Abstract
Iron deficiency (ID), measured via serum ferritin (SF), is a common issue for female athletes due to inadequate dietary iron intakes, menstruation and exercise-induced iron losses. Elite female rugby sevens players are no exception with the high contact nature of the game leading to severe muscle damage which provokes an inflammatory response. It has previously been shown that inflammation artificially raises SF concentration, and as such, could cause a misdiagnosis of ID in athletes. This could lead to health and performance consequences such as fatigue, lack of energy, apathy, impaired adenosine triphosphate (ATP) synthesis and reduced exercise capacity.
Hepcidin, the negative regulator of iron levels, has been indicated as a potential diagnostic tool for assessing iron status in athletes who are in inflammatory states. This is because hepcidin is an acute phase protein (APP) which is elevated during the 24 hours after exercise, subsequent to inflammation. Therefore, adjusting raised SF concentrations in athletes with hepcidin will remove the confounding effect of inflammation and expose true SF concentrations, providing a more accurate diagnosis of iron status. This will enable better treatment and prevention strategies that can be applied to each athlete individually. However, due to the lack of haematological and inflammatory data available on elite female rugby sevens athletes, the assessment of hepcidin in these players has not been explored, until now.
The aim of this longitudinal observational study is to analyse the relationship between hepcidin and indices of iron status in elite female rugby sevens players.
Venepuncture blood samples were analysed from 17 elite female rugby sevens players in February and July 2018 and analysed for iron, SF, soluble transferrin receptor (sTfR), high sensitivity C-reactive Protein (CRP) and hepcidin. Dietary intakes were also measured via five-day diet records to assess average iron and energy intakes.
The novel findings from this study show that ID is a common issue in elite female rugby sevens players with 18 % of players identified as iron deficient based on SF < 30 μg/L. A further 29 – 35 % of players were identified with sub-optimal iron stores at some point during the study (SF < 45 μg/L). Serum hepcidin was strongly correlated with SF (r = 0.61, P = 0.0001). Further, mean SF concentration dropped from 67.0 to 54.5 μg/L in February and 62.8 to 51.4 μg/L in July after adjusting for hepcidin, suggesting inflammation confounded true mean SF concentrations resulting in an underestimation of the prevalence of ID. This also highlights the benefit of adding hepcidin to the repertoire of indices used for assessing iron status.
In conclusion, this is the first study to describe the relationship between hepcidin and indices of iron status in the New Zealand women’s rugby sevens team. We showed inflammation confounds true SF concentration and hepcidin is a beneficial tool when used to adjust SF for inflammation. By more accurately diagnosing ID in these players, this could improve their health and performance and long-term lower the prevalence of ID.