Time sequence of autonomic changes induced by daily slow-breathing sessions

Modesti, Pietro Amedeo; Ferrari, Antonella; Bazzini, Cristina; Boddi, Maria

doi:10.1007/s10286-014-0255-9

Cited by 20 publications

(10 citation statements)

References 35 publications

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“…Modesti et al . () reported that daily session of slow‐breathing increased parasympathetic modulation. Regular exercise improves HRV and parasympathetic activity, and reduces sympathetic activity.…”

Section: Discussionmentioning

confidence: 98%

Breathing exercise combined with cognitive behavioural intervention improves sleep quality and heart rate variability in major depression

Chien

Chung

Yeh

et al. 2015

Journal of Clinical Nursing

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Section: Discussionmentioning

confidence: 98%

Breathing exercise combined with cognitive behavioural intervention improves sleep quality and heart rate variability in major depression

Chien

Chung

Yeh

et al. 2015

Journal of Clinical Nursing

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“…Under physiological conditions RRI assay could detect phasic increase in renal vascular resistance induced by sympathetic activation obtained by cold pressor test or handgrip; in the same subjects the increase of blood volume by acute hydration resulted in an RRI decrease [27]. Repeated daily sessions of music-guided slow-breathing increased parasympathetic modulation and decreased RRI early in the study .These changes were being followed by a positive modulation of baroflex sensitivity and decrease in blood pressure [50]. In patients with heart failure high RRI values were associated with increased intrarenal vascular resistance due to neurohormonal hyperactivity and independently predicted heart failure progression [51].…”

Section: Role Of Arterial Vascular Resistancementioning

confidence: 95%

Renal Ultrasound (and Doppler Sonography) in Hypertension: An Update

Boddi

2016

Advances in Experimental Medicine and Biology

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Ultrasound (US) allows the non-invasive evaluation of morphological changes of kidney structure (by means of B-Mode) and patterns of renal and extrarenal vascularization (by means of color-Doppler and contrast-enhanced US). In hypertensive subjects it offers a relevant contribution to the diagnosis of early renal damage, acute or chronic nephropathies and nephrovascular disease. However, morphological changes are often detected late and non-specific and in recent years evidence has increased regarding the clinical relevance of renal resistive index (RRI) for the study of vascular and renal parenchymal renal abnormalities. RRI is measured by Doppler sonography in an intrarenal artery, as the difference between the peak systolic and end-diastolic blood velocities divided by the peak systolic velocity. At first RRI was proved to be a marker of renal disease onset and progression; later the influence of systemic vascular properties on RRI was shown and authors claimed its use as an independent predictor of cardiovascular risk rather than of renal damage. Indeed, renal vascular resistance is only one of several renal (vascular compliance, interstitial and venous pressure), and extrarenal (heart rate, pulse pressure) determinants that concur to determine RRI individual values but not the most important one. The clinical relevance of RRI measurement as a surrogate endpoint of specific renal damage or/and as surrogate endpoint of atherosclerotic diffuse vascular damage is still debated.To summarize, from the literature: (a) In hypertensives with normal renal function and no albuminuria, especially in younger people, RRI is an early marker of renal damage that is especially useful when hypertension and diabetes concur in the same subjects. In these subjects RRI could improve current clinical scores used to stratify early renal damage. In older subjects RRI increases in accordance with the increase in systemic vascular stiffness and, because of this close relationship, RRI is also a marker of systemic atherosclerotic burden and the role of renal determinants can weaken. The clinical relevance was not specifically investigated. (b) In transplant kidney and in chronic renal disease high (>0.80) RRI values can independently predict renal failure. The recent claim that systemic (pulse pressure) rather than renal hemodynamic determinants sustain this predictive role of RRI, does not significantly reduce this predictive role of RRI. (c) Doppler ultrasound allows diagnosis and grading of renal stenosis in both fibromuscolar dysplastic and atherosclerotic diseases. Moreover, by RRI assay Doppler ultrasound can indirectly measure the hemodynamic impact of renal artery stenosis on the homolateral kidney, by virtue of the stenosis-related decrease in pulse pressure. However, in elderly subjects with atherosclerotic renal artery stenosis coexisting renal diseases can independently increase RRI by the augmentation in renal vascular stiffness and tubulo-interstitial pressure and hidden changes due to renal artery stenosis.

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“…Controlled clinical trials in patients with hypertension have shown reductions in resting blood pressure and heart rate by long-term practice of SDB (Zou et al, 2017). Improvement in baroreflex sensitivity, increased parasympathetic modulation, and decreased sympathetic tone are proposed as possible underlying mechanisms (Cernes & Zimlichman, 2015;Modesti, Ferrari, Bazzini, & Boddi, 2015). In a recent clinical trial, hypertensive patients practiced controlled breathing at 0.1 Hz with or without inspiratory load of 20 cmH 2 O for 8 weeks.…”

Section: Clinical Applications Of Slow Deep Breathing With Inspiramentioning

confidence: 99%

Influence of inspiratory threshold load on cardiovascular responses to controlled breathing at 0.1 Hz

et al. 2019

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Slow, deep breathing is being used as a self‐management intervention for various health conditions including pain and hypertension. Stimulation of the arterial baroreceptors and increased vagal modulation are among the proposed mechanisms for the therapeutic effects of slow, deep breathing. We investigated whether adding inspiratory threshold load can enhance the cardiovascular responses to controlled breathing at the frequency of 0.1 Hz, a common form of slow, deep breathing. Healthy volunteers (N = 29) performed controlled breathing at 0.1 Hz (6 breaths/minute) without load and with inspiratory threshold loads of 5 cmH2O and 10 cmH2O. Respiratory airflow, heart rate, and blood pressure were continuously recorded. The amplitude of the systolic blood pressure variation during respiratory cycles increased with increasing loads. Respiratory sinus arrhythmia was higher during controlled breathing at 0.1 Hz with the load of 10 cmH2O compared to without load. Baroreflex sensitivity was not affected by loads. The effect of loads on respiratory sinus arrhythmia was mediated by increasing the amplitude of systolic blood pressure variation during respiratory cycles. These results suggest that applying small inspiratory threshold loads during controlled breathing at 0.1 Hz increases cardiac vagal modulation by this breathing exercise. This effect seems to be mediated by stronger stimulation of the arterial baroreceptors because of larger systolic blood pressure swings along the respiratory cycle. The potential benefit of long‐term practice of controlled breathing at 0.1 Hz with inspiratory threshold loads on baroreflex function and cardiac vagal control needs to be investigated, particularly in pain and hypertension patients.

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Time sequence of autonomic changes induced by daily slow-breathing sessions

Abstract: Repeated daily session of music-guided SB increased parasympathetic modulation and decreased renal resistive index early in the study. These changes were being followed by a positive modulation of BRS and blood pressure reduction.

Cited by 20 publications

References 35 publications

Breathing exercise combined with cognitive behavioural intervention improves sleep quality and heart rate variability in major depression

Breathing exercise combined with cognitive behavioural intervention improves sleep quality and heart rate variability in major depression

Renal Ultrasound (and Doppler Sonography) in Hypertension: An Update

Influence of inspiratory threshold load on cardiovascular responses to controlled breathing at 0.1 Hz

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