Author: Harika Pingali1, Stacy D Hunter2
Affiliation: <sup>1</sup> Texas State University Department of Health & Human Performance, San Marcos, TX, USA.
<sup>2</sup> Texas State University Department of Health & Human Performance, San Marcos, TX, USA. Electronic address: stacy.d.hunter@gmail.com.
Conference/Journal: Auton Neurosci
Date published: 2022 Nov 14
Other:
Volume ID: 244 , Pages: 103050 , Special Notes: doi: 10.1016/j.autneu.2022.103050. , Word Count: 311
Background:
Hypertension is a widespread disease that, if persistent, increases the risks of coronary heart disease mortality and morbidity. Slow breathing is a recommended blood pressure-lowering strategy though the mechanisms mediating its effects are unknown.
Objective:
This review aims to evaluate autonomic and vascular function as potential mediators driving BP adaptive responses with slow breathing.
Methods:
We searched EBSCO host, Web of Science, Cochrane Central Register of Controlled Trials, and PubMed using key words for optimized search results.
Results:
Nineteen studies were included in this review (11 device-guided; 8 non-device-guided breathing). Though some studies showed increased vagally mediated components of heart rate variability during slow breathing, results from acute and long-term studies were incongruent. Increases in baroreflex sensitivity (BRS) following a single device-guided slow breathing bout were noted in normotensive and hypertensive adults. Long-term (4 weeks to 3 months) effects of slow breathing on BRS were absent. Device-guided breathing resulted in immediate reductions in muscle sympathetic nerve activity (MSNA) in normo- and hyper-tensive adults though results from long-term studies yielded inconsistent findings. Non-device-guided slow breathing posed acute and chronic effects on vascular function with reductions in arterial stiffness in adults with type I diabetes and increases in microvascular endothelial function in adults with irritable bowel syndrome. Non-device guided breathing also reduced pro-inflammatory cytokines in healthy and hypertensive adults in acute and chronic studies. No adverse effects or non-adherence to treatment were noted in these trials.
Conclusion:
Device-guided slow breathing is a feasible and effective modality in improving BRS, HRV, and arterial stiffness though its long-term effects are obscure. Though less evidence exists supporting the efficacy of non-device-guided slow breathing, acute and chronic studies demonstrate improvements in vascular function and inflammatory cytokines. More studies are needed to further explore the long-term effects of slow breathing in general and non-device-guided breathing in particular.
Keywords: Heart rate variability; Inflammation; Pranayama; Slow breathing; Sympathetic activity.
PMID: 36410208 DOI: 10.1016/j.autneu.2022.103050