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The effects of slow breathing on

affective responses to pain stimuli: An
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Alex Zautra

Pain

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PAIN 149 (2010) 12–18

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Research papers

The effects of slow breathing on affective responses to pain stimuli:

An experimental study
Alex J. Zautra a,*, Robert Fasman a, Mary C. Davis a, Arthur D. (Bud) Craig b
a
Department of Psychology, Arizona State University, Tempe, AZ, USA
b
Atkinson Research Laboratory, Barrow Neurological Institute, Phoenix, AZ, USA

a r t i c l e i n f o a b s t r a c t

Article history: This study examined whether breathing rate affected self-reported pain and emotion following thermal
Received 15 March 2009 pain stimuli in women with fibromyalgia syndrome (FM: n = 27) or age-matched healthy control women
Received in revised form 8 September 2009 (HC: n = 25). FM and HC were exposed to low and moderate thermal pain pulses during paced breathing
Accepted 2 October 2009
at their normal rate and one-half their normal rate. Thermal pain pulses were presented in four blocks of
four trials. Each block included exposure to both mild and moderate pain trials, and periods of both nor-
mal and slow paced breathing. Pain intensity and unpleasantness were recorded immediately following
Keywords:
each pain trial, and positive and negative affect were assessed at the end of each block of trials. Compared
Slow breathing
Pain
to normal breathing, slow breathing reduced ratings of pain intensity and unpleasantness, particularly for
Fibromyalgia moderately versus mildly painful thermal stimuli. The effects of slow breathing on pain ratings were less
Affect reliable for FM patients than for HCs. Slow versus normal breathing decreased negative affect ratings fol-
lowing thermal pain pulses for both groups, and increased positive affect reports, but only for healthy
controls with high trait negative affect. Participants who reported higher levels of trait positive affect
prior to the experiment showed greater decreases in negative affect as a result of slow versus normal
breathing. These experimental findings provide support for prior reports on the benefits of yogic breath-
ing and mindful Zen meditation for pain and depressed affect. However, chronic pain patients may
require more guidance to obtain therapeutic benefit from reduced breathing rates.
Ó 2009 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

1. Introduction of the two opposing components of the efferent Autonomic Ner-

Meditation has recently been advanced as a self-regulation strat-
egy particularly beneficial to those in chronic pain [13,15,21,27,33].
Neural models of how meditative techniques might work, however,
are underdeveloped. In this experiment, we applied a model of pain
as a homeostatic emotion [5] to test whether a key component of
meditation, slow breathing, reduces pain unpleasantness for a group
of chronic pain patients and healthy controls.
Pain can be regarded as a negative emotion that is part of the
arousal/stress system characterized by increased sympathetic acti-
vation [5,16,19]. This conceptualization builds on the James-Lange
tradition by positing that the neurobiological basis for emotion in
the human forebrain is directly and neuroanatomically related to
the organization of homeostatic afferent and efferent processing.
A progression of re-representations of the homeostatic condition
of the body is present in the insular cortex of humanoid primates
that becomes lateralized to parallel the asymmetric representation
* Corresponding author. Address: Department of Psychology, Box 871104, Ari-
zona State University, Tempe, AZ 85287, USA. Tel.: +1 480 727 8227; fax: +1 480
965 8544.
E-mail address: alex.zautra@asu.edu (A.J. Zautra).
vous System (ANS), the sympathetic and the parasympathetic sys-
tems, respectively, in the right and left anterior insular and
anterior cingulate cortices. The homeostatic neuroanatomical
model of emotion [4] proposes that the left forebrain is associated
predominantly with parasympathetic activity, and thus with nour-
ishment, safety, positive affect, approach (appetitive) behavior, and
group-oriented (affiliative) emotions, while the right forebrain is
associated predominantly with sympathetic activity, and thus with
arousal, danger, negative affect, withdrawal (aversive) behavior,
and individual-oriented (survival) emotions.
Individuals vary in the homeostatic regulation of pain experi-
ence, leading in some cases to a diagnosis of chronic pain syn-
dromes. The connection between pain and emotion dysregulation
is particularly evident among patients diagnosed with fibromyalgia
syndrome (FM) [32]. FM is characterized by persistent pain in all
four quadrants of the body (without evidence of inflammation or
lesion; [26]), depressed affect, and abnormally high levels of fati-
gue, pointing to possible disturbances of central mechanisms that
regulate sensitization to pain stimuli [10,26]. Chief among those
central pain mechanisms potentially responsible for FM hyperalge-
sia and allodynia are those involved in the regulation of emotional
states [11]. Rates of depression can exceed 50%, leading some to

