Effect of the “Race Across The Alps” in elite cyclists on plasma cardiac troponins I and T

Prolonged aerobic exercise such as marathon running produces supraphysiological hemodynamic stress that can potentially affect the athlete's cardiac homeostasis. While cardiac structural and functional adaptations in professional athletes are well characterized, only a limited information is available for recreational runners undergoing this supraphysiological stress.

Premarathon and post-marathon echocardiography was performed in 50 recreational marathon runners [age 40.8 ± 7.5 years, 44 (88%) males; running distance 42.195 km]. All the runners received 4-month training for the marathon. The baseline echocardiogram and N-terminal B-type natriuretic peptide (NT-proBNP) were obtained before training, whereas the post-marathon study was performed within 10 days (7.27 ± 0.92 days) of completion of marathon. Two-dimensional speckle-tracking echocardiography was used for characterizing the changes in myocardial mechanics.

There was a significant reduction in heart rate post-marathon, whereas the levels of NT-proBNP increased significantly (86.0 ± 9.5 pg/ml vs 106.5 ± 24.2 pg/ml, p = 0.001). The left ventricular (LV) end-diastolic volume (61.8 ± 16.5 ml vs 72.8 ± 5.1 ml, p < 0.001), LV mass (120.2 ± 30.0 gm vs 160.3 ± 43.0 gm, p < 0.001), and LV ejection fraction (64.9 ± 5.6% vs 72.0 ± 5.7%, p < 0.001) also increased significantly. However, there was a significant attenuation in LV global longitudinal (−19.3 ± 2.71% vs −16.5 ± 4.6%, p = 0.003) and circumferential strain (−17.2 ± 2.41% vs −15.2 ± 2.6%, p = 0.001) post-marathon. The LV global radial strain showed a nonsignificant reduction.

Recreational marathon runners have reduced longitudinal and circumferential shortening of the left ventricle with elevation of NT-proBNP. However, the LV ejection performance remains maintained because of an increase in the LV end-diastolic volume and mass. These changes suggest the possibility of “myocardial fatigue” occurring in response to supraphysiological hemodynamic stress of marathon running.

Cardiac troponins are the preferred biomarkers in diagnostic of myocardial infarction, but these markers also can rise in response to exercise. Multiple studies have assessed troponins post-exercise, but the results have varied and there have been disagreements about the mechanism of troponin release. The aim of this paper was to review the literature, and to consider factors and mechanisms regarding exercise-induced increase of troponin.

145 studies were found after a search in pubmed and inclusion of additional articles found in the reference list of the first articles.

Results showed that troponin rises in 0–100% of subjects after prolonged heavy exercise like marathon, but also after short-term and intermittent exercise like 30 min of running and basketball. The variation can be due to factors like intensity, age, training experience, variation in sample size, blood sample timing and troponin assay.

The pattern of troponin level post-exercise corresponds to release from the cytosolic compartment of cardiomyocytes. Increased membrane permeability might be caused by production of reactive oxygen species or alterations in calcium, pH, glucose/fat metabolism or in communication between integrins. Other suggested mechanisms are increased cardiovascular stress, inflammation, vasculitis, release of troponin degradation products in “blebs”, dehydration, impaired renal clearance and expression of cardiac troponin in skeletal muscle.

It can be concluded that both heavy and light exercise may cause elevated troponin, which have to be considered when patient are suspected to have a myocardial infarction. Several factors probably influence post-exercise levels of troponin, but the mechanism of release is most likely physiologic.

Habitual physical activity and regular exercise training improve cardiovascular health and longevity. A physically active lifestyle is, therefore, a key aspect of primary and secondary prevention strategies. An appropriate volume and intensity are essential to maximally benefit from exercise interventions. This document summarizes available evidence on the relationship between the exercise volume and risk reductions in cardiovascular morbidity and mortality. Furthermore, the risks and benefits of moderate- versus high-intensity exercise interventions are compared. Findings are presented for the general population and cardiac patients eligible for cardiac rehabilitation. Finally, the controversy of excessive volumes of exercise in the athletic population is discussed.

