Effect of One Session of Physical Activity on Cardiac Troponin T and Free Fatty Acids

Although regular and moderate exercise reduces cardiovascular risk, recent studies have shown an increase in biomarkers compatible with heart damage (e.g., cardiac troponin T after prolonged periods of exercise in healthy individuals without cardiovascular disease) (1–3). Studies show that strenuous physical activity may cause acute cardiovascular and hemodynamic stress, which can be assessed through necrosis of myocytes and myocardial infarction. Research shows that exercise is an effective factor in changing the levels of indicators Heart damage includes cardiac troponin T.Prolonged exercise is associated with an acute increase in cardiac biomarkers. Cardiac troponin T is a very specific marker of myocardial damage. Which is released from the myocardium during different periods of stress and heart damage(9). Cardiac troponin I and cardiac troponin T are proteins present in the contractile system of heart cells and are very sensitive and specific indicators of cardiac cell necrosis.As a result, these indicators are a good tool for assessing the potential damage to heart muscle cells in athletes. Prolonged exercise also leads to increased plasma free fatty acid concentrations(10). The aim of this study was to explain Effect of physical activityon cardiac troponin T and free fatty acids.

20 professional Sky Running athletes with an average age of 27-37 years from Tehran participated in this competition voluntarily and purposefully. The race was held in the valleys of Central Alborz, the total distance traveled was 21 km and 200 m, the starting point was 1650 m above sea level and the maximum altitude was 3150 m. 5 ml of blood was taken from the subjects 30 minutes before the start of the race. Immediately after the race and 1 hour later, 5 ml of blood was taken from the subjects again. To isolate serum after blood sampling, blood was poured into sterile test tubes labeled with each sample that did not contain any anticoagulants and incubated at room temperature for 60 minutes. They were then centrifuged at 2000 rpm for 20 minutes. The clear supernatant (serum) was carefully separated by a sampler 1000 so that it did not mix with the red blood cells, and the serum was kept at -80 ° C until the experiment was performed. Cardiac troponin T was injected by ELISA with a high-sensitive kit with1.56 ng / L sensitivity of Zellbio brand made in Germany and free fatty acids were measured by colorimetric method with a hypersensitive kit with a sensitivity of 5 µmol/ L by Zellbio brand made in Germany. Correlated t-test at the significance level of 0.05 alpha was used to evaluate the changes in the studied variables.

The amount of cardiac troponin T immediately after and one hour after the end of the race increased significantly compared to before the race (P <0.05). The amount of free fatty acids immediately and one hour after the end of the race increases significantly compared to before the race (P <0.05).

The results of this study showed that immediately and 1 hour after the end of the Sky Running competition, the amount of cardiac troponin T increased significantly. These changes identified in our study are in accordance with the results of previous studies performed in athletes completing endurance competitions. Richardson et al. reported an increase in cardiac troponin T after the marathon, stating that an increase in cardiac troponin T was related to exercise intensity associated with ventilation threshold and maximal oxygen consumption, but it has nothing to do with a person's cardiovascular fitness, training status or exercise history(16). Similarly, Dapont et al. reported that cardiac troponin I was elevated in all marathon runners(17). Lagzaras et al. showed an increase in troponin levels in all participants in the triple race (18).While Kim et al. Moreover, Park et al. Did not observe a significant increase in cardiac troponin T after prolonged exercise(19,20). Physiological mechanisms of cardiac biomarker enhancement associated with endurance activities include increased permeability of the cardiomyocyte membrane, which causes the release of cardiac troponin T in the cytosol on a concentration gradient from intracellular to extracellular. The initial peak represents the release of cardiac troponin T through the sarcolemma membrane, the level of which decreases after 24 hours and reflects the half-life and subsequent clearance of cardiac troponin T subunits. It has been suggested that mechanical or oxidative stress through Transient disorder (wounding) of sarcolemma may be responsible for this increase in membrane permeability and increase troponin secretion(21).Therefore; it seems that the increase in troponin following exercise may be a reflection of the adaptation of cellular cascades seen in exercise-induced remodeling and cardiac hypertrophy. Another result observed in the present study was a significant increase in free fatty acids immediately and 1 hour after the race compared to before the race. Which was in line with previous studies in this field. Vincent et al. 2020 showed that long-term high-intensity exercise could deplete the heart fat basin(24). Waskiwisk et al. 2011 showed that prolonged exercise significantly increased free fatty acids immediately, 12 and 24 hours after competition(35). Pak and Walk 2019 showed that cardiac troponin T did not change significantly, but free fatty acids immediately after Completion of triple and triple ultra competitions increased significantly(20). Bilt et al. 2011 showed that a 2-hour cycle of fasting cycling in 11 men untrain, tripled plasma free fatty acid concentrations while increasing cardiac lipid content, but did not impair systolic function(36). Elevated cardiac troponin T and elevated free fatty acids can indicate a degree of "cardiac fatigue." Increased free fatty acids after competition and long-term exercise appear to play an important role in reducing cardiac inotropic.Due to the multifaceted nature of heart fatigue, two main hypotheses have been proposed: A reversible process of heart damage is often referred to as “stunning “; Myocardial injury can underlie left ventricular diastolic and systolic dysfunction; transient ischemia has a mechanism similar to cardiac fatigue, and can lead to a process called stunning, stunning theory because it leads to necrosis or injury.It does not become a permanent cell, it has a transient nature.It is called cardiac beta-adrenergic receptor desensitization. A wide range of studies have identified biomarkers of increased heart damage after prolonged exercise and have linked them to functional changes(29–32). Increased catecholamine concentrations, increased plasma free fatty acids, and accumulation of oxygen free radicals may lead to decreased blood flow to the heart through increased vascular tone and endothelial dysfunction(33). Physical activity increase heart injury biomarkers in professional athletes. Elevated cardiac troponin T and elevated free fatty acids can indicate a degree of "cardiac fatigue". Increased free fatty acids after competition and long-term exercise appear to play an important role in reducing cardiac inotropic.