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499
Hypertens Res
Vol.28 (2005) No.6
p.499-504
Original Article
How Does Deep Breathing Affect Office
Blood Pressure and Pulse Rate?
Hisao MORI, Hareaki YAMAMOTO, Masaomi KUWASHIMA, Saburo SAITO,
Hiroshi UKAI, Kouichi HIRAO, Mikio YAMAUCHI*, and Satoshi UMEMURA**
Little is known about the relation between deep breathing (DB) and blood pressure (BP). We studied the rela-
tionship between DB and BP in a large Japanese population. The subjects were recruited from randomly
selected clinics and hospitals that were members of a medical association, and divided into two groups. In
one group, BP was measured before and after taking 6 DB over a period of 30 s, and in the other group BP
was measured before and after a 30-s rest in a sitting position without DB. Before these measurements, all
patients rested 10 min or more in the waiting room and another 2 min or more in the doctor’s office. Anal-
yses were performed on data collected from 21,563 subjects. In both groups, systolic blood pressure (SBP),
diastolic blood pressure (DBP) and pulse rate (PR) were significantly reduced after DB or a 30-s rest com-
pared with the baseline measurements (p
<
0.001). SBP reductions were greater in the DB group than in the
30-s rest group (normotensives:
-
6.4±8.3 vs.
-
3.0±7.4 mmHg, p
<
0.001; untreated hypertensives:
-
9.6±10.2
vs.
-
5.9±9.1 mmHg, p
<
0.001; treated hypertensives:
-
8.3±9.6 vs.
-
4.4±8.3 mmHg, p
<
0.001). Greater BP
reductions were found in patients with a higher baseline BP in both the DB and 30-s rest groups. In con-
clusion, the present study showed a baseline BP-dependent BP reduction by DB, suggesting that BP mea-
surement should be done without DB in the office because DB lowers BP. (Hypertens Res 2005; 28: 499–504)
Key Words: office blood pressure, deep breathing, 30-s rest
Introduction
Deep breathing (DB) is believed to lower blood pressure
(BP), but no large population study has been conducted to
clarify the relationship between DB and office BP and pulse
rate (PR). Although the sixth report of the Joint National
Committee (JNC 6) (1) recommended that as a BP measure-
ment method, “two or more readings separated by 2 minutes
should be averaged,” and the seventh report of the Joint
National Committee (JNC 7) (2) recommendation was that at
least two measurements should be made and the average
recorded, there have been few reports of BP differences
between the first and second readings, which are generally
separated by a few min of rest in a sitting position in the
office. The aim of the present study was to clarify the effect of
DB and a 30-s rest in a sitting position on the office BP and
PR in both hypertensive and normotensive patients.
Methods
Collection of Data
We asked 19,055 clinics or hospitals in Japan that were mem-
bers of Japanese Medical and Dental Practitioners for the
Improvement of Medical Care (JMDPIMC) to participate in
the study. The clinics and hospitals were randomly selected
from locations throughout Japan to minimize the regional dif-
ferences in prevalence, treatment and control of hypertension
between rural and urban area (3) and comprised about 30% of
From Japanese Medical and Dental Practitioners for the Improvement of Medical Care, Tokyo, Japan; *Health Education Center Science Clinic, Yoko-
hama, Japan; and **Second Department of Internal Medicine, Yokohama City University, Yokohama, Japan.
Address for Reprints: Satoshi Umemura, M.D., Second Department of Internal Medicine, Yokohama City University, 3−9 Fukuura, Kanazawa-ku,
Yokohama 236−0004, Japan. E-mail: umemuras@med.yokohama-cu.ac.jp
Received December 8, 2004; Accepted in revised form April 12, 2005.
500
Hypertens Res Vol. 28, No. 6 (2005)
all the members of JMDPIMC. The study period was from
Jan 10 to Jan 31, 2002. The enrolled patients were divided
into two groups (Fig. 1). One group was instructed to take 6
DB at about 80% maximum capacity over a period of 30 s
(Deep Breathing Group: DBG) and the other was instructed to
sit quietly for 30 s without DB (Control Group: CG). Each
doctor was asked to enroll at least 5 normotensives, at least 5
untreated hypertensives and at least 10 treated hypertensive
patients in the DBG, and at least one of each of these types of
subjects in the CG.
Informed consent was obtained from all enrolled patients.
