Abstract

It is under debate whether the cumulative effects of intensive endurance exercise induce chronic cardiac damage. The aim of this study was to examine the cardiac structure and function in long-term master endurance athletes with special focus on cardiac fibrosis by contrast-enhanced cardiovascular magnetic resonance (CMR), myocardial extracellular volume fraction (ECV) quantified by CMR and global longitudinal strain (GLS) at rest and at exercise evaluated with echocardiography. Ten healthy competitive male master endurance athletes (age range: 41–55 years, current training volume: 9 ± 1 h/week) with a training history of 27 ± 7 years, and 8 control subjects pair-matched for age, height, and weight underwent exercise echocardiography including speckle tracking at rest and peak exercise, and cardiovascular magnetic resonance. Right ventricular (RV) mass (33 ± 4 and 23.2 ± 6 g/m 2 , P = 0.005), right ventricular end-diastolic volume 94 ± 21 and 67 ±15 mL/m 2 , P = 0.04) and left atrial volume (35.5 ± 4 and 28.6 ± 6 mL/m 2 , P = 0.04) were significantly increased in athletes in comparison with control subjects. Left ventricular (LV) mass (81.5 ± 16 and 74 ± 14 g/m 2 ·NS) LV end-diastolic volume (92 ± 24 and 75 ± 9 mL/m 2 ·NS) left and right ventricular ejection fraction (EF) did not differ between athletes and control subjects (LVEF: 61 ± 3 and 58 ± 8% NS; RVEF: 48.5 ± 3 and 50.3 ± 5% NS). Pathological late enhancement was not observed. ECV was normal in athletes (21.7 ± 0.7%) and control subjects (23.2 ± 2.6% NS). LV GLS at rest was higher in athletes (−19.4 ± 1.4 vs 17.1 ± 0.9; P = 0.005) but mean increase at peak exercise was similar (−4.6 ± 3.3 vs −4.2 ± 1.8%·NS). RV GLS was not significantly different between athletes and control subjects at rest (−24.1 ± 2.2 and −22.2 ± 2.4%·NS) and at peak exercise (increase of −3 ± 1.6 and −4.3 ± 3%·NS). Based on our results, cardiac fibrosis and chronic LV or RV damage in endurance master athletes with lifelong high training volumes seems to be unlikely.

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