Mysteries of the Right Ventricle in Sports and Exercise

The Right Ventricle (RV) and Exercise – Physiological Considerations

Exercise, particularly intense endurance exercise, necessitates substantial increases in cardiac output. For example, the author of this Expert Analysis article has measured cardiac outputs of just under 40 litres/ min in elite cyclists during near-maximal exercise.1 This requires an increase in cardiac work, and the amount of work required of the two ventricles is not necessarily equal. The left ventricle (LV) pumps into a systemic circulation that has significant reserve to decrease resistance and increase compliance during exercise, owing to greatly increased flow through the large vascular bed which supplies the working muscles. In contrast, the RV empties into the pulmonary circulation, which is near maximally perfused at rest, and already has low resistance and high compliance. Thus, there is more limited capacity for the pulmonary circulation to adapt and accommodate exercise blood flow. Put simply, the same cardiac output that is pushed around the entire body must also be pushed through a circulation confined only to the chest – the latter requiring a greater proportionate increase in work. The increase in RV work during exercise has been demonstrated by multiple investigators. Investigators from Boston, Belgium, Italy, and Australia have used echocardiography and invasive measures to consistently demonstrate a near-linear increase of 1-3 mmHg in mean pulmonary arterial pressure (PAP) for every litre increase in cardiac output. In highly trained athletes, this represents a considerable pressure and work load (keeping in mind that ventricular work can be approximated as Pressure x Stroke Volume).2 To assess the relative load on the RV, the authors of this Expert Analysis article compared systolic wall stress in both ventricles during exercise using a combination of resting cardiac magnetic resonance (CMR) and real-time exercise echocardiography, and documented a substantially greater increase in wall stress of the RV as compared with the LV (Figure 1).3

Figure 1: Disproportionately Greater RV Pressures and Wall Stress Give Rise to RV Remodelling

Figure 1
a. During exercise, there is a near linear increase in PAPs during exercise with cardiac output; this relationship is similar for athletes (brown) and non-athletes (green). In healthy subjects, greater exercise capacity predicts higher PAPs, with well-trained athletes generating the highest pressures of all.
b. As compared with the LV, relative increases in wall stress are greater for the RV during intense exercise, the result of which is healthy cardiac remodelling with a very slight RV dominance, which diminishes with de-training. Repeated bouts of excessive and prolonged RV wall stress may result in cumulative RV damage, which may predispose to arrhythmias. The degree to which this adverse remodelling may recover with de-training is unclear.
Reproduced with permission from Heidbuchel H, Prior DL, La Gerche A. Ventricular arrhythmias associated with long-term endurance sports: what is the evidence? Br J Sports Med 2012;46 Suppl 1:i44-50.

Greater RV Remodelling in Athletes

As a result of the excess work and wall stress, the RV undergoes disproportionate structural, functional, and electrical remodelling proportionate to the amount of exercise that is undertaken. This is evident in the general population in which physical activity has been demonstrated to be associated with greater RV mass, independent of the associations with LV mass.4 This is also true of athletes in whom all four cardiac chambers increase in size to accommodate the high-output requirements of intensive exercise (the so-called "athlete's heart"); however, the degree of remodelling is even greater for the RV, resulting in higher RV to LV mass and volume ratios.3

Athletes have a higher prevalence of electrocardiogram (ECG) changes, reflecting relatively larger right-sided heart chambers. T-wave inversion in the septal leads, incomplete and complete right-bundle branch block, and ECG criteria for RV hypertrophy are all more common in athletes, particularly endurance trained athletes.5-7 Finally, RV functional remodelling is also prominent in athletes. Partly as a consequence of larger RV volumes, many resting measures of RV function are reduced, such as RV ejection fraction and strain.8,9

RV Fatigue After Prolonged Intense Exercise

During brief maximal exercise, the RV has the capacity to increase contractility to compensate for the disproportionate increases in work.10,11 However, after intense endurance exercise, numerous studies have demonstrated acute RV dysfunction, usually in spite of apparently normal LV function.12 This may be explained by prolonged exposure to the greater wall stress and work requirements of the RV relative to the LV. This also explains why greater RV dysfunction has been associated with longer endurance events in a "dose-response" manner.13 It is also intriguing to note that while studies have failed to identify a relationship between biomarkers of cardiac injury and exercise-induced LV dysfunction, a number of investigators have demonstrated a relatively strong relationship between troponin and B-type natriuretic peptides and acute RV dysfunction.13,14

Clinical Relevance of RV Remodelling and Fatigue

The clinical consequence of repeated bouts of RV dysfunction after intense prolonged exercise is yet to be determined. Hein Heidbuchel coined the term "exercise-induced right ventricular cardiomyopathy" after observing mild RV structural and functional changes associated with a pro-arrhythmic tendency in highly trained endurance athletes,15 but this concept remains to be validated in a large prospective population. One critique was that this observation reflected selection of athletes with early familial disease. That is, the athletes may have had the well described autosomal dominant condition arrhythmogenic right ventricular cardiomyopathy (ARVC), given the clear phenotypic overlap. However, subsequent studies have shown that athletes with an ARVC phenotype tend not to have a history of familial involvement, and the yield from genetic testing is much lower than would be expected in familial disease.16,17 Thus, although there is much research still required to understand the association between exercise-induced RV remodelling and arrhythmias, there is a strong physiological rationale and evolving circumstantial evidence to support a link.