Before BP measurement, patients rested in the waiting room
for at least 10 min and in the office for 2 min. In the DBG, BP
and PR were measured before and after the taking of 6 DB in
30 s. In the CG, BP and PR were measured before and after
the 30-s rest in a seated position.
Hypertension was defined as a systolic blood pressure
(SBP) of 140 mmHg or more and/or a diastolic blood pressure
(DBP) of 90 mmHg or more. Patients who had fever, diar-
rhea, atrial fibrillation, frequent arrhythmias, liver cirrhosis,
glaucoma or chronic renal failure, and those who took minor
or major tranquilizers were excluded from the study.
Fig. 1. Study profile.
Table 1. Baseline Data of Deep Breathing Group and Control Group
DBG CG
p value
between
DBG and CG
Male ratio test 1
Normotensives 31.30%
*
NS
33.70%
*
NS
NS
Untreated hypertensives 42.60% * 43.60% * NS
Treated hypertensives 40.60% 40.50% NS
Age (years) test 2
Normotensives 57.3±16.5
*
*
56.8±17.0
*
*
NS
Untreated hypertensives 63.7±12.3 * 63.5±12.6 * NS
Treated hypertensives 67.5±10.7 67.5±10.9 NS
SBP test 2
Normotensives 124.0±15.8 (n
=
4,347) 122.5±15.1 (n
=
1,095)
<
0.01
Untreated hypertensives 158.0±16.9 (n
=
3,064) 156.0±15.9 (n
=
587)
<
0.01
Treated hypertensives 148.7±17.7 (n
=
11,203) 145.5±16.4 (n
=
1,220)
<
0.001
DBP test 2
Normotensives 73.5±10.3 (n
=
4,374) 72.6±10.3 (n
=
1,095)
<
0.05
Untreated hypertensives 89.3±12.3 (n
=
3,064) 88.4±12.1 (n
=
587) NS
Treated hypertensives 82.6±11.5 (n
=
11,203) 81.3±11.6 (n
=
1,220)
<
0.001
PR test 2
Normotensives 72.5±10.6 (n
=
4,342) 71.8±9.8 (n
=
1,092)
<
0.05
Untreated hypertensives 74.4±11.1 (n
=
3,060) 74.3±11.3 (n
=
585) NS
Treated hypertensives 73.5±11.2 (n
=
11,131) 73.0±11.3 (n
=
1,209) NS
DBG, deep breathing group; CG, control group; SBP, systolic blood pressure; DBP, diastolic blood pressure; PR, pulse rate; test 1,
χ
2
test; test 2, unpaired t-test; NS, not significant. *p
<
0.001 by one-way analysis of variance and a post-hoc multiple comparison test.
Mori et al: Deep Breathing and Blood Pressure
501
Table 2. Baseline Measurements of SBP, DBP and PR and Measurements after DB or a 30-s Rest
DB group Control group
Before DB After DB np value
First
measurements
Second
measurements
after 30-s
rest
np value
NOR
SBP 124.0±15.8 117.6±14.7 4,373
<
0.001 122.4±15.0 119.4±15.0 1,091
<
0.001
DBP 73.5±10.3 71.2±10.1 4,373
<
0.001 72.6±10.3 71.6±10.0 1,091
<
0.001
PR 72.5±10.6 71.8±10.4 4,334
<
0.001 71.8±9.8 71.0±9.6 1,087
<
0.001
UNT
SBP 158.0±16.9 148.4±16.7 3,060
<
0.001 156.0±15.9 150.1±16.0 586
<
0.001
DBP 89.3±12.3 86.3±12.0 3,060
<
0.001 88.4±12.1 86.4±12.2 586
<
0.001
PR 74.4±11.1 73.2±10.7 3,048
<
0.001 74.3±11.3 73.3±10.9 584
<
0.001
TRE
SBP 148.6±17.7 140.3±16.9 11,200
<
0.001 145.5±16.4 141.1±16.1 1,217
<
0.001
DBP 82.6±11.5 79.8±11.3 11,200
<
0.001 81.2±11.6 79.7±11.6 1,217
<
0.001
PR 73.5±11.2 72.1±10.9 11,111
<
0.001 73.0±11.3 71.9±10.7 1,204
<
0.001
SBP, systolic blood pressure; DBP, diastolic blood pressure; PR, pulse rate; DB, deep breathing; NOR, normotensive patients; UNT,
untreated hypertensives; TRE, treated hypertensives. Paired t-test.
