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      The physiological effects of slow breathing in the healthy human

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      Breathe
      European Respiratory Society

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          Abstract

          Slow breathing practices have been adopted in the modern world across the globe due to their claimed health benefits. This has piqued the interest of researchers and clinicians who have initiated investigations into the physiological (and psychological) effects of slow breathing techniques and attempted to uncover the underlying mechanisms. The aim of this article is to provide a comprehensive overview of normal respiratory physiology and the documented physiological effects of slow breathing techniques according to research in healthy humans. The review focuses on the physiological implications to the respiratory, cardiovascular, cardiorespiratory and autonomic nervous systems, with particular focus on diaphragm activity, ventilation efficiency, haemodynamics, heart rate variability, cardiorespiratory coupling, respiratory sinus arrhythmia and sympathovagal balance. The review ends with a brief discussion of the potential clinical implications of slow breathing techniques. This is a topic that warrants further research, understanding and discussion.

          Key points
          • Slow breathing practices have gained popularity in the western world due to their claimed health benefits, yet remain relatively untouched by the medical community.

          • Investigations into the physiological effects of slow breathing have uncovered significant effects on the respiratory, cardiovascular, cardiorespiratory and autonomic nervous systems.

          • Key findings include effects on respiratory muscle activity, ventilation efficiency, chemoreflex and baroreflex sensitivity, heart rate variability, blood flow dynamics, respiratory sinus arrhythmia, cardiorespiratory coupling, and sympathovagal balance.

          • There appears to be potential for use of controlled slow breathing techniques as a means of optimising physiological parameters that appear to be associated with health and longevity, and that may extend to disease states; however, there is a dire need for further research into the area.

          Educational aims
          • To provide a comprehensive overview of normal human respiratory physiology and the documented effects of slow breathing in healthy humans.

          • To review and discuss the evidence and hypotheses regarding the mechanisms underlying slow breathing physiological effects in humans.

          • To provide a definition of slow breathing and what may constitute “autonomically optimised respiration”.

          • To open discussion on the potential clinical implications of slow breathing techniques and the need for further research.

          Abstract

          Slow breathing techniques have been used in asthma but are there effects in healthy individuals? http://ow.ly/gCPO30eQOPZ

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          Most cited references106

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          Impact of Reduced Heart Rate Variability on Risk for Cardiac Events: The Framingham Heart Study

          Although heart rate variability (HRV) is altered in a variety of pathological conditions, the association of reduced HRV with risk for new cardiac events has not been studied in a large community-based population. The first 2 hours of ambulatory ECG recordings obtained on subjects of the Framingham Heart Study who were free of clinically apparent coronary heart disease or congestive heart failure were reprocessed to assess HRV. Five frequency-domain measures and three time-domain measures were obtained. The associations between HRV measures and the incidence of new cardiac events (angina pectroris, myocardial infarction, coronary heart disease death, or congestive heart failure) were assessed with proportional hazards regression analyses. There were 2501 eligible subjects with a mean age of 53 years. During a mean follow-up of 3.5 years, cardiac events occurred in 58 subjects. After adjustment for age, sex, cigarette smoking, diabetes, left ventricular hypertrophy, and other relevant risk factors, all HRV measures except the ratio of low-frequency to high-frequency power were significantly associated with risk for a cardiac event (P = .0016 to .0496). A one-standard deviation decrement in the standard deviation of total normal RR intervals (natural log transformed) was associated with a hazard ratio of 1.47 for new cardiac events (95% confidence interval of 1.16 to 1.86). The estimation of HRV by ambulatory monitoring offers prognostic information beyond that provided by the evaluation of traditional cardiovascular disease risk factors.
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            Prospective Study of Heart Rate Variability and Mortality in Chronic Heart Failure: Results of the United Kingdom Heart Failure Evaluation and Assessment of Risk Trial (UK-Heart)

            Patients with chronic heart failure (CHF) have a continuing high mortality. Autonomic dysfunction may play an important role in the pathophysiology of cardiac death in CHF. UK-HEART examined the value of heart rate variability (HRV) measures as independent predictors of death in CHF. In a prospective study powered for mortality, we recruited 433 outpatients 62+/-9.6 years old with CHF (NYHA functional class I to III; mean ejection fraction, 0.41+/-0.17). Time-domain HRV indices and conventional prognostic indicators were related to death by multivariate analysis. During 482+/-161 days of follow-up, cardiothoracic ratio, SDNN, left ventricular end-systolic diameter, and serum sodium were significant predictors of all-cause mortality. The risk ratio for a 41.2-ms decrease in SDNN was 1.62 (95% CI, 1.16 to 2.44). The annual mortality rate for the study population in SDNN subgroups was 5.5% for >100 ms, 12.7% for 50 to 100 ms, and 51.4% for <50 ms. SDNN, creatinine, and serum sodium were related to progressive heart failure death. Cardiothoracic ratio, left ventricular end-diastolic diameter, the presence of nonsustained ventricular tachycardia, and serum potassium were related to sudden cardiac death. A reduction in SDNN was the most powerful predictor of the risk of death due to progressive heart failure. CHF is associated with autonomic dysfunction, which can be quantified by measuring HRV. A reduction in SDNN identifies patients at high risk of death and is a better predictor of death due to progressive heart failure than other conventional clinical measurements. High-risk subgroups identified by this measurement are candidates for additional therapy after prescription of an ACE inhibitor.
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              The enigma of Mayer waves: Facts and models.

              Mayer waves are oscillations of arterial pressure occurring spontaneously in conscious subjects at a frequency lower than respiration (approximately 0.1 Hz in humans). Mayer waves are tightly coupled with synchronous oscillations of efferent sympathetic nervous activity and are almost invariably enhanced during states of sympathetic activation. For this reason, the amplitude of these oscillations has been proposed as a surrogate measure of sympathetic activity, although in the absence of a clear knowledge of their underlying physiology. Some studies have suggested that Mayer waves result from the activity of an endogenous oscillator located either in the brainstem or in the spinal cord. Other studies, mainly based on the effects of sinoaortic baroreceptor denervation, have challenged this view. Several models of dynamic arterial pressure control have been developed to predict Mayer waves. In these models, it was anticipated that the numerous dynamic components and fixed time delays present in the baroreflex loop would result in the production of a resonant, self-sustained oscillation of arterial pressure. Recent analysis of the various transfer functions of the rat baroreceptor reflex suggests that Mayer waves are transient oscillatory responses to hemodynamic perturbations rather than true feedback oscillations. Within this frame, the amplitude of Mayer waves would be determined both by the strength of the triggering perturbations and the sensitivity of the sympathetic component of the baroreceptor reflex.
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                Author and article information

                Journal
                Breathe (Sheff)
                Breathe (Sheff)
                BREATHE
                breathe
                Breathe
                European Respiratory Society
                1810-6838
                2073-4735
                December 2017
                : 13
                : 4
                : 298-309
                Affiliations
                [1 ]Hunter Pain Clinic, Broadmeadow, Australia
                [2 ]ATUNE Health Centres, Warners Bay, Australia
                Author notes
                Article
                EDU-0098-2017
                10.1183/20734735.009817
                5709795
                c4f9fcee-c364-42f8-bc46-a2a2cc8aee54
                Copyright ©ERS 2017

                Breathe articles are open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.

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