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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Sympathetic hyperactivity differentially affects skeletal muscle mass in developing heart failure: role of exercise training

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Author(s):
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Bacurau, Aline V. N. ; Jardim, Maira A. ; Ferreira, Julio C. B. ; Bechara, Luiz R. G. ; Bueno, Jr., Carlos R. ; Alba-Loureiro, Tatiana C. [1] ; Negrao, Carlos E. [2] ; Casarini, Dulce E. [3] ; Curi, Rui [1] ; Ramires, Paulo R. ; Moriscot, Anselmo S. [4] ; Brum, Patricia C. [5]
Total Authors: 12
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, BR-05508900 Sao Paulo - Brazil
[2] Univ Sao Paulo, Sch Med, Heart Inst InCor, BR-05508900 Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Med, Div Nephrol, Sao Paulo - Brazil
[4] Univ Sao Paulo, Inst Biomed Sci, Dept Cell & Dev Biol, BR-05508900 Sao Paulo - Brazil
[5] Univ Sao Paulo, Dept Biodinam Movimento Corpo Humano, Escola Educacao Fis & Esporte, BR-05508900 Sao Paulo - Brazil
Total Affiliations: 5
Document type: Journal article
Source: Journal of Applied Physiology; v. 106, n. 5, p. 1631-1640, MAY 2009.
Web of Science Citations: 53
Abstract

Bacurau AV, Jardim MA, Ferreira JC, Bechara LR, Bueno CR Jr, Alba-Loureiro TC, Negrao CE, Casarini DE, Curi R, Ramires PR, Moriscot AS, Brum PC. Sympathetic hyperactivity differentially affects skeletal muscle mass in developing heart failure: role of exercise training. J Appl Physiol 106: 1631-1640, 2009. First published January 29, 2009; doi:10.1152/japplphysiol.91067.2008.-Sympathetic hyperactivity (SH) is a hallmark of heart failure (HF), and several lines of evidence suggest that SH contributes to HF-induced skeletal myopathy. However, little is known about the influence of SH on skeletal muscle morphology and metabolism in a setting of developing HF, taking into consideration muscles with different fiber compositions. The contribution of SH on exercise tolerance and skeletal muscle morphology and biochemistry was investigated in 3- and 7-mo-old mice lacking both alpha(2A)- and alpha(2C)-adrenergic receptor subtypes (alpha(2A)/alpha(2C)ARKO mice) that present SH with evidence of HF by 7 mo. To verify whether exercise training (ET) would prevent skeletal muscle myopathy in advanced-stage HF, alpha(2A)/alpha(2C)ARKO mice were exercised from 5 to 7 mo of age. At 3 mo, alpha(2A)/alpha(2C)ARKO mice showed no signs of HF and preserved exercise tolerance and muscular norepinephrine with no changes in soleus morphology. In contrast, plantaris muscle of alpha(2A)/alpha(2C)ARKO mice displayed hypertrophy and fiber type shift (IIA -> IIX) paralleled by capillary rarefaction, increased hexokinase activity, and oxidative stress. At 7 mo, alpha(2A)/alpha(2C)ARKO mice displayed exercise intolerance and increased muscular norepinephrine, muscular atrophy, capillary rarefaction, and increased oxidative stress. ET reestablished alpha(2A)/alpha(2C)ARKO mouse exercise tolerance to 7-mo-old wild-type levels and prevented muscular atrophy and capillary rarefaction associated with reduced oxidative stress. Collectively, these data provide direct evidence that SH is a major factor contributing to skeletal muscle morphological changes in a setting of developing HF. ET prevented skeletal muscle myopathy in alpha(2A)/alpha(2C)ARKO mice, which highlights its importance as a therapeutic tool for HF. (AU)

FAPESP's process: 06/56321-6 - Involvement of protein kinase C βII and ε isoforms in heart failure induced by myocardial infarction
Grantee:Julio Cesar Batista Ferreira
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 05/59740-7 - Physical exercise and autonomic control in cardiovascular physiopathology
Grantee:Carlos Eduardo Negrão
Support type: Research Projects - Thematic Grants