that control the red cell mass RCM and plasma volume PV.

Estimation of body iron stores Serum Ferr concentration is one of the most frequently used indices in iron status examination. Estimation of plasma or serum iron status Iron concentration, together with Total Iron Binding Capacity TIBC and TS provide information about iron status in plasma or serum.

Estimation of erythropoiesis into the bone marrow Erythrocyte Protoporphyrin EP or Zinc Protoporphyrin ZPP , and the soluble Transferrin Receptor sTfR reflect the adequacy or inadequacy of iron for erythropoiesis into the bone marrow and tissues. Estimation of hemolysis Haptoglobin Hp is used as an index of hemolysis.

Table 1. Chronic exercise There is a great body of evidence indicating that several hematological and iron status parameters often appear altered as a result of chronic exercise Table 2 giving the impression that athletes may be iron-deficient [ 14 - 17 , 22 , 43 ].

Acute exercise Not only chronic exercise, but also acute strenuous physical activity may alter several indices of iron status. Study Study protocol Subjects Estimated indices Results Compromised iron status Chronic exercise Kohler et al Retrospective estimation of iron status in athletes from 25 different events 96 males Table 2.

Iron status in competitive athletes. Iron supplementation in iron-deficient individuals Whether the increased uptake of iron through diet or supplements improves iron status in athletes is still under debate. Iron supplementation in individuals with normal iron status Supplementation of iron is commonly used, not only in iron-deficient athletes, but also in athletes with normal iron status.

Studies Study protocol Subjects Estimated Indices Results Improvement in iron status Nachtigal et al. Table 3. Iron supplementation in iron-deficient individuals There is no doubt that iron-deficiency anemia, which amongst other indicators e.

Iron supplementation in individuals with normal iron status In one of the very few studies that used healthy, non-iron-depleted and non-anemic adolescent swimmers, the enhanced iron intake either through supplement or diet ranging from one to five times the RDA, did not change iron status or result in favorable changes of physical performance [ 25 ].

References 1. Fontecave M, Pierre JL. Iron - Metabolism, Toxicity and Therapy. Biochimie ;75 9 : Crichton RR, Ward RJ. An overview of iron metabolism: molecular and cellular criteria for the selection of iron chelators. Curr Med Chem ; 10 12 : Bacic G, Spasojevic I, Secerov B, Mojovic M.

Spin-trapping of oxygen free radicals in chemical and biological systems: new traps, radicals and possibilities. Spectrochim Acta A Mol Biomol Spectrosc ; 69 5 : Nachtigall D, Nielsen P, Fischer R, Engelhardt R, Gabbe EE.

Iron deficiency in distance runners. A reinvestigation using Fe-labelling and non-invasive liver iron quantification. Int J Sports Med ; 17 7 : Stewart JG, Ahlquist DA, Mcgill DB, Ilstrup DM, Schwartz S, Owen, RA. Gastrointestinal Blood-Loss and Anemia in Runners.

Annals of Internal Medicine ; 6 : de Oliveira EP, Burini RC. The impact of physical exercise on the gastrointestinal tract. Current Opinion in Clinical Nutrition and Metabolic Care ; Brune M, Magnusson B, Persson H, Hallberg L. Iron losses in sweat. Am J Clin Nutr ; DeRuisseau KC, Cheuvront SN, Haymes EM, Sharp RG.

Sweat Iron and Zinc Losses During Prolonged Exercise. International Journal of Sport Nutrition and Exercise Metabolism ; Harvey LJ, Armah CN, Dainty JR, Foxall RJ, Lewis DJ, Langford NJ, Fairweather-Tait SJ.

Impact of menstrual blood loss and diet on iron deficiency among women in the UK. British Journal of Nutrition ; 94 4 : doi: Doi Lyle RM, Weaver CM, Sedlock DA, Rajaram S, Martin B, Melby CL. Iron status in exercising women: the effect of oral iron therapy vs increased consumption of muscle foods.

Am J Clin Nutr ; 56 6 : Hurrell R, Egli I. Iron bioavailability and dietary reference values.

In severe cases and in cases where the nutrition approach is ineffective the use of parenteral iron therapy iron infusions or injections may be considered and this is what we will explore in this blog. Multiple mechanisms are related to iron loss during exercise, including sweating, gastrointestinal blood loss, haemolysis, and changes in iron regulatory hormone hepcidin that controls iron absorption from post-exercise feeding 1.

