Blood coagulation activation and fibrinolysis during a downhill marathon run.

Prolonged physical exercise is associated with multiple changes in blood hemostasis. Eccentric muscle activation induces microtrauma of skeletal muscles, inducing an inflammatory response. Since there is a link between inflammation and coagulation we speculated that downhill running strongly activates the coagulation system. Thirteen volunteers participated in the Tyrolean Speed Marathon (42,195 m downhill race, 795 m vertical distance). Venous blood was collected 3 days (T1) and 3 h (T2) before the run, within 30 min after finishing (T3) and 1 day thereafter (T4). We measured the following key parameters: creatine kinase, myoglobin, thrombin-antithrombin complex, prothrombin fragment F1 + 2, D-dimer, plasmin-alpha(2)-antiplasmin complexes, tissue-type plasminogen activator antigen, plasminogen-activator-inhibitor-1 antigen and thrombelastography with ROTEM [intrinsic pathway (InTEM) clotting time, clot formation time, maximum clot firmness, alpha angle]. Thrombin generation was evaluated by the Thrombin Dynamic Test and the Technothrombin TGA test. Creatine kinase and myoglobin were elevated at T3 and further increased at T4. Thrombin-antithrombin complex, prothrombin fragment F1 + 2, D-dimer, plasmin-alpha(2)-antiplasmin complexes, tissue-type plasminogen activator antigen and plasminogen-activator-inhibitor-1 antigen were significantly increased at T3. ROTEM analysis exhibited a shortening of InTEM clotting time and clot formation time after the marathon, and an increase in InTEM maximum clot firmness and alpha angle. Changes in TGA were indicative for thrombin generation after the marathon. We demonstrated that a downhill marathon induces an activation of coagulation, as measured by specific parameters for coagulation, ROTEM and thrombin generation assays. These changes were paralleled by an activation of fibrinolysis indicating a preserved hemostatic balance.

Austrian Moderate Altitude Study (AMAS 2000): erythropoietic activity and Hb-O(2) affinity during a 3-week hiking holiday at moderate altitude in persons with metabolic syndrome.

Moderate altitude hypoxia (1500 to 2500 m) is known to stimulate erythropoiesis and to improve oxygen transport to tissue by a reduction of Hb-O(2) affinity. Whether this adaptation also occurs in tourists with metabolic syndrome has not yet been investigated sufficiently. Thus, we performed a prospective field study to measure erythropoietic parameters and oxygen transport properties in 24 male volunteers with metabolic syndrome during a 3- week holiday program at 1700 m consisting of four guided, individually adapted hiking tours per week. The following examinations were performed: baseline investigations at 500 m (T1); examinations at moderate altitude on day 1 (T2), day 4 (T3), day 9 (T4), and day 19 (T5); and postaltitude tests (T6) 7 to 10 days after return. On day 1 and day 19, a walk on a standardized hiking test route with oxygen saturation (SpO(2)) measure points was performed. Hemoglobin, packed cell volume, and red cell count showed changes over time, with higher values at T5 as compared to baseline. Reticulocyte count and erythropoietin (EPO) were increased at T2 and increased further until T5. EPO declined toward prealtitude values. P50-value (blood PO(2) at 50% hemoglobin oxygen saturation at actual pH) increased during the altitude sojourn (maximum increase at T5 by +0.40 kPa). At T5 all volunteers had a higher SpO(2) before, during, and at the end of the test route compared to T1. During adaptation to moderate altitude, persons with metabolic syndrome exhibit an increase in EPO and a rightward shift of the oxygen dissociation curve that is similar to healthy subjects.

Changes of biochemical markers and functional tests for clot formation during long-haul flights.

