Effect of Slow Breathing on Normal and Overweight Prehypertensives
Authors: Idowu Florence Olawunmi , Shekh Vera Evgenievna , Chima Esther Chinwenmeri , Ahmad Rukaya Ahouiza 
Published: April 2020

One of the pathological conditions employing the heart rate variability analysis is a dysregulation of the autonomic nervous system that leads to the development of hypertension. It was shown that slow breathing can reduce blood pressure (BP) in hypertensive patients but not in normotensives. Very little is known if it reduces blood pressure in prehypertensives and if body weight influences the effect of slow breathing.

A total of 194 men were recruited from the international student population of the V.N. Karazin Kharkiv National University. The cohort was subdivided into four groups with systolic blood pressure (SBP) 114.8±0.7 mm Hg referred as normotensive and 129.0±0.5 mm Hg as prehypertensive, with BMI 21.3±0.2kg/m2 labelled as normal weigh and 27.7±0.3 kg/m2 as overweight. Written informed consent was obtained from all participants.

After 5 minutes resting stage breathing rate was slowed to 6 breaths per minute (CardioLab CS, XAI‐Medica, Ukraine) for 5 minutes.The ECG was continually recorded, LF and HF HRV power was expressed in absolute units. The HF power was interpreted as a measure of cardiovagal outflow, LF power as an index of baroreflex activity and possibly as a sympathoinhibitory arm of baroreflex according to our hypothesis described previously. Measurements of SBP and DBP were conducted using an automatic digital sphygmomanometer (Nissei WS‐1011, Japan). Blood pressure was measured at 4.5 minute of each stage. MANOVA with Bonferroni correction was used to test for effects of slow breathing, prehypertension, and body weight on cardiovascular and HRV variables. All analyses were conducted using SPSS 22.

The resting SBP was higher in overweight than in normal weight prehypertensives at rest and at the end of slow breathing stage. Slow breathing reduced significantly SBP in prehypertensives with normal weight and overweight but not in normotensive participants (Fig.
).

The prehypertensives with normal weight had higher resting LnLF and LnHF than normotensives with normal weight (7.1±0.1 vs. 6.7±0.1 and 7.4±0.1 vs. 7.0±0.1 Lnms2, P=0.004 and P=0.002, respectively). Possibly young men with normal weight only developing hypertension used their resources of baroreflex (or sympathoinhibitory) and cardiovagal activity for the controlling of blood pressure. No difference in LnLF and LnHF were found between overweights.

The LnLF and LnHF power increased more in normal weight normotensives than in prehypertensives indicating higher reserves of baroreflex (or sympathoinhibitory) and cardiovagal activities (Fig.
).

Overweight normotensives had the increment of LnLF power significantly lower compared with normal weight normotensives (Fig.
). This finding may be explained by exhausted function of baroreflex or by depletion of resources inhibiting sympathetic nervous system activity.

In conclusion, slowing the respiratory rate to 6 breaths per minute led to the significant reduction of SBP in prehypertensives with normal weight and overweight. The resting cardiovagal and baroreflex (or sympathoinhibitory) activities were more in prehypertensives than in normotensives with normal weight, but during breathing these differences were no longer significant. Between overweight normotensives and prehypertensives, no difference in HRV was found.

Effect of slow breathing and body weight on SBP in normotensive (A) and prehypertensive (B) young men. *P<0.05, ** P<0.01, *** P<0.001. Data are expressed as means±SE.

Figure 1

Effect of slow breathing, prehypertension, and body weight on LnLF (A) and LnHF power (B).* P<0.05, ** P<0.01. Data are expressed as means±SE.

Figure 2