Alterations in coagulatory and fibrinolytic systems following an ultra-marathon

• Published in: European journal of applied physiology 2013-11, Vol.113 (11), p.2705-2712
• Main Authors: Kupchak, Brian R., Volk, Brittanie M., Kunces, Laura J., Kraemer, William J., Hoffman, Martin D., Phinney, Stephen D., Volek, Jeff S.
• Format: Article
• Language: English
• Subjects: Adult; Altitude; Antigens; Biomedical and Life Sciences; Biomedicine; Creatine Kinase - blood; Female; Fibrinolysis; Human Physiology; Humans; Male; Marathons; Middle Aged; Myoglobin - blood; Occupational Medicine/Industrial Medicine; Original Article; Physical Endurance - physiology; Plasminogen Inactivators - blood; Prothrombin - analysis; Running - physiology; Sports Medicine; Thrombin - analysis; Trails; Ultramarathon; Women
• ISSN: 1439-6319; 1439-6327
• DOI: 10.1007/s00421-013-2709-5

Purpose 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. Methods 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. Results 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. Conclusion 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.