INTRODUCTION: Long-haul flights have been suggested to be associated with an increased risk for thromboembolic events. Until now, changes in the coagulation system during an actual flight have not been investigated. MATERIALS AND METHODS: To explore whether any changes occur in the coagulation system during a real long-haul flight molecular markers for coagulation and fibrinolysis were measured in 20 volunteers (10 subjects with a low and 10 with a moderate risk for venous thromboembolism (VTE)) during and after a return flight from Vienna to Washington. In addition, functional measurements of coagulation were performed using activated thrombelastography. RESULTS: Thrombelastographic measurements revealed activation of coagulation in all passengers, who showed an increased activity of FVII and FVIII as well as suppressed fibrinolysis. There was no evidence of a pronounced thrombin and fibrin formation. We did not find any differences between both groups concerning coagulation changes. CONCLUSION: Long-haul flights induce a certain activation of the coagulation system. This activated coagulation could be a risk factor for VTE during long-haul flights mainly when other risk factors are present.

Coagulation changes and edema formation during long-distance bus travel.

Long-distance travel in a cramped position by aircraft or by bus and car has been suggested to be associated with an increased risk for thromboembolic events. Recently, we demonstrated moderate activation of coagulation after a long-haul flight. At present the single contributing factors (i.e. hypoxia and low humidity on board an aircraft and prolonged sitting in an aircraft, car or bus inducing venous stasis) have not yet been investigated. Therefore we measured markers of coagulation and fibrinolysis as well as functional parameters of coagulation using activated thrombelastography in 19 healthy volunteers before, during and after a real 10-h bus journey. In addition, changes in leg volume were measured. Thrombelastography revealed moderate activation of coagulation in all travelers, which was accompanied by a significant increase in prothrombin fragment F1 + 2. Thrombin-antithrombin III complexes and D-dimer remained unchanged, and tissue-type plasminogen activator and plasminogen-activator inhibitor 1 decreased after travel. After the travel we found a significant increase in leg volume that was exclusively distributed in the calf. We conclude that beside long-haul flights also long-distance bus travel induces a certain activation of the coagulation system. Thus, it is questionable whether hypoxia is the crucial risk factor for thromboembolic events after long-haul flights.

Formation of edema and fluid shifts during a long-haul flight.

BACKGROUND: More than 1.5 billion passengers travel by aircraft every year. Leg edema, as a sign of venous stasis, is a well-known problem among passengers during and after long-haul flights. Until now, no studies have been done on the development of leg edema and fluid shifts under real flight conditions. The aim of our study was to evaluate edema formation in the leg and to investigate possible fluid shifts to the interstitial space under real flight conditions. METHODS: Twenty participants, 10 without risk and 10 with moderate risk for venous thrombosis, were selected. They flew from Vienna to Washington, flight time 9 h, and returned 2 days later. Investigations were done 48 h before the flight, between the fifth and eighth flight hour on board to Washington and back to Vienna, immediately after arrival in Vienna, and 1 and 3 days after arrival. Plethysmographic measurements were carried out using an optoelectronic scanner system (Perometer). Thickness of the skin was measured at the forehead and in front of the tibia. RESULTS: There were no differences in all measurements between both groups. The volume of the leg increased from 8242 +/- 1420 mL to 8496 +/- 1474 mL after the flight (p <.001). Volume accumulation was distributed to the lower leg as well as to the thigh. Skin thickness in front of the tibia increased significantly during the flight (p <.05), and remained elevated 1 day after arrival. CONCLUSION: We have demonstrated that long-haul flights induce significant fluid accumulation in the lower extremity, involving the lower leg and thigh. This increase in tissue thickness was maintained for some days after the flights.

Travel-related thromboembolism: mechanisms and avoidance.

Evidence regarding the existence of travel-related venous thrombosis and pulmonary embolism is building. Research suggests that travel of all kinds increases the risk by two- to four-fold. Risks are not restricted to air travel alone. For travelers without any known risk factors, the risk of experiencing venous thromboembolism is likely to be very low. However, risks increase significantly in the presence of known risk factors, such as age over 60 years, thrombophilic disorders, varicose veins, history of thromboembolism, obesity, women taking oral contraceptives and travel duration over 12 h. A combination of one or more of these risk factors raises the probability of developing travel-related thromboembolism. Possible contributing factors, such as cramped sitting (with suppressed leg venous flow), moderate hypoxia, low humidity in the aircraft and dehydration, are discussed. Depending on the risk profile of individuals, the use of graduated compression stockings and/or pharmacological interventions (low-molecular-weight heparins are preferred) may be recommended.