Niemelä Markus, Niemelä Onni, Bloigu Risto, Bloigu Aini, Kangastupa Päivikki, Juvonen Tatu
Department of Surgery, Oulu University Hospital, Oulu 90029, Finland.
Department of Laboratory Medicine and Medical Research Unit, Seinäjoki Central Hospital and Tampere University, Seinäjoki 60220, Finland.
J Inflamm Res. 2020 May 22;13:223-231. doi: 10.2147/JIR.S250675. eCollection 2020.
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.
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.
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 = 0.720, p < 0.01), IL-10 = 0.615, p < 0.05), TNF-α = 0.594, p < 0.05), suPAR = 0.587, p < 0.05) and blood leukocytes = 0.762, p < 0.01).
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.
虽然已知极端体力消耗会引起炎症状态的变化,但对于高强度运动急性发作后各种炎症介质反应的比较却很有限。
我们检测了12名身体活跃的志愿者(10名男性,2名女性,平均年龄37±14岁)在完成各种类型的极端体力消耗(马拉松跑、半程马拉松跑或24小时越野滑雪)前后,新型炎症蛋白、钙卫蛋白、可溶性尿激酶型纤溶酶原激活物受体(suPAR)、CD163以及促炎和抗炎细胞因子的血清水平反应。为作比较,还在30名低活动量或久坐不动的健康对照者(25名男性,5名女性,平均年龄42±12岁)静息时测量了生物标志物的水平。
极端体力消耗导致血清钙卫蛋白(p<0.0005)、suPAR(p<0.01)、CD163(p<0.05)、白细胞介素-6(IL-6,p<0.0005)、白细胞介素-8(IL-8,p<0.01)和白细胞介素-10(IL-10,p<0.0005)显著升高(运动前与运动后3小时比较)。这些反应在48小时内恢复正常。虽然不同类型运动后血白细胞的增加幅度相似,但在活动强度更大的人群中,血清肿瘤坏死因子-α(TNF-α,p<0.01)、IL-8(p<0.01)和CD163(p<0.05)的反应明显更显著。在运动后3小时的样本中,观察到血清钙卫蛋白与IL-6(r = 0.720,p<0.01)、IL-10(r = 0.615,p<0.05)、TNF-α(r = 0.594,p<0.05)、suPAR(r = 0.587,p<0.05)和血白细胞(r = 0.762,p<0.01)之间存在显著相关性。
目前的结果表明,极端体力消耗后炎症介质(包括钙卫蛋白、suPAR和CD163)存在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性影响。