Acute effects of device-guided slow breathing on sympathetic nerve activity and baroreflex sensitivity in posttraumatic stress disorder

Abstract

Patients with posttraumatic stress disorder (PTSD) have elevated sympathetic nervous system reactivity and impaired sympathetic and cardiovagal baroreflex sensitivity (BRS). Device-guided slow breathing (DGB) has been shown to lower blood pressure (BP) and sympathetic activity in other patient populations. We hypothesized that DGB acutely lowers BP, heart rate (HR), and improves BRS in PTSD. In 23 prehypertensive veterans with PTSD, we measured continuous BP, ECG, and muscle sympathetic nerve activity (MSNA) at rest and during 15 min of DGB at 5 breaths/min ( n = 13) or identical sham device breathing at normal rates of 14 breaths/min (sham; n = 10). Sympathetic and cardiovagal BRS was quantified using pharmacological manipulation of BP via the modified Oxford technique at baseline and during the last 5 min of DGB or sham. There was a significant reduction in systolic BP (by -9 ± 2 mmHg, P < 0.001), diastolic BP (by -3 ± 1 mmHg, P = 0.019), mean arterial pressure (by -4 ± 1 mmHg, P = 0.002), and MSNA burst frequency (by -7.8 ± 2.1 bursts/min, P = 0.004) with DGB but no significant change in HR ( P > 0.05). Within the sham group, there was no significant change in diastolic BP, mean arterial pressure, HR, or MSNA burst frequency, but there was a small but significant decrease in systolic BP ( P = 0.034) and MSNA burst incidence ( P = 0.033). Sympathetic BRS increased significantly in the DGB group (-1.08 ± 0.25 to -2.29 ± 0.24 bursts·100 heart beats·mmHg, P = 0.014) but decreased in the sham group (-1.58 ± 0.34 to -0.82 ± 0.28 bursts·100 heart beats·mmHg, P = 0.025) (time × device, P = 0.001). There was no significant difference in the change in cardiovagal BRS between the groups (time × device, P = 0.496). DGB acutely lowers BP and MSNA and improves sympathetic but not cardiovagal BRS in prehypertensive veterans with PTSD. NEW & NOTEWORTHY Posttraumatic stress disorder is characterized by augmented sympathetic reactivity, impaired baroreflex sensitivity, and an increased risk for developing hypertension and cardiovascular disease. This is the first study to examine the potential beneficial effects of device-guided slow breathing on hemodynamics, sympathetic activity, and arterial baroreflex sensitivity in prehypertensive veterans with posttraumatic stress disorder.

Acute effects of resonance frequency breathing on cardiovascular regulation

“…In the healthy state, MSNA represents global sympathetic outflow to the skeletal muscle linked to BP regulation with strong feedback from the arterial baroreceptors (Wallin, ) and respiratory modulation (Habler, Janig, & Michaelis, ). The reduction in MSNA observed during slow breathing at either RF or RF + 1 was similar to that demonstrated in previous studies where slow breathing was of 10–15 min duration (Fonkoue et al, ; Harada et al, ; Hering et al, ; Oneda et al, ). Two prior studies in healthy subjects indicated no effect of slow breathing on MSNA but the duration of the breathing exercise was much shorter being 3 (Limberg et al, ) or 4 min (Raupach et al, ).…”

“…Tzeng et al () demonstrated that slow breathing in healthy subjects did not affect the arterial baroreflex when measured using the gold standard modified Oxford method and suggested that results indicating improvement in baroreflex function during slow breathing may have occurred as commonly used baroreflex assessment techniques may not be accurate in this setting. The sympathetic baroreflex function was also explored as a possible contributor to the changes in MSNA as Fonkue and colleagues observed that slow breathing improved the sympathetic baroreflex function (Fonkoue et al, ). However, this was not observed in our study as neither RF nor RF + 1 improved the slope of the sympathetic baroreflex function.…”

“…Slow breathing has long been recognized to exert beneficial effects in a range of disorders including those related to the cardiovascular system and those associated with anxiety. Breathing at a low pace (5–6 breaths per min) has been shown to acutely decrease blood pressure (BP) in patients with post‐traumatic stress disorder (Fonkoue et al, ), and in the longer term decrease BP in patients with hypertension (Hering et al, ). In patients with heart failure, slow breathing either performed acutely or chronically reduced the cardiovascular reactivity to mental stress and improved various aspects of health‐related quality of life (Lachowska, Bellwon, Morys, Gruchala, & Hering ).…”

“…Interventions aiming at altering the breathing frequency may affect the within‐breath modulation of MSNA and hence modulate steady state sympathetic tone. Acute slow breathing for 10–15 min was found to decrease MSNA in patients with hypertension (Hering et al, ; Oneda, Ortega, Gusmao, Araujo, & Mion, ), post‐traumatic stress disorder (Fonkoue et al, ) and those with heart failure (Harada et al, ), but failed to induce any change in healthy subjects when the breathing exercise was of 3 min duration (Limberg et al, ).…”

Sympathoexcitation and impaired arterial baroreflex sensitivity are linked to vascular inflammation in individuals with elevated resting blood pressure

“…; Fonkoue et al. ) and endothelial remodeling (Savoia et al. ) may have a role in impairing arterial BRS at the level of the nucleus tractus solitarii in the brainstem, or the baroreceptor nerve endings within the vasculature, thereby contributing to the maintenance of SNS overactivation and subsequent development of hypertension (Bristow et al.…”