Table 3. Changes in SBP, DBP and PR after DB and after a 30-s Rest
DB group Control group
p value
Change of
measurements
n
Change of
measurements
n
NOR
SBP
-
6.4±8.3 4,373
-
3.0±7.4 1,091
<
0.001
DBP
-
2.3±5.9 4,373
-
1.1±6.0 1,091
<
0.001
PR
-
0.8±5.6 4,334
-
0.8±4.7 1,087 NS
UNT
SBP
-
9.6±10.2 3,060
-
5.9±9.1 586
<
0.001
DBP
-
3.0±6.7 3,060
-
2.0±6.0 586
<
0.001
PR
-
1.2±5.7 3,048
-
1.0±5.0 584 NS
TRE
SBP
-
8.3±9.6 11,200
-
4.4±8.3 1,217
<
0.001
DBP
-
2.8±6.1 11,200
-
1.6±5.7 1,217
<
0.001
PR
-
1.4±5.6 11,111
-
1.1±4.8 1,204
<
0.05
SBP, systolic blood pressure; DBP, diastolic blood pressure; PR, pulse rate; NOR, normotensive patients; UNT, untreated hypertensives;
TRE, treated hypertensives; DB, deep breathing; NS, not significant. Unpaired t-test.
Table 4. Changes of Measurements after DB
SBP reduction
after DB
DBP reduction
after DB
PR reduction
after DB
Untreated hypertensives
-
9.6±10.2
*
*
-
3.0±6.7
NS
*
-
1.2±5.7
NS
*
Treated hypertensives
-
8.3±9.6
*
-
2.8±6.1
*
-
1.4±5.6
**
Normotensives
-
6.4±8.3
-
2.3±5.9
-
0.8±5.6
*p
<
0.001, **p
<
0.01 by one-way analysis of variance and a post-hoc multiple comparison test. SBP, systolic blood pressure; DBP, dias-
tolic blood pressure; PR, pulse rate; DB, deep breathing.
502
Hypertens Res Vol. 28, No. 6 (2005)
Statistical Analysis
Statistical analyses were carried out with Student’s t-test,
χ
2
test, or one-way analysis of variance and post-hoc multiple
comparison test using SPSS Version 10 software. Values of
p
<
0.05 were considered to indicate statistical significance.
All values were expressed as the mean±SD.
Results
Characteristics of Study Populations
The enrolled cases comprised 25,022 patients from 1,186
clinics and hospitals throughout Japan, and in 21,563 of these
cases, all the data necessary for analysis were available. The
DBG consisted of 4,377 normotensives, 3,066 untreated
hypertensives and 11,217 treated hypertensives. The CG con-
sisted of 1,096 normotensives, 587 untreated hypertensives
and 1,220 treated hypertensives (Fig. 1).
There were no significant differences in the sex ratio or age
of normotensives, untreated hypertensives, or treated hyper-
tensives between the DBG and CG groups. The percentage of
men was significantly lower in the normotensives than in the
hypertensives in both the DBG and CG. The mean age was
significantly different among the normotensives and hyper-
tensives in both the DBG and CG (Table 1).
Blood Pressure and Pulse Rate
Baseline SBP and DBP were significantly different among
the three groups in both the DBG and CG. PR in normoten-
sives was significantly different between the DBG and CG
(Table 1).
SBP, DBP and PR were significantly reduced after DB in
the normotensive, untreated hypertensive and treated hyper-
tensive patients (p
<
0.001). Moreover, in the CG, the second
measurements of SBP, DBP and PR were significant lower
than the first measurements (Table 2, p
<
0.001). Both DB and
a 30-s rest reduced BP and PR, and the reductions were
greater in the DBG than in the 30-s-rest group. A significantly
greater reduction in PR was found only in treated hyperten-
sive patients (Table 3). The reductions in BP and PR by DB
were greater in hypertensives than in normotensives (Table
4).
The decreases in SBP, DBP and PR following DB were sig-
nificantly correlated with the baseline SBP (r
=
-
0.349,
p
<
0.001, n
=
18,633), DBP (r
=
-
0.300, p
<
0.001, n
=
18,633), and PR (r
=
-
0.05, p
<
0.001, n
=
18,518), respec-
tively. In the treated patients of both groups, similar correla-
tions were found for SBP (r
=
-
0.351, p
<
0.001, n
=
11,200),
DBP (r
=
-
0.300, p
<
0.001, n
=
11,200), and PR (r
=
-
0.312,
p
<
0.001, n
=
11,111).
