The findings of this thesis demonstrate that the modulation of immune capacity and iron-related parameters is dependent on the specific training stimulus adopted. Superposition of different training stimuli may limit training adaptation through activation of opposing signalling pathways. Further, the simultaneous introduction of normobaric hypoxia andi iron supplementation to training partially suppressed resting serum levels of hepcidin. The up-regulation of hepcidin as a response to the training-induced inflammation may limit the haematological responses to LHTL, suggesting that a less intense training stimulus be adopted during periods of LHTL. Findings from this thesis provide new insights for the interactions between iron availability, inflammation and hypoxia within the pathways regulating hepcidin expression.
|Date of Award||7 Oct 2017|
|Sponsors||Australian Institute of Sport & QIMR-Berghofer Medical Research Institute|
|Supervisor||Bon Gray (Supervisor), Gregory J. Anderson (Supervisor), Nicola Bullock (Supervisor) & Chris P McLellan (Supervisor)|