Related Experiment Video
Updated: Jun 9, 2026
A Minimally Invasive Model of Aortic Stenosis in Swine
Published on: October 20, 2023
Low-intensity aerobic interval training attenuates pathological left ventricular remodeling and mitochondrial
Craig A Emter1, Christopher P Baines
1Dept. of Biomedical Science, Univ. of Missouri, 1600 E. Rollins, E117 Veterinary Medicine, Columbia, MO 65211, USA. emterc@missouri.edu
Insights
Exercise training improved heart function in pigs with cardiac hypertrophy by reducing fibrosis and preventing mitochondrial dysfunction. This suggests exercise may be a valuable therapy for heart failure patients.
Area of Science:
- Cardiovascular Physiology
- Exercise Science
- Mitochondrial Biology
Background:
- Cardiac hypertrophy is a pathological response to hypertension and myocardial infarction, often leading to heart failure.
- Cardiomyocyte loss through cell death pathways involving mitochondria is a key aspect of cardiac remodeling.
- Exercise training has shown potential to reverse or attenuate pathological cardiac remodeling.
Purpose of the Study:
- To investigate the effects of exercise training on left ventricular (LV) function, cardiac remodeling, and cardiomyocyte mitochondrial function in an animal model of cardiac hypertrophy.
- To compare sedentary, aortic-banded (heart failure) swine with exercise-trained, aortic-banded swine and control swine.
Main Methods:
- Male Yucatan miniature swine underwent aortic banding (AB) to induce hypertrophy. Groups included sedentary AB (HFSED), exercise-trained AB (HFTR), and sedentary controls.
- Left ventricular function, remodeling parameters (volumes, dimensions, heart/ventricular weights, cardiomyocyte size), fibrosis, collagen content, and mitochondrial permeability transition were assessed.
- Exercise training consisted of low-intensity interval training over 15 weeks.
Main Results:
- Exercise training prevented further increases in LV end-systolic volume and dimension in AB swine.
- Despite maintained hypertrophy (increased heart weight, cardiomyocyte size), exercise training preserved LV function, including fractional shortening and ejection fraction.
- Exercise attenuated LV fibrosis and collagen accumulation and prevented mitochondrial dysfunction (increased Ca(2+)-induced permeability transition) observed in sedentary HF animals.
Conclusions:
- Low-intensity interval exercise training preserves left ventricular function in the setting of cardiac hypertrophy.
- Exercise training mitigates pathological remodeling by reducing fibrosis and inhibiting mitochondrial dysfunction.
- These findings support the therapeutic potential of exercise for managing heart failure and related cardiac conditions.
Abstract:
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.
