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Resumen de Right Ventricular Fatigue Developing during Endurance Exercise: An Exercise Cardiac Magnetic Resonance Study.

Guido Claessen, Hein Heidbüchel, Piet Claus, Stefan Ghysels, Pieter Vermeersch, Steven Dymarkowski, André La Gerche

  • AB Introduction: Prolonged intense exercise has often been associated with the impairment of right ventricular (RV) function after activity, whereas this is rare for the left ventricle (LV). The effect of prolonged exercise on the heart has not been adequately measured during exercise itself. Methods: We performed real-time cardiac magnetic resonance imaging at rest and during incremental exercise in 14 male endurance athletes (mean +/- SD; age = 36 +/- 6 yr, BMI = 23.1 +/- 1.94 kg[middle dot]m-2) 1-3 wk before (baseline) and immediately after a 150-km cycling event (end-of-race) to measure LV and RV end-diastolic and end-systolic volumes (EDV and ESV), ejection fraction (EF), and ventricular-arterial coupling (stroke volume [SV]/ESV). Results: End-of-race RV EDV was unchanged from baseline at rest but was significantly increased during near-maximal exercise (235 +/- 18 vs 217 +/- 24 mL, P < 0.0001). Resting RV ESV was higher end-of-race (100 +/- 16 vs 93 +/- 15 mL, P = 0.009), which became more appreciable during near-maximal exercise (75 +/- 15 vs 60 +/- 14 mL, P < 0.0001). RV EF, although unchanged at rest, was significantly decreased during near-maximal exercise (68% +/- 5% vs 73% +/- 4%, P = 0.001). LV volume measures were similar at baseline and end-of-race. Therefore, the effect of endurance activity on the RV and LV was significantly different (P < 0.0001). Cardiac output increased to similar values at near-maximal exertion before and at the end of the race. However, whereas LV SV/ESV was unchanged, RV SV/ESV was attenuated end-of-race (P = 0.02 for interaction with race setting). Conclusions: Intense endurance exercise does not affect LV volume or function but results in RV dilatation and reduced RV EF, which becomes even more significant during exercise. Alterations in RV ventricular-arterial coupling suggest that this may be an expression of exercise-induced RV contractile impairment rather than changes in autonomic or loading conditions.


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