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Obes Res Clin Pract ; 18(2): 131-140, 2024.
Article in English | MEDLINE | ID: mdl-38594124

ABSTRACT

OBJECTIVE: To identify subclinical left ventricle dysfunction (LVD) in obese rats by speckle-tracking echocardiography, and to evaluate the effects of 12-week Moderate-Intensity Continuous Training (MICT) or High-Intensity Interval Training (HIIT) on LV geometry, histology and function in obese rats. METHODS: Eighteen male standard or obese Sprague-Dawley rats were randomly divided into the Control group, the MICT group, and the HIIT group. Exercise interventions were conducted for 12 weeks, with equal total load and increased intensity gradient. Using dual-energy X-ray, two-dimensional speckle-tracking echocardiography, pulse Doppler, and HE staining to evalucate body shape, LV morphology, structure, and myocardial mechanics function. RESULTS: (1) Both MICT and HIIT have good weight loss shaping effect. (2) The LV of obese rats underwent pathological remodeling, with decreased longitudinal contractility and synchrony, and increased circumferential contractility and synchrony. (3) Exercise can inhibit LV pathological remodeling, improve myocardial mechanical function. HIIT is superior to MICT. (4) The global longitudinal strain of obese rats in the HIIT group showed a significant correlation with Fat% and Lean%. CONCLUSION: Obesity can induce LV pathological remodeling and subclinical dysfunction. Compared with MICT, 12-week HIIT can effectively inhibit the pathological remodeling of LV and promote the benign development of myocardial mechanical function in obese rats.


Subject(s)
Echocardiography , Obesity , Physical Conditioning, Animal , Rats, Sprague-Dawley , Ventricular Dysfunction, Left , Animals , Obesity/physiopathology , Obesity/therapy , Obesity/complications , Male , Rats , Ventricular Dysfunction, Left/physiopathology , Ventricular Dysfunction, Left/diagnostic imaging , Physical Conditioning, Animal/methods , Echocardiography/methods , High-Intensity Interval Training/methods , Ventricular Remodeling , Disease Models, Animal
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