Document Detail


Porcine cardiac myocyte power output is increased after chronic exercise training.
MedLine Citation:
PMID:  16565350     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chronic exercise training increases the functional capacity of the heart, perhaps by increased myocyte contractile function, as has been observed in rodent exercise models. We examined whether cardiac myocyte function is enhanced after chronic exercise training in Yucatan miniature swine, whose heart characteristics are similar to humans. Animals were designated as either sedentary (Sed), i.e., cage confined, or exercise trained (Ex), i.e., underwent 16-20 wk of progressive treadmill training. Exercise training efficacy was shown with significantly increased heart weight-to-body weight ratios, skeletal muscle citrate synthase activity, and exercise tolerance. Force-velocity properties were measured by attaching skinned cardiac myocytes between a force transducer and position motor, and shortening velocities were measured over a range of loads during maximal Ca2+ activation. Myocytes (n = 9) from nine Ex pigs had comparable force production but a approximately 30% increase in peak power output compared with myocytes (n = 8) from eight Sed. Interestingly, Ex myofibrillar samples also had higher baseline PKA-induced phosphorylation levels of cardiac troponin I, which may contribute to the increase in power. Overall, these results suggest that enhanced power-generating capacity of porcine cardiac myofibrils contributes to improved cardiac function after chronic exercise training.
Authors:
Aaron C Hinken; F Steven Korte; Kerry S McDonald
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2006-03-24
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  101     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2006 Jul 
Date Detail:
Created Date:  2006-06-19     Completed Date:  2006-08-28     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  40-6     Citation Subset:  IM    
Affiliation:
Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Biomechanics
Cardiac Output / physiology*
Carrier Proteins / analysis,  physiology
Cell Separation
Male
Myocardial Contraction / physiology
Myocytes, Cardiac / chemistry,  cytology,  physiology*
Myofibrils / chemistry,  physiology*
Myosin Heavy Chains / analysis,  physiology
Phosphorylation
Physical Conditioning, Animal / physiology*
Swine
Swine, Miniature
Time Factors
Troponin T / analysis,  physiology
Grant Support
ID/Acronym/Agency:
HL-52490/HL/NHLBI NIH HHS; HL-57852/HL/NHLBI NIH HHS; K02 HL-71550/HL/NHLBI NIH HHS; R01 HL-57852/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/Myosin Heavy Chains; 0/Troponin T; 0/myosin-binding protein C

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


Previous Document:  Ischemia induces aggravation of baseline repolarization abnormalities in left ventricular hypertroph...
Next Document:  Components and mechanisms of thermal hyperpnea.