Abstract
Introduction: Left ventricular hypertrophy (LVH) is a risk factor for developing heart failure (HF). Exercise training decreases LV stiffness in individuals with LVH, but the effects of exercise training on LV relaxation in these individuals are unknown. Methods: Patients with LVH (> 11 mm) and elevated cardiac biomarkers (N-terminal pro- B-type natriuretic peptide [>40 pg/mL] or high-sensitivity troponin T [>0.6 pg/mL]) were randomized 2:1 to 1 year of monitored exercise training 4-5 days a week, including high intensity intervals, and 1-2 days of strength training or an attention control. Isovolumetric relaxation time (IVRT) was measured with pulse wave Doppler echocardiography and pulmonary capillary wedge pressure (PCWP) was consecutively measured with right heart catheterization before and after intervention. LV relaxation time constant, Tau, was estimated by Tau = IVRT / (Ln End-systolic pressure (ESP) - Ln PCWP) (Figure). Maximal oxygen uptake (VO 2 Max; Douglas bags) was measured with an incremental treadmill test. LV Stiffness was significantly improved in exercise arm, previously reported. Results: Thirty-one participants completed the study (Control: n=11, 51±6 years, 55% men, Exercise: n=20 53±6, 65% men). VO 2 Max increased by 18.2% in the exercise arm (2.2±0.6 L/min to 2.5±0.6, but not in controls; group x time p<0.001). Exercise training did not change Tau (exercise 38.2±6.5 to 39.8±8.7 ms) compared to control(40.3 ± 5.9 to 39.2±6.8 ms, group x time p = 0.84, Figure ). Exercise training resulted in no significant changes in IVRT (p = 0.35), SBP (p=0.89) or PCWP (p=0.69). Conclusions: In patients with LVH at risk for HF, one year of high intensity exercise training did not improve LV relaxation despite significant improvement in ventricular stiffness and exercise capacity. These results suggest the primary mechanism for HF risk reduction with exercise training is by lowering LV stiffness, and not necessarily altering LV relaxation.
Published Version
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