|Heart failure with preserved ejection fraction: chronic low-intensity interval exercise training preserves myocardial O2 balance and diastolic function.|
|PMID: 23104696 Owner: NLM Status: MEDLINE|
|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.|
|Kurt D Marshall; Brittany N Muller; Maike Krenz; Laurin M Hanft; Kerry S McDonald; Kevin C Dellsperger; Craig A Emter|
Related Documents :
|21195376 - Usefulness of at rest and exercise hemodynamics to detect subclinical myocardial diseas...
2009846 - The y-intercept of the critical power function as a measure of anaerobic work capacity.
1797696 - An examination of the hemodynamic and metabolic effects of carteolol during different w...
8357576 - Portable system for continuous ex vivo measurements of lactate.
2515246 - The broad-specificity, membrane-bound lactate dehydrogenase of neisseria gonorrhoeae: t...
1168656 - Influence of timing and intensity of musclar exercise on temporal patterns of plasma co...
|Type: Journal Article; Research Support, American Recovery and Reinvestment Act; Research Support, N.I.H., Extramural Date: 2012-10-25|
|Title: Journal of applied physiology (Bethesda, Md. : 1985) Volume: 114 ISSN: 1522-1601 ISO Abbreviation: J. Appl. Physiol. Publication Date: 2013 Jan|
|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|
|Languages: eng Pagination: 131-47 Citation Subset: IM|
|APA/MLA Format Download EndNote Download BibTex|
Arterial Pressure / genetics, physiology
Citrate (si)-Synthase / genetics, metabolism
Collagen Type III / genetics, metabolism
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
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
Tissue Inhibitor of Metalloproteinases / genetics, metabolism
Ventricular Function, Left / genetics, physiology
Ventricular Remodeling / genetics, physiology
|P30 HL101332/HL/NHLBI NIH HHS; R01 HL057852/HL/NHLBI NIH HHS|
|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 22.214.171.124/Citrate (si)-Synthase; EC 2.7.-/Protein Kinases; EC 126.96.36.199/Proto-Oncogene Proteins c-akt; EC 188.8.131.52/MAP Kinase Kinase 4; EC 184.108.40.206/Matrix Metalloproteinase 2; S88TT14065/Oxygen|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Separating in vivo mechanical stimuli for postpneumonectomy compensation: physiological assessment.
Next Document: Oxygen, pH, and mitochondrial oxidative phosphorylation.