ORIGINAL ARTICLE Regular slow-breathing exercise effects on blood pressure and breathing patterns at rest DE Anderson, JD McNeely and BG Windham Clinical Research Branch, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA Previous studies reported that a device-guided slow- breathing (DGB) exercise decreases resting blood pressure (BP) in hypertensive patients. This study investigated the effects of daily practice of DGB on (a) 24-h BP and breathing patterns in the natural environ- ment, as well as (b) BP and breathing pattern during clinic rest. Altogether, 40 participants with pre-hyperten- sion or stage 1 hypertension were trained to decrease breathing rate through DGB or to passively attend to breathing (control, CTL) during daily 15-min sessions. The participants practiced their breathing exercise at home for 4 weeks. The DGB (but not the CTL) interven- tion decreased clinic resting BP, mid-day ambulatory systolic BP (in women only) and resting breathing rate, and increased resting tidal volume. However, 24-h BP level was not changed by DGB or CTL interventions, nor was overnight breathing pattern. These findings are consistent with the conclusion that a short-term, autonomic mechanism mediated the observed changes in resting BP, but provided no evidence that regular DGB affected factors involved in long-term BP regu- lation. Additional research will be needed to determine whether 24-h BP can be lowered by a more prolonged intervention. Journal of Human Hypertension advance online publication, 4 March 2010; doi:10.1038/jhh.2010.18 Keywords: BP; breathing; tidal volume Introduction Several previous studies have reported that regular practice of device-guided breathing (DGB) decreases resting blood pressure (BP) of hyper- tensive patients. 1–8 However, only three of the studies reported to date involved randomized clinical trials. Two of those did not measure BP in the natural environment, 3,8 and the third was unable to confirm greater effects than in a control group. 7 Whether the effects of DGB observed in the clinic setting extend to the natural environment is an important issue that needs to be investigated in a randomized clinical trial with 24-h BP monitoring preceding and following the DGB intervention. A study with 24-h BP monitoring would also be relevant to the mechanism by which the enduring BP changes are generated. Performance of DGB itself is accompanied by increased cardiopulmonary stretch receptor stimulation that reduces sympathetic efferent fibre discharge, resulting in peripheral vasodilation. 9 Thus, acute decreases in BP during DGB are mediated, at least in part, by decreases in sympathetic and increases in parasympathetic nervous system activity. 10 Long-term changes in BP are mediated, however, not by changes in autonomic nervous system activity, but by factors that change the set point for BP. 11 Renal sodium regulation is sensitive to changes in breathing pattern that alter blood gas concentrations. Previous studies of DGB have found not only that tidal volume increases as breathing rate falls, but also that end tidal CO 2 (PetCO 2 ) decreases, apparently because of improved gas transfer associated with deeper breath- ing. 12 To date, however, no studies have examined possible changes in resting breathing rate, tidal volume, minute ventilation or PetCO 2 in response to regular practice of DGB. If PetCO 2 chronically decreased in response to regular DGB, long-term effects on BP could involve alterations in blood gases and acid–base balance that alter total body sodium levels. The effectiveness of DGB depends on the fre- quency of practice. For example, Elliott et al. 6 found that a 180-min practice of DGB over an 8-week interval was a threshold for the occurrence of significant decreases in systolic BP. Although pre- vious interventions were each of 8 weeks duration, several found that BP decreased during the first 3–4 weeks before levelling off. 3–5 Received 11 June 2009; revised 11 September 2009; accepted 5 November 2009 Correspondence: Dr DE Anderson, Osher Center for Integrative Medicine, Campus Box 1726, University of California at San Francisco, San Francisco, CA 94143-1726, USA. E-mail: Andersod@mail.nih.gov Journal of Human Hypertension (2010), 1–7 & 2010 Macmillan Publishers Limited All rights reserved 0950-9240/10 $32.00 www.nature.com/jhh