For example, serum ferritin has recently been reported to dictate hepcidin activity

in athletes [17]. Here, Peeling and colleagues [17] demonstrated that low serum ferritin levels RG-7388 molecular weight (<30 μg.L−1) were linked to the suppression of pre-exercise levels of hepcidin, and the magnitude of hepcidin response to an acute exercise stimulus. Additionally, concerns were raised for individuals with ‘suboptimal’ iron stores (serum ferritin 30–50 μg.L−1), as the post-exercise hepcidin response in these individuals was still evident after 3 h of recovery, at a similar magnitude to those athletes presenting with more healthy iron stores. Considering that both the running and control groups in Ma et al. [26]

presented with poor iron stores (at the time of biological sampling; serum ferritin of < 35 ug.L−1), they would also be classified as Stage One Iron Deficient according to MK5108 supplier numerous published guidelines for athletes [2, 28]. Consequently, these previous findings may only be relevant to populations displaying a poor iron status. Karl et al. [25] also reported that serum hepcidin levels were unchanged in female soldiers who had performed a nine week BCT training program while receiving an iron fortified food bar (twice daily) or a placebo equivalent. However, when soldiers were regrouped according to their iron status (either

Normal [NORM], Iron Deficient [ID] or Iron Deficient Anemic [IDA]), post-BCT basal hepcidin levels were significantly lower in IDA as compared to NORM, while the ID group showed similar decreases without Givinostat molecular weight reaching significance (p = 0.06). Most importantly, it should be highlighted that during the aforementioned investigations, basal hepcidin samples were obtained at the end of specific training phases [14, 25] or at a single time point [26], without measuring any acute changes over the course of the training period. In our investigation, basal hepcidin levels were measured on five occasions (D1, D2, R3, D6, R7), in addition to 3 h post-exercise PAK6 samples (D1, D2, D6) to highlight the acute hepcidin response. Additionally, this is the first investigation to explore if any benefits associated with iron metabolism might be present after completing a series of non-weight-bearing exercise (cycling) sessions as compared to weight-bearing activity (running) in active males. Numerous exercise investigations have explored the hepcidin response acutely [3–9], showing that the hormone levels are significantly elevated 3 h post-exercise (as compared to baseline) after each exercise session. However, such a response was only recorded here on D1 of RTB, with moderate to large ES recorded for the majority of the other running and cycling sessions.