As a result, there are numerous approaches to addressing an iron deficiency, ranging from dietary adjustments to oral or parenteral iron supplementation 2. However, the appropriate approach to addressing an iron deficiency is generally dictated by the severity of the issue. Consumption of iron in food or via oral iron supplements can be used to address low iron stores, although the propensity of the gut to absorb iron via these approaches can be influenced by numerous factors, including exercise itself 3.

Accordingly, studies emphasise the importance of timing iron consumption within 30 minutes of exercise before or after for optimal absorption 4, 5. Furthermore, morning intake seems more effective than afternoon, likely due to diurnal variations in hepcidin activity that impact iron absorption 4.

In addition to issues with absorption at the gut, it might also be noted that it takes ~ weeks of consistent oral supplementation to achieve significant improvements in iron status, and even then, the improvement may be small i. Accordingly, for athletes with severe iron deficiency anaemia , parenteral iron provision i.

Parenteral iron administration through intravenous IV delivery has become an increasingly used approach to address an iron deficiency in athletes, with formulations having evolved over the last decade to offer safe doses into circulation in a single infusion.

Formulations such as ferric carboxymaltose and ferumoxytol, have a favourable safety profile with limited serious adverse effects; however, intramuscular iron treatment, while effective, is a less favoured approach to IV iron administration, a result of negative indications such as pain, skin staining, and the potential for adverse impact on immediate post-treatment training or competition.

The efficacy of IV formulations in rapidly normalizing haematological parameters is a significant advantage, especially in severe cases of iron deficiency. The impact of parenteral iron approaches on performance outcomes in athletes varies based on iron deficiency severity.

In non-anaemic athletes, studies demonstrate that IV iron supplementation does not significantly enhance performance 8. Accordingly, efficacy on performance is notably greater in anaemic athletes with low pre-infusion serum ferritin concentrations i. Long-term impacts and decay rates of serum ferritin following IV iron infusion vary among athletes, necessitating individualized follow-up and potential subsequent treatments Research exploring the decay rates of serum ferritin subsequent to parenteral iron administration recommends blood screening at 4 weeks and 6 months post-infusion to assess the efficacy of approach on an individual basis In summary, parenteral iron therapy is valuable for athletes, particularly in severe cases or when rapid repletion is required.

However, indiscriminate use of IV iron is unwarranted, and therefore, this treatment approach should only be recommended and overseen by a trained medical physician ensuring compliance with any anti-doping regulations. Webinar recording of Managing iron in athletes available on mysportscience academy.

Peeling, P. Athletic induced iron deficiency: new insights into the role of inflammation, cytokines and hormones. Eur J Appl Physiol, 4 , McCormick, R.

Refining treatment strategies for iron deficient athletes. Sports Medicine, 50 12 , Barney, D. A Prolonged Bout of Running Increases Hepcidin and Decreases Dietary Iron Absorption in Trained Female and Male Runners.

J Nutr, 9 , The Impact of Morning versus Afternoon Exercise on Iron Absorption in Athletes. Med Sci Sports Exerc, 51 10 , McKay, A. Iron absorption in highly-trained runners: Does it matter when and where you eat your iron? Under Review.

Garvican, L. Intravenous iron supplementation in distance runners with low or suboptimal ferritin. Med Sci Sports Exerc, 46 2 , Baird-Gunning, J. Correcting iron deficiency. IL-6 is a key regulator of not only the inflammatory response but also the activity of the iron-regulating hormone hepcidin [ 23 ].

This hormone adversely affects the activity of the main iron export protein, ferroportin, which leads to a decrease of iron absorption in the intestine, and inhibition of iron release from hemolyzed red blood cells and internal organs that store iron [ 24 ]. Also, hemopexin and lactoferrin are involved in the regulation of iron levels.

They capture free heme or iron ions, and thus contribute to the regulation of inflammation [ 25 , 26 ]. Both proteins reduce macrophage production of pro-inflammatory cytokines, including IL They thus affect the activity of ferroportin — positively; and ferritin — negatively, preventing intracellular iron overload and inhibiting the development of inflammation [ 26 ].