0304-3959/$36.00 Ó 2009 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
doi:10.1016/j.pain.2009.10.001
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A.J. Zautra et al. / PAIN 149 (2010) 12–18
conclude that FM is one of a cluster of ‘‘affective spectrum” disor-
ders [14]. FM patients have been distinguished from healthy con-
trols and other pain patients in their reduced capacity for
positive emotion [7,34] and lower emotional complexity [8,23],
leading to less differentiation in awareness of emotive states, and
less efficacy in coping with adverse states. The homeostatic neuro-
anatomical model of emotion suggests that central sensitization of
pain in FM patients results in part from a relative deficit of activity
in the parasympathetic branch of the ANS required for down-reg-
ulation of negative emotion and pain experience.
We tested the effect of a natural method for enhancing para-
sympathetic afferent activation, slow breathing, on pain intensity
and unpleasantness reports. Slow breathing increases activation
of bronchiopulmonary vagal afferents and produces enhanced
heart rate variability, which reflects increased parasympathetic
tone [1]. The homeostatic neuroanatomical model of emotion pre-
dicts that slow breathing will result in reduced pain unpleasant-
ness and subjective ratings of intensity.
2. Methods
2.1. Overview
In the current study, we manipulated breathing rate directly to
examine the association between breathing rate and pain ratings
in age-matched healthy control subjects (HCs) and FM patients
during induced pain. Furthermore, we tested whether the effect
of slow breathing covaried with changes in negative and positive
affective states compared with normal breathing. We hypothe-
sized that FM patients would differ from HCs, showing fewer ef-
fects of slow breathing on pain sensation because prior studies
revealed that they have difficulties in positive affect regulation
[32].
The study was designed as a balanced two-factorial experiment,
in which FM and HC participants breathed comfortably at their
own normal rate or at one-half of that rate, by following a visual
command signal displayed on a laptop computer screen. Two lev-
els (mild, moderate) of individually calibrated painful thermal heat
stimuli were delivered during the two breathing periods in a coun-
terbalanced, pseudorandom protocol, and verbal reports of pain
intensity and unpleasantness were recorded immediately follow-
ing each stimulus. We expected that ratings of the intensity and
unpleasantness of pain would be reduced during periods of slow
breathing in normal subjects, but less so in FM patients.
2.2. Participants
Participants were 27 women with a physician-confirmed diag-
nosis of FM and 25 age-matched healthy women without FM. FM
participants were recruited from a previous multiyear project
assessing a wide range of mental and physical health variables in
a community-based sample of FM patients in the Phoenix, AZ
metropolitan area. Participants who had been diagnosed with FM
by a physician and previously given permission to be contacted
for future research studies were called by telephone and screened
for eligibility. HC participants were recruited via flyers posted in
public areas at and near the medical office building where the
study was conducted. All participants were paid $50 for the study.
All participants were right-handed women aged 45–65,
(M = 55.44, SD = 6.3 for the FM sample, M = 55.58, SD = 5.7 for
the HC sample). Exclusionary criteria were a reported diagnosis
of rheumatoid arthritis, systemic lupus, polymalgia rheumatica,
or multiple sclerosis. For all FM participants, we obtained confir-
mation of their diagnosis from their rheumatologist/physician.
Tender point examinations were conducted by research staff to
13
