Iron deficiency promotes a shift towards a more glycolytic metabolism, without detectable effect on mitochondrial bioenergetics, which can be corrected with iron supplements.
The methodology of this prospective, case-control, clinical physiology study involved two series of testing. Thirteen iron-deficient individuals and thirteen iron-replete control participants were chosen for the study, and they underwent P-magnetic resonance spectroscopy of their exercising calf muscles to investigate the differences in oxidative phosphorylation. This testing was followed by a whole-body cardiopulmonary exercise test. After these assessments, individuals were given an intravenous infusion, which was randomised to be either iron or saline.
The results showed no significant influence of either baseline iron levels or the intravenous iron infusion on the high-energy phosphate metabolism. In the case of submaximal cardiopulmonary exercise, the rate of decline in blood lactate concentration was slower for the iron deficient group, which shows signs of abnormal energy metabolism on a whole-body level. Remarkably, this anomaly was corrected after an intravenous iron infusion. Furthermore, the intravenous iron also increased the lactate threshold during maximal cardiopulmonary exercise by around 10%, no matter what the baseline iron status of the individual was.
