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Alterations in the Coagulation and Fibrinolytic Systems following an Ultra‐marathon

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The aim of this study was to examine coagulation and fibrinolytic responses in runners competing in the Western States Endurance Run (WSER, June 23 to 24, 2012). The WSER is a 160‐km trail foot race through the Sierra Nevada Mountains that involves 15,540 ft of climb and 22,970 ft of descent. We examined 12 men and 4 women (mean±SE, age 44.6±3.0 y), who completed the race (24.64±1.07 hrs). 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 hr, and 75 – 78 hr from the start of the race, respectively). Muscle damage was assessed by serum creatine kinase (CK) and myoglobin. Hypercoagulable state was characterized by prothrombin fragment 1+2 (PTF 1+2) and thrombin‐antithrombin complex. Fibrinolytic state was assessed by plasminogen activator inhibitor antigen (PAI‐1 Ag), tissue plasminogen activator antigen (tPA Ag), and D‐Dimer. Significant increases were measured immediate post‐race for thrombin generation markers, PTF 1+2 and TAT; markers of fibrinolysis, tPA Ag, PAI‐1 Ag, and D‐Dimer; muscle damage markers, CK and myoglobin. Most markers returned to baseline levels at D1, except for PTF 1+2 and D‐Dimer. Muscle damage markers, CK and myoglobin; also continued to be elevated at D1 and D2 time points. In spite of these increases, no clinical evidence of vascular occlusion was observed following the race. In conclusion, the WSER produced extensive muscle damage and activated both the coagulation and fibrinolytic systems. Moreover, these systems are in balance thus limiting the potential of a thrombotic episode.
Title: Alterations in the Coagulation and Fibrinolytic Systems following an Ultra‐marathon
Description:
The aim of this study was to examine coagulation and fibrinolytic responses in runners competing in the Western States Endurance Run (WSER, June 23 to 24, 2012).
The WSER is a 160‐km trail foot race through the Sierra Nevada Mountains that involves 15,540 ft of climb and 22,970 ft of descent.
We examined 12 men and 4 women (mean±SE, age 44.
6±3.
0 y), who completed the race (24.
64±1.
07 hrs).
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 hr, and 75 – 78 hr from the start of the race, respectively).
Muscle damage was assessed by serum creatine kinase (CK) and myoglobin.
Hypercoagulable state was characterized by prothrombin fragment 1+2 (PTF 1+2) and thrombin‐antithrombin complex.
Fibrinolytic state was assessed by plasminogen activator inhibitor antigen (PAI‐1 Ag), tissue plasminogen activator antigen (tPA Ag), and D‐Dimer.
Significant increases were measured immediate post‐race for thrombin generation markers, PTF 1+2 and TAT; markers of fibrinolysis, tPA Ag, PAI‐1 Ag, and D‐Dimer; muscle damage markers, CK and myoglobin.
Most markers returned to baseline levels at D1, except for PTF 1+2 and D‐Dimer.
Muscle damage markers, CK and myoglobin; also continued to be elevated at D1 and D2 time points.
In spite of these increases, no clinical evidence of vascular occlusion was observed following the race.
In conclusion, the WSER produced extensive muscle damage and activated both the coagulation and fibrinolytic systems.
Moreover, these systems are in balance thus limiting the potential of a thrombotic episode.

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