re-confirm FM diagnosis. Five of the study participants did not re-
port pain in 11 or more of 18 possible tender points, and were ex-
cluded from the analyses. Healthy control participants were also
excluded if they reported a diagnosis of FM or osteoarthritis, or
the aforementioned autoimmune conditions, and if they reported
an ‘‘average level of bodily pain” of greater than 20 on a 0–100 nu-
meric rating scale in the last months. Participants were asked to re-
frain from consuming alcohol for 24 h prior to participation, and to
refrain from caffeine for four hours prior to participation. One FM
participant did not complete the laboratory session due to her
ongoing pain.
The majority of participants were Caucasian (86%), and the
average income for both groups fell within the $60,000–$69,999
range. Most participants completed high school (92% HC, 96%
FM) and approximately half had four years of college or post grad-
uate study (60% HC, 44% FM). Most participants also were em-
ployed (83% HC, 60% FM) and married (52% HC, 74% FM).
2.3. Study design
This study utilized a 2  2  2 repeated measures nested de-
sign. Prior to beginning the runs, ‘‘normal” respiration rate (no
instruction given regarding breathing) was measured with a nasal
cannula connected to a device measuring carbon dioxide exhala-
tion (Ohmeda 520; General Electric Healthcare, London, UK). Sub-
sequently, FM patients and normal controls were instructed to
breathe at either their normal rate or 1/2 that rate during four
blocks of four trials. During each trial, participants were subjected
to a mild or a moderately painful heat pulse at temperatures corre-
sponding to individual subjective assessments of mild and moder-
ate pain during a preceding test (described below). Participants
rated the intensity and unpleasantness of the noxious heat stimu-
lus at each trial and positive and negative affect after each block of
trials.
2.4. Study procedures
After arrival at the lab, participants completed an initial ques-
tionnaire to obtain demographic data and information on pain lev-
els, current physical and psychological functioning, and trait affect.
Participants were told that they would be receiving a series of heat
pulses and were informed about the distinction between pain
intensity and unpleasantness based on a standardized script
adapted from Price et al. [22]. Next, pain thresholds to heat stimuli
were assessed, and normal breathing rate recorded. Participants
then practiced slow paced breathing. Finally, participants were ex-
posed to four blocks of four trials each; each trial consisted of
exposure to two mild and two moderate pain stimuli during either
Normal or Slow breathing. Participants made ratings of pain inten-
sity and unpleasantness following each trial and of positive and
negative affect following each block of trials. Fig. 1 provides sche-
matics that detail the conduct of the pain trials.
2.4.1. Thermal pain threshold assessment
Subjective pain thresholds were assessed for each participant
using a TSA II thermoelectric device (Medoc; Ramat Yishai, Israel).
The 30  30 mm thermode was placed on the right thenar emi-
nence (soft fleshy area under the thumb) of participants, and a Vel-
cro strap was affixed to maintain constant pressure between the
hand and the thermode. The Medoc device has received FDA 510
clearance, and was developed to be used safely in pain research
for the delivery of thermally-induced heat and cold pain stimula-
tion. Following standard methods [17], ‘mild’ and ‘moderate’ pain
thresholds were established for each participant by delivering suc-
cessive 10 s stimuli, beginning from a non-painful temperature (38
degrees centigrade), at gradually higher temperatures (2 degree
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14 A.J. Zautra et al. / PAIN 149 (2010) 12–18

