1 Department for Internal Medicine III, Cardiology, Angiology and Intensive Care Medicine, Saarland University, Homburg/Saar, Germany.
2 Department of Neurology, Charité - Universitätsmedizin Berlin, Germany.
Eur J Prev Cardiol. 2018 Feb;25(3):317-324. doi: 10.1177/2047487317744364. Epub 2017 Nov 29.
Background Acute vascular effects of high intensity physical activity are incompletely characterized. Circulating microparticles are cellular markers for vascular activation and damage. Methods Microparticles were analysed in 99 marathon runners (49 ± 6 years, 22% female) of the prospective Berlin Beat of Running study. Blood samples were taken within three days before, immediately after and within two days after the marathon run. Endothelial-derived microparticles were labelled with CD144, CD31 and CD62E, platelet-derived microparticles with CD62P and CD42b, leukocyte-derived microparticles with CD45 and monocyte-derived microparticles with CD14. Results Marathon running induced leukocytosis (5.9 ± 0.1 to 14.8 ± 0.3 10/l, p < 0.0001) and increased platelet counts (239 ± 4.6 to 281 ± 5.9 10/l, p < 0.0001) immediately after the marathon. Blood monocytes increased and lymphocytes decreased after the run ( p < 0.0001). Endothelial-derived microparticles were acutely increased ( p = 0.008) due to a 23% increase of apoptotic endothelial-derived microparticles ( p = 0.007) and returned to baseline within two days after the marathon. Thrombocyte-derived microparticles acutely increased by 38% accompanied by an increase in activated and apoptotic thrombocyte-derived microparticles ( p ≤ 0.0001) each. Both monocyte- and leukocyte-derived microparticles were decreased immediately after marathon run ( p < 0.0001) and remained below baseline until day 2. Troponin T increased from 12 to 32 ng/l ( p < 0.0001) immediately after the run and returned to baseline after two days. Conclusion Circulating apoptotic endothelial- and thrombocyte-derived microparticles increased after marathon running consistent with an acute pro-thrombotic and pro-inflammatory state. Exercise-induced vascular damage reflected by microparticles could indicate potential mechanisms of post-exertional cardiovascular complications. Further studies are warranted to investigate microparticles as markers to identify individuals prone to such complications.
背景 高强度体力活动的急性血管效应尚不完全明确。循环微颗粒是血管激活和损伤的细胞标志物。
方法 在前瞻性柏林跑步研究的 99 名马拉松跑者(49±6 岁,22%为女性)中分析了微颗粒。在马拉松比赛前三天内、比赛后立即和两天内采集血样。用 CD144、CD31 和 CD62E 标记内皮衍生的微颗粒,用 CD62P 和 CD42b 标记血小板衍生的微颗粒,用 CD45 标记白细胞衍生的微颗粒,用 CD14 标记单核细胞衍生的微颗粒。
结果 马拉松比赛后即刻白细胞增多(5.9±0.1 至 14.8±0.3×10 /L,p<0.0001)和血小板计数增加(239±4.6 至 281±5.9×10 /L,p<0.0001)。跑步后血液单核细胞增加,淋巴细胞减少(p<0.0001)。内皮衍生的微颗粒急性增加(p=0.008),凋亡的内皮衍生的微颗粒增加了 23%(p=0.007),并在马拉松赛后两天内恢复到基线。血小板衍生的微颗粒急性增加 38%,同时激活和凋亡的血小板衍生的微颗粒增加(p≤0.0001)。马拉松赛后即刻单核细胞和白细胞衍生的微颗粒减少(p<0.0001),直到第 2 天仍低于基线。肌钙蛋白 T 从 12 增加到 32ng/L(p<0.0001),马拉松赛后即刻增加,并在两天后恢复到基线。
结论 马拉松赛后循环凋亡的内皮和血小板衍生的微颗粒增加,提示急性促血栓和促炎状态。微颗粒反映的运动引起的血管损伤可能表明潜在的运动后心血管并发症的机制。需要进一步研究微颗粒作为识别易发生此类并发症个体的标志物。