Disproportionate Exercise Load and Remodeling of the Athlete's Right Ventricle

LA GERCHE, ANDRÉ1,2; HEIDBÜCHEL, HEIN2; BURNS, ANDREW T.3; MOONEY, DON J.3; TAYLOR, ANDREW J.4; PFLUGER, HEINZ B.4; INDER, WARRICK J.1; MACISAAC, ANDREW I.3; PRIOR, DAVID L.1,3

Medicine & Science in Sports & Exercise: June 2011 - Volume 43 - Issue 6 - pp 974-981
doi: 10.1249/MSS.0b013e31820607a3
Basic Sciences

Purpose: There is evolving evidence that intense exercise may place a disproportionate load on the right ventricle (RV) when compared with the left ventricle (LV) of the heart. Using a novel method of estimating end-systolic wall stress (ES-σ), we compared the RV and LV during exercise and assessed whether this influenced chronic ventricular remodeling in athletes.

Methods: For this study, 39 endurance athletes (EA) and 14 nonathletes (NA) underwent resting cardiac magnetic resonance (CMR), maximal oxygen uptake (V˙O2), and exercise echocardiography studies. LV and RV end-systolic wall stress (ES-σ) were calculated using the Laplace relation (ES-σ = Pr/(2h)). Ventricular size and wall thickness were determined by CMR; invasive and Doppler echo estimates were used to measure systemic and pulmonary ventricular pressures, respectively; and stroke volume was quantified by Doppler echocardiography and used to calculate changes in ventricular geometry during exercise.

Results: In EA, compared with NA, resting CMR measures showed greater RV than LV remodeling. The ratios RV ESV/LV ESV (1.40 ± 0.23 vs 1.26 ± 0.12, P = 0.007) and RV mass/LV mass (0.29 ± 0.04 vs 0.25 ± 0.03, P = 0.012) were greater in EA than in NA. RVES-σ was lower at rest than LVES-σ (143 ± 44 vs 252 ± 49 kdyn·cm−2, P < 0.001) but increased more with strenuous exercise (125% vs 14%, P < 0.001), resulting in similar peak exercise ES-σ (321 ± 106 vs 286 ± 77 kdyn·cm−2, P = 0.058). Peak exercise RVES-σ was greater in EA than in NA (340 ± 107 vs 266 ± 82 kdyn·cm−2, P = 0.028), whereas RVES-σ at matched absolute workloads did not differ (P = 0.79).

Conclusions: Exercise induces a relative increase in RVES-σ which exceeds LVES-σ. In athletes, greater RV enlargement and greater wall thickening may be a product of this disproportionate load excess.

1Department of Medicine, St. Vincent's Hospital, University of Melbourne, Melbourne, AUSTRALIA; 2Cardiology Department, University Hospital, University of Leuven, Leuven, BELGIUM; 3Cardiology Department, St. Vincent's Hospital Melbourne, Melbourne, AUSTRALIA; and 4Alfred Hospital and Baker IDI Heart and Diabetes Institute, Melbourne, AUSTRALIA

Address for correspondence: André La Gerche, M.B.B.S., Ph.D., Department of Cardiology, St. Vincent's Hospital, PO Box 2900, Fitzroy 3065, Australia; E-mail: Andre.LaGerche@svhm.org.au.

Submitted for publication October 2010.

Accepted for publication November 2010.

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©2011The American College of Sports Medicine