Iron metabolism may undergo changes during exercise, with reductions in classical iron status
markers due to a variety of postulated mechanism which include hemodilution, increased iron
loss, hemolysis and increased iron storage in muscles. Furthermore, it has been reported that
vigorous training increases hepcidin, a central regulatory peptide in iron metabolism. This
increase has been ascribed to the presence of subclinical inflammation. Increased hepcidin
levels may reduce iron bioavailability and iron incorporation in erythrocytes.
Twenty healthy men subjects will be recruited as subjects for this study. Subjects should be
generally healthy, with no history of blood donation in the last 6 months, should weigh less
than 85 Kg, and not take iron supplements and/or multivitamin supplements. Subjects should
have familiarity to sports and running, but not currently (i.e. in the past 3 months)
training for more than 1h per week on average.
The aim of this study is to measure an iron bioavailability during a resting and an exercise
phase lasting approx. 14 days with training sessions on alternate days. Subjects will
participate in both restign and exercising protocols and act as their own controls during the
study. Iron bioavailability will be measured via the incorporation of stable isotopic labels
14 days after administration. To control for changes in blood volume during the course of the
study, blood volume of the participating subjects will be measured before and after the
exercise phase with the CO-rebreathing method.
Measurement of iron bioavailability and iron incorporation in a resting and exercising phase
will allow determine if the increased level of hepcidin seen in in exercise will induce a
lower iron bioavailability and iron incorporation during exercise.