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Exploring mechanisms of blood pressure regulation in response to device-guided and non-device-guided slow breathing: A mini review

Published:November 14, 2022DOI:https://doi.org/10.1016/j.autneu.2022.103050

      Highlights

      • While acutely, device-guided slow breathing lowers muscle sympathetic nerve activity, results are minimized long-term.
      • Results from most studies deploying direct and indirect measures of autonomic function are consistent.
      • A small body of evidence also suggests that non-device-guided breathing is effective in improving vascular function.

      Abstract

      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

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