Low-intensity aerobic interval training prevented further increases in left ventricular end-systolic volume, preserved left ventricular function, and attenuated fibrosis in aortic-banded miniature swine.
Does low-intensity aerobic interval training attenuate pathological left ventricular remodeling and mitochondrial dysfunction in aortic-banded miniature swine?
Low-intensity interval exercise training preserves LV function by attenuating fibrosis and inhibiting mitochondrial dysfunction in a swine model of pressure overload.
Absolute Event Rate: 4.5% vs 6.4%
p-value: p=<0.05
Cardiac hypertrophy in response to hypertension or myocardial infarction is a pathological indicator associated with heart failure (HF). A central component of the remodeling process is the loss of cardiomyocytes via cell death pathways regulated by the mitochondrion. Recent evidence has indicated that exercise training can attenuate or reverse pathological remodeling, creating a physiological phenotype. The purpose of this study was to examine left ventricular (LV) function, remodeling, and cardiomyocyte mitochondrial function in aortic-banded (AB) sedentary (HFSED; n = 6), AB exercise-trained (HFTR, n = 5), and control sedentary (n = 5) male Yucatan miniature swine. LV hypertrophy was present in both AB groups before the start of training, as indicated by increases in LV end-diastolic volume, LV end-systolic volume (LVESV), and LV end-systolic dimension (LVESD). Exercise training (15 wk) prevented further increases in LVESV and LVESD (P < 0.05). The heart weight-to-body weight ratio, LV + septum-to-body weight ratio, LV + septum-to-right ventricle ratio, and cardiomyocyte cross-sectional area were increased in both AB groups postmortem regardless of training status. Preservation of LV function after exercise training, as indicated by the maintenance of fractional shortening, ejection fraction, and mean wall shortening and increased stroke volume, was associated with an attenuation of the increased LV fibrosis (23%) and collagen (36%) observed in HFSED animals. LV mitochondrial dysfunction, as measured by Ca(2+)-induced mitochondrial permeability transition, was increased in HFSED (P < 0.05) but not HFTR animals. In conclusion, low-intensity interval exercise training preserved LV function as exemplified by an attenuation of fibrosis, maintenance of a positive inotropic state, and inhibition of mitochondrial dysfunction, providing further evidence of the therapeutic potential of exercise in a clinical setting.
Emter et al. (Sat,) conducted a other in Heart failure (pressure overload) (n=16). Low-intensity aerobic interval training vs. Sedentary was evaluated on Left ventricular end-systolic volume (LVESV) at 6 months (p=<0.05). Low-intensity aerobic interval training prevented further increases in left ventricular end-systolic volume, preserved left ventricular function, and attenuated fibrosis in aortic-banded miniature swine.