The higher the baseline SBP, the greater the reduction in
SBP after DB, although patients whose baseline SBP was less
than 100 mmHg showed an increase in SBP after DB (Fig. 2).
Fig. 2. Baseline SBP and change of SBP after deep breathing.
Mori et al: Deep Breathing and Blood Pressure
503
Discussion
In the present study, we found that DB decreased BP and PR,
and these decreases correlated with the baseline BP and PR,
respectively. Furthermore, we found that a 30-s rest in a sit-
ting position also decreased BP and PR, but to a lesser degree
than DB.
It is not clear why the DBG showed a higher baseline BP
than the CG. One possibility is that the instructions on how to
perform DB made the patients nervous and increased their
baseline BP. Even after adjusting for this difference in base-
line BP between the DBG and CG, the reduction in BP was
still greater in the former group.
DB is often used to examine the autonomic nervous system.
In such studies, the DB method used entails breathing deeply
five (4) or six times (5−10) in 1 min. In the present study, we
instructed the patients to take 6 DB at about 80% maximum
capacity over a period of 30 s. This protocol was used
because, in our pilot study, when patients were asked to 6 DB
over a period of 1 min, they sometimes held their breath,
resulting in increased BP and PR (Tables 5, 6).
The autonomic nervous system, through stimulation of the
arterial baroreceptor, pulmonary stretch receptors, and low-
pressure baroreceptors, may play important roles in the
changes of BP and PR associated with DB, although the
actual mechanisms are unknown.
Bernardi et al. reported that baroreflex activity could be
enhanced by slow breathing not only in healthy people but
also in patients with congestive heart failure, and they noted
that BP decreased with slower or deeper breathing due to the
relative increase of vagal activity, decreased sympathetic
activity and reduced afterload (11). Rajeev et al. pointed out
that the increments of SBP, DBP and PR in response to stress
were greater in hypertensives than in normal controls, and
that sympathetic nervous system activity was increased in
patients with essential hypertension (8). Yoshihara et al.
reported that there was no significant reduction of DBP in
sustained hypertensive patients after DB, but that patients
with white coat hypertension showed a significant reduction
of DBP after DB. They also showed that office SBP fell sig-
nificantly after DB in both sustained and white coat hyperten-
sives, and that there was no significant difference in the
degree of reduction between the two groups; these findings
suggested that measurements taken after DB are useful for
identifying white coat hypertensive patients in the office (4).
In the present study, because we did not measure home BP,
we were unable to confirm the efficacy of measurement after
DB for identifying white coat hypertension at the office. Our
study revealed a significant reduction in SBP, DBP and PR in
normotensives, untreated hypertensives and treated hyperten-
sives after DB, and also in the CG. We found a baseline-BP-
dependent BP decrease by DB. Though the actual reason for
the relationship between BP and DB is unknown, a similar
result (12) has been reported in a study using a device-guided
breathing exercise, which suggests the involvement of
increased sympathetic activity (13, 14), decreased baroreflex
function (15−17), and reduced arterial wall compliance (18).
In conclusion, the present study showed a baseline BP-
dependent BP reduction by DB, suggesting that office BP
measurement should be done without DB because DB lowers
BP.
References
1. Joint National Committee on Prevention, Detection, Evalu-
Table 5. Changes of Measurements before and after Deep Breathing in Pilot Study
Normotensives Untreated hypertensives Treated hypertensives
(n
=
118) (n
=
81) (n
=
217)
BDB ADB p value BDB ADB p value BDB ADB p value
SBP 117.6±15.2 111.1±13.2
<
0.001 151.1±20.1 142.9±20.6
<
0.001 145.3±17.3 136.5±16.6
<
0.001
DBP 70.5±10.1 68.3±10.4
<
0.001 87.5±14.6 84.8±11.2
<
0.05 81.0±11.4 77.6±10.6
<
0.01
PR 69.9±9.8 69.5±10.0 NS 74.9±10.4 71.7±10.0
<
0.001 73.0±11.9 71.6±10.9
<
0.02
Paired t-test. BDB, before deep breathing; ADB, after deep breathing; SBP, systolic blood pressure; DBP, diastolic blood pressure; PR,
pulse rate.
