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

2015 ◽  
Vol 308 (9) ◽  
pp. H1096-H1102 ◽  
Author(s):  
Raphaela V. Groehs ◽  
Edgar Toschi-Dias ◽  
Ligia M. Antunes-Correa ◽  
Patrícia F. Trevizan ◽  
Maria Urbana P. B. Rondon ◽  
...  

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.

2018 ◽  
Vol 103 (10) ◽  
pp. 1318-1325 ◽  
Author(s):  
Lauro C. Vianna ◽  
Igor A. Fernandes ◽  
Daniel G. Martinez ◽  
André L. Teixeira ◽  
Bruno M. Silva ◽  
...  

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Anthony V Incognito ◽  
Milena Samora ◽  
Andrew D Shepherd ◽  
Roberta A Cartafina ◽  
Gabriel MN Guimarães ◽  
...  

2001 ◽  
Vol 281 (4) ◽  
pp. R1134-R1139 ◽  
Author(s):  
Atsunori Kamiya ◽  
Daisaku Michikami ◽  
Qi Fu ◽  
Yuki Niimi ◽  
Satoshi Iwase ◽  
...  

To examine effects of static exercise on the arterial baroreflex control of vascular sympathetic nerve activity, 22 healthy male volunteers performed 2 min of static handgrip exercise at 30% of maximal voluntary force, followed by postexercise circulatory arrest (PE-CA). Microneurographic recording of muscle sympathetic nerve activity (MSNA) was made with simultaneous recording of arterial pressure (Portapres). The relationship between MSNA and diastolic arterial pressure was calculated for each condition and was defined as the arterial baroreflex function. There was a close relationship between MSNA and diastolic arterial pressure in each subject at rest and during static exercise and PE-CA. The slope of the relationship significantly increased by >300% during static exercise ( P < 0.001), and the x-axis intercept (diastolic arterial pressure level) increased by 13 mmHg during exercise ( P< 0.001). These alterations in the baroreflex relationship were completely maintained during PE-CA. It is concluded that static handgrip exercise is associated with a resetting of the operating range and an increase in the reflex gain of the arterial barorelex control of MSNA.


2000 ◽  
Vol 279 (2) ◽  
pp. H536-H541 ◽  
Author(s):  
Philippe Van de Borne ◽  
Silvia Mezzetti ◽  
Nicola Montano ◽  
Krzysztof Narkiewicz ◽  
Jean Paul Degaute ◽  
...  

Interactions between mechanisms governing ventilation and blood pressure (BP) are not well understood. We studied in 11 resting normal subjects the effects of sustained isocapnic hyperventilation on arterial baroreceptor sensitivity, determined as the α index between oscillations in systolic BP (SBP) generated by respiration and oscillations present in R-R intervals (RR) and in peripheral sympathetic nerve traffic [muscle sympathetic nerve activity (MSNA)]. Tidal volume increased from 478 ± 24 to 1,499 ± 84 ml and raised SBP from 118 ± 2 to 125 ± 3 mmHg, whereas RR decreased from 947 ± 18 to 855 ± 11 ms (all P < 0.0001); MSNA did not change. Hyperventilation reduced arterial baroreflex sensitivity to oscillations in SBP at both cardiac (from 13 ± 1 to 9 ± 1 ms/mmHg, P < 0.001) and MSNA levels (by −37 ± 5%, P < 0.0001). Thus increased BP during hyperventilation does not elicit any reduction in either heart rate or MSNA. Baroreflex modulation of RR and MSNA in response to hyperventilation-induced BP oscillations is attenuated. Blunted baroreflex gain during hyperventilation may be a mechanism that facilitates simultaneous increases in BP, heart rate, and sympathetic activity during dynamic exercise and chemoreceptor activation.


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