a. Jitter Length and Pain Stimulus Intensity for Trials within Blocks

Block Jitter Trial 1 Jitter Trial 2 Jitter Trial 3 Jitter Trial 4

(sec) (sec) (sec) (sec)

1 0 L 4 L 2 M 6 M

2 2 M 6 M 0 L 4 L

3 2 L 0 M 6 M 4 L

4 4 M 6 L 0 L 2 M

Note: L=Mild Pain, M=Moderate Pain stimulus. Blocks were randomly ordered for each
participant.

b. Structure of Trials within a Block

Block ~6:00 mins

Breathing Pain Pain Pain Pain End

Instruction Trial 1 Trial 2 Trial 3 Trial 4 Screen

16s ~85s ~85s ~85s ~85s 4s

c. Structure of a Trial

Pain Trial ~85secs

Baseline Jitter Ramp Pain Pulse Ramp Pain Recovery

20s 4s 10s 4s 44s

Fig. 1. Structure of pain stimulus and breathing trials.

step) until the participant selected a ‘3’ (for mild pain) and a ‘6’ (for
moderate pain) on an 11-point pain unpleasantness visual analog
scale (from 0 to 10 where 0 = ‘‘not bad at all” and 10 = ‘‘the most
unpleasant feeling possible”). Participants were informed that they
could terminate the heat stimulus at any time by saying ‘‘stop,”
and the experimenter would terminate the stimulus by pushing a
key on the computer terminal. After participants reported an
unpleasantness level of 6 on the 0–10 scale, they were asked if they
were willing to receive another pulse two degrees higher. If the
participant did not want to be exposed to a heat stimulus two de-
grees higher, then she was asked if she would allow administration
of a stimulus heat pulse one degree higher. This procedure was
continued until the participant rated a temperature above a level
of 6 or until she chose not to continue. This procedure ensured that
pain levels were appropriate for participants of varying pain
thresholds.
sured normal rate or 1/2 each participant’s normal rate. Partici-
pants practiced this paced breathing at the beginning of the
session prior to the stimulus trials. For each six minute block of
four trials, breathing was set at either Normal or Slow. Each partic-
ipant had two trials at a normal breathing rate and two trials at a
slow breathing rate. The order of these breathing rates across
blocks was alternated at random.
2.4.3. Pain trials
Within each 6-min block, heat stimuli were delivered during
four 85-s trials. The heat stimuli alternated between mild and
moderate levels in a pseudorandom schedule (see Fig. 1). Whether
the pain pulse was mild or moderate (i.e., an individually cali-
brated ‘3’ or ‘6’) and the time of delivery during the jitter interval
(between 20 and 26 s following the onset of each trial) was deter-
mined randomly to reduce expectation effects [17].

2.4.2. Breathing rate manipulation 2.5. Measures

Breathing rate at rest was assessed over a 10 min period for
each participant. Normal and slow breathing epochs were then
paced by a specially designed PowerPoint display of colored ellip-
ses that expanded and contracted on a screen mounted in front of
participants, at a rate set to be equivalent to the participant’s mea-
2.5.1. Pain intensity and unpleasantness
Ratings of pain intensity and unpleasantness were based on re-
sponses to an 11-point pain scale, where 0 = ‘‘not bad at all” and
10 = ‘‘the most intense (unpleasant) feeling possible.”
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A.J. Zautra et al. / PAIN 149 (2010) 12–18 15

2.5.2. Positive and negative affect (PANAS) [30] Table 1

The PANAS consists of 10 adjectives that describe an individ- Hierarchical multilevel regression predicting pain intensity.

ual’s levels of positive affect (PA: 5 items) and negative affect Covariance Estimate SE Z p
(NA: 5 items). Trait affects were assessed by referring to affective parameter
experience during the past 4 weeks, whereas state affects were as- estimated

sessed by referring to current experience. Internal consistency for Random effects: prediction of pain intensity
the PA and NA subscales is excellent for ratings of current affect Variance:intercept UN (1, 1) 2.77 0.76 3.63 <.001
(In)
and affect over the preceding 30 days (alpha > .83) [30].
PS by In UN (2, 1) 1.16 0.39 2.96 <.003
PS UN (2, 2) 0.88 0.25 3.56 <.001
2.6. Statistical analyses Auto-regressive AR (1) 0.35 0.04 7.86 <.001
component
Residual 1.36 0.93 14.55 <.001
Preliminary multilevel regression analyses were conducted to
determine whether there was systematic error in pain ratings Predictor variables Num df Denom df F p
due to trial effects or order of presentation effects. Study hypothe-
Type 3 tests of fixed effects
ses then were tested in a series of multilevel models that examined Diagnosis (D) 1 44 2.44 .13
differences in pain and affect ratings as a function of breathing rate Breathing rate (BR) 1 668 .03 .86
(BR: Slow or Normal), diagnosis (D: FM or HC), and Pain Stimulus D  BR 1 668 9.09 .003
(PS: mild or moderate); an auto-regressive function (AR-1) was Pain Stimulus (PS) 1 668 50.86 .001
D  PS 1 668 .19 .67
used to estimate and account for variance shared by ratings made
PS  BR 1 668 4.94 .03
on adjacent trials, and PS was treated as a random effect.

