Impaired left and right ventricular function following prolonged exercise in young athletes: influence of exercise intensity and responses to dobutamine stress

Abstract

We examined the effect of intensity during prolonged exercise (PE) on left (LV) and right ventricular (RV) function. Subjects included 18 individuals (mean +/- SE: age = 28.1 +/- 1.1 yr, maximal aerobic power = 55.1 +/- 1.6 ml . kg(-1) . min(-1)), who performed 150 min of exercise at 60 and 80% maximal aerobic power on two separate occasions. Transthoracic echocardiography assessed systolic and diastolic performance, and blood sampling assessed hydration status and noradrenaline levels before (pre), during (15 and 150 min), and 60 min following (post) PE. beta-Adrenergic sensitivity pre- and post-PE was assessed by dobutamine stress. High-intensity PE (15 vs. 150 min) induced reductions in LV ejection fraction (69.3 +/- 1.3 vs. 63.5 +/- 1.3%, P = 0.000), LV strain (-23.5 +/- 0.6 vs. -22.3 +/- 0.6%, P = 0.034), and RV strain (-26.3 +/- 0.6 vs. -23.0 +/- 0.6%, P < 0.01). Both exercise intensities induced diastolic reductions (pre vs. post) in the ratio of septal early wave of annular tissue velocities to late/atrial wave of annular tissue velocities (2.15 +/- 0.15 vs. 1.62 +/- 0.09; 2.21 +/- 0.15 vs. 1.48 +/- 0.10), ratio of lateral early wave of annular tissue velocities to late/atrial wave of annular tissue velocities (3.84 +/- 0.42 vs. 2.49 +/- 0.20; 3.56 +/- 0.32 vs. 2.08 +/- 0.18), ratio of early to late LV strain rate (2.42, +/- 0.16 vs. 1.97 +/- 0.13; 2.30 +/- 0.15 vs. 1.81 +/- 0.11), and ratio of early to late RV strain rate (2.03 +/- 0.17 vs. 1.51 +/- 0.09; 2.16 +/- 0.16 vs. 1.44 +/- 0.11) (P < 0.001). Evidence of beta-adrenergic sensitivity was supported by a decreased strain, strain rate, ejection fraction, and systolic pressure-volume ratio response to dobutamine (P < 0.05) with elevated noradrenaline (P < 0.01). PE-induced reductions in LV and RV systolic function were related to exercise intensity and beta-adrenergic desensitization. The clinical significance of exercise-induced cardiac fatigue warrants further research.