Effects of acute and long-term slow breathing exercise on muscle sympathetic nerve activity in untreated male patients with hypertension

Hering, Dagmara; Kucharska, W.; Kára, Tomáš; Somers, Virend K.; Parati, Gianfranco; Narkiewicz, Krzysztof

doi:10.1097/hjh.0b013e32835eb2cf

Cited by 43 publications

(45 citation statements)

References 47 publications

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“…In the healthy state, MSNA represents global sympathetic outflow to the skeletal muscle linked to BP regulation with strong feedback from the arterial baroreceptors (Wallin, ) and respiratory modulation (Habler, Janig, & Michaelis, ). The reduction in MSNA observed during slow breathing at either RF or RF + 1 was similar to that demonstrated in previous studies where slow breathing was of 10–15 min duration (Fonkoue et al, ; Harada et al, ; Hering et al, ; Oneda et al, ). Two prior studies in healthy subjects indicated no effect of slow breathing on MSNA but the duration of the breathing exercise was much shorter being 3 (Limberg et al, ) or 4 min (Raupach et al, ).…”

Section: Discussionsupporting

confidence: 89%

“…Slow breathing has long been recognized to exert beneficial effects in a range of disorders including those related to the cardiovascular system and those associated with anxiety. Breathing at a low pace (5–6 breaths per min) has been shown to acutely decrease blood pressure (BP) in patients with post‐traumatic stress disorder (Fonkoue et al, ), and in the longer term decrease BP in patients with hypertension (Hering et al, ). In patients with heart failure, slow breathing either performed acutely or chronically reduced the cardiovascular reactivity to mental stress and improved various aspects of health‐related quality of life (Lachowska, Bellwon, Morys, Gruchala, & Hering ).…”

Section: Introductionmentioning

confidence: 99%

“…Interventions aiming at altering the breathing frequency may affect the within‐breath modulation of MSNA and hence modulate steady state sympathetic tone. Acute slow breathing for 10–15 min was found to decrease MSNA in patients with hypertension (Hering et al, ; Oneda, Ortega, Gusmao, Araujo, & Mion, ), post‐traumatic stress disorder (Fonkoue et al, ) and those with heart failure (Harada et al, ), but failed to induce any change in healthy subjects when the breathing exercise was of 3 min duration (Limberg et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Acute effects of resonance frequency breathing on cardiovascular regulation

Pagaduan

Kameneva

et al. 2019

Physiol Rep

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Acute slow breathing may have beneficial effects on cardiovascular regulation by affecting hemodynamics and the autonomic nervous system. Whether breathing at the resonance frequency (RF), a breathing rate that maximizes heart rate oscillations, induces differential effects to that of slow breathing is unknown. We compared the acute effects of breathing at either RF and RF + 1 breaths per minute on muscle sympathetic nervous activity (MSNA) and baroreflex function. Ten healthy men underwent MSNA, blood pressure (BP), and heart rate (HR) recordings while breathing for 10 min at their spontaneous breathing (SB) rate followed by 10 min at both RF and RF + 1 randomly assigned and separated by a 10‐min recovery. Breathing at either RF or RF + 1 induced similar changes in HR and HR variability, with increased low frequency and decreased high frequency oscillations (p < .001 for both). Both respiration rates decreased MSNA (−5.6 and −7.3 bursts per min for RF and RF + 1 p < .05), with the sympathetic bursts occurring more often during mid‐inspiration to early expiration (+57% and + 80%) and longer periods of silence between bursts were seen (p < .05 for RF + 1). Systolic BP was decreased only during RF (−4.6 mmHg, p < .05) but the decrease did not differ to that seen during RF + 1 (−3.1 mmHg). The sympathetic baroreflex function remained unchanged at either breathing rates. The slope of the cardiac baroreflex function was unaltered but the cardiac baroreflex efficiency was improved during both RF and RF + 1. Acute breathing at either RF or RF + 1 has similar hemodynamic and sympatho‐inhibitory effects in healthy men.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Acute effects of resonance frequency breathing on cardiovascular regulation

Pagaduan

Kameneva

et al. 2019

Physiol Rep

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“…Device-guided breathing has been used to treat hypertension and heart failure with mixed results (Hering et al, 2013; Howorka et al, 2013; Landman et al, 2013; de Barros, da Silva et al, 2014; Harada et al, 2014; van Hateren et al, 2014). The mixed result sparked a debate on what constitutes device-guided breathing (Huang and Subak, 2014; Landman et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Increased cardio-respiratory coupling evoked by slow deep breathing can persist in normal humans