3. Results
3.1. Preliminary analyses
3.1.1. Group differences on study variables
Initial analyses examined possible sources of confounding due
to group differences on key variables under study. There were no
diagnostic group differences in temperatures for mild and moder-
ate pain, trait positive affect, trait negative affect, and ratings of
intensity and unpleasantness on the initial trial (all t’s < 1.2,
p > .25).
3.1.2. Medication use
The use of analgesics was a potential confounding influence on
measures of pain [28]. Opioid analgesics were prescribed to 10 of
the FM participants. No HC participants were taking analgesics.
Within the FM group, there were no differences in reports of pain
intensity or unpleasantness as a function of medication use. Study
analyses were initially conducted including all participants, and
then rerun without the 10 FM participants taking opioid analgesics,
with comparable results. The findings reported below are for the
FM sample not on opioid medications, but do not differ except
where noted from results obtained when including those on opioid
medications.
3.2. Breathing rate effects
3.2.1. Pain intensity ratings
Results of the combined analyses that included diagnosis,
breathing rate, and pain stimulus and their interactions as predic-
tors are displayed in Table 1. (Separate analyses controlling for ac-
tual rate of slow breathing yielded the same results and are not
reported further.) The contrasting effects are displayed in Fig. 2a
and 2b.
Higher heat stimulus levels produced higher pain intensity rat-
ings, but a slow breathing rate dampened this effect, as evidenced
by a significant two-way interaction between PS and BR (see Ta-
ble 1). Table 1 also shows a significant interaction between diagno-
sis and breathing rate in their influence on intensity ratings.
Inspection of the means revealed that slower breathing lowered
intensity ratings only for HC participants. A three-way interaction
was not predicted and also was not significant (p’s > .40) for inten-
sity and also unpleasantness. In addition to these fixed effects,
noteworthy variability between subjects in response to the pain
stimulus (PS) was found, as shown in the analysis of variance com-
ponents. This variability was lower for those who on average had
higher intensity ratings, as shown in Table 1 as PS by Intercept
variance.

3.2.2. Pain unpleasantness ratings

3.1.3. Trial and order effects
For pain intensity ratings, there was a marginal but non-signif-
icant effect comparing the four blocks of trials (F(3, 132) = 2.39,
p < .10), and no effects of order of presentation of stimuli
(p > .20). The actual temperatures established as mild and moder-
ate pain stimuli for each participant were also examined as poten-
tial confounds and found to have no effect on intensity ratings of
participants (all p’s > .12).
For pain unpleasantness ratings, there was a marginal non-sig-
nificant effect when comparing the four blocks of trials
(F(3, 132) = 2.49, p < .10). Order of presentation of pain stimuli
within each block did not show a significant effect on pain
unpleasantness ratings (F(3, 132) = 1.79, p = .15). Unpleasantness
ratings were lower overall for participants who selected higher
temperatures for mild pain stimuli/threshold [t(44) = 2.07,
p < .05] In analyses of the effects of diagnosis and breathing rate
on unpleasantness ratings, we tested for and did not find effects
of differences in temperatures selected by participants for pain
stimuli.
The findings for pain unpleasantness were similar to those
found for pain intensity: the benefits of slower breathing were
more pronounced at higher pain stimulus levels, reflected in a
two-way interaction between BR and PS shown in Table 2. The
two-way interaction of breathing rate by diagnosis in prediction
of unpleasantness ratings was also significant. These findings are
reported in Table 2 and displayed in Fig. 3a and 3b. In addition
to these fixed effects, variability was found between subjects in
unpleasantness ratings in response to the pain stimulus (PS), sim-
ilar to that found for intensity ratings. This variability was lower
for those who on average had higher unpleasantness ratings.
The differences observed between FM and HC groups led to an
examination of differences between groups in the temperatures
of the stimuli used for mild and moderate pain, but no group differ-
ences were found (p’s > .2). Additional analyses did not reveal any
differential effects of the temperatures of mild and moderate pain
stimuli on pain ratings for FMs, and no other interactions with
study variables. An inspection of resting breathing rates for the
two groups revealed no differences between groups: an average
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16 A.J. Zautra et al. / PAIN 149 (2010) 12–18

6 Table 2
Multilevel regression predicting pain unpleasantness.
5.5
Pain Intensity Rating

5 Covariance Estimate SE Z p
parameter
4.5 estimated
4 Random effects: prediction of pain unpleasantness
3.5 Variance:intercept UN (1, 1) 3.02 0.79 3.79 <.001
(In)
3 Slow Breathing PS  In UN (2, 1) 1.45 0.47 3.05 <.00
2.5 Normal Breathing PS UN (2, 2) 1.50 0.37 4.01 <.001
Auto-regressive AR (1) 0.33 0.04 7.51 <.001
2
component
Mild Pain Moderate Pain Residual 1.20 0.08 14.81 <.001
Pain Stimulus Level
Predictor variables Num df Denom df F p
Fig. 2a. Effects of breathing rate on pain intensity ratings in healthy controls. Type 3 tests of fixed effects
Diagnosis (D) 1 44 1.84 .18
6 Breathing rate (BR) 1 668 .22 .64
D  BR 1 668 4.07 .04
5.5
Pain stimulus (PS) 1 668 39.45 .001
Pain Intensity Rating

