VENTILATORY CONTROL OF HEART RATE DURING INHALATION OF 5% CO1 AND TYPES OF PANIC ATTACKS
Studies
designed
to
evoke
panic-disorder
patients S’%
inhalation
of
challenge)
reveal
heart
While
rate.
and Heninger of
CO1
did not panic,
Roth
increase
of
“panicked”.
subjects
who CO?.
reported from period
but
of about
patients
5.5%
(IY87).
a small
increase
of CO1
l-1 patients
6 b/min who
did
not.
heart
on
one bimin
each.
both
“panicked” And (M
of inhalation
other for
two
which
during and
75.X
of 5.5%
CO1 (M
for
a group
of Iti patients
with
of panic
attacks
during
seven
through = 76.0
of
changes
in
from
the poini
there
with will
I ‘Ji
or
of 5%
of
which
a
arc reported The
purthese
of respiratory
of view
no
that
rccog-
nature
(Lcy,
of
in press).
tiir.cpc.f physiological
increases
without
increase
in ventilation
by the :tddition
of view
prolonged
and .sigrl[fi’crrrlt
rate
in
and reflexive
is
these
the absence
attacks?
to CO,
between
people
creases
of whom
of
of diffcr-
is to address
;I point
responses
heart
no history
a
tight
among
studies
study
ventilatory
for
range
for
panic
present
the volitional
S’%, CO2
a
with
sleep.
of the subjects
experienced the
Although
b/
CO? (A4 =
16 patients
increases
accounts
portion
connection
rate
.SI>
the large
nizcs both
of
(IYYO)
in heart
b/min)
sleep.
contained
in
b/min.
during
what
psychophysiology. of
inhalation
rate
questions
rc-
groups
Barlow
no increase =
hand,
non-significant
of
Craske
essentially
baseline
the
rate
And
have
post
statistically
for
heart
significant to
attacks
incrcasc
of 5.5%
11.8) for
accounts in
studies?
and
=
M = 77.3
“panicked”.
ences
patients
(M
inhalation
SLI
of panic
What
a uniform
for
b/min,
whom
who
baseline
I I .7) through
history
and
absolutely
and
rate from
77.3
patients
reported
patients
in
increase
eight
=
CO2
normals.
Sanderson ported
min)
about
the
a mean
for
“panicked”, heart
Goodman.
inhalation
(IYYO)
in
of increase
for
of I6 bimin
asymptomatic
IO
(bimin) during
(i.e.
Charney,
( 198X) reported
a mean increase
who
air
attacks
of prolonged
range
Woods.
“panicked”
mean
in
a large
25 beats/minute
who
panic
by means
in
of
in heart
rate
panic
disorder,
proportion
beyond CO2
inhalation
that
to room
to
in-
demanded air.
Thus,
R0NAI.I)
104
one explanation
for
sonle.
if
not
aII.
of
the
in heart rate during
inhalation of 5% CO1 may lie in voluntary hypcrncic breathing (overbrcathing) i.e. an increase in ventilation beyond the involuntal-y cupneic level (reflesivc breathing) demanded by the addition of 5% increase
(‘02.
The
following
cicmonstr~rtion
was designed
for the purpose of illustrating how changes in heart rate can be controlled through (a) voluntury changes in breathing during prolonged inhalation of 5?0 CO2 and (h) voluntary changes in breathing during prolonged brea thing of room air. This clcmonstr~ltio~~ was not designed to test :I hypothesis: it is offered hel-c as a first-hand empirical illustration of the 1’sy’ti(‘physioloFic~li process by Lvhich partial control of heart rate can be achievccl through simple voluntary ventilatory mancuvcrs. This case study provides tangential data on the connection between respiration and panic (a) by demonstrating that involuntar! brea ovcrbreathin~ (i.e. thing and voluntary hypcrpnea) during prolonged inhalation of 5% CO2 in air produce respiratory and cardiac changes associated with primary panic attacks and (b) by demonstrating that voluntary hypcrventilatory breathing and involuntary rcspiratory effects immediately following prolonged CO2 in air produce acute inhalation of 5% hyperventilatory
hypocapnea
sudden drop in pC02 increase in heart rate.
and
iI11
marked cqu;dIy
by
:I
sudden
I.1.Y
history of respiratory clisorders. and was not experiencing an\ acute rcspiratorq clistrcss. The subject understood the physiology of t-cspiration and the purpose of the experiment.
