Iron metabolism in athletes - achieving a gold standard (original) (raw)
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Iron Status and the Acute Post-Exercise Hepcidin Response in Athletes
PLoS ONE, 2014
This study explored the relationship between serum ferritin and hepcidin in athletes. Baseline serum ferritin levels of 54 athletes from the control trial of five investigations conducted in our laboratory were considered; athletes were grouped according to values ,30 mg/L (SF,30), 30-50 mg/L (SF30-50), 50-100 mg/L (SF50-100), or .100 mg/L (SF.100). Data pooling resulted in each athlete completing one of five running sessions: (1) 863 min at 85% vVO 2peak ; (2) 564 min at 90% vVO 2peak ; (3) 90 min continuous at 75% vVO 2peak ; (4) 40 min continuous at 75% vVO 2peak ; (5) 40 min continuous at 65% vVO 2peak . Athletes from each running session were represented amongst all four groups; hence, the mean exercise duration and intensity were not different (p.0.05). Venous blood samples were collected pre-, post-and 3 h post-exercise, and were analysed for serum ferritin, iron, interleukin-6 (IL-6) and hepcidin-25. Baseline and post-exercise serum ferritin levels were different between groups (p,0.05). There were no group differences for pre-or post-exercise serum iron or IL-6 (p.0.05). Post-exercise IL-6 was significantly elevated compared to baseline within each group (p,0.05). Pre-and 3 h post-exercise hepcidin-25 was sequentially greater as the groups baseline serum ferritin levels increased (p,0.05). However, post-exercise hepcidin levels were only significantly elevated in three groups (SF30-50, SF50-100, and SF.100; p,0.05). An athlete's iron stores may dictate the baseline hepcidin levels and the magnitude of post-exercise hepcidin response. Low iron stores suppressed post-exercise hepcidin, seemingly overriding any inflammatory-driven increases.
The role of hepcidin in iron metabolism in athletes
Fizicka kultura, 2019
Hepcidin is a peptide that was discovered in 2000, it is synthesized in the liver and it goes into circulation. There are three forms of hepcidin, hepcidin-25, hepcidin-22 and hepcidin-20. The first form is the most studied and its role is the most significant. Hepcidin-25 is considered to be a major regulator of the absorption of dietary iron as well as its release from cells. It achieves its regulatory function by preventing the function of ferroportin, the major cellular iron exporter. Ferroportin is a protein whose function is to release iron from the cells on which it is located (macrophages, hepatocytes and enterocytes). Hepcidin-25 induces degradation of ferroportin, resulting in an increase in intracellular iron stores. It also reduces the absorption of iron from food and thus reduces the concentration of circulating iron. During physical activity, the concentration of hepcidin increases at an intensity of 65% VO 2 max, and maximum values are reached at 90-95% VO 2 max. Not only intensisty, but also the volume of physical activity influence its concentration. Sudies showed that hepcidin expression during physical activity is influenced by inflammation, iron status, erythropoiesis and hypoxia. It is considered one of the causes of anemia in athletes. There are potential methods for neutralizing hepcidin (monoclonal antibodies and antagonists) and reducing its expression (erythropoietin doping, wich is forbbiden in sport, anti-IL-6 antibodies, STAT and BMP modulators). Given its important role in iron metabolism, which is essential for the transport of oxygen in the body, it can affect sports performance. It is still the subject of many research.
Exercise-Induced Changes in Iron Status and Hepcidin Response in Female Runners
PLoS ONE, 2013
Background and Aims: Exercise-induced iron deficiency is a common finding in endurance athletes. It has been suggested recently that hepcidin may be an important mediator in this process. Objective: To determine hepcidin levels and markers of iron status during long-term exercise training in female runners with depleted and normal iron stores. Methods: Fourteen runners were divided into two groups according to iron status. Blood samples were taken during a period of eight weeks at baseline, after training and after ten days' recovery phase. Results: Of 14 runners, 7 were iron deficient at baseline and 10 after training. Hepcidin was lower at recovery compared with baseline (p,0.05). The mean cell haemoglobin content, haemoglobin content per reticulocyte and total iron binding capacity all decreased, whereas soluble transferrin receptor and hypochromic red cells increased after training and recovery (p,0.05 for all). Conclusion: The prevalence of depleted iron stores was 71% at the end of the training phase. Hepcidin and iron stores decreased during long-term running training and did not recover after ten days, regardless of baseline iron status.
