Tryfonos Andrea, Cocks Matthew, Browning Nicola, Dawson Ellen A
Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool L3 3AF, UK.
Department of Laboratory Medicine, Division of Clinical Physiology, Karolinska Institutet, Stockholm, Sweden.
Appl Physiol Nutr Metab. 2023 Feb 1;48(2):209-218. doi: 10.1139/apnm-2022-0278. Epub 2022 Dec 3.
Acute exercise can result in temporary decrease in endothelial functions, which may represent a transient period of risk. Numerous mechanisms underpinning these responses included release of extracellular vesicles (EVs) derived from apoptotic or activated endothelial cells and platelets. This study aims to compare the time course of endothelial responses to moderate-intensity continuous exercise (MICE) and high-intensity interval exercise (HIIE) and the associations with EV release. Eighteen young healthy males (age: 22.6 ± 3.7 years, BMI: 25.6 ± 2.5 m/kg, and VO: 38.6 ± 6.5 mL/kg/min) completed two randomly assigned exercises: HIIE (10 × 1 min-@-90% heart rate reserve (HRR) and 1 min passive recovery) and MICE (30 min-@-70% HRR) on a cycle ergometer. Flow-mediated dilation (FMD) was used to assess endothelial function and blood samples were collected to evaluate endothelial cell-derived EV (CD62E) and platelet-derived EV (CD41a), 10, 60, and 120 min before and after exercise. There were similar increases but different time courses ( = 0.017) in FMD (increased 10 min post-HIIE, < 0.0001 and 60 min post-MICE, = 0.038). CD62E remained unchanged ( = 0.530), whereas overall CD41a release was reduced 60 min post-exercise ( = 0.040). FMD was not associated with EV absolute release or change ( > 0.05). Acute exercise resulted in similar improvements, but different time course in FMD following either exercise. Whilst EVs were not associated with FMD, the reduction in platelet-derived EVs may represent a protective mechanism following acute exercise.
急性运动可导致内皮功能暂时下降，这可能代表一个短暂的风险期。支撑这些反应的众多机制包括源自凋亡或活化内皮细胞及血小板的细胞外囊泡（EVs）的释放。本研究旨在比较内皮对中等强度持续运动（MICE）和高强度间歇运动（HIIE）反应的时间进程以及与EV释放的关联。18名年轻健康男性（年龄：22.6±3.7岁，体重指数：25.6±2.5 m/kg，摄氧量：38.6±6.5 mL/kg/min）在功率自行车上完成两项随机分配的运动：HIIE（10×1分钟，运动强度为心率储备（HRR）的90%，随后1分钟被动恢复）和MICE（30分钟，运动强度为HRR的70%）。采用血流介导的血管舒张（FMD）评估内皮功能，并在运动前及运动后10、60和120分钟采集血样，以评估内皮细胞衍生的EV（CD62E）和血小板衍生的EV（CD41a）。FMD有相似的增加但时间进程不同（P = 0.017）（HIIE后10分钟增加，P < 0.0001；MICE后60分钟增加，P = 0.038）。CD62E保持不变（P = 0.530），而运动后60分钟血小板衍生的EV总体释放减少（P = 0.040）。FMD与EV的绝对释放或变化无关（P > 0.05）。急性运动导致FMD有相似的改善，但两种运动后FMD的时间进程不同。虽然EV与FMD无关，但血小板衍生的EV减少可能代表急性运动后的一种保护机制。