To date, studies into the changes in iron levels or the levels of proteins responsible for the regulation of iron homeostasis have primarily focused on pre- and post-exercise values and, predominantly, on the restitution period 24 h post-exercise [ 4 , 15 , 16 ].

Only few studies have focused on the early restitution period. Such studies mainly consider the relationship between iron status and the levels of hepcidin [ 9 , 39 ]. However, as a caveat to interpreting the results of such studies, the reported data hold for athletes during periods of high-stress training, and the observed levels of iron metabolism markers were not compared with those in completely rested athletes.

Little is known about whether these changes are also sustained at the end of the competition period, when the training loads are greatly reduced, and rest and recovery are emphasized. We hypothesized that the changes in the level of iron and its regulatory proteins may depend not only on the acuity of exercise but also on the training load.

Accordingly, the current study aimed to assess the impact of acute exercise performed at the end of the competition period on iron levels and selected parameters related to the regulation of serum iron homeostasis in trained basketball players.

Twenty-seven female trained basketball players participated in the study. Inclusion criteria consisted of female athletes participant minimum of 6 years of training experience , free from iron homeostasis disturbances e. Exclusion criteria consisted of: the presence of acute or chronic inflammation of pain disability, fever, infections, iron supplementation, use of any anti-inflammatory drugs.

All participants belong to the youth groups of ENEA AZS AJP Gorzów Wielkopolski 1st League and Premier League. Table 1 shows the anthropometric characteristics of the study participants.

The research was conducted at the end of the competition period, two weeks after the last competition games. All players were on the same team and were subjected to the same training regime. In this study, the participants performed acute exercise until exhaustion. The experiment was designed for assessing the disturbances in iron homeostasis caused by an acute exercise thus biochemical assays were performed using blood collected at three time-points: at rest Pre-exercise , immediately after the exercise post-exercise and after 3 h of rest 3 h Recovery Fig.

All participants performed an incremental exercise test on HP Cosmos Treadmill serial no. cosva04; Nussdorf—Traunstein Germany. The test protocol was as follows: the starting speed of the treadmill for the participants was 8. The test ended with voluntary exhaustion of the subjects.

During the test, minute ventilation VE , oxygen uptake VO 2 , and carbon dioxide production VCO 2 were determined continuously using the exhaled air analyzer MES measurement system contains of a pneumotach headpiece patented by MES and fast analyzers of carbon dioxide and oxygen fit for applying "breath-by-breath" method to each exhalatory phase.

Table 2 shows the basic characteristics of the exercise. The participants were verbally encouraged to continue for as long as possible. Heart rate bpm was recorded using a sport tester Polar PE This model of acute exercise until exhaustion is often used in research focused on the observation of changes in biochemical parameters in response to the short-term but very intense effort [ 16 ].

Hematological variables, such as red blood cell count RBC , hemoglobin Hb , hematocrit HCT , mean corpuscular hemoglobin MCH , mean corpuscular hemoglobin concentration MCHC , mean corpuscular volume MCV , red cell distribution width RDW , mean platelet volume MPV , and platelet count PLT , were analyzed using the MYTHIC 18 Haematology Analyser Orphee Medical, Geneva, Switzerland.

Iron concentration and TIBC Total Iron-Binding Capacity were determined using colorimetric method with chromogens cat. Enzyme-linked immunosorbent assay kits and Thermo Scientific Multiscan GO microplate spectrophotometer Fisher Scientific, Vantaa, Finland were used to determine serum levels of the following molecules: IL-6, transferrin, hemopexin, and lactate dehydrogenase LDH SunRed Biotechnology Co.

Descriptive statistics, including mean and SD, were used to visualize immediate trends and patterns. Shapiro—Wilk test was used to examine the normal distribution of variables. Lactoferrin level was not normally distributed, and was log transformed for further analysis.

One-way analysis of variance with repeated measures ANOVA , with Tukey's post-hoc analysis was used to asses differences in measured variables of the three assessments points pre-exercise, post-exercise and 3 h recovery respectively.

Post-exercise ; in the following 3 h of restitution, the iron level decreased and reached values close to the baseline. No significant changes in the serum concentration of hepcidin and IL-6 were observed during the study Fig. The effect of intense exercise on iron, hepcidin and IL-6 plasma concentration.