Cardiac troponin I (cTnI) and T (cTnT) are the most important biomarkers in the diagnosis of acute myocardial infarction (AMI). Nevertheless, they can be elevated in the absence of AMI. It is unclear if such elevations represent irreversible cardiomyocyte-damage or leakage from viable cardiomyocytes. Our objective is to evaluate whether cTn is released from viable cardiomyocytes in response to ischemia and to identify differences in the release of cTn and its molecular forms.

HL-1 cardiomyocytes (mouse) were subjected to ischemia (modeled by anoxia with glucose deprivation). The total contents and molecular forms of cTn were determined in culture media and cell lysates. Cell viability was assessed from the release of lactate dehydrogenase (LDH). Before the release of LDH, the intracellular cTn content in ischemic cells decreased significantly compared to control (52% for cTnI; 23% for cTnT) and was not matched by a cTn increase in the medium. cTnI decreased more rapidly than cTnT, resulting in an intracellular cTnT/cTnI ratio of 25.5 after 24 h of ischemia. Western blots revealed changes in the relative amounts of fragmented cTnI and cTnT in ischemic cells.

HL-1 cardiomyocytes subjected to simulated ischemia released cTnI and cTnT only in combination with the release of LDH. We find no evidence of cTn release from viable cardiomyocytes, but did observe a significant decrease in cTn content, before the onset of cell death. Intracellular decrease of cTn in viable cardiomyocytes can have important consequences for the interpretation of cTn values in clinical practice.

The objective of this study was to examine the association between cortisol response to mental stress and high-sensitivity cardiac troponin T (hs-cTnT) in healthy older individuals without history of cardiovascular disease (CVD).

Mental stress is a recognized risk factor for CVD, although the mechanisms remain unclear. Cortisol, a key stress hormone, is associated with coronary atherosclerosis and may accentuate structural and functional cardiac disease.

This cross-sectional study involved 508 disease-free men and women aged 53 to 76 years drawn from the Whitehall II epidemiological cohort. We evaluated salivary cortisol response to standardized mental stress tests (exposure) and hs-cTnT plasma concentration using a high-sensitivity assay (outcome). We measured coronary calcification using electron-beam dual-source computed tomography and Agatston scores.

After adjustment for demographic and clinical variables associated with CVD as well as for inflammatory factors, we found a robust association between cortisol response and detectable hs-cTnT (odds ratio [OR]: 3.98; 95% confidence interval [CI]: 1.60 to 9.92; p = 0.003). The association remained when we restricted the analysis to participants without coronary calcification (n = 222; OR: 4.77; 95% CI: 1.22 to 18.72; p = 0.025) or when we further adjusted for coronary calcification in participants with positive Agatston scores (n = 286; OR: 7.39; 95% CI: 2.22 to 26.24; p = 0.001).

We found that heightened cortisol response to mental stress was associated with detectable plasma levels of cTnT using high-sensitivity assays in healthy participants, independently of coronary atherosclerosis. Further research is needed to understand the role of psychosocial stress in the pathophysiology of cardiac cell damage.

Cardiac troponin increases are common in adult marathon finishers. However, data on troponin values for young marathon runners are scarce. Forty young runners (20 healthy male and 20 female) 13 to 17 years old participated in this study. Blood samples were taken before, immediately after, and 24 hours after the race for determination of cardiac troponin T (cTnT) and troponin I (cTnI). Thirty-seven runners completed the race with a mean finishing time of 4 hours 53 minutes. No participant developed an adverse medical event during or after the race. In 30 of 37 participants, levels of cTnT and/or cTnI exceeded upper reference limits of 0.01 and 0.1 ng/ml immediately after the race, and in 3 participants these levels were even higher than the reference range for acute myocardial infarction (>0.1 and >0.5 ng/ml for cTnT and cTnI, respectively). Twenty-four hours after the race no participant had troponin levels exceeding the upper reference limits. Average increases of troponin levels did not differ between sexes. In conclusion, this is the first study to show that cardiac troponin levels increase to a similar extent in male and female adolescent marathon runners as observed in adults. Rapid recovery of troponin levels after a race is indicative of a physiologic rather than a pathologic response.