Can We Identify "At Risk" Athletes?

Assessment of the athlete with palpitations, ventricular ectopics, or non-sustained ventricular arrhythmias can be very challenging. In general, ventricular arrhythmias in the absence of structural heart disease are not associated with an adverse prognosis. However, the exclusion of structural heart disease in athletes can be more difficult, especially in endurance athletes in whom pronounced remodelling is common. In athletes in whom cardiac imaging raises suspicion of cardiac pathology, a more comprehensive evaluation is necessary. The ARVC Task Force Criteria18 provide an excellent framework for evaluation which consider clinical, electrophysiological, and imaging markers of pathology. Regardless of the debate between whether RV arrhythmias are due to a genetic tendency, or exercise in its own right, the ARVC Task Force Criteria can identify athletes at greater risk of potentially life threatening arrhythmic events during follow-up.15 Electrophysiological studies with or without electro-anatomical mapping have been promoted as having value in predicting "at-risk" athletes, but are relatively invasive techniques.15,19 The authors of this Expert Analysis article have recently promoted the use of exercise imaging (echocardiographic and magnetic CMR) as a means of identifying athletes with subtle RV dysfunction which only becomes apparent under the hemodynamic stress of exercise.11 This may prove to be a useful means of identifying the very small proportion of athletes who are at greater risk of serious arrhythmias.


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  2. Lewis GD, Bossone E, Naeije R, et al. Pulmonary vascular hemodynamic response to exercise in cardiopulmonary diseases. Circulation 2013;128:1470-9.
  3. La Gerche A, Heidbuchel H, Burns AT, et al. Disproportionate exercise load and remodeling of the athlete's right ventricle. Med Sci Sports Exerc 2011;43:974-81.
  4. Aaron CP, Tandri H, Barr RG, et al. Physical activity and right ventricular structure and function. The MESA-Right Ventricle Study. Am J Respir Crit Care Med 2011;183:396-404.
  5. Kim JH, Noseworthy PA, McCarty D, et al. Significance of electrocardiographic right bundle branch block in trained athletes. Am J Cardiol 2011;107:1083-9.
  6. Wasfy MM, DeLuca J, Wang F, et al. ECG findings in competitive rowers: normative data and the prevalence of abnormalities using contemporary screening recommendations. Br J Sports Med 2015;49:200-6.
  7. Brosnan M, La Gerche A, Kalman J, et al. Comparison of frequency of significant electrocardiographic abnormalities in endurance versus nonendurance athletes. Am J Cardiol 2014;113:1567-73.
  8. Zaidi A, Sheikh N, Jongman JK, et al. Clinical Differentiation Between Physiological Remodeling and Arrhythmogenic Right Ventricular Cardiomyopathy in Athletes With Marked Electrocardiographic Repolarization Anomalies. J Am Coll Cardiol 2015;65:2702-11.
  9. Teske AJ, Prakken NH, De Boeck BW, et al. Echocardiographic tissue deformation imaging of right ventricular systolic function in endurance athletes. Eur Heart J 2009;30:969-77.
  10. La Gerche A, Burns AT, D'Hooge J, Macisaac AI, Heidbüchel H, Prior DL. Exercise strain rate imaging demonstrates normal right ventricular contractile reserve and clarifies ambiguous resting measures in endurance athletes. J Am Soc Echocardiogr 2012;25:253-62 e1.
  11. La Gerche A, Claessen G, Dymarkowski S, et al. Exercise-induced right ventricular dysfunction is associated with ventricular arrhythmias in endurance athletes. Eur Heart J 2015;36:1998-2010.
  12. Elliott AD, La Gerche A. The right ventricle following prolonged endurance exercise: are we overlooking the more important side of the heart? A meta-analysis. Br J Sports Med 2014;49:724-9.
  13. La Gerche A, Burns AT, Mooney DJ, et al. Exercise-induced right ventricular dysfunction and structural remodelling in endurance athletes. Eur Heart J 2012;33:998-1006.
  14. Neilan TG, Januzzi JL, Lee-Lewandrowski E, et al. Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon. Circulation 2006;114:2325-33.
  15. Heidbuchel H, Hoogsteen J, Fagard R, et al. High prevalence of right ventricular involvement in endurance athletes with ventricular arrhythmias. Role of an electrophysiologic study in risk stratification. Eur Heart J 2003;24:1473-80.
  16. La Gerche A, Robberecht C, Kuiperi C, et al. Lower than expected desmosomal gene mutation prevalence in endurance athletes with complex ventricular arrhythmias of right ventricular origin. Heart 2010;96:1268-74.
  17. Sawant AC, Bhonsale A, Te Riele AS, et al. Exercise has a disproportionate role in the pathogenesis of arrhythmogenic right ventricular dysplasia/cardiomyopathy in patients without desmosomal mutations. J Am Heart Assoc 2014;3:e001471.
  18. Marcus FI, McKenna WJ, Sherrill D, et al. Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the Task Force Criteria. Circulation 2010;121:1533-41.
  19. Corrado D, Basso C, Leoni L, et al. Three-dimensional electroanatomical voltage mapping and histologic evaluation of myocardial substrate in right ventricular outflow tract tachycardia. J Am Coll Cardiol 2008;51:731-9.

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