Table 6. Percentage of Measurements Increment before and after Deep Breathing in Pilot Study
Normotensives Untreated hypertensives Treated hypertensives
SBP 15/118 (12.7%) 8/81 (9.9%) 31/217 (14.3%)
DBP 8/118 (6.8%) 13/81 (16.0%) 45/217 (20.7%)
PR 38/118 (32.2%) 13/81 (16.0%) 63/217 (29.0%)
SBP, systolic blood pressure; DBP, diastolic blood pressure; PR, pulse rate.
504
Hypertens Res Vol. 28, No. 6 (2005)
ation, and Treatment of High Blood Pressure: The sixth
report of the Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pres-
sure. Arch Intern Med 1997; 157: 2413−2446.
2. Joint National Committee on Prevention, Detection, Evalu-
ation, and Treatment of High Blood Pressure: The seventh
report of the Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pres-
sure. JAMA 2003; 289: 2560−2572.
3. Wang Z, Wu Y, Zhao L, Li Y, Yang J, Zhou B, for the
Cooperative Research Group of the Study on Trends of Car-
diovascular Diseases in China and Preventive Strategy for
the 21st Century: Trends in prevalence, awareness, treat-
ment and control of hypertension in the middle-aged popu-
lation of China, 1992−1998. Hypertens Res 2004; 27: 703−
709.
4. Yoshihara K, Fukui T, Osawa H, et al: Deep breathing test
(DBT) in predicting white coat hypertension. Fukuoka
Igaku Zasshi 1993; 84: 395−401.
5. May O, Arildsen H, Moller M: Parasympathetic function
during deep breathing in the general population: relation to
coronary risk factors and normal range. J Intern Med 1999;
245: 267−294.
6. Torok T, Rudas L, Kardos A, Paprika D: The effects of pat-
terned breathing and continuous positive airway pressure on
cardiovascular regulation in healthy volunteers. Acta Phys-
iol Hung 1997−1998; 85: 1−10.
7. Diehl RR, Linden D, Berlit P: Determinants of heart rate
variability during deep breathing: basic findings and clinical
applications. Clin Auton Res 1997; 7: 131−135.
8. Kaushik RM, Mahajan SK, Rajesh V, Kaushik R: Stress
profile in essential hypertension. Hypertens Res 2004; 27:
619−624.
9. Igresias GM, Arauxo VD, Mallo FF, Cabezas CJ: The
baroreflex pathway and essential arterial hypertension. Rev
Clin Esp 1999; 186: 11−14.
10. Igresias GM, Arauxo VD, Cabezas CJ: Aging and efficacy
of the baroreflex arc. Analysis of a large sample of normal
individuals studied with a computerized technic. Rev Esp
Cardiol 1990; 43: 29−34.
11. Bernardi L, Porta C, Spicuzza L, et al: Slow breathing
increases arterial baroreflex sensitivity in patients with
chronic heart failure. Circulation 2002; 105: 143−145.
12. Talma R, Ariela A, Endna P, Benjamin G: Device-guided
breathing exercise reduce blood pressure: ambulatory and
home measurements. Am J Hypertens 2001; 14: 74−76.
13. Esler MD, Turner AG, Kaye DM, et al: Ageing effects on
human sympathetic neuronal function. Am J Physiol 1995;
268 (Regul Integr Comp Physiol 37): R278−R285.
14. Ng AV, Callister R, Johnson DG, Seals DR: Age and gen-
der influence sympathetic nerve activity at rest in healthy
humans. Hypertension 1986; 8: 147−153.
15. Eckberg DL, Drabinsky M, Braunwald E: Defective cardiac
parasympathetic control in patients with heart disease. N
Engl J Med 1971; 282: 877−883.
16. Gribbin B, Pickering TG, Sleight P, Peto R: Effect of age
and high blood pressure on baroreflex sensitivity in man.
Circ Res 1971; 29: 424−431.
17. Laitinen T, Hartikainen J, Vanninen E, Niskanen L, Geelen
G, Lansimies E: Age and gender dependency of baroreflex
sensitivity in healthy subjects. J Appl Physiol 1998; 84:
576−583.
18. Randall O, Esler M, Culp B, Julius S, Zweifler A: Determi-
nants of baroreflex sensitivity in man. J Lab Clin Med 1978;
91: 514−519.
