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Long‐Term Effects of Device‐Guided Slow Breathing on Autonomic Control of Blood Pressure at Rest and During Stress in Post‐Traumatic Stress Disorder
Author(s) -
Fonkoue Ida T,
Jones Toure N,
Vemulapalli Monica,
Kankam Melanie,
Park Jeanie
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.745.7
Subject(s) - blood pressure , medicine , heart rate , baroreflex , breathing , respiratory rate , heart rate variability , sympathetic nervous system , cardiology , autonomic nervous system , biofeedback , anesthesia , physical therapy
Post‐traumatic stress disorder (PTSD) is characterized by augmented sympathetic nervous system (SNS) reactivity, impaired baroreflex sensitivity (BRS), and an increased risk for developing hypertension and cardiovascular disease. We recently showed that device‐guided slow breathing (DGB) using the RESPeRATE device acutely lowers blood pressure (BP) and muscle sympathetic activity (MSNA) and improves sympathetic BRS in PTSD. The aim of this study was to determine if long‐term daily DGB leads to sustained improvements in resting MSNA, BP, sympathetic BRS, and neurocirculatory reactivity during mental stress in combat veterans with PTSD. 19 post 9/11 veterans with PTSD (age, 36±2 years) were enrolled and randomized to either 8 weeks of DGB (n=9) versus an identical Sham device (n=10) for 15 minutes daily. Using biofeedback and musical tones, DGB guided respiratory rate (RR) to a subphysiologic rate of 5–6 breaths/min, while Sham guided RR to a normal rate of 12–14 breaths/min. BP, heart rate (HR), RR and MSNA were measured at rest and during 3 minutes of mental arithmetic (MA). Sympathetic and cardiovagal BRS were assessed with pharmacologic manipulation of BP using the modified Oxford technique. All physiologic measures were obtained before, and after 8 weeks of breathing intervention. Age, BMI, BP and HR were similar between the groups, while baseline MSNA at rest was greater in the DGB group pre‐intervention (p=0.048). Contrary to our hypothesis, there was no difference in the change in resting systolic BP (visit*group, p=0.097), diastolic BP (visit*group, p=0.571), HR (visit*group, p=0.323) and RR (visit*group, p=0.304) after 8 weeks of DGB versus Sham. There was a trend towards a difference in change in resting MSNA between the groups (visit*group, p=0.081). However, contrary to our hypothesis, there was no change in resting MSNA from pre to post 8 weeks of DGB (19±4 vs 20±2 burst/min, p>0.05), while there was an increase in resting MSNA after 8 weeks of Sham (9±2 vs 19±3 burst/min, p<0.001). There was no difference in change in cardiovagal BRS between the groups (visit*group, p= 0.139). Meanwhile, sympathetic BRS (visit*group, p=0.031) was not altered by 8 weeks of DGB (−1.47±0.5 vs 1.13±0.4, p=0.401), but improved with 8 weeks of Sham (−0.63±0.3 vs 1.45±0.4, p=0.032). During stress, neural and hemodynamic responses to MA (time*visit*group, p >0.05 for BP, HR and MSNA) were not different between the treatment groups. In summary, although our previous data showed that DGB acutely improves SNS activity and regulation in PTSD, we observed no sustained improvements in resting MSNA, BRS, hemodynamics, or neurocirculatory reactivity during mental stress with long‐term DGB in PTSD. Support or Funding Information Supported by NIH HL‐098744, NIH DK‐00756, VA Merit I01CX001065, AHA 15CSA24340001 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .