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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.)

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

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Antunes-Correa, Ligia M. [1] ; Nobre, Thais S. [1] ; Groehs, Raphaela V. [1] ; Alves, Maria Janieire N. N. [1] ; Fernandes, Tiago [2] ; Couto, Gisele K. [3] ; Rondon, Maria Urbana P. B. [2] ; Oliveira, Patricia [1] ; Lima, Marta [1] ; Mathias, Wilson [1] ; Brum, Patricia C. [2] ; Mady, Charles [1] ; Almeida, Dirceu R. [4] ; Rossoni, Luciana V. [3] ; Oliveira, Edilamar M. [2] ; Middlekauff, Holly R. [5] ; Negrao, Carlos E. [2, 1]
Total Authors: 17
[1] Univ Sao Paulo, Heart Inst InCor, Sch Med, Sao Paulo - Brazil
[2] Univ Sao Paulo, Sch Phys Educ & Sport, Sao Paulo - Brazil
[3] Univ Sao Paulo, Inst Biomed Sci, Sao Paulo - Brazil
[4] Univ Fed Sao Paulo, Dept Med, Sao Paulo - Brazil
[5] Univ Calif Los Angeles, Geffen Sch Med, Dept Med Cardiol & Physiol, Los Angeles, CA - USA
Total Affiliations: 5
Document type: Journal article
Web of Science Citations: 29

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. (AU)

FAPESP's process: 10/50048-1 - Cellular and functional bases of exercise in cardiovascular diseases
Grantee:Carlos Eduardo Negrão
Support type: Research Projects - Thematic Grants