Appmtus otltl ptwcdrrt~c~. ‘l‘hc apparatu\ consistcd of ;i flowp;ist system hy which ;I stream of gas wfl;is conducted past the distal Cnd of the mouthpiece through which the \ut3Ject breathctl. I’he t’low t-ate was such that it exceeded the inspiratory flow ralcs ot the subject so that by controlling the composition of the gas stream the cxpcrimcntcl- was able to control the inspired ga4 concentrations ol the sut>,icct. The expired gases were car-rid ;I\\;I\ in the gas stream. Ail- ~;IS drawm 1’1roni the room and pumped at ;I stcadv rate of 75 limin into ;I mi\ing chamber. .lud prior to entering the chamber. put-c (‘(I1 coiIIc1 bc 2ctdecl to tlic ait- stream. A mass spectt-ometcr prcdw Iving in the g;14 stream just distal to lhc mixing chamhe~ allowed the Icvcl of (‘0, IO lx mcasuretl. The experimenter was ;ible to adjust the flop r-ate of the pure CO1 to produce ;I mixed gas concentration of 5’!/,, (‘0, 93”!4, ail-. Ilie flom ot (‘0, could bc turned on or off using a tap thus allowing the gas stream to bc changed from ait onlv (tap closed) to 5% (‘0, in air (tap open). Th&c gas rnixturcs u’ct-c then conductccl through and
subject
of this
to
past the mouthpiece
the
rroom.
A
length
ot
was ad&d on the down-stream 4icle of the mouthpiece to act as ;I dead space so that if peak inspiratory flow rates excet~~cd 73 Vmin inspired gas would still be dl-awn in from the tubing
ml). The
tubing
vented
flow-past system and not the room. The subJect wore a noes clip and breathed through the mouthpiece; this in turn was conncctcti to the flow-pat system \,i;t ;I l”icumot~lchograph (Fleisch #3. ctuaclspacu 1X.i
Method Srrl?jcct.
wide-bore
then
single-case
study
was ;I healthy %-year-old male volunteer recruitcti from the staff of the Charing Cross Hospital and Westminster Medical College staff, who had no history of panic attacks. no
Thi\
allowed
inspir-atory
and
the
mcasurcmcnt
expiratorq’
was recorded and integration a record of inspirccl
flow
prmiuwd (VI
flows.
). Hand
chart
records
analysis allowed
both
ot’ this signal tidal
of these signals inspired
of
Inspirator)i volume
f’rom paper
respiration
rate,
tidal
volume.
and minute
volume
to be calcu-
lated. respiratory
mass
MGA200)
allowing
both
just to
single
was
lead
recorded
CO,
allow
lips
(lead
rate
to
VS)
be
re-
corded.
volume. for
each
Figure fksign.
Respiration
liters
-
per
minute. (beats
breath.
minute
and pCOl
throughout
the
first
sisted
were
six
and
phase,
which
period
were breathed
during
followed
during
which
the
5%
CO,
in air i.e..
effort
to control
no voluntary
no effort
respiration third without
which
interruption. during
which
voluntary fourth
i.e..
effort phase
which
consisted the subject
attempting
to
on room
air),
without
interruption.
period
during
breathed while
room
attempting
each
lowed
which
breath. the
fifth
;I
S-min
breathed
of
room
made
on
5%
followed
which
period
tidal
5% while
volume
of
(hyperventilating the fourth
consisted the
dur-
breathed
the
in
without
of 30 breathdmin phase
no The
CO1
phase
of a 5-min
fifth
The phase
breathing.
