Document Detail


Low-intensity aerobic interval training attenuates pathological left ventricular remodeling and mitochondrial dysfunction in aortic-banded miniature swine.
MedLine Citation:
PMID:  20817828     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Craig A Emter; Christopher P Baines
Related Documents :
7362328 - Protective effect of hyaluronidase after long-term aortic cross-clamping: initial exper...
21037848 - The use of exercise echocardiography in the evaluation of mitral regurgitation.
7587418 - Acute alterations of oxygen uptake and symptom-limited exercise time in patients with m...
10634948 - In vivo behavior of epoxy-crosslinked porcine heart valve cusps and walls.
8091048 - Gender differences in substrate utilisation during exercise.
19484698 - Anthropometry as a predictor of high speed performance.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-09-03
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-01     Completed Date:  2010-11-29     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1348-56     Citation Subset:  IM    
Affiliation:
Dept. of Biomedical Science, Univ. of Missouri, 1600 E. Rollins, E117 Veterinary Medicine, Columbia, MO 65211, USA. emterc@missouri.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Aorta, Thoracic
Cell Death / physiology
Disease Models, Animal
Heart Failure / pathology,  physiopathology,  therapy*
Hypertrophy, Left Ventricular / pathology,  physiopathology*
Ligation
Male
Mitochondria, Heart / physiology*
Myocytes, Cardiac / pathology
Physical Conditioning, Animal / physiology*
Swine
Swine, Miniature
Ventricular Function, Left
Ventricular Remodeling / physiology*
Grant Support
ID/Acronym/Agency:
HL-093982-01/HL/NHLBI NIH HHS; HL-094404/HL/NHLBI NIH HHS; HL-52490/HL/NHLBI NIH HHS; R01 HL094404/HL/NHLBI NIH HHS; R01 HL094404-02/HL/NHLBI NIH HHS; R01 HL094404-03/HL/NHLBI NIH HHS
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Extracellular transsulfuration generates hydrogen sulfide from homocysteine and protects endothelium...
Next Document:  Novel role of endothelial BKCa channels in altered vasoreactivity following hypoxia.