Dick

Mims

Hsieh

et al. 2014

Respiratory Physiology & Neurobiology

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Slow deep breathing (SDB) has a therapeutic effect on autonomic tone. Our previous studies suggested that coupling of the cardiovascular to the respiratory system mediates plasticity expressed in sympathetic nerve activity. We hypothesized that SDB evokes short-term plasticity of cardiorespiratory coupling (CRC). We analyzed respiratory frequency (fr), heart rate and its variability (HR&HRV), the power spectral density (PSD) of blood pressure (BP) and the ventilatory pattern before, during, and after a 20-min epoch of SDB. During SDB, CRC and the relative PSD of BP at fr increased; mean arterial pressure decreased; but HR varied; increasing (n=3), or decreasing (n=2) or remaining the same (n=5). After SDB, short-term plasticity was not apparent for the group but for individuals differences existed between baseline and recovery periods. We conclude that a repeated practice, like pranayama, may strengthen CRC and evoke short-term plasticity effectively in a subset of individuals.

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“…Likely mechanisms contributing include elevated reflex afferent drive from both peripheral chemoreceptors 14,15 and kidney, 16,17 saltangiotensin II, [18][19][20][21] inflammation, [22][23][24] and respiration. 13,[25][26][27][28][29] Respiratory modulation of sympathetic activity or respiratory-sympathetic coupling has been observed in many sympathetic postganglionic outflows. 13,21,[28][29][30][31][32][33] Clinical studies have purported that by controlling breathing depth and rate (using RespeRate) blood pressure can be lowered 34 in patients with hypertension.…”

mentioning

confidence: 99%

Specific Respiratory Neuron Types Have Increased Excitability That Drive Presympathetic Neurones in Neurogenic Hypertension

2014

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H igh sympathetic activity is associated with hypertension 1-6 and many other diseases including heart failure, 7,8 insulin resistance, 9 and obesity. 10,11 Sympathetic nerve activity increases progressively as blood pressure rises from normal to moderate to severe hypertension in humans. 12 Interestingly, in both animal models of hypertension 13 and in patients with hypertension 3,6 elevated sympathetic activity precedes hypertension. The mechanisms driving excessive sympathetic activity in hypertension remain unresolved. Likely mechanisms contributing include elevated reflex afferent drive from both peripheral chemoreceptors 14,15 and kidney, 16,17 saltangiotensin II, 18-21 inflammation, [22][23][24] and respiration. 13,[25][26][27][28][29] Respiratory modulation of sympathetic activity or respiratory-sympathetic coupling has been observed in many sympathetic postganglionic outflows. 13,21,[28][29][30][31][32][33] Clinical studies have purported that by controlling breathing depth and rate (using RespeRate) blood pressure can be lowered 34 in patients with hypertension. 35 Recently, we found that in the spontaneously hypertensive (SH) rats, a genetic animal model of hypertension, 13 as well in rats submitted to chronic intermittent hypoxia, 27,29,36 there is augmented coupling of the central respiratory network to sympathetic circuits. This is expressed as elevations in sympathetic bursts in the late inspiratory (or beginning of postinspiratory; post-I) phases in the thoracic sympathetic nerve relative to age/sex-matched normotensive rats and is present before rats develop hypertension. 13 Simms et al 13 focused only on phrenic (central inspiratory) related modulation of sympathetic nerve activity and did not consider changes in expiratory neuronal activity at either the motor or neuronal level, so the central neural mechanisms for enhancing this coupling are unknown. In other models of hypertension (angiotensin II-salt hypertension), rostral ventrolateral medulla (RVLM) presympathetic neurons also show enhanced respiratory-related activity, 28 suggesting that this fundamental mechanism exists in both genetic and environmental induced hypertensive animal models. The unknown issue is whether enhanced respiratory-sympathetic coupling reflects either enhanced excitability of RVLM premotor sympathetic Abstract-A major aspect of hypertension is excessive sympathetic activity but the reasons for this remain elusive.Sympathetic tone is increased in the spontaneously hypertensive (SH) rat reflecting, in part, enhanced respiratorysympathetic coupling. We aimed to identify which respiratory cells might have altered properties. Using the working heart-brain stem preparation, we monitored simultaneously sympathetic and respiratory nerve activity in combination with intracellular recordings of physiologically characterized medullary presympathetic or respiratory neurons. In SH rats, respiratory modulation of both inspiratory and postinspiratory phases of sympathetic activity was larger relative to Wistar rats. An additiona...

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Effects of acute and long-term slow breathing exercise on muscle sympathetic nerve activity in untreated male patients with hypertension

Cited by 43 publications

References 47 publications

Acute effects of resonance frequency breathing on cardiovascular regulation

Acute effects of resonance frequency breathing on cardiovascular regulation

Increased cardio-respiratory coupling evoked by slow deep breathing can persist in normal humans

Specific Respiratory Neuron Types Have Increased Excitability That Drive Presympathetic Neurones in Neurogenic Hypertension

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