third
maximize
The
he
either
second
voluntarily
in air at the rate
each breath.
of
the
made
volume.
his
(overbrcathing followed
interruption, ing which CO1
to control
subject
of
phase
;I
S-min
voluntarily
air at the rate of 30 brenthdmin to maximize The phase
sixth
the tidal phase.
without
rate
of
arc given
the in
data
for
in Figure
2.
the respiration
a pattern
of
standard
measures
breathing
normal Table
respiration I. which
deviations
volume
which interruption.
fol-
-_
Of
I I
I
I
of the
of room contains of
the
I
air)
under
period breathed
subject
heart
without
or &a-case
the
the
phases
tidal
pCOZ)
25) are given
sat
his breathing;
consisted
three
second
phase
the subject
first
baseline
IS-min
the
All
conditions.
con-
the subject
followed
rate.
and end-tidal
one through
(ad libitum
and
The
tidal
phase
means
reflexively
or
Phu.sc~ I. first
relaxed
air)
the all of
experiment.
the subject
;I
to increase
reflexively
air).
subject
frequency
phase,
period
of
while
show
which
the first
consisted
I,
of
(min
continuously
ad libitum.
interruption. (eupnea)
per rate
room
made while
the
in
in liters
of the -
volume
and heart
recorded
(baseline
of a S-min
upright
Hg)
phases
phase
measurements
made
min
(respiration
volume,
each min of all six phases
(respiration
tidal
volume
in mm
per minute)
The
measures
beats per minute,
measures
minute
experiment
frequency
which
reflexively.
Results Respiration
heart
during
air
and O7
be recorded. electrocardiogram
to
period
room
from
to the subject’s
and expired
breathed
(Centro-
gas continuously
distal
inspired
concentrations A
spectrometer
sampled
the mouthpiece
air
of a S-min
subject
A nits
consisted
I
the
respir-
ation measures and heart rates for each ot‘ the six phases, provides ;I statistical profile. During Phase I, hasclinc mcasurcs show ;I respiration rate of IO brcathsimin. tidal volume of .X0 I/breath, minute volume of 7.83 liniin. pC@ of 38.22 mm Hg. and heart rate of 69.2 Mnin (a rate consistent with the subject’s personal record of heart rate during relaxed
wnkefulncss
taken
over
;I
period
of several
years).
I’IIUSf’ 2. nc cffccts of adding 5% c01 to room air can be seen in min 0 through 20 of Figure 2 and in the data of the second Phae of Table I. All respiration measures showed a sharp increase (incan respiration rate rose
from 10 to 17.27 breathdmin. mean tidal volume rose from .X0 to 1.25 I/breath, mean minute volume rose from 7.84 to 23.23 Vmin. and mean pC0, rose from 3X.22 to 47.41 mm Hg) while mean heart rate remained virtually constant from Phase 1 (6Y.2 b/mill) to Phase 2 (6Y.Y b/min). P/~rr.sc~3. The termination of 5% CO? at the end of the second Phase (20th min) and the resumption of reflexive ad lib. breathing of room air in Phase 3 (min 21 through 25) resulted in a reduction in the respiration measures. However. comparisons with the baseline mcasurcs indicate that the reduction in respiration to a mean of 14 breaths/min was still significantly greater than the mean of IO breathdmin during Phase 1. evidence of the “afterdischarge” or “flywheel” phenomenon (Folgering, lYX8). Mean tidal volume (.72 I/ breath) and mean pCOl (35.02 mm Hg) were slightly lower than corresponding mean baseline measures of Phase I. Minute volume. a correlate of respiration rate and the variable underlying pCOI, also showed evidence of the flywheel phenomenon i.e., the mean volume of Y.Y6 I/min was L greater than the mean baseline of 7.84 limin. Although heart rate rose from 6Y.Y b/min during Phase 2 to 70.X b/min during Phase 3. the singular datum of this phase was the level of pCOl during the first min following terminatier: of 5% CO? (30.1 mm Hg). Compared with the level of pCOz of the last min of Phase 2 (47.4 mm Hg), this sudden decrement (47.430.1 = 17.3) represents a 36% drop in pC02. Pl~nse 4. Respiration measures for the last min of Phase 3 (25th min) and for each min of the last three phases of the experiment (min 26 through 40) are given in Figure 3. The effects of voluntary forced overbreathing (30 breaths/ min plus voluntary effort to maximize tidal volume of each breath) of 5% CO? in air can be seen in the second panel of Figure 3. where all four respiratory measures show a sharp rise from the 25th min (the last min of Phase 4).
