72-h Kinetics of High-Sensitive Troponin T and Inflammatory Markers after Marathon
72-h Kinetics of High-Sensitive Troponin T and Inflammatory Markers after Marathon
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DOI：
10.1249/mss.0b013e31821b12eb
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发表时间：
2011-10-01
影响因子：
4.1
通讯作者：
Halle, Martin
中科院分区：
文献类型：
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作者：
Scherr, Johannes;Braun, Siegmund;Halle, Martin
谢尔，J.，S. T·布劳恩舒斯特角哈特曼B.莫伦坎普沃尔法特和M.哈尔。马拉松后高敏肌钙蛋白T和炎症标志物的72小时动力学。医学科学体育锻炼：第43卷，第10期，第110页。1819-1827年，2011年。简介：剧烈运动导致心脏生物标志物显著增加。然而，目前尚不清楚这是由心肌细胞坏死或继发机制，如缺血，心脏能量不足，炎症增加，或肾功能不全。研究方法：因此，我们研究了心脏生物标志物，（高敏心肌肌钙蛋白T（hs-cTnT）、N末端脑钠肽前体（NT-proBNP）、心脏型脂肪酸结合蛋白（h-FABP））、炎症标志物（高敏C反应蛋白（hs-CRP）、白细胞介素-6（IL-6）、白细胞介素-10、肿瘤坏死因子-α），102名42 +/- 9岁健康男性在马拉松前、后0、24和72小时的肾功能（胱抑素C）。结果如下：hs-cTnT的动力学显示，比赛后（V3）立即出现峰值，在72 h内（V5）迅速降至试验前值（V3时中位数（四分位距）= 31.07（19.25-46.86）ng.L-1，V5时为3.61（3.20-6.70）ng.L-1，P < 0.001）。NT-proBNP和h-FABP的动力学表现出相似的模式（V3和34.9时NT-proBNP = 92.6（56.9-149.7）ng.L-1（21.7-54.5）ng.L-1（V5）; h-FABP = 44.99（32.19-64.42）μ g.L-1（V3）和7.66（5.64-10.60）μ g.L-1（V5）;始终P < 0.001）。促炎标志物，如IL-6和hs-CRP，和肾功能不全在比赛后立即显著增加（比赛前与比赛后最大值相比：IL-6 = 15.5倍，hs-CRP = 28倍，胱抑素C = 1.22倍，所有P < 0.001）。这些升高与hs-cTnT升高无关。同样，训练史、完成时间和运动强度与hs-cTnT的变化无关。结论：心脏生物标志物在马拉松比赛后立即增加。有趣的是，数值在72小时内恢复到正常水平。这些具有尖峰的动力学表明，在马拉松跑步过程中心肌坏死似乎不太可能，但可能是由肌细胞代谢的改变来解释的。
SCHERR, J., S. BRAUN, T. SCHUSTER, C. HARTMANN, S. MOEHLENKAMP, B. WOLFARTH, A. PRESSLER, and M. HALLE. 72-h Kinetics of High-Sensitive Troponin T and Inflammatory Markers after Marathon. Med. Sci. Sports Exerc., Vol. 43, No. 10, pp. 1819-1827, 2011. Introduction: Strenuous exercise induces significant increases in cardiac biomarkers. However, it is still unclear whether this is caused by cardiomyocyte necrosis or secondary mechanisms such as ischemia, cardiac energy deficiency, increased inflammation, or renal dysfunction. Methods: Therefore, we investigated cardiac biomarkers (high-sensitive cardiac troponin T (hs-cTnT), N-terminal pro-brain natriuretic peptide (NT-proBNP), heart-type fatty acid-binding protein (h-FABP)), inflammation markers (high-sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), interleukin-10, tumor necrosis factor-alpha), and renal function (cystatin C) in 102 healthy men age 42 +/- 9 yr before and 0, 24, and 72 h after a marathon. Results: Kinetics of hs-cTnT revealed a peak immediately after the race (V3) that decreased rapidly to pretest values within 72 h (V5) (median (interquartile range) = 31.07 (19.25-46.86) ng.L-1 at V3 and 3.61 (3.20-6.70) ng.L-1 at V5, P < 0.001). NT-proBNP and h-FABP kinetics showed a similar pattern (NT-proBNP = 92.6 (56.9-149.7) ng.L-1 at V3 and 34.9 (21.7-54.5) ng.L-1 at V5; h-FABP = 44.99 (32.19-64.42) mu g.L-1 at V3 and 7.66 (5.64-10.60) mu g.L-1 at V5; always P < 0.001). Proinflammatory markers, such as IL-6 and hs-CRP, and renal dysfunction were significantly augmented immediately after the race (before the race compared with maximum after the race: IL-6 = 15.5-fold, hs-CRP = 28-fold, cystatin C = 1.22-fold, all P < 0.001). These increases were not related to the increase of hs-cTnT. Similarly, training history, finishing time, and exercise intensity were not associated with changes of hs-cTnT. Conclusions: Cardiac biomarkers were increased immediately after a marathon race. Interestingly, values returned to normal levels within 72 h. These kinetics with a sharp peak indicate that cardiac necrosis during marathon running seems very unlikely but may be explained by altered myocyte metabolism.