Abstract
The effects of polyphenol-rich foods on the iron status of athletes, as well as the effect of physical training on the hormone hepcidin, implicated in iron metabolism, are not clear. We investigated the influence on iron metabolism of a long-term training intervention of 120 days, measuring the hepcidin concentration in the plasma of 16 elite triathletes, and the effect of the ingestion of 200 mL of either aronia-citrus juice or a placebo drink for 45 days, in a crossover design. The highest plasma hepcidin concentrations were observed at the beginning of the study (116 ± 63 nM) and levels steadily decreased until the end of the intervention (final value 10 ± 7.5 nM). Long-term training might reduce inflammation and, hence, could be responsible for the decrease in hepcidin in triathletes. Polyphenols from aronia-citrus juice did not interfere in iron absorption, as we did not observe significant differences between the intake of the placebo drink or juice with regard to hepcidin levels. Further studies are required to ascertain the time and conditions necessary to restore hepcidin levels, which reflect the iron status of triathletes.
Highlights
Hepcidin is a peptide hormone synthesized mainly in the liver and the active form consists of 25 amino acids
The aim of the present study is to investigate a citrus-based juice, rich in polyphenols and vitamin C, along with long-term exercise affect iron status, considering changes in serum hepcidin levels, in a sample of elite triathletes
The increase in hepcidin would probably have been followed by inhibition of both intestinal iron absorption and the release would probably have been followed by inhibition of both intestinal iron absorption and the release of iron from macrophages, both contributing to the development of iron deficiency in these athletes
Summary
Hepcidin is a peptide hormone synthesized mainly in the liver and the active form consists of 25 amino acids. Some studies have demonstrated the relationship between hepcidin and iron. Nicolas et al observed a severe iron overload in mice that were knockout for the gene encoding hepcidin [1]. It has been shown that hepcidin is regulated by hemojuvelin, a protein produced in the liver and whose gene expression is responsible for juvenile hemochromatosis, causing excessive accumulation of iron in different organs, mainly in the liver [2], and promoting the development of certain infectious diseases [3]. The maintenance of iron levels involves regulation of iron absorption from the diet and its storage in hepatic and splenic macrophages. Iron is taken up by enterocytes, where it will bind to ferroportin or be incorporated into intracellular ferritin for storage [4,5]
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