Cardiac Biomarkers and Autoantibodies in Endurance Athletes: Potential Similarities with Arrhythmogenic Cardiomyopathy Pathogenic Mechanisms

Abstract

The “Extreme Exercise Hypothesis” states that when individuals perform training beyond the ideal exercise dose, a decline in the beneficial effects of physical activity occurs. This is due to significant changes in myocardial structure and function, such as hemodynamic alterations, cardiac chamber enlargement and hypertrophy, myocardial inflammation, oxidative stress, fibrosis, and conduction changes. In addition, an increased amount of circulating biomarkers of exercise-induced damage has been reported. Although these changes are often reversible, long-lasting cardiac damage may develop after years of intense physical exercise. Since several features of the athlete’s heart overlap with arrhythmogenic cardiomyopathy (ACM), the syndrome of “exercise-induced ACM” has been postulated. Thus, the distinction between ACM and the athlete’s heart may be challenging. Recently, an autoimmune mechanism has been discovered in ACM patients linked to their characteristic junctional impairment. Since cardiac junctions are similarly impaired by intense physical activity due to the strong myocardial stretching, we propose in the present work the novel hypothesis of an autoimmune response in endurance athletes. This investigation may deepen the knowledge about the pathological remodeling and relative activated mechanisms induced by intense endurance exercise, potentially improving the early recognition of whom is actually at risk.

Inherited and Acquired Rhythm Disturbances in Sick Sinus Syndrome, Brugada Syndrome, and Atrial Fibrillation: Lessons from Preclinical Modeling

“…They show variable manifestations, which render often unpredictable the prognosis definition and the anticipation of adverse events. Congenital diseases may eventually manifest during adulthood in response to specific stresses, remaining undiscovered until a dramatic or fatal episode occurs, even in agonistic athletes routinely submitted to ECG to practice [102][103][104][105][106][107][108][109][110][111]. Acquired rhythm pathologies might be induced by several causes, among which drug cardiotoxicity, cardiomyopathies, myocarditis or systemic infections, valve diseases, and interventional/surgical maldeployment of cardiac valve replacements [112][113][114][115][116][117][118][119][120][121][122][123][124][125][126][127][128].…”

Inflammation in the Pathogenesis of Arrhythmogenic Cardiomyopathy: Secondary Event or Active Driver?

“…The next challenge is to translate all the results in the field of exercise to the clinics. In particular it will be necessary to better clarify the definition of "intense/strenuous exercise" in patients, to be able to provide clear, and maybe patient-tailored, recommendation to balance between a good quality of life and the risk of sudden cardiac death (137,138).…”

Beyond the Finish Line: The Impact and Dynamics of Biomarkers in Physical Exercise—A Narrative Review

“…Previous data showed that cardiac biomarkers such as troponins or natriuretic peptides are increased after prolonged and/or intense physical exercise, usually followed by a normalization of their serum levels within the next 24–72 h [ 86 ]. In the case of persistently elevated biomarkers in athletes, multiple mechanisms are incriminated, such as myocardial hypertrophy with subsequent fibrosis, chamber enlargement, oxidative stress or myocardial inflammation [ 87 ].…”