Purpose: While extreme physical exertion is known to induce changes in the status of inflammation comparisons of the responses for various mediators of inflammation after acute bouts of high-intensity exercise have been limited.
Subjects and Methods: We examined the responses in serum levels of novel inflammatory proteins, calprotectin, suPAR, CD163, and pro- and anti-inflammatory cytokines in 12 physically active volunteers (10 men, 2 women, mean age 37± 14 years) before and after completing various types of extreme physical exertion (marathon run, half-marathon run or 24-h cross-country skiing). For comparisons, the levels of the biomarkers were also measured at rest in 30 healthy controls (25 men, 5 women, mean age 42 ± 12 years) with low or sedentary activity.
Results: Extreme physical exertion induced significant increases in serum calprotectin (p < 0.0005), suPAR (p < 0.01), CD163 (p < 0.05), IL-6 (p < 0.0005), IL-8 (p < 0.01) and IL-10 (p < 0.0005) (pre- vs 3h-post-exercise). These responses were found to normalize within 48 hours. While the increases in blood leukocytes were of similar magnitude following the different types of exercise, markedly more pronounced responses occurred in serum TNF-α (p < 0.01), IL-8 (p < 0.01) and CD163 (p < 0.05) in those with more intense activity. In 3-h post-exercise samples significant correlations were observed between serum calprotectin and IL-6 (r_s = 0.720, p < 0.01), IL-10 (r_s = 0.615, p < 0.05), TNF-α (r_s = 0.594, p < 0.05), suPAR (r_s = 0.587, p < 0.05) and blood leukocytes (r_s = 0.762, p < 0.01).
Conclusion: The present results suggest distinct exercise-intensity dependent changes in mediators of inflammation (including calprotectin, suPAR and CD163) following extreme physical exertion. Our findings indicate that there is a major reversible impact of high-intensity physical exertion on the status of inflammation.

Keywords: acute exercise, cytokine, immune status, leukocyte, oxidative stress



中文翻译：

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血清钙卫蛋白，中性粒细胞活化的标志物，以及其他炎症介质，以应对健康志愿者的各种极端体力消耗。

目的：虽然已知极端的体力消耗会引起炎症状态的变化，但对急性高强度运动后各种炎症介质的反应进行比较是有限的。
受试者和方法：我们检查了 12 名体力活动志愿者（10 名男性，2 名女性，平均年龄 37±14 岁）的血清中新型炎症蛋白、钙卫蛋白、suPAR、CD163 和促炎和抗炎细胞因子的反应。并在完成各种极限体力消耗（马拉松跑、半程马拉松跑或24小时越野滑雪）后。为了进行比较，还测量了 30 名健康对照者（25 名男性，5 名女性，平均年龄 42 ± 12 岁）在休息时的生物标志物水平，他们的活动量较低或久坐不动。
结果：剧烈运动导致血清钙卫蛋白 (p < 0.0005)、suPAR (p < 0.01)、CD163 (p < 0.05)、IL-6 (p < 0.0005)、IL-8 (p < 0.01) 和 IL-10 显着增加（p < 0.0005）（运动前与运动后 3 小时）。发现这些反应在 48 小时内恢复正常。虽然在不同类型的运动后血液白细胞的增加幅度相似，但血清 TNF-α (p < 0.01)、IL-8 (p < 0.01) 和 CD163 (p < 0.05) 的反应明显更明显。与更激烈的活动。在运动后 3 小时的样本中，观察到血清钙卫蛋白与 IL-6 （r _s = 0.720，p < 0.01）、IL-10 （r _s = 0.615，p < 0.05）、TNF-α （r _s = 0.594, p < 0.05),(rs = _0.587 , p < 0.05) 和血液白细胞₍ rs = 0.762, p < 0.01)。
结论：目前的结果表明，剧烈运动后炎症介质（包括钙卫蛋白、suPAR 和 CD163）发生明显的运动强度依赖性变化。我们的研究结果表明，高强度体力消耗对炎症状态有重大的可逆影响。

关键词：急性运动，细胞因子，免疫状态，白细胞，氧化应激