5 D  PS 1 668 .14 .71

4.5
4
3.5
3
Slow Breathing
2.5 Normal Breathing
2 ported at the end of each block of trials.
Mild Pain Moderate Pain
Pain Stimulus Level
Fig. 2b. Effects of breathing rate on pain intensity ratings in FM patients.
rate of 13.68 (SD = 3.54) breaths per minute for FM patients, and
13.63 (SD = 2.17) for HCs. Controlling for resting breathing rates
also did not affect the results of the breathing manipulation.
3.2.3. Affect ratings
Because existing evidence suggests that FM patients exhibit less
emotional complexity than other pain patients [7,23], preliminary
analyses tested and did not find differences in the size of the in-
verse relationship between positive and negative affect between
groups.1 In all subsequent analyses probing the effects of breathing
rate on affective state, the main effect of the opposing affect were in-
cluded in the prediction of both positive and negative affects.
Overall, slow breathing led to lower negative affect during pain
trials compared to normal breathing (t(663) = 5.45, p < .001), and
there were no significant differences of the effects of BR due to
diagnosis. Negative affects were not uniform across blocks of trials,
however: there were higher negative affect ratings following later
trials, if those blocks of trials called for normal versus slow breath-
ing (BR by block number interaction: F(3, 121) = 7.96, p < .001).
There were also differences in the reporting of negative affects over
blocks of trials as a function of diagnosis: FM status by block num-
ber: F(3, 121) = 6.30, p < .001. FM patients showed a tendency to
PS  BR 1 668 5.88 .02
F(3, 121) = 4.61, p < .005. For FMs, positive affect tended to drift
downward over the course of the experiment. There was no down-
ward trend in positive affect for HCs. Level of pain was equivalent
across each block of trials and thus would not affect NA or PA re-
Individual differences in the influences of trait PA and NA were
examined using data collected by questionnaire on emotional well-
being prior to the experiment. The two trait affects were correlated
.422 for the entire sample. Because of variance restrictions when
including trait affects as predictors of state level affects of the same
valence, only trait PA was tested as a predictor of NA across trials,
and only trait NA was included in the prediction of PA levels across
trials. There was a significant two-way interaction between BR and
trait PA, (F(1, 662) = 7.33, p < .007) predicting state NA. Those with
high trait PA were more likely to show lower NA during slow
breathing, regardless of diagnosis. There was a significant three-
way interaction between BR, diagnosis, and Trait NA in the predic-
tion of PA across trials (F(1, 662) = 33.66, p < .0001). Only HCs
showed higher PA during slow breathing, and only if they reported
higher trait level NA. Those with low trait NA from either group
were unaffected by the breathing rate. Because of these findings
for trait level affects, the analyses of BR on pain intensity and
unpleasantness were repeated including trait level affects as pre-
dictors. A four-way interaction was found between BR, PS, trait
PA, and trait NA predicting pain unpleasantness: F(1, 661) = 7.99,
p < .005, and pain intensity ratings: F(1, 661) = 4.55, p = .033. In
both analyses, participants with higher trait level PA combined
with higher trait level NA had slightly lower pain ratings in re-
sponse to the moderate pain stimulus when breathing more
slowly. These effects did not vary by diagnosis.
5
Pain Unpleasantness Rating

report more negative affect than controls on later blocks of trials. 4.5
Variation in PA did not show a consistent pattern across trials. 4
The effect of breathing rate on PA varied as a function of diagnosis,
3.5
similar to what was found for pain ratings. PA was sustained by
slower breathing during pain trials for healthy controls, but not 3
for FM patients: t = 2.62, p = .009. A three-way interaction was 2.5
also found when probing further: diagnosis by BR by Block, 2 Slow Breathing
1.5 Normal Breathing