Transitory hematologic effects of moderate exercise are not influenced by iron supplementation
European Journal of Applied Physiology and Occupational Physiology, 1983
A young women's exercise/fitness class tested the idea that administration of supplemental iron would prevent "sports anemia" that may develop during exercise and training and improve iron status of exercising females of menstrual age. Fifteen women (aged 18-37) were selected for each of three treatment groups: (1) no supplemental iron; (2) 9 mg-d-1 of Fe; and (3) 18 rag. d-1 of Fe (1 US Recommended Daily Allowance). Women exercised at approximately 85% of maximal heartrate for progressively increasing lengths of time in a jogging program and worked up to 45 min of exercise 4 d. week-1 for 8 weeks. Hematologic analysis was performed in weeks 1, 5, and 8. A significant decline in hemoglobin (Hb) concentration and hematocrit (Hct) was observed at week 5 when all data were examined without regard for iron intake; these red cell indices returned to pre-exercise levels by week 8. Reduction of mean cell hemoglobin concentration (MCHC) indicated that the midpoint decline was not caused by simple hemodilution during exercise. Serum ferritin (SF) concentration changed in parallel with Hb and Hct. Although the midpoint decline in SF was not statistically significant, it ruled out the possibility that turnover of red cell iron was directed to storage. Lowered MCHC and SF suggested lower availability of iron during the synthesis of a new generation of red cells. Few iron treatment effects of magnitude were observed. Iron did not prevent the midpoint decline in Hb concentration. Iron intake did not affect SF, serum iron, transferrin saturation, or final Hb, and Hct. Dietary iron availability thus does not appear to play a role in the phenomenon of "sports anemia". Temporary alteration of priorities for iron needs during exercise, perhaps for muscle myoglobin, may be responsible fo r this transitory" anemia".
Baltic Journal of Health and Physical Activity, 2019
Background: The aim of the study was to compare the influence of exercise on iron metabolism and hepcidin concentration between carriers of His63Asp mutation (H63D polymorphism) and wild type HFE gene males. Iron is an essential micronutrient required for various biological processes. Systemic iron homeostasis is maintained in a hormone-like negative feedback mechanism by the 25-amino acid peptide hepcidin. Hepcidin controls duodenal iron absorption and iron recycling from senescent erythrocytes using tissue macrophages through the down-regulation of the sole known iron cell exporter, ferroportin-1. Exercise may induce an inflammatory response that leads to changes in iron metabolism. Material and methods: Iron, ferritin, hepcidin concentration and transferrin saturation were measured in carriers of His63Asp mutation of HFE and wild type teenagers before and after cycle ergometer exercise. Results: His63Asp carriers had higher basal hepcidin concentration than wild type probands (p < 0.05). Interestingly, the analysis of the correlation between iron and hepcidin concentration showed a positive tendency in H63D carriers, while the wild type group showed a negative tendency at the basal and post-exercise point. Conclusions: This study demonstrates that exercise has a distinct impact on iron metabolism through the hepcidin pathway with regard to the HFE gene status.
European Journal of Haematology, 2013
Inhibition of hepcidin expression by erythropoietic signals is of great physiological importance; however, the inhibitory pathways remain poorly understood. To investigate (i) the direct effect of erythropoietin (Epo) and (ii) the contribution of putative mediators on hepcidin repression, healthy volunteers were injected with a single dose of Epo, either low (63 IU/kg, n = 8) or high (400 IU/kg, n = 6). Low-dose Epo provoked hepcidin down-modulation within 24 h; the effect was not immediate as hepcidin circadian variations were still present following injection. High-dose Epo induced no additional effect on the hepcidin response, that is hepcidin diurnal fluctuations were not abolished in spite of extremely high Epo levels. We did not find significant changes in putative mediators of hepcidin repression, such as transferrin saturation, soluble transferrin receptor, or growth differentiation factor 15. Furthermore, the potential hepcidin inhibitor, soluble hemojuvelin, was found unaltered by Epo stimulation. This finding was consistent with the absence of signs of iron deficiency observed at the level of skeletal muscle tissue. Our data suggest that hepcidin repression by erythropoietic signals in humans may not be controlled directly by Epo, but mediated by a still undefined factor.