Evidence that voluntary forced overbreathing increased ventilation beyond that produced by eupneic breathing of 5% CO, in air can be seen in a comparison of the respiratory data of Phase 4 with those of Phase 2. Table 1 shows that mean tidal volume during Phase 4 (1.63 I/ breath) was greater than mean tidal volume during Phase 2 (1.25 I/breath); mean minute volume during Phase 4 (4Y. IY Vmin) was more than twice mean minute volume during Phase 2 (23.23 I/min); while pCOl was about the same (46.86 mm Hg during Phase 4 vs 47.41 mm Hg during Phase 2). For the purposes of the present paper. the most significant datum was the sharp increase in heart rate (set Figure 2 and Table 1) from ;I mean of 6Y.Y bimin during Phase 2 (eupneic breathing of 5% CO1 in air) to 81.2 b/min during Phase 4 (overbreathing 5% CO1 in air.
li0NAl.l)
I ‘JS
I’/IN.Y~ lation
5. The
effects
(maintaining
hreathsimin) ing
when
in
Phase
of
the
sharp
5 in
tidal
and minute
tory
drive.
(‘(I7
decrcasc volume
which
addition
room
5%
IO
indicate
of
5”/;,
the
C‘O,
tlowevcr,
to to
the
to to
cotiipat-iaon
during
hc
the
mm
3O.S-l).
cstcnt
contrihutcs
I .13)
can
Phax
limin
30
follow-
air.
I .h3 l/breath
(4X.
4 to
close to those of the baselines of Phase I. It should he noted. however. that while minute volume slows down quickly to baseline levels during Phase I. pc‘O1 does not. Although pc’0, shows ;I steady rise from 3.4 mm Hg
at
air
in t’t-om
(
volume
reductions the
hypcrvcnfirate
breathing
overhreathing
seen
of voluntary respiration
I.LJ\r’
Hg
first
during
min
of
the
fifth
the
final and
phase finai
of minute
short of 07% of resting pC’02 prior \,entilation. thi5 condition indicates
23.7.3 limin).
h5l”t-\,‘“til~rtioti.
during
I’h;isc
Tidal cotiipirccl
ingfully qucnq
bxs
with
5
minute
volumes Ixx~ruse
t-cstrictecl
cannot be nieantrc9piration (I-C2 coti4tant of 30 it w;15 pct-tiiit-
10
hreathdmin
dur-iny
ted
frcclv during I’haw 2. significant rcspit-ation datum of the dramatic cleclinc in pC’O1 from during the last min of I’Ii;~sc 4 to
to vat-> I‘he most I’hasc 5 M’;IS 47.5 tiini t1g
35.5
mm
I’hasc
tlg during
decline csccc& mm fig
5 while
the
i’ir4t
min
of
I’Ii;iw
5.
;I
of -IO?,, ’ I‘hi4 drop of 22 mm kig the 17.3 111111liy drop from the -17.1 of the last miti 01‘ I’hax 2 (cupncic
breathing of 5”‘c1 C’O1 in air) to 30. I nini 1 l,c ot the first miti of I%:Iw 3 (ad lit>. tlreathing ot room ail-). The theorelical \ignificancc of thee
ant1 dramatic
sudden acute the
onset
of
termination
cspcciallb in
of
if one
dir.
rate
In
the 90 himin
of
ot
the
room
by air
the
Ihc
in
air.
