Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs, CT, USA,
Eur J Appl Physiol. 2013 Nov;113(11):2705-12. doi: 10.1007/s00421-013-2709-5. Epub 2013 Aug 22.
The aim of this study was to examine coagulatory and fibrinolytic responses to the Western States Endurance Run (WSER, June 23 to 24, 2012). The WSER is a 161-km (100 mile) trail foot race through the Sierra Nevada Mountains that involves 6,030 m of climb and 7,001 m of descent.
We examined 12 men and 4 women [mean (95 % CI), age 44.6 years (38.7-50.6)] who completed the race (24.64 h; range 16.89-29.46). Blood samples were collected the morning before the race, immediately post-race, and 1 (D1) and 2 (D2) days post-race (corresponding to 51-54 h and 75-78 h from the start of the race, respectively). Hypercoagulable state was characterized by prothrombin fragment 1+2 (PTF 1+2) and thrombin-antithrombin complex (TAT). Fibrinolytic state was assessed by plasminogen activator inhibitor antigen (PAI-1 Ag), tissue plasminogen activator antigen (tPA Ag), and D-Dimer. Muscle damage was assessed by serum creatine kinase (CK) and myoglobin concentrations.
Significant (P ≤ 0.05) increases were observed immediately post-race for thrombin generation markers, PTF 1+2 (3.9-fold) and TAT (2.4-fold); markers of fibrinolysis, tPA Ag (4.0-fold), PAI-1 Ag (4.5-fold), and D-Dimer (2.2-fold); and muscle damage markers, CK (154-fold) and myoglobin (114-fold). Most markers continued to be elevated at D1, as seen by PTF 1+2, TAT (1.5- and 1.3-fold increase at D1), and D-Dimer (2.5- and 2.1-fold increase at D1 and D2, respectively). Additionally, PTF 1+2:tPA and TAT:tPA ratios, which assessed balance between coagulation and fibrinolysis, were slightly, but significantly increased at D1 (69 and 36 %) and D2 (19 and 31 %). CK and myoglobin also remained elevated at D1 (54- and 7-fold) and D2 (25- and 2-fold) time points.
The WSER produced extensive muscle damage and activated the coagulation and fibrinolytic systems. Since we observed a slight imbalance response between the two systems, a limited potential for thrombotic episodes is apparent in these highly trained athletes.
本研究旨在探讨西方耐力跑(WSER,2012 年 6 月 23 日至 24 日)对凝血和纤维蛋白溶解反应的影响。WSER 是一项穿越内华达山脉的 161 公里(100 英里)的越野长跑比赛,涉及 6030 米的爬升和 7001 米的下降。
我们检查了 12 名男性和 4 名女性[平均(95%置信区间),年龄 44.6 岁(38.7-50.6)],他们完成了比赛(24.64 小时;范围 16.89-29.46)。在比赛前一天早上、比赛后立即以及比赛后第 1 天(D1)和第 2 天(D2)(分别对应比赛开始后 51-54 小时和 75-78 小时)采集血液样本。高凝状态通过凝血酶原片段 1+2(PTF 1+2)和凝血酶-抗凝血酶复合物(TAT)来描述。纤溶状态通过纤溶酶原激活物抑制剂抗原(PAI-1 Ag)、组织型纤溶酶原激活物抗原(tPA Ag)和 D-二聚体来评估。肌肉损伤通过血清肌酸激酶(CK)和肌红蛋白浓度来评估。
比赛后立即观察到凝血酶生成标志物 PTF 1+2(3.9 倍)和 TAT(2.4 倍);纤溶标志物 tPA Ag(4.0 倍)、PAI-1 Ag(4.5 倍)和 D-二聚体(2.2 倍);以及肌肉损伤标志物 CK(154 倍)和肌红蛋白(114 倍)显著升高(P≤0.05)。大多数标志物在 D1 时仍持续升高,如 PTF 1+2、TAT(D1 时分别增加 1.5 倍和 1.3 倍)和 D-二聚体(D1 和 D2 时分别增加 2.5 倍和 2.1 倍)。此外,凝血和纤溶之间平衡的 PTF 1+2:tPA 和 TAT:tPA 比值在 D1(69%和 36%)和 D2(19%和 31%)时略有但显著升高。CK 和肌红蛋白在 D1(54-和 7 倍)和 D2(25-和 2 倍)时也持续升高。
WSER 导致了广泛的肌肉损伤,并激活了凝血和纤维蛋白溶解系统。由于我们观察到两个系统之间的反应略有失衡,因此在这些训练有素的运动员中,血栓形成事件的潜在风险有限。