The American Journal of Clinical Nutrition
Background Iron status is a determinant of physical performance, but training may induce both low-grade inflammation and erythropoiesis, exerting opposing influences on hepcidin and iron metabolism. To our knowledge, the combined effects on iron absorption and utilization during training have not been examined directly in humans. Objective We hypothesized that 3 wk of exercise training in recreational male runners would decrease oral iron bioavailability by increasing inflammation and hepcidin concentrations. Design In a prospective intervention, nonanemic, iron-sufficient men (n = 10) completed a 34-d study consisting of a 16-d control phase and a 22-d exercise-training phase of 8 km running every second day. We measured oral iron absorption and erythroid iron utilization using oral 57Fe and intravenous 58Fe tracers administered before and during training. We measured hemoglobin mass (mHb) and total red blood cell volume (RCV) by carbon monoxide rebreathing. Iron status, interleuki...
The Journal of sports medicine and physical fitness, 2013
Exercise may induce an inflammatory response that may lead to changes in iron metabolism. The aim of this study was to examine the relationship between the inflammation induced by a 100 km run and the level of hepcidin, which is a hormone regulating iron metabolism. Six males, age 44.5±13.5 years, running 100 km. the CRP protein, IL-6 and leucocyte count were measured as an index of inflammation. A 100 km run caused a progressive increase in blood IL-6 concentration, which reached the highest values after 75 km. Furthermore, an increase in levels of CRP, a marker of inflammation, was observed after the 100 km run and continued to increase after a 14 h recovery period. Leucocyte number and markers of muscle damage were significantly elevated after the 100 km run. This was accompanied by a decrease in transferrin saturation and an increase in blood haemoglobin and ferritin. Despite all these changes, the 100 km race did not affect blood hepcidin concentration either during the run or ...
Effects of an Acute Exercise Bout on Serum Hepcidin Levels
Nutrients, 2018
Iron deficiency is a frequent and multifactorial disorder in the career of athletes, particularly in females. Exercise-induced disturbances in iron homeostasis produce deleterious effects on performance and adaptation to training; thus, the identification of strategies that restore or maintain iron homeostasis in athletes is required. Hepcidin is a liver-derived hormone that degrades the ferroportin transport channel, thus reducing the ability of macrophages to recycle damaged iron, and decreasing iron availability. Although it has been suggested that the circulating fraction of hepcidin increases during early post-exercise recovery (~3 h), it remains unknown how an acute exercise bout may modify the circulating expression of hepcidin. Therefore, the current review aims to determine the post-exercise expression of serum hepcidin in response to a single session of exercise. The review was carried out in the Dialnet, Elsevier, Medline, Pubmed, Scielo and SPORTDiscus databases, using h...
International Journal of Sport Nutrition and Exercise Metabolism, 2012
Exercise-associated iron deficiency is a common disorder in endurance athletes. The authors investigated the effects of long-term endurance exercise on hepcidin concentrations, inflammatory parameters, and iron status in moderately trained female long-distance runners. Eighteen runners were assigned to either an interval-or a continuous-training exercise group. The physical training consisted of two 3-week progressive overload periods, each followed by a week's recovery, and concluded with a 10-or 21-km competitive run. Samples were taken 6 times during the 8-wk training program, first at baseline (BPre), then after the first and second 3-wk training loads (TPost1, TPost2), after each recovery week (Recovery1 and Recovery2), and poststudy (BPost). Soluble transferrin receptor (sTfR) concentrations were increased in Recovery2 and BPost compared with BPre (p = .02), hemoglobin decreased in TPost1 and TPost2 (p < .001), and red blood cells decreased in TPost2 (p = .01). Hepcidin decreased with time in TPost1 and in BPost compared with BPre (p < .001) and increased in TPost2 compared with TPost1 (p < .001). No differences over time were found for high-sensitivity C-reactive protein. The main findings of the current study indicate that serum hepcidin and sTfR were affected after 8 weeks of endurance running in women. No positive relation was found with inflammation.