1
1
In the full sample consisting of all FM participants regardless of tender point
Mild Pain Moderate Pain
count or opioid medication use, FM participants showed a stronger inverse
relationship between positive and negative affect across trials, t(859) = 3.29, Pain Stimulus Level
p < .002, indicating that affect reports were more uni-dimensional for FM patients,
and suggesting less emotional complexity for the FM group. Fig. 3a. Effects of breathing rate on pain unpleasantness ratings in healthy controls.
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A.J. Zautra et al. / PAIN 149 (2010) 12–18
5 comes and as predictors, but to test for interactions between these
Pain Unpleasantness Rating
4.5
4
3.5
3 als in which higher levels of pain were administered. The changes
2.5
2 Slow Breathing
1.5 Normal Breathing
1
Mild Pain Moderate Pain
Pain Stimulus Level
Fig. 3b. Effects of breathing rate on pain unpleasantness ratings in FM patients.
3.2.4. Post hoc analyses
A series of pos-hoc tests were conducted to rule out potential
confounding sources of variance that might be due to differences
between FM and control participants unrelated to their diagnosis.
Age, income, and education were entered into prediction equations
used above to examine their influence. These demographic vari-
ables were uncorrelated with intensity and unpleasantness ratings
made during the pain trials.
4. Discussion
This study sought to examine the benefits of an experimental
analog to meditation. Participants were guided through epochs of
paced breathing at one-half their normal respiration rate during
which mild and moderately painful heat pulses were delivered to
their palms. We recorded the participants’ ratings of pain intensity
and unpleasantness following each trial and found an overall
reduction in pain ratings when healthy control participants were
paced to breathe slowly. These findings are consistent with those
of an observational investigation, which found lower breathing
rates were associated with reduced pain intensity and unpleasant-
ness ratings when participants meditated while receiving pulses of
painful heat [12].
Analyses of these ratings across conditions revealed that slow
breathing had its greatest effects on ratings of pain stimuli of mod-
erate in comparison to mild intensity. The salubrious effects of
slow breathing also extended to ratings of negative affect that were
made at the end of each block of four trials. After blocks in which
participants were paced to breathe at one-half their normal rate,
they rated their negative affect significantly lower.
FM participants benefited less from slow breathing than HCs, as
predicted. Their ratings of pain intensity appeared unaffected by
changes in breathing rate, and there was a similar suggestive find-
ing for pain unpleasantness. There were no differences between
HCs and FMs in the effects of breathing rate on negative affect,
but there were differences found with positive affect. Positive af-
fect ratings were overall unaffected by slow breathing, but there
was a three-way interaction suggesting that FM participants were
less able to sustain positive affect gains from slow breathing than
were HCs. Both trait level negative affect and trait level positive af-
fect enhanced the effects of slow breathing. There was only a mod-
est correlation between trait level negative affect and trait level
positive affect suggesting that these two influences on the interac-
tion between pain and emotion were independent. In analyses of
both pain intensity and unpleasantness, participants with greater
negative affect disturbance coupled with a greater capacity for po-
sitive emotions benefited most from slow breathing. These findings
call attention to the central though complex role that affect regu-
lation plays in amelioration of pain. It was useful not only to assess
positive and negative affective responses separately, both as out-
17
affective states.
The use of experimental arrangements to vary breathing rate at
different pain levels played an important part in determining the
benefits of slow breathing. Slow breathing helped most during tri-
in negative affect observed and the more modest changes in posi-
tive affect found here during slow breathing may depend on condi-
tions in which homeostasis is disturbed with a painful stimulus.
The study could not examine whether any affective benefits of
slow breathing would accrue for participants not in pain, since
all participants received trials where pain was administered. For
example, slow breathing might have a greater influence on positive
affects in the absence of a painful stimulus. Such studies would be
valuable to conduct in the future.
To what extent might the effects observed have been due to dif-
ferences in attention or expectation introduced by slow breathing
and not the slow breathing itself? With regard to attention biases,
we doubt the instructions led to greater distraction in either con-
dition since participants in all conditions were asked to pace their
breathing in accordance with the visual stimuli displayed. It is con-
ceivable that greater effort was required to breathe at a slower
rate, but increased effort would likely to have led to more negative
affect [9], and we found less negative affect during slow breathing
overall. Further, differences in response to slow breathing found
between groups and between pain stimuli are inconsistent with
a general bias in expectations introduced by experimental arrange-
ments. Left unassessed was the degree of compliance with experi-
menter instructions for participants to pace their breathing rate by
following the visual cues. Although we doubt that there was a dif-
ference in compliance with breathing rates for the two conditions
