The purpose of the present study was to verify whether impaired iron metabolism in young athletes is a consequence of an excessive workload during the tournament season. Low levels of ferritin (under 25 µg·L(-1)) have been frequently observed in young tennis players. We considered this finding to be related to the high-intensity workload or to insufficient rest, which both trigger a strong immune response. Groups of male, well-trained young tennis players (16 ± 0.9 years old, average of 10-year training experience) and a control peer group participated in this study. The research consisted of two examination sessions (March and September 2010). Blood samples were collected to determine haematological and immunological parameters. Additionally, body composition and physical capacity were assessed. In both periods of the study, the trained groups were characterised by low levels of ferritin, but also elevated levels of pro- inflammatory cytokine IL-1β. Moreover, an inverse correlation between IL-1β and blood ferritin was observed. Additionally, an increased concentration of the iron homeostasis regulator hepcidin was found in blood samples (mean 71 ng·ml(-1); range from 48 to 100 ng·ml(-1)). We concluded that the pro- inflammatory cytokine IL-1β, most likely induced by an extensive workload during the tournament season, was responsible for the low level of ferritin in young, professional athletes. Key PointsThe first research demonstrating low grade inflammation-induced iron deficiency to be associated with elevated blood hepcidin levels in young tennis athletes.Evaluation of immunological response after the complete tournament season in young male tennis players.Conclusion to introduce the assessment of hepcidin to monitor trainings as well as symptoms of overreaching more effectively.Research providing practical information for coaches that changes in diet and modifications in workloads applied in physical training could be more effective than iron supplementation in iron deficient athletes.
Keywords: Pro-inflammatory cytokine; hepcidin; overreaching.