The Impact of Endurance Exercise Training on Left Ventricular Torsion

ObjectivesWe sought to examine the effect of endurance exercise training (EET) on peak systolic left ventricular torsion (LVT) and peak early diastolic untwisting rate (UTR).BackgroundLeft ventricular (LV) structural adaptations to EET have been well characterized. LVT, a recognized marker of LV function in numerous cardiac diseases, has recently been investigated in the setting of exercise. However, longitudinal data characterizing the impact of sustained exercise training on LVT have not been reported.MethodsA prospective, longitudinal study design examined the impact of a 90-day period of training on LV twist mechanics in university male rowers (n = 15, mean age 18.6 ± 0.5 years). Conventional LV structural measurements, LV apical and basal rotation, peak systolic LVT, and peak early diastolic UTR were measured by 2-dimensional and speckle tracking echocardiography before and after the EET study period.ResultsParticipants experienced LV eccentric hypertrophy, characterized by increased LV end-diastolic volume (80.8 ± 8.7 ml/m2 vs. 91.3 ± 8.0 ml/m2, p < 0.001) and LV mass (101.3 ± 11.4 g/m2 vs. 115.7 ± 12.6 g/m2, p = 0.001). There was a significant increase in peak systolic apical rotation (8.9 ± 4.2° vs. 12.7 ± 3.9°, p = 0.002) but no change in basal rotation. This translated into a highly significant increase in peak systolic LVT after EET (14.1 ± 5.0° vs. 18.0 ± 3.6°, p = 0.002). The impact of EET on LV twist mechanics was not confined to ventricular systole, as peak early diastolic UTR (−110.6 ± 41.8°/s vs. −148.0 ± 29.8°/s, p = 0.003) and the percentage of untwisting that occurred by the end of isovolumic relaxation (31.2 ± 12.0% vs. 39.9 ± 14.9%, p = 0.04) increased.ConclusionsParticipation in EET was associated with significant changes in LV twist mechanics characterized by increased apical rotation, LVT, and UTR. These findings suggest that LVT and UTR augmentation may be an important and previously unrecognized component of exercise-induced cardiac remodeling.