| Low-intensity aerobic interval training attenuates pathological left ventricular remodeling and mitochondrial dysfunction in aortic-banded miniature swine. | |
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MedLine Citation:
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PMID: 20817828 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Craig A Emter; Christopher P Baines |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2010-09-03 |
Journal Detail:
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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:
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Created Date: 2010-11-01 Completed Date: 2010-11-29 Revised Date: 2011-11-01 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1348-56 Citation Subset: IM |
Affiliation:
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Dept. of Biomedical Science, Univ. of Missouri, 1600 E. Rollins, E117 Veterinary Medicine, Columbia, MO 65211, USA. emterc@missouri.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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HL-093982-01/HL/NHLBI NIH HHS; HL-094404/HL/NHLBI NIH HHS; HL-52490/HL/NHLBI NIH HHS; R01 HL094404-02/HL/NHLBI NIH HHS; R01 HL094404-03/HL/NHLBI NIH HHS |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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