Post-exercise Fig. The effect of intense exercise on transferrin, TIBC and transferrin saturation. The effect of intense exercise on myoglobin and haemoglobin. No significant changes in ferritin concentration, transferrin, and UIBC saturation values were observed Table 3.

We here aimed to assess the impact of intense exercise performed at the end of the competition period when the low-load exercises are applied, and athletes have had the time to rest and recover after a heavy starting period on iron and iron regulatory proteins level.

We found that intense exercise performed by rested athletes caused a short-term increase in iron ion levels, with a simultaneous increase in transferrin saturation and a slight increase in TIBC without a significant response from IL-6 or hepcidin.

The increased iron level after the exercise observed in this study indicates that the test used was a stimulus strong enough to elicit a hemolytic or non-hemolytic response.

The increase of iron level after a bout of acute exercise was observed in a few studies, i. Moreover, the authors suggested that an increased iron levels as a result of vigorous exercise is one of the important factors responsible for triggering a sequence of reactions to regulate iron levels involving IL-6 and hepcidin.

In recent years, many studies have been conducted to determine the potential impact of intense exercise on hepcidin levels [ 4 , 28 ]. The obtained data indicate that hepcidin levels are associated with an observable increase in iron levels and reach a maximum value 3—6 h after exercise.

Hepcidin levels are also associated with a post-exercise increase in IL-6 levels [ 28 ]. According to Newlin et al. However, this phenomenon was not confirmed in the current study, as we observed a significant post-exercise increase in iron levels, with a simultaneous small, non-significant increase in IL-6 and lack of hepcidin responses.

The lack of a significant increase in IL-6 levels after the exercise test was surprising but not implausible. Literature data suggested that plasma Il-6 concentration may increase up to fold after exercise.

Moreover, the concentration of pro-inflammatory cytokines, including IL-6, in the serum significantly increased after a long-term endurance effort, e. This response may be significantly less pronounced after a short vigorous exercise [ 32 ]. Cullen et al. Additionally, exercise training may reduce basal IL-6 production as well as the magnitude of the acute exercise IL-6 response.

A decreased plasma IL-6 concentration at rest as well as in response to exercise appears to characterize normal training adaptation [ 34 ]. In addition, the training frequency of elite athletes is often so high that the short time between consecutive sessions may not be sufficient to achieve full recovery; this, in turn, may lead to the accumulation of harmful metabolites and an increase in the inflammatory response [ 35 ].

It is worth emphasizing that the current study involved young, but highly trained athletes. It has been proved that trained individuals have a lower level of IL-6 in serum [ 34 ].

Furthermore, our study was conducted at the final stage of the starting period, when the exercise load was reduced. Athletes who participated in the study had time to rest and recover after basketball gaming season.

The lack of significant changes in IL-6 levels may be responsible for the lack of hepcidin level increase observed in other studies.

It is also important to note that trained athletes show a specific adaptation to exercise, i. Sandström et al. Similar to our findings, no significant changes in IL-6 and hepcidin levels were observed by Troadec et al. In turn, Kasprowicz et al. A major involvement of hepcidin in the regulation of iron homeostasis was also demonstrated by Peeling et al.

In athletes with lower baseline iron and ferritin levels, the increase in hepcidin was significantly lower than that in athletes with higher baseline iron and ferritin levels.

Whereas the results of the current study suggest that the observed significant increase in post-exercise iron levels is not a strong enough stimulus to activate hepcidin dependent mechanism of iron regulation in well-rested athletes. The disturbance of iron metabolism, resulting from the presence of inflammation manifested by increased IL-6 levels, is, as mentioned above, associated with training periods characterized by high loads preparation and competition period.

In the current study, all measurements were conducted at the final stage of the starting period. This stage of training is characterized, as already mentioned, by a reduced training load and, therefore, may impact the biochemical and morphological parameters of the subjects.

Ostojic and Ahmetovic [ 39 ] showed that in highly trained athletes footballers during the preconditioning period, most of the parameters related to iron management are higher than those in the playing season associated with higher loads and, thus, fatigue. Importantly, Banfi et al.

It can be assumed that the management of iron ions during the restitution period may be regulated by different mechanisms than those operational during intense training or competition period. We did not note any changes in ferritin levels in the current study.

