Document Detail


Heart failure with preserved ejection fraction: chronic low-intensity interval exercise training preserves myocardial O2 balance and diastolic function.
MedLine Citation:
PMID:  23104696     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have previously reported chronic low-intensity interval exercise training attenuates fibrosis, impaired cardiac mitochondrial function, and coronary vascular dysfunction in miniature swine with left ventricular (LV) hypertrophy (Emter CA, Baines CP. Am J Physiol Heart Circ Physiol 299: H1348-H1356, 2010; Emter CA, et al. Am J Physiol Heart Circ Physiol 301: H1687-H1694, 2011). The purpose of this study was to test two hypotheses: 1) chronic low-intensity interval training preserves normal myocardial oxygen supply/demand balance; and 2) training-dependent attenuation of LV fibrotic remodeling improves diastolic function in aortic-banded sedentary, exercise-trained (HF-TR), and control sedentary male Yucatan miniature swine displaying symptoms of heart failure with preserved ejection fraction. Pressure-volume loops, coronary blood flow, and two-dimensional speckle tracking ultrasound were utilized in vivo under conditions of increasing peripheral mean arterial pressure and β-adrenergic stimulation 6 mo postsurgery to evaluate cardiac function. Normal diastolic function in HF-TR animals was characterized by prevention of increased time constant of isovolumic relaxation, normal LV untwisting rate, and enhanced apical circumferential and radial strain rate. Reduced fibrosis, normal matrix metalloproteinase-2 and tissue inhibitors of metalloproteinase-4 mRNA expression, and increased collagen III isoform mRNA levels (P < 0.05) accompanied improved diastolic function following chronic training. Exercise-dependent improvements in coronary blood flow for a given myocardial oxygen consumption (P < 0.05) and cardiac efficiency (stroke work to myocardial oxygen consumption, P < 0.05) were associated with preserved contractile reserve. LV hypertrophy in HF-TR animals was associated with increased activation of Akt and preservation of activated JNK/SAPK. In conclusion, chronic low-intensity interval exercise training attenuates diastolic impairment by promoting compliant extracellular matrix fibrotic components and preserving extracellular matrix regulatory mechanisms, preserves myocardial oxygen balance, and promotes a physiological molecular hypertrophic signaling phenotype in a large animal model resembling heart failure with preserved ejection fraction.
Authors:
Kurt D Marshall; Brittany N Muller; Maike Krenz; Laurin M Hanft; Kerry S McDonald; Kevin C Dellsperger; Craig A Emter
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Publication Detail:
Type:  Journal Article; Research Support, American Recovery and Reinvestment Act; Research Support, N.I.H., Extramural     Date:  2012-10-25
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  114     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-01-02     Completed Date:  2013-07-08     Revised Date:  2014-01-09    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  131-47     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Arterial Pressure / genetics,  physiology
Citrate (si)-Synthase / genetics,  metabolism
Collagen Type III / genetics,  metabolism
Connectin
Diastole / genetics,  physiology*
Extracellular Matrix / genetics,  metabolism
Fibrosis / genetics,  metabolism,  physiopathology
Heart / physiology*
Heart Failure / genetics,  metabolism,  physiopathology*,  rehabilitation*
Hypertrophy, Left Ventricular / genetics,  metabolism,  physiopathology
MAP Kinase Kinase 4 / genetics,  metabolism
Male
Matrix Metalloproteinase 2 / genetics,  metabolism
Muscle Proteins / genetics,  metabolism
Myocardial Contraction / genetics,  physiology
Myocardium / metabolism*
Natriuretic Peptide, Brain / genetics,  metabolism
Oxygen / metabolism*
Oxygen Consumption / genetics,  physiology
Physical Conditioning, Animal / physiology*
Protein Kinases / genetics,  metabolism
Proto-Oncogene Proteins c-akt / genetics,  metabolism
RNA, Messenger / genetics
Regional Blood Flow / genetics,  physiology
Sarcomeres / genetics,  metabolism,  physiology
Swine
Tissue Inhibitor of Metalloproteinases / genetics,  metabolism
Ventricular Function, Left / genetics,  physiology
Ventricular Remodeling / genetics,  physiology
Grant Support
ID/Acronym/Agency:
P30 HL101332/HL/NHLBI NIH HHS; R01 HL057852/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Collagen Type III; 0/Connectin; 0/Muscle Proteins; 0/RNA, Messenger; 0/Tissue Inhibitor of Metalloproteinases; 0/tissue inhibitor of metalloproteinase-4; 114471-18-0/Natriuretic Peptide, Brain; EC 2.3.3.1/Citrate (si)-Synthase; EC 2.7.-/Protein Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.12.2/MAP Kinase Kinase 4; EC 3.4.24.24/Matrix Metalloproteinase 2; S88TT14065/Oxygen
Comments/Corrections

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