title: Disproportionate exercise load and remodeling of the athlete's right ventricle.
abstract: OBJECTIVE
  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 (VO2), 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, 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, P = 0.058). Peak exercise RVES-σ was greater in EA than in NA (340 ± 107 vs 266 ± 82 kdyn · cm, 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.
authors.affiliation: Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Australia. Andre.LaGerche@svhm.org.au
authors.forename: André
authors.initials: A
authors.lastname: La Gerche
authors.forename: Hein
authors.initials: H
authors.lastname: Heidbüchel
authors.forename: Andrew T
authors.initials: AT
authors.lastname: Burns
authors.forename: Don J
authors.initials: DJ
authors.lastname: Mooney
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Taylor
authors.forename: Heinz B
authors.initials: HB
authors.lastname: Pfluger
authors.forename: Warrick J
authors.initials: WJ
authors.lastname: Inder
authors.forename: Andrew I
authors.initials: AI
authors.lastname: Macisaac
authors.forename: David L
authors.initials: DL
authors.lastname: Prior
mesh_terms: D000328:Adult; D056352:Athletes; D016022:Case-Control Studies; D015444:Exercise / Q000502:physiology*; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology*; D006801:Humans; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D010101:Oxygen Consumption / Q000502:physiology; D005082:Physical Exertion / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D013599:Systole / Q000502:physiology; D018608:Ultrasonography, Doppler; D016277:Ventricular Function, Left / Q000502:physiology; D016278:Ventricular Function, Right / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology*