| Aerobic exercise training improves skeletal muscle function and Ca2+ handling-related protein expression in sympathetic hyperactivity-induced heart failure. | |
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MedLine Citation:
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PMID: 20595538 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The cellular mechanisms of positive effects associated with aerobic exercise training on overall intrinsic skeletal muscle changes in heart failure (HF) remain unclear. We investigated potential Ca2+ abnormalities in skeletal muscles comprising different fiber compositions and investigated whether aerobic exercise training would improve muscle function in a genetic model of sympathetic hyperactivity-induced HF. A cohort of male 5-mo-old wild-type (WT) and congenic alpha2A/alpha2C adrenoceptor knockout (ARKO) mice in a C57BL/6J genetic background were randomly assigned into untrained and trained groups. Exercise training consisted of a 8-wk running session of 60 min, 5 days/wk (from 5 to 7 mo of age). After completion of the exercise training protocol, exercise tolerance was determined by graded treadmill exercise test, muscle function test by Rotarod, ambulation and resistance to inclination tests, cardiac function by echocardiography, and Ca2+ handling-related protein expression by Western blot. alpha2A/alpha2CARKO mice displayed decreased ventricular function, exercise intolerance, and muscle weakness paralleled by decreased expression of sarcoplasmic Ca2+ release-related proteins [alpha1-, alpha2-, and beta1-subunits of dihydropyridine receptor (DHPR) and ryanodine receptor (RyR)] and Ca2+ reuptake-related proteins [sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)1/2 and Na+/Ca2+ exchanger (NCX)] in soleus and plantaris. Aerobic exercise training significantly improved exercise tolerance and muscle function and reestablished the expression of proteins involved in sarcoplasmic Ca2+ handling toward WT levels. We provide evidence that Ca2+ handling-related protein expression is decreased in this HF model and that exercise training improves skeletal muscle function associated with changes in the net balance of skeletal muscle Ca2+ handling proteins. |
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Authors:
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C R Bueno; J C B Ferreira; M G Pereira; A V N Bacurau; P C Brum |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-07-01 |
Journal Detail:
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Title: Journal of applied physiology (Bethesda, Md. : 1985) Volume: 109 ISSN: 1522-1601 ISO Abbreviation: J. Appl. Physiol. Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-09-10 Completed Date: 2011-01-12 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8502536 Medline TA: J Appl Physiol Country: United States |
Other Details:
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Languages: eng Pagination: 702-9 Citation Subset: IM |
Affiliation:
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School of Physical Education and Sport, University of São Paulo, SP, CEP 05508-900 Brazil. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blotting, Western Calcium / metabolism* Disease Models, Animal Exercise Tolerance Heart Failure / genetics, metabolism, physiopathology*, ultrasonography Male Mice Mice, Inbred C57BL Mice, Knockout Muscle Proteins / metabolism* Muscle Strength Muscle Weakness / metabolism, physiopathology Muscle, Skeletal / metabolism, physiopathology* Physical Exertion* Receptors, Adrenergic, alpha-2 / deficiency, genetics Sarcoplasmic Reticulum / metabolism* Sympathetic Nervous System / physiopathology* Time Factors Ventricular Function, Left |
| Chemical | |
Reg. No./Substance:
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0/Adra2a protein, mouse; 0/Adra2c protein, mouse; 0/Muscle Proteins; 0/Receptors, Adrenergic, alpha-2; 7440-70-2/Calcium |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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