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Athlete’s Heart: The cardiac biomarkers that point to damage sustained during endurance training

What is Athlete’s Heart?

In simple terms, this is a syndrome afflicting athlete’s that refers to an increase in cardiac mass due to systematic endurance training. This article will look at the precise manner in which this syndrome develops, considering the most significant implications.

The cardiac biomarkers pointing to damage during endurance training

Sports that require sustained elevations in cardiac work – like marathons, rowing, swimming, cycling – naturally require prolonged/chronic endurance training from their athlete’s. This imposes a higher hemodynamic demand on the heart that alters the loading condition of the heart(1). One may observe structural changes such as enlarged left ventricle and right ventricle volumes, increased left ventricle wall thickness, or higher cardiac mass with increased left atrial size(2-4). Although highly trained athletes tend to adapt to these structural deformations, when these conditions are paired with a preserved left ventricular ejection fraction, they are associated with poor cardiac prognosis in the general population (5). This adaptation that has become typical amongst highly trained athlete’s was aptly named Athlete’s Heart.

The factor of concern regarding this topic is that these structural cardiac adaptations in athletes do not completely regress to normal levels even several years after retirement from competitive strength training for endurance(10).

The most commonly observed structural and functional alterations in the physiology of endurance athletes tend to be in cardiac and renal regions. Serologic markers that are indicators of cardiac damage – like cardiac troponin, creatine kinase MB, and B-type natriuretic peptide –have been documented to be elevated in up to 50% of participants during and after marathons and other extreme endurance activities.

The renal biomarkers pointing to damage

In addition to cardiac damage, transient renal dysfunction has also been correlated with extreme muscular endurance training as it can cause volume depletion and diminished renal filtration, and increased levels of serum urea nitrogen, serum creatinine, and cystatin C. Increased levels of these cardiac biomarkers is an indication of myocardial cell damage in any endurance athlete. However, the significance of the elevated cardiac biomarkers is not 100% certain, and some argue that these may be entirely benign increases resulting from cardiovascular adaptations to long-term endurance training (2-5).

In our article titled ‘Endurance Training: The Best Heart Health Drug There Is?’, we discuss informative  statistics regarding increased cardiac output (2) during endurance training. One should consider these statistics and the fact that some individuals may be prone to developing chronic structural changes over time that occur due to the recurrent volume overload and excessive cardiac strain. (6,7,10) These abnormalities are often asymptomatic and develop over many years, but they might predispose you to serious arrhythmias such as atrial fibrillation and/or ventricular arrhythmias.

References

  1. Middleton N., Shave R., George K. Altered left ventricular diastolic filling following a marathon is a reproducible phenomenon. Int J Cardiol. 2007;122(1):87–89. 
  2. Pelliccia A., Culasso F., Di Paolo F.M., Maron B.J. Physiologic left ventricular cavity dilatation in elite athletes. Ann Intern Med. 1999;130(1):23–31.
  3. Pelliccia A., Maron B.J., Di Paolo F.M. Prevalence and clinical significance of left atrial remodeling in competitive athletes. J Am Coll Cardiol. 2005;46(4):690–696. 
  4. Pelliccia A., Maron B.J., Spataro A., Proschan M.A., Spirito P. The upper limit of physiologic cardiac hypertrophy in highly trained elite athletes. N Engl J Med. 1991;324(5):295–301.
  5. Patel D.A., Lavie C.J., Milani R.V., Ventura H.O. Left atrial volume index predictive of mortality independent of left ventricular geometry in a large clinical cohort with preserved ejection fraction. Mayo Clin Proc. 2011;86(8):730–737.
  6. Pluim B.M., Zwinderman A.H., van der Laarse A., van der Wall E.E. The athlete's heart: a meta-analysis of cardiac structure and function. 2000;101(3):336–344.
  7. Maron B.J., Pelliccia A. The heart of trained athletes: cardiac remodeling and the risks of sports, including sudden death. 2006;114(15):1633–1644.
  8. Spirito P., Pelliccia A., Proschan M.A. Morphology of the ”athlete's heart” assessed by echocardiography in 947 elite athletes representing 27 sports. Am J Cardiol. 1994;74(8):802–806.
  9. Maron B.J. Hypertrophic cardiomyopathy and other causes of sudden cardiac death in young competitive athletes, with considerations for preparticipation screening and criteria for disqualification. Cardiol Clin. 2007;25(3):399–414. vi.
  10. Maron B.J., Pelliccia A., Spirito P. Cardiac disease in young trained athletes: insights into methods for distinguishing athlete's heart from structural heart disease, with particular emphasis on hypertrophic cardiomyopathy. Circulation. 1995;91(5):1596–1601.