Exercise training prevents the deterioration in the arterial baroreflex control of sympathetic nerve activity in chronic heart failure patients

Author:

Groehs Raphaela V.1,Toschi-Dias Edgar1,Antunes-Correa Ligia M.1,Trevizan Patrícia F.1,Rondon Maria Urbana P. B.2,Oliveira Patrícia1,Alves Maria J. N. N.1,Almeida Dirceu R.3,Middlekauff Holly R.4,Negrão Carlos E.12

Affiliation:

1. Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil;

2. School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil,

3. Division of Cardiology, Department of Medicine, Federal University of Sao Paulo, Sao Paulo, Brazil;

4. Department of Medicine (Cardiology) and Physiology, Geffen School of Medicine at UCLA, University of California, Los Angeles, California

Abstract

Arterial baroreflex control of muscle sympathetic nerve activity (ABRMSNA) is impaired in chronic systolic heart failure (CHF). The purpose of the study was to test the hypothesis that exercise training would improve the gain and reduce the time delay of ABRMSNA in CHF patients. Twenty-six CHF patients, New York Heart Association Functional Class II-III, EF ≤ 40%, peak V̇o2 ≤ 20 ml·kg−1·min−1 were divided into two groups: untrained (UT, n = 13, 57 ± 3 years) and exercise trained (ET, n = 13, 49 ± 3 years). Muscle sympathetic nerve activity (MSNA) was directly recorded by microneurography technique. Arterial pressure was measured on a beat-to-beat basis. Time series of MSNA and systolic arterial pressure were analyzed by autoregressive spectral analysis. The gain and time delay of ABRMSNA was obtained by bivariate autoregressive analysis. Exercise training was performed on a cycle ergometer at moderate intensity, three 60-min sessions per week for 16 wk. Baseline MSNA, gain and time delay of ABRMSNA, and low frequency of MSNA (LFMSNA) to high-frequency ratio (HFMSNA) (LFMSNA/HFMSNA) were similar between groups. ET significantly decreased MSNA. MSNA was unchanged in the UT patients. The gain and time delay of ABRMSNA were unchanged in the ET patients. In contrast, the gain of ABRMSNA was significantly reduced [3.5 ± 0.7 vs. 1.8 ± 0.2, arbitrary units (au)/mmHg, P = 0.04] and the time delay of ABRMSNA was significantly increased (4.6 ± 0.8 vs. 7.9 ± 1.0 s, P = 0.05) in the UT patients. LFMSNA-to-HFMSNA ratio tended to be lower in the ET patients ( P < 0.08). Exercise training prevents the deterioration of ABRMSNA in CHF patients.

Funder

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (Coordination for the Improvement of Higher Education Personnel)

Conselho Nacional de Pesquisa (CNPq)

São Paulo Research Foundation (FAPESP)

HHS | National Institutes of Health (NIH)

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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