University of Glasgow, Division of Cardiovascular and Medical Sciences, Gardiner Institute, Western Infi rmary,Glasgow, UK.
Br J Sports Med. 2010 Jun;44(8):573-8. doi: 10.1136/bjsm.2008.053306.
Physical fitness may confer protection from thrombosis; however, exercise-induced platelet activation may be involved in the triggering of acute vascular events. This study aimed to assess haemostatic responses to acute exercise in trained and sedentary middle-aged subjects.
21 first class Scottish football referees and 15 sedentary controls performed a treadmill exercise test. Blood sampling was performed before, immediately after and 30 minutes post-exercise. Samples were analysed for platelet count, prothrombin time, activated partial thromboplastin time (APTT) and serum fibrinogen. Platelet activation was assessed using flow cytometry with CD62 (P-selectin) and antifibrinogen antibodies at rest and in response to ADP and epinephrine.
Mean maximal oxygen consumption (Vo2) (ml/kg per minute) achieved was 47.23 (5.02) in the referees and 30.1 (5.2) in sedentary controls. Total platelet count (x10(-9)/l) increased immediately post-exercise (228.2 (40.5), 278.6 (48.9) p=0.001) remaining elevated at 30 minutes in both groups. APTT (s) was reduced immediately post-exercise (32.15 (3.1), 29.7 (3.94) p=0.001) with a further reduction seen at 30 minutes (32.15 (3.1), 28.4 (3.31) p=0.001). In the referees, percentage CD62 expression increased immediately post-exercise (0.688 (0.52), 1.42 (1.3) p=0.008). Percentage antifibrinogen expression increased post-exercise (5.19 (4.31), 13.01 (14.24) p=0.017), with a further increase at 30 minutes (5.19 (4.31), 20.47 (26.8) p=0.02). Similar trends were seen in sedentary controls.
This study suggests that in an older athletic population, physical fitness does not protect against the prothrombotic effects of exercise. These data suggest that during a football match when referees achieve approximately 80% of peak VO2 (23) they may be at risk of significant platelet activation. Prophylactic platelet inhibition should be considered in this group after appropriate screening and risk stratification.
身体活动可能有助于预防血栓形成;然而,运动引起的血小板激活可能参与了急性血管事件的触发。本研究旨在评估训练有素和久坐的中年受试者在急性运动后的止血反应。
21 名一级苏格兰足球裁判和 15 名久坐的对照组进行了跑步机运动测试。在运动前、运动后即刻和运动后 30 分钟进行采血。用流式细胞术检测血小板计数、凝血酶原时间、活化部分凝血活酶时间(APTT)和血清纤维蛋白原。在静止状态和响应 ADP 和肾上腺素时,使用 CD62(P-选择素)和抗纤维蛋白原抗体评估血小板活化。
裁判的平均最大耗氧量(Vo2)(ml/kg/min)为 47.23(5.02),久坐对照组为 30.1(5.2)。运动后即刻总血小板计数(x10(-9)/l)升高(228.2(40.5),278.6(48.9),p=0.001),两组均在 30 分钟时仍升高。APTT(s)运动后即刻降低(32.15(3.1),29.7(3.94),p=0.001),30 分钟时进一步降低(32.15(3.1),28.4(3.31),p=0.001)。在裁判中,CD62 表达的百分比在运动后即刻增加(0.688(0.52),1.42(1.3),p=0.008)。运动后抗纤维蛋白原表达的百分比增加(5.19(4.31),13.01(14.24),p=0.017),30 分钟时进一步增加(5.19(4.31),20.47(26.8),p=0.02)。久坐对照组也出现了类似的趋势。
本研究表明,在年龄较大的运动员人群中,身体活动并不能预防运动引起的血栓形成效应。这些数据表明,在足球比赛中,当裁判达到大约 80%的最大摄氧量峰值(23)时,他们可能面临显著的血小板激活风险。在适当的筛查和风险分层后,应考虑在这群人中预防性血小板抑制。