Training Surface and Intensity :  Inflammation, Hemolysis, and Hepcidin Expression

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Abstract

This investigation assessed the effects of training intensity and ground surface type on hemolysis, inflammation, and hepcidin activity during running. Ten highly trained male endurance athletes completed a graded exercise test, two continuous 10-km runs on a grass (GRASS) and a bitumen road surface (ROAD) at 75%-80% peak VO2 running velocity, and a 10 x 1-km interval running session (INT) at 90%-95% of the peak VO2 running velocity. Venous blood and urine samples were collected before, immediately after, and at 3 and 24 h after exercise. Serum samples were analyzed for circulating levels of IL-6, free hemoglobin (Hb), haptoglobin (Hp), iron, and ferritin. Urine samples were analyzed for changes in hepcidin expression. After running, the IL-6 and free Hb were significantly greater, and serum Hp was significantly lower than preexercise values in all three conditions (P < 0.05). Furthermore, IL-6 levels and the change in free Hb from baseline were significantly greater in the INT compared with those in the GRASS (P < 0.05). There were no differences between the GRASS and ROAD training surfaces (P > 0.05). Serum iron and ferritin were significantly increased after exercise in all three conditions (P < 0.05) but were not different between trials. Greater running intensities incur more inflammation and hemolysis, but these variables were not affected by the surface type trained upon.

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Most cited references 37

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Hepcidin regulates cellular iron efflux by binding to ferroportin and inducing its internalization.

E Németh (2004)

Hepcidin is a peptide hormone secreted by the liver in response to iron loading and inflammation. Decreased hepcidin leads to tissue iron overload, whereas hepcidin overproduction leads to hypoferremia and the anemia of inflammation. Ferroportin is an iron exporter present on the surface of absorptive enterocytes, macrophages, hepatocytes, and placental cells. Here we report that hepcidin bound to ferroportin in tissue culture cells. After binding, ferroportin was internalized and degraded, leading to decreased export of cellular iron. The posttranslational regulation of ferroportin by hepcidin may thus complete a homeostatic loop: Iron regulates the secretion of hepcidin, which in turn controls the concentration of ferroportin on the cell surface.

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Exercise and the immune system: regulation, integration, and adaptation.

Bente Pedersen, Laurie Hoffman-Goetz (2000)

Stress-induced immunological reactions to exercise have stimulated much research into stress immunology and neuroimmunology. It is suggested that exercise can be employed as a model of temporary immunosuppression that occurs after severe physical stress. The exercise-stress model can be easily manipulated experimentally and allows for the study of interactions between the nervous, the endocrine, and the immune systems. This review focuses on mechanisms underlying exercise-induced immune changes such as neuroendocrinological factors including catecholamines, growth hormone, cortisol, beta-endorphin, and sex steroids. The contribution of a metabolic link between skeletal muscles and the lymphoid system is also reviewed. The mechanisms of exercise-associated muscle damage and the initiation of the inflammatory cytokine cascade are discussed. Given that exercise modulates the immune system in healthy individuals, considerations of the clinical ramifications of exercise in the prevention of diseases for which the immune system has a role is of importance. Accordingly, drawing on the experimental, clinical, and epidemiological literature, we address the interactions between exercise and infectious diseases as well as exercise and neoplasia within the context of both aging and nutrition.

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Pro- and anti-inflammatory cytokine balance in strenuous exercise in humans.

K. Ostrowski, T Rohde, S Asp … (1999)

1. The present study investigates to what extent and by which time course prolonged strenuous exercise influences the plasma concentration of pro-inflammatory and inflammation responsive cytokines as well as cytokine inhibitors and anti-inflammatory cytokines. 2. Ten male subjects (median age 27.5 years, range 24-37) completed the Copenhagen Marathon 1997 (median running time 3 : 26 (h : min), range 2 : 40-4 : 20). Blood samples were obtained before, immediately after and then every 30 min in a 4 h post-exercise recovery period. 3. The plasma concentrations of tumour necrosis factor (TNF)alpha, interleukin (IL)-1beta, IL-6, IL-1ra, sTNF-r1, sTNF-r2 and IL-10 were measured by enzyme-linked immunosorbent assay (ELISA). The highest concentration of IL-6 was found immediately after the race, whereas IL-1ra peaked 1 h post exercise (128-fold and 39-fold increase, respectively, as compared with the pre-exercise values). The plasma level of IL-1beta, TNFalpha, sTNF-r1 and sTNF-r2 peaked in the first hour after the exercise (2. 1-, 2.3-, 2.7- and 1.6-fold, respectively). The plasma level of IL-10 showed a 27-fold increase immediately post exercise. 4. In conclusion, strenuous exercise induces an increase in the pro-inflammatory cytokines TNFalpha and IL-1beta and a dramatic increase in the inflammation responsive cytokine IL-6. This is balanced by the release of cytokine inhibitors (IL-1ra, sTNF-r1 and sTNF-r2) and the anti-inflammatory cytokine IL-10. The study suggests that cytokine inhibitors and anti-inflammatory cytokines restrict the magnitude and duration of the inflammatory response to exercise.