The effect of carbohydrate ingestion on plasma interleukin-6, hepcidin and iron concentrations following prolonged exercise
| Autor: | Paula Robson-Ansley, Ian H. Walshe, Douglas G. Ward |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
Adult
Male medicine.medical_specialty Iron Immunology Carbohydrates Carbohydrate metabolism Placebo Biochemistry Placebos Time trial Hepcidins Hepcidin Internal medicine medicine Humans Immunology and Allergy Aerobic exercise Ingestion Exercise physiology Exercise Molecular Biology biology Interleukin-6 business.industry Feeding Behavior Hematology Iron deficiency medicine.disease Endocrinology biology.protein business Antimicrobial Cationic Peptides |
| Zdroj: | Cytokine. 53:196-200 |
| ISSN: | 1043-4666 |
| DOI: | 10.1016/j.cyto.2010.10.001 |
| Popis: | The aim of our study was twofold, firstly to examine the relationship between plasma concentrations of IL-6, hepcidin and iron following prolonged exercise and secondly, to assess the effect of carbohydrate ingestion on circulating hepcidin concentration post-exercise. The study was a randomised double-blind cross-over design, with participants consuming either a carbohydrate (CHO) or an isovolumetric placebo drink throughout the trial. Nine healthy, trained males completed a treadmill run at 60% vVO(2max) for 120 min followed by a 5 km time trial. Plasma concentrations of both IL-6 and hepcidin significantly increased post-exercise following both trials (p.05) and returned to baseline by 24 h post (p.05). A positive correlation between hepcidin and IL-6 was demonstrated immediately following exercise during PLA while there was a trend for a moderate correlation during CHO (PLA trial rho=0.81, p0.001; CHO trial rho=0.36, p=0.07). Plasma iron was unaffected immediately post-exercise but significantly reduced by 24 h post-exercise compared to baseline. CHO ingestion significantly reduced post-exercise IL-6 (p.05) but this had no effect on plasma hepcidin or iron concentration. Our data demonstrate CHO supplementation does not alter the rapid hepcidin response associated with exercise and does not prevent a subsequent fall in plasma iron concentration. This finding adds further support to the theory that an exercise-induced, up-regulation of hepcidin activity is a mechanism causing iron deficiency in endurance athletes. |
| Databáze: | OpenAIRE |
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