Molecular basis for the improvement in muscle metaboreflex and mechanoreflex control in exercise-trained humans with chronic heart failure

Molecular basis for the improvement in muscle metaboreflex and mechanoreflex control in exercise-trained humans with chronic heart failure

Author Antunes-Correa, Ligia M. Google Scholar
Nobre, Thais S. Google Scholar
Groehs, Raphaela V. Google Scholar
Alves, Maria Janieire N. N. Google Scholar
Fernandes, Tiago Google Scholar
Couto, Gisele K. Google Scholar
Rondon, Maria Urbana P. B. Google Scholar
Oliveira, Patricia Google Scholar
Lima, Marta Google Scholar
Mathias, Wilson Google Scholar
Brum, Patricia C. Google Scholar
Mady, Charles Google Scholar
Almeida, Dirceu R. Autor UNIFESP Google Scholar
Rossoni, Luciana V. Google Scholar
Oliveira, Edilamar M. Google Scholar
Middlekauff, Holly R. Google Scholar
Negrao, Carlos E. Google Scholar
Institution Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Univ Calif Los Angeles
Abstract Previous studies have demonstrated that muscle mechanoreflex and metaboreflex controls are altered in heart failure (HF), which seems to be due to changes in cyclooxygenase (COX) pathway and changes in receptors on afferent neurons, including transient receptor potential vanilloid type-1 (TRPV1) and cannabinoid receptor type-1 (CB1). the purpose of the present study was to test the hypotheses: 1) exercise training (ET) alters the muscle metaboreflex and mechanoreflex control of muscle sympathetic nerve activity (MSNA) in HF patients. 2) the alteration in metaboreflex control is accompanied by increased expression of TRPV1 and CB1 receptors in skeletal muscle. 3) the alteration in mechanoreflex control is accompanied by COX-2 pathway in skeletal muscle. Thirty-four consecutive HF patients with ejection fractions <40% were randomized to untrained (n = 17; 54 +/- 2 yr) or exercise-trained (n = 17; 56 +/- 2 yr) groups. MSNA was recorded by microneurography. Mechanoreceptors were activated by passive exercise and metaboreceptors by postexercise circulatory arrest (PECA). COX-2 pathway, TRPV1, and CB1 receptors were measured in muscle biopsies. Following ET, resting MSNA was decreased compared with untrained group. During PECA (metaboreflex), MSNA responses were increased, which was accompanied by the expression of TRPV1 and CB1 receptors. During passive exercise (mechanoreflex), MSNA responses were decreased, which was accompanied by decreased expression of COX-2, prostaglandin-E-2 receptor-4, and thromboxane-A(2) receptor and by decreased in muscle inflammation, as indicated by increased miRNA-146 levels and the stable NF-kappa B/I kappa B-alpha ratio. in conclusion, ET alters muscle metaboreflex and mechanoreflex control of MSNA in HF patients. This alteration with ET is accompanied by alteration in TRPV1 and CB1 expression and COX-2 pathway and inflammation in skeletal muscle.
Keywords heart failure
muscle sympathetic nervous system
metaboreflex
mechanoreflex
exercise training
Language English
Sponsor Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Fundacao Zerbini
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
National Heart, Lung, and Blood Institute
Grant number FAPESP: FAPESP-2010/50048-1
National Heart, Lung, and Blood Institute: RO1-HL084525
Date 2014-12-01
Published in American Journal of Physiology-heart and Circulatory Physiology. Bethesda: Amer Physiological Soc, v. 307, n. 11, p. H1655-H1666, 2014.
ISSN 0363-6135 (Sherpa/Romeo, impact factor)
Publisher Amer Physiological Soc
Extent H1655-H1666
Origin http://dx.doi.org/10.1152/ajpheart.00136.2014
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000346019900013
URI http://repositorio.unifesp.br/handle/11600/38477

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