Thrombosis refers to the formation of a blood clot (thrombus) within a blood vessel, obstructing the normal flow of blood [23]. Blood clotting is a natural process that helps prevent excessive bleeding when an injury occurs. However, when a clot forms within a blood vessel without a clear cause, it can lead to serious health complications. There are two main types of thrombosis: arterial and venous. Arterial occurs when a blood clot forms in an artery
and may lead to severe conditions such as heart attack, stroke, or peripheral arterial disease [24, 25]. Venous thrombosis on the other hand occurs in veins, in deep veins (deep vein thrombosis or DVT) or in superficial veins close to the skin's surface (superficial thrombophlebitis) [26, 27]. If a clot in the deep veins dislodges and travels to the lungs, it can cause a life-threatening condition called pulmonary embolism [28].
Several factors can contribute to the development of thrombosis, such as: prolonged immobility [29, 30], trauma or injury [31, 32], surgery [33], genetics factors [34, 35, 36] as well as hormonal changes [37, 38] and certain medical conditions e.g., cancer, heart disease or obesity [39, 40, 41]. Thrombosis can occur also in athletes, although they are generally considered to have a lower risk of thrombosis due to their active lifestyle and better cardiovascular health. However, certain factors and circumstances can increase the risk of thrombosis in this group (Fig. 2). The most common among them are dehydration, intense effort and trauma or injury (Fig. 2) [42]. Dehydration occurs during intense physical activity and makes the blood more likely to form clots [43, 44, 45]. Similarly to dehydration, trauma or injury can trigger clotting mechanisms, leading to thrombosis [46]. Overtraining of the body, on the other hand may lead to myocardial damage, which is additional risk factor for thrombosis [47]. Myocardial damage can be manifested by a heart attack or cardiac arrest, what may result in embolism and ischemia of internal organs [49, 50]. The degree of heart muscle damage is determined on the basis of the H-FABP level, considered as a cardiac damage marker [51]. H-FABP is found in the heart muscle cells and is released into bloodstream when there is injury or acute myocardial infarction (AMI) [52]. H-FABP is released earlier than other cardiac markers [53]. It is particularly valuable in situations such as the early hours of a heart attack, when there is a delay in other cardiac marker elevation e.g., troponin [54]. In our study, we observed that in both cases before (2.75 ± 1.32 ng/mL vs. 4.14 ± 1.30 ng/mL, p < 0.01) and after training (2.75 ± 1.32 ng/mL vs. 3.94 ± 1.47ng/mL, p < 0.01) the amount of H-FABP is higher in athletes when compared to the control group. These results confirm that athletes in our experimental group were at greater risk of cardiac microtrauma when we compared them to the control group, which doesn’t practice sport professionally. Myocardial damage is a common phenomen in sportspeople, particularly in those engaged in intense training. It is often referred to as exercise-induced cardiac injury [55]. Myocardial damage in athletes may occur for several reasons. The first one is a long-term stress associated with high-intensity exercise, which increases workload and may lead to the structural changes in the heart muscle, including myocardial damage [56]. Another one is a coronary artery issue, intense trainings can contribute to the development of coronary artery disease, potentially leading to myocardial damage [57]. Genetic factors can also be involved, and some athletes may have underlying genetic predisposition to cardiac issues e.g. arrhythmias [58]. Performance-enhancing substances, such as anabolic steroids may have detrimental effects on the heart [59]. Last but not least, dehydration and what follows electrolyte imbalance, inadequate fluid intake can place additional stress on the heart [60]. In reference to above, appropriate training, monitoring workload and allowing sufficient recovery periods are crucial for athletes to avoid a possible myocardial damages, which in turn may lead to thrombosis. Also, H-FABP level as a cardiac marker should be checked routinely in athletes.
Beside tissue damage parameters, such as H-FABP, in diagnosis and prevention of thrombosis blood clotting parameters are the most important, among them: prothrombin time (PT), activated partial thromboplastin clotting time (APTT), thrombin time (TT), fibrinogen (Fb) and international normalized ratio (INR) [61, 62]. PT primarily evaluates the activity of clotting factors in the extrinsic pathway, including fibrinogen, prothrombin and factors V, VII, X. The results are provided as the INR, that helps for standardized interpretation [63]. APTT, on the other hand evaluates the activity of clotting factors in intrinsic pathway, including fibrinogen, prothrombin, V, VIII, IX, X, XI and XII factors. The APTT is commonly used to monitor the effectiveness of heparin therapy [64]. For patients with prolonged PT and APTT, TT is additionally determined. It is a coagulation test that detects abnormalities in the conversion of fibrinogen to fibrin [6]. Fibrinogen (Fb) is a glycoprotein produced in the liver [6]. It is a key factor in the blood clotting process. After its cleavage by thrombin, fibrin is formed as the main component of the clot [6]. Fluctuations in fibrinogen levels may be related to its accelerated production as well as slowed down degradation. Typically, an elevated value indicates an acute phase effect, endothelial damage, or activation of fibrinolysis. Its level also increases in the case of atherosclerosis and in the elderly. Low fibrinogen values are often observed in athletes [7]. Overall conclusion from our study is that the studied athletes display adverse results regarding blood clotting parameters after training when compared to control group or to the results before the training. We observed a significant difference in PT, INR, APTT, Fb and TT levels before and after training. After the training, all parameters were elevated in relation to the values measured before the exercise (Fig. 1). Interestingly before the training PT and APTT levels were lower in athletes when compared to control group (p = 0.06 and p < 0.01 respectively). After the physical effort of training the values of PT, INR and TT increased in the sportsmen group (p = 0.02, p = 0.02 and p < 0.01 respectively, Fig. 1.). In connection with the above results we assume that similarly to the myocardial damages, certain factors associated with intense or endurance exercise can lead to temporary changes in clotting parameters, which may result in thrombosis. In addition to the factors already mentioned as dehydration, performance-enhancing substances or genetic factors, that may contribute the elevated clotting parameters in athletes, we should also add exercise-induced muscle damage and environmental factors. Exercise-induced muscle damage, causes the release of substances that promote blood clotting, such as coagulation and fibrinolytic factors. Hemostatic system activation, manifesting by temporary elevation of clotting parameters is a normal body’s response to injury and healing process [69, 70, 71]. Environmental factors on the other hand include e.g., high altitude or extreme cold, since such conditions can affect blood clotting parameters [68]. An interesting aspect in the occurrence of thrombosis in athletes is traveling long distances. It is commonly referred to as travel-related thrombosis or economy class syndrome [65]. Deep vein thrombosis (DVT) can be caused by prolonged periods of sitting e.g., long flights or bus rides. Immobility can lead to slower blood flow, potentially causing blood clots to form in the deep veins of the legs [66]. Typical symptoms that athletes experience during DVT are: leg pain, swelling, redness, tenderness as well as warmth. However, DVT may also occur asymptomatic [48]. Another factor, examined in our study is the activity of HMGCR: 3-hydroxy-3-methylglutaryl-coenzyme A reductase. This enzyme is involved in the mevalonate pathway, responsible for the synthesis of cholesterol. It plays a critical role in the production of cholesterol in the liver [67]. The level of HMGCR in tested group of athletes was, independently from exercise, always significantly lower when compared to the control group (p < 0.01). This indicates a positive effect of training on the appropriate level of cholesterol, regardless of the degree of exercise intensity.