overall, because we monitored each subject’s breathing visually,
we did not quantitatively measure rate or compliance. Future stud-
ies could benefit from measurements of actual breathing rates as
well as the compliance.
Among the study limitations are possible lack of representative-
ness in the samples of FM and HCs. A different sample of FM patients
may reveal group differences not apparent here. In comparison to
controls, FM patients did not have lower thresholds for pain and
did not display a consistent pattern of more affective disturbance,
in contrast to findings reported in other research [11]. The sample
size in the current study led to relatively low power to detect small
differences between groups, and there may have been other influ-
ences in recruitment and screening that led to a non-representative
sample of FMs and controls. In any case, our results indicate that
slow breathing can reduce pain and negative emotion for some indi-
viduals. Since all participants were administered trials where pain
was administered, the potential benefit of interventions that include
the practice of meditation in the treatment of pain patients is sup-
ported. However, the mixed findings for FM patients give us pause.
It may be more difficult to engender states of relaxation needed to
endure pain in FM patients through slow paced breathing alone.
4.1. Theoretical implications
From these results we may infer that slow breathing facilitates
emotional regulation and the maintenance of homeostasis under
the challenging conditions of acute pain induction. The effects of
breathing rate on pain responses varied as a function of both level
of pain and FM diagnosis. Indeed, the relative weak effects of slow
breathing on outcomes for FM patients suggests that this group has
particular difficulty in the maintenance of emotional equilibrium,
due perhaps in part to a less differentiated affect system.
Taken together these findings are consistent with the model of
pain as a homeostatic emotion. In this model, the neurophysiologi-
cal processes that underlie how slow breathing influences pain be-
 Author's personal copy
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18 A.J. Zautra et al. / PAIN 149 (2010) 12–18
gins with the increased bronchiopulmonary afferent activity. This
activity produces increased activation in the left mid-insula and
anterior insula [24], as well as increased activation in the left ante-
rior cingulate associated directly with increased heart rate variabil-
ity [18], corresponding with a shift in sympathovagal tone. This
activation counterbalances the acute activation in the right ante-
rior insula produced by painful stimulation [2] by virtue of oppo-
nent interaction [4]. This model fits psychophysiological evidence
of forebrain affective and autonomic asymmetry [6,20,31], pro-
vides a structural complement for the bivalent concept of positive
and negative emotion [23], and instantiates neurobiologically the
psychological proposal that a ‘‘calm and connection system” op-
poses the arousal/stress system [29]. Increased activity in the para-
sympathetic branch of the ANS thus might provide a natural means
for homeostatic down-regulation of activity in the stress system
and a reduction in pain. The same explanation can be used to ex-
plain the reduction of pain by hearing subjectively pleasant music
[25], and by maternal contact [29].
4.2. Clinical implications
Our study is the first to directly examine the benefits in pain re-
ports and affect using experimental methods to manipulate both
breathing rate and pain exposure, adding strength to our causal
inferences regarding the value of slow breathing in pain adapta-
tion. By testing chronic pain patients as well as normal controls,
we were also able to further extend the reach of our study and per-
mit generalizing to a chronic pain population. The findings indicate
that a slower breathing rate is a useful target in interventions for
patients in pain. Reductions in pain and negative affect may be ex-
pected when people are guided to halve their respiration rate. Our
findings provide direct support for prior reports describing effects
of yogic breathing on depression [3] and mindful Zen meditation
on pain [12]. However, for FM patients, the data suggest that med-
itative breathing alone is insufficient. Clinical interventions that
address positive affective disregulation, appear necessary to assist
FM patients in the management of their chronic pain.
The hypotheses here are based on a model of emotion regulation
that posits connectivity among processes from the highest levels of
neural organization to those responsible for the most fundamental,
the human breath. Our paradigmatic approach opens the whole of
mind–body exploration to more precise and effective interventions
that may ultimately strengthen the capacity for emotion regulation
among chronic pain patients and also those suffering from affective
disorders such as depression and generalized anxiety. The methods
we have devised allow us to study the salutary effects of simple
emotion-regulation tools, such as mindful breathing, directly and
invite new applications. More generally, the model and supporting
data presented here, extend beyond the stress/distress quadrant
to permit testable hypotheses regarding how forces within the body
and also those originating outside ourselves communicate to re-
store and sustain the organism’s vitality.
Acknowledgements
The authors have no conflict of interest that could compromise
the conduct of this study or the reporting of the results. They thank
The Arizona Institute for Mental Health Research for their research
grant (Arthur (Bud) Craig, PI) that provided the funding for this
study.
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