Abstract
Background: Prevalence of iron deficiency is commonly reported among athletic population groups. It impairs physical performance due to insufficient oxygen delivery to target organs and low energy production. This is due to the high demand of exercise on oxygen delivery for systemic metabolism by the erythrocytes in the blood. Hepcidin, the key regulator of iron homeostasis, decreases to facilitate iron efflux into the circulation during enhanced erythropoiesis. However, acute anaemia of exercise is caused by increased hepcidin expression that is induced by stress and inflammatory signal. The study aimed to systematically review changes in serum hepcidin levels during resistance and aerobic exercise programmes. Methods: A systemic literature search from 2010 to April 2020 across seven databases comprised of Cochrane library, PubMed, Web of Science, Scopus, Embase, MEDLINE, and OpenGrey. The primary outcome was increased or decreased serum hepcidin from baseline after the exercise activity. Risks of bias were evaluated by using the National Institutes of Health (NIH) for quality assessment of before and after different exercise programmes. Results: Overall, twenty-three studies met the inclusion criteria. Out of the 23 studies, 16 studies reported significantly exercise-induced serum hepcidin elevation. Of the 17 studies that evaluated serum interleukin (IL)-6 levels, 14 studies showed significant exercise-induced serum IL-6 elevation. Changes in exercise-induced serum hepcidin and IL-6 levels were similar in both resistance and endurance exercise. Significant correlations were observed between post-exercise hepcidin and baseline ferritin levels (r = 0.69, p < 0.05) and between post-exercise hepcidin and post-exercise IL-6 (r = 0.625, p < 0.05). Conclusion: Resistance and endurance training showed significant increase in serum hepcidin and IL-6 levels in response to exercise. Baseline ferritin and post-exercise IL-6 elevation are key determining factors in the augmentation of hepcidin response to exercise.
Highlights
Changes in exercise-induced serum hepcidin and IL-6 levels were similar in both resistance and endurance exercise
The inclusion criteria were as follows: (a) experimental studies that examined the effect of exercise on serum hepcidin and IL6 levels that were determined by valid methods, (b) studies conducted with athletes or recreationally trained participants, and (c) studies published in the English language
The current review found a similar elevation in serum hepcidin in response to different exercise intensities from 60% to 90% of VO2max, indicating that exercise intensity may not be vital in the response of hepcidin to endurance training
Summary
Iron is an essential mineral for a number of physiological processes, and it is crucial for health and physical performance It plays an essential role in the human body because it is involved in the production of oxygen-carrying proteins, haemoglobin, and myoglobin, which deliver oxygen to target tissues. Iron is involved in energy formation within the electron transport chain, DNA synthesis, and in oxidative phosphorylation in the mitochondria [1] These functions make iron an essential element that is relevant to physical performance. Iron deficiency (ID) leads to impaired energy metabolism due to reduced cytochrome production. It impairs physical performance due to insufficient oxygen delivery to target organs and low energy production This is due to the high demand of exercise on oxygen delivery for systemic metabolism by the erythrocytes in the blood.
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