Changes in ferritin levels, especially their reduction, are frequently observed among athletes and indicate iron store depletion [ 40 ]. Ferritin levels positively correlate with tissue iron stores, including the bone marrow, and hence, they are a good indicator of iron reserves in the body [ 41 ].

Since muscle oxygen consumption increases during intense exercise, which increases ROS levels, it is likely that ROS may contribute to the release of some of the iron stored in ferritin [ 42 ].

An interesting observation of the current study was the lack of changes in transferrin levels during the analyzed period, with a simultaneous change in the parameters directly related to its activity, i.

Transferrin saturation significantly increased immediately after exercise, while changes in TIBC reflecting changes in iron levels increased immediately after exercise and then significantly decreased after a 3 h rest period. In addition, we observed a significant positive correlation between TIBC and iron levels, and a negative correlation between TIBC and hepcidin.

Apotransferrin is responsible for capturing free iron ions, including those from damaged hemoglobin [ 43 ]. The increase in transferrin saturation and changes in TIBC levels observed in the current study in parallel with the increased iron levels may indicate that iron capture by apotransferrin is the main mechanism responsible for the reduction of serum iron levels to the baseline values during the restitution period.

The decrease in TIBC observed after a 3 h rest suggests that the iron levels have returned to the baseline values. According to Hymes et al. The TIBC values increase with decreasing iron stores indicating that the iron is being moved to the stored iron pool.

Considering that the observed changes in iron ion level occurred within 3 h of exercise, it can be concluded that capturing iron by apotransferrin is a relatively rapid mechanism of iron level regulation and may be related to the high training level of the participants. The iron released during exercise was entirely captured by the circulating transferrin in the serum, without the need to activate additional regulatory mechanisms, e.

Changes in transferrin saturation or TIBC are often used to characterize the dynamic changes in iron levels during training, or to observe the effects of a single, intense exercise [ 44 , 45 ].

However, the reports on TIBC and transferrin saturation in athletes are inconsistent. Whereas we have observed changes in TIBC similar to those reported here in a previous study involving a group of rowers [ 16 ], others have observed the involvement of the IL-6—hepcidin axis.

Deruisseu et al. On the other hand, Podgórski et al. Lactoferrin is another protein that regulates the concentration of iron ions in the body. Its levels rapidly increase in response to inflammation [ 47 ]. The data presented herein indicated lack of inflammation in the study participants in the first few hours after exercise, which would explain the lack of the expected increase in lactoferrin levels after exercise.

The iron balance is also characterized by red cell parameters, such as RBC, HTC, Hb, and myoglobin. The intense physical effort that the basketball players were subjected to in the current study resulted in a significant but short-term increase in RBC, Hb, and HTC, and their levels were comparable with the baseline values during the 3 h rest period.

The hemolysis that occurs during intense exercise may lead to disturbances in both, hematological parameters, and iron metabolism, leading to iron deficiency. Hence, iron supplementation is often recommended for athletes, especially for women, even in the absence of anemia symptoms [ 49 , 50 ].

The observed increase in RBC and Hb values after physical exertion, along with simultaneously increased iron levels, may indicate a response that is not disturbed by inflammation.

They may also suggest that the initial iron levels in the group of female players selected for the current study were sufficient and stable. Intense exercise performed by highly qualified athletes during the training period focused on regeneration caused a short-term increase in iron ion levels, with a simultaneous increase in transferrin saturation and a slight increase in TIBC.

Both parameters returned to baseline values during the 3 h recovery period. However, no changes in the levels of IL-6 and hepcidin, and transferrin and ferritin, were observed. Post-exercise increase in hematological parameters suggests that ferritin, and not post-exercise hemolysis, may be the source of iron ions.

This could indicate that the study participants were not iron-deficient. Considering the study results within the context of existing literature it seems that the threshold level required for the induction of Il-6 and hepcidin response in highly trained, but rested athletes is higher than in athletes during their routine training program.

Latunde-Dada GO. Iron metabolism in athletes—achieving a gold standard. Eur J Haematol. Article CAS PubMed Google Scholar. Damian MTVR, Login CC, Damian L, Chis A, Bojan A. Life basel. Life , 11 9 Murray-Kolb LE, Beard JL. Iron treatment normalizes cognitive functioning in young women.

