Abstract：
BACKGROUND: Cardiovascular safety of marathon running middle-aged amateurs remains unclear. We previously hypothesized that transient release of cardiac troponin I (cTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), in addition to an acute inflammatory response to exercise, may be the cause.
OBJECTIVE: To evaluate the effects of running a marathon on inflammatory biomarkers, and its impact on cardiovascular function.
METHODS: Thirty-three healthy male amateur runners aged ≥50 (mean age: 57 ±7 years) were enrolled in the study. Venous blood samples were obtained before the marathon, just after the race, and 2-4 days and 7 days after the marathon. Using novel single molecule counting (SMC) technology, we measured plasma concentrations of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). White blood cell (WBC) count was measured using a certified hematology analyzer. The results were related to previous analyses on cardiovascular stress and endothelial function biomarkers. Transthoracic echocardiography (TTE) and cardiac magnetic resonance (CMR) were used to determine myocardial function.
RESULTS: We observed a sharp rise of all studied biomarkers after the race, which subsequently normalized after 2-4 days and stayed within the normal range 7 days after the race. We found no correlation between inflammatory and cardiovascular stress biomarkers. Transthoracic echocardiography and CMR did not show ischemic or inflammatory myocardial damage.
CONCLUSIONS: Marathon running is associated with a sharp and significant rise in inflammatory and cardiovascular stress biomarkers. We found no connection between immune activation and cardiac biomarker release. Cardiovascular imaging showed no myocardial damage due to ischemia or inflammation.
OBJECTIVE: To evaluate the effects of running a marathon on inflammatory biomarkers, and its impact on cardiovascular function.
METHODS: Thirty-three healthy male amateur runners aged ≥50 (mean age: 57 ±7 years) were enrolled in the study. Venous blood samples were obtained before the marathon, just after the race, and 2-4 days and 7 days after the marathon. Using novel single molecule counting (SMC) technology, we measured plasma concentrations of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). White blood cell (WBC) count was measured using a certified hematology analyzer. The results were related to previous analyses on cardiovascular stress and endothelial function biomarkers. Transthoracic echocardiography (TTE) and cardiac magnetic resonance (CMR) were used to determine myocardial function.
RESULTS: We observed a sharp rise of all studied biomarkers after the race, which subsequently normalized after 2-4 days and stayed within the normal range 7 days after the race. We found no correlation between inflammatory and cardiovascular stress biomarkers. Transthoracic echocardiography and CMR did not show ischemic or inflammatory myocardial damage.
CONCLUSIONS: Marathon running is associated with a sharp and significant rise in inflammatory and cardiovascular stress biomarkers. We found no connection between immune activation and cardiac biomarker release. Cardiovascular imaging showed no myocardial damage due to ischemia or inflammation.
摘要：
背景：马拉松中年爱好者的心血管安全性尚不清楚。我们先前假设心肌肌钙蛋白I（cTnI）和N末端B型利钠肽前体（NT-proBNP）的瞬时释放，除了对运动的急性炎症反应，可能是原因。
目的：为了评估马拉松对炎症生物标志物的影响，以及它对心血管功能的影响。
方法：33名年龄≥50岁（平均年龄：57±7岁）的健康男性业余跑步者被纳入研究。在马拉松比赛前采集静脉血样本,比赛刚结束,以及马拉松后2-4天和7天。采用新型单分子计数(SMC)技术,我们测量了白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的血浆浓度。使用经认证的血液学分析仪测量白细胞(WBC)计数。结果与先前对心血管压力和内皮功能生物标志物的分析有关。经胸超声心动图（TTE）和心脏磁共振（CMR）用于确定心肌功能。
结果：我们观察到所有研究的生物标志物在比赛后急剧上升，随后在2-4天后恢复正常，并在比赛后7天保持在正常范围内。我们发现炎症和心血管应激生物标志物之间没有相关性。经胸超声心动图和CMR未显示缺血性或炎性心肌损害。
结论：马拉松跑步与炎症和心血管应激生物标志物的急剧和显著升高相关。我们发现免疫激活和心脏生物标志物释放之间没有联系。心血管成像显示没有因缺血或炎症引起的心肌损伤。
目的：为了评估马拉松对炎症生物标志物的影响，以及它对心血管功能的影响。
方法：33名年龄≥50岁（平均年龄：57±7岁）的健康男性业余跑步者被纳入研究。在马拉松比赛前采集静脉血样本,比赛刚结束,以及马拉松后2-4天和7天。采用新型单分子计数(SMC)技术,我们测量了白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的血浆浓度。使用经认证的血液学分析仪测量白细胞(WBC)计数。结果与先前对心血管压力和内皮功能生物标志物的分析有关。经胸超声心动图（TTE）和心脏磁共振（CMR）用于确定心肌功能。
结果：我们观察到所有研究的生物标志物在比赛后急剧上升，随后在2-4天后恢复正常，并在比赛后7天保持在正常范围内。我们发现炎症和心血管应激生物标志物之间没有相关性。经胸超声心动图和CMR未显示缺血性或炎性心肌损害。
结论：马拉松跑步与炎症和心血管应激生物标志物的急剧和显著升高相关。我们发现免疫激活和心脏生物标志物释放之间没有联系。心血管成像显示没有因缺血或炎症引起的心肌损伤。
