Is the effect of slow breathing on blood pressure a function of prehypertension and body weight?

Abstract

Overweight and obesity are well‐known risk factors for hypertension, but some few subjects have a high prevalence of obesity but a relatively low prevalence of hypertension. The reduction of respiratory rate lowers blood pressure (BP) in hypertensive and prehypertensive subjects by a modulation of autonomic nervous system (ANS) activity at both central and peripheral (baroreflex) levels. HRV is a noninvasive and useful tool for assessment of ANS function. The Valsalva ratio (VR) may be used as a surrogate marker of baroreflex activity. The aim of this study was to evaluate the effect of slow breathing on cardiovascular variables, HRV indices and VR in overweights with normal and increased BP.113 men recruited from V.N. Karazin Kharkiv National University international student population were divided into four groups according to blood pressure and body weight into normotensives with normal weight and overweight and prehypertensives with normal weight and overweight (Table 1). The written informed consents were obtained. The ECG was continually recorded during 5 min resting and slow breathing (6 breaths/min) stages and HR, LF and HF power expressed in absolute units were obtained by CardioLab software (Ukraine). The measurements of systolic and diastolic BP (SBP and DBP) were conducted at the end of each stage (Nissei WS‐1011, Japan). The VR was the ratio of max/min RR interval during the maneuver performed after resting and slow breathing stages. Three‐way repeated measures MANOVA with Bonferroni correction was used to test for possible effects of PHT, overweight, slow breathing, and their interaction on cardiovascular and HRV variables. All analyses were conducted using SPSS 22.In congruence with previous reports prehypertensive subjects with normal weight and overweight demonstrated reduction of SBP from 129.72±1.29 to 125.33±1.45 mm Hg (P=0.008) and from 131.43±1.03 to 128.54±1.16 mm Hg (P=0.029), respectively, as a result of slowing breathing rate. In both normotensive groups SBP did not change significantly. The VR increased in normotensives with normal weight from 1.89±0.05 to 2.00±0.06 (P=0.013), in prehypertensives with normal weight from 1.77±0.08 to 1.95±0.09 (P=0.005), and in prehypertensives with overweight from 1.73±0.06 to 1.85±0.07 (P=0.026), indicating improvement of baroreflex regulation during slow breathing, in congruence with previous reports. However, in normotensive overweights VR did not change significantly. The LnLF HRV power increased in all the groups. However, LnHF HRV power increased only in normotensive overweight subjects from 6.81±0.18 to 7.31±0.16 Lnms2 (P=0.008) indicating increased parasympathetic lability in this group.The effect of slow breathing is a function of prehypertension but not of body weight. Prehypertensives with normal weight and overweight demonstrated reduction of SBP as a result of slow breathing. Only normotensive overweight subjects demonstrated an increase of LnHF power in addition to LF HRV power indicating increased parasympathetic lability in this group, the advantage preventing from increased blood pressure despite presence of overweight. Why only in this group VR did not change due to slow breathing remains unclear and require study.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.