Am J Clin Nutr. Auersperger I, Skof B, Leskosek B, et al. Exercise-induced changes in iron status and hepcidin response in female runners. PLoS One. Article CAS PubMed PubMed Central Google Scholar. Pate RR, Miller BJ, Davis JM, et al. Iron status of female runners. Int J Sport Nutr. Alaunyte I, Stojceska V, Plunkett A.

Iron and the female athlete: a review of dietary treatment methods for improving iron status and exercise performance. J Int Soc Sports Nutr. Milic R, Martinovic J, Dopsaj M, et al.

Eur J Appl Physiol Dellavalle DM, Haas JD. Iron status is associated with endurance performance and training in female rowers. Med Sci Sports Exerc. Peeling P, Dawson B, Goodman C, et al. Athletic induced iron deficiency: new insights into the role of inflammation, cytokines and hormones.

Eur J Appl Physiol. Troadec MB, Laine F, Daniel V, et al. Daily regulation of serum and urinary hepcidin is not influenced by submaximal cycling exercise in humans with normal iron metabolism.

Banfi G, Del Fabbro M, Mauri C, et al. Haematological parameters in elite rugby players during a competitive season. Clin Lab Haematol.

Banfi G, Dolci A, Freschi M, et al. Immature reticulocyte fraction irf monitored in elite athletes during a whole season. Candau R, Busso T, Lacour JR. Effects of training on iron status in cross-country skiers.

Eur J Appl Physiol Occup Physiol. Malcovati L, Pascutto C, Cazzola M. Hematologic passport for athletes competing in endurance sports: a feasibility study. PubMed Google Scholar. Zugel M, Treff G, Steinacker JM, et al. Increased hepcidin levels during a period of high training load do not alter iron status in male elite junior rowers.

Front Physiol. Article PubMed Google Scholar. Skarpanska-Stejnborn A, Basta P, Trzeciak J, et al. Effect of intense physical exercise on hepcidin levels and selected parameters of iron metabolism in rowing athletes.

Yusof ALR, Roth HJ, Finkernagel H, Wilson MT, Beneke R. Exercise-induced hemolysis is caused by protein modification and most evident during the early phase of an ultraendurance race. J Appl Physiol Article CAS Google Scholar.

Lippi G, Sanchis-Gomar F. Epidemiological, biological and clinical update on exercise-induced hemolysis. Ann Transl Med. Barros MP, Ganini D, Lorenco-Lima L, et al. Effects of acute creatine supplementation on iron homeostasis and uric acid-based antioxidant capacity of plasma after wingate test.

Orino K, Lehman L, Tsuji Y, et al. Ferritin and the response to oxidative stress. Biochem J. Soldin OP, Bierbower LH, Choi JJ, et al. Serum iron, ferritin, transferrin, total iron binding capacity, hs-crp, ldl cholesterol and magnesium in children; new reference intervals using the dade dimension clinical chemistry system.

Clin Chim Acta. Ponka P. Tissue-specific regulation of iron metabolism and heme synthesis: Distinct control mechanisms in erythroid cells. Dominguez R, Sanchez-Oliver AJ, Mata-Ordonez F, et al. Nutrients , Nemeth E and Ganz T: Hepcidin-ferroportin interaction controls systemic iron homeostasis. Int J Mol Sci , Lin T, Sammy F, Yang H, et al.

Identification of hemopexin as an anti-inflammatory factor that inhibits synergy of hemoglobin with hmgb1 in sterile and infectious inflammation. J Immunol. Rosa L, Cutone A, Lepanto MS, et al. Schumacher YO, Jankovits R, Bultermann D, et al.

Hematological indices in elite cyclists. Scand J Med Sci Sports. Larsuphrom P, Latunde-Dada GO: Association of serum hepcidin levels with aerobic and resistance exercise: a systematic review.

Newlin MK, Williams S, McNamara T, et al. The effects of acute exercise bouts on hepcidin in women. Int J Sport Nutr Exerc Metab. Peake JM, Della Gatta P, Suzuki K, et al. Cytokine expression and secretion by skeletal muscle cells: regulatory mechanisms and exercise effects.

Exerc Immunol Rev. Villar-Fincheira P, Paredes AJ, Hernandez-Diaz T, et al. Soluble interleukin-6 receptor regulates interleukindependent vascular remodeling in long-distance runners.

Article PubMed PubMed Central Google Scholar.