Long‐term Device Guided Slow Breathing Decreases Sympathetic Nervous Reactivity to Stress in Post‐Traumatic Stress Disorder

Abstract

Posttraumatic stress disorder is characterized by augmented sympathetic reactivity, impaired baroreflex sensitivity, and an increased risk for developing hypertension and cardiovascular disease. We recently showed that device‐guided slow breathing (DGB), in which breathing rates are lowered to subphysiologic levels using a biofeedback device, acutely lowers blood pressure (BP) and muscle sympathetic activity (MSNA) and improves sympathetic baroreflex sensitivity (BRS) in post‐traumatic stress disorder (PTSD). The aim of this study was to assess the potential long‐term benefits of DGB on MSNA, hemodynamics, and BRS in patients with PTSD at rest and during stress. We hypothesized that long‐term DGB will further improve sympathetic BRS, lower BP and MSNA in PTSD. Twenty five young adults, clinically diagnosed with PTSD, were studied and randomized to either 8 weeks of DGB (n=12; age, 36±2 years; BMI, 30±2 Kg/m2) or 8 weeks of an identically looking Sham device (n=13; age, 34±2 years; BMI, 28±2 Kg/m2). DGB guided the participants to a breathing rate of 5–6 breaths/min while Sham guided breathing to 14 breaths/min. BP, heart rate (HR) and MSNA was measured at rest and during 3 min of mental arithmetic. Sympathetic and cardiovagal BRS were assessed using the modified oxford technique. Measurements were done during two laboratory visits, before and after 8 weeks of 15 min of at‐home breathing daily. Both groups (DGB and Sham) were matched for age, BMI, resting MSNA, BP and heart rate (HR). Resting MSNA, BP and HR remain comparable (condition*device, p>0.05) before and after the 8 weeks (condition effect) in both breathing groups. Likewise, the change in sympathetic and cardiovagal BRS was not different between the two groups (condition*device, p>0.05). Interestingly, 8 weeks of DGB significantly decreased minute by minute (time effect) MSNA reactivity to mental arithmetic when expressed as burst frequency (time*condition*device, p= 0.006) or burst incidence (time*condition*device, p= 0.004) compared to 8 weeks of sham, suggesting a sustained effect of chronic DGB on sympathetic reactivity to mental stress in PTSD. Contrary to our hypothesis, long term DGB did not lower (time*condition*device, p>0.05) systolic BP, diastolic BP or HR responses to stress compared to sham. However, DGB but not sham tended to decrease pulse pressure reactivity after 8 weeks of intervention (time*condition*device, p= 0.06), due to the tendency for low systolic BP reactivity post DBG. In summary, our data suggest that the long‐term use of DGB leads to a sustained dampening of sympathetic reactivity and trend towards improved pulse pressure reactivity to mental stress. Taken together, these results suggest that long term use of DGB may have beneficial effects on neurocardiovascular reactivity in individuals with PTSD.Support or Funding InformationThis work was supported by National Institutes of Health (NIH) Grant R01 HL135183; NIH R61 AT010457, VA Merit I01CX001065, the Department of Veterans Affairs, Veterans Health Administration and the Office of Research and Development, Decatur, Georgia.