3”%
sui-gc
C‘O,
in hear1
Pliasc -I to of I’hasc 5 Icncls
last
min
miti lhc
in the follows
(‘(IT
during of
hvpocapnic
volitntarv
when
in
to
lies that
5%)
fourth
support
producccI CO,
breathing
o\,ct-hr’cathc\
S3 tdmiti
additional
in p(‘02 alkatosis
conncctic~n.
this
from
drops
rcspir;ttorv
II\
ot
o\et-ht-edthing
normal
and
.5?,
ait-.
forced
h. In this
lib.
breathing
and
l‘ahle and
sutu
of
final room
phase ait-).
the
data
of
Figure
I treveat heart
recocery
pet-iod
oral
an
fixation
of
following
Since
report
panic during
Harclonk
that
if after
three
min
the
subject
coiilcl
Ixcathecl the
not
be
espcri-
obtained
trial w;14 tcrniinated. the end of Phiisc 0. the he felt no ansictv during pha4ck and expct-icticcd of the DSILI-IIIK cl:t\\iattacl\s pha~
esccpt 5. the
for lightpcrioci ot
for-cccl
voluntary h~l~~rv~~itil~ttion ot room ait-. mild dysptlc;i during Phase 7. eupncic inhalation of 5% (‘(IT in air. Esccpt for sonic clisconitort in the jam m~iscles and ;I dr\ mouth. conditions cotiltiio~i to prc~loiipd hr-eathins \,ia 3 nioitthpiecc. the onlv itnpleas;rnt sensalion espcricticed L\;IS the sense of loss of volittitat-v control of tlreathing dut-ing the I--niin pet-iod of inhalation ot .TJ”~, and
CO2
in air (l’hasc
2). The suhjcct repot-tccl that an Ltncontrollahtc and for-cccl increase in frquenc\ and depth of ventilation was unplcos;ant and might ha\ e tx~n ;I stimulus i’or fear if hc had not knc~n what to anticipate sensation
of
t7re~tthing
.S”,,,
(‘0,
in
air.
Discussion
4
iiic;i-
to
levels
ot
falls to hyxrchronic
pC‘02
throughout
until the cxperiniental Initiiccliatel~ I’ollowing sithicxt t-cported that any part of the 4i\ none of the scnsationk llc~~dedticss
by
maintain
h~l”t-\‘entilation.
.Ylrl~jc~.l‘.s ~por’f. through ii mouthpiccc 111ent,
specified
who
of ad
(t-esumpfion
that the respiration rate show ;I return
of recovery
( 1979).
voluntary
when /‘/zK\c
range
Beunicr
a 5-min
the
eft’ccb
hV}‘ct-v”itilation
prcccded
36.6 pCO1
falls ,just short of the lowest measure during Phase I, namely. 36.5 mm 1lg. This relativeI>, sIow rccovcry is. howe\,er. well within the
which vcntila-
\~oIum~~ during I’hasc ? (rei’lcsivc breathing of 5”L C‘O, in air) makes it clear that voluntary hypcr\,cntilation of room air result5 in ;I significantI) greatctventilation (tiw3;it1 = 3h.M limiti) than reflexive breathing ot 5’!4, (‘0, in air (tiic;iti = volume
to
tnin
The
results
of
the
clcmonstratior~
present4
here illustrate the psychophysiological process by which voluntary overbreathing during prolonged inhalation of 5% CO1 in air can lead to a significant increase in heart rate. The results of this demonstration also indicate that voluminous voluntary hyperventilatory breathing can produce an even greater increase in heart rote. The implications of these results bear directly on the differences in heart rate reported in studies that have employed the 5% CO, and thus provide the basis for the challenge, hypothesis that some of the variance in heart rate data may be attributable to variability in volitional overbreathing