Effect of exercise on inflammation, hepcidin regulation and iron metabolism

[Truncated abstract] Iron deficiency has been reported to affect up to 36% of the athletic population. This condition has previously been attributed solely to exercise-induced iron losses (e.g. sweating, haematuria, gastrointestinal bleeding and haemolysis), often in combination with poor dietary intake. Recently, a new hormonal pathway has been discovered, involving the master iron regulatory hormone, hepcidin. Largely due to exercise-induced increases in interleukin-6 (IL-6), circulating hepcidin levels are subsequently increased, and have been shown to peak ~3-6 h post-exercise. When hepcidin levels are elevated above basal levels, iron recycling and absorption may be compromised. To date, most investigations studying these responses have used male participants where hormonal fluctuations in response to the menstrual cycle are not present. Additionally, these studies have also predominately been performed using weight-bearing exercise modalities (such as running) that are typically associated with increased haemolysis. Finally, it is also evident that these studies have generally been of an acute nature, thus ignoring the chronic influences of elevated hepcidin levels in athletic populations. Therefore, it was the aim of this thesis to examine if factors such as female hormonal fluctuations, weight-bearing vs. non-weight-bearing exercise, and exercise training conducted over an extended period of time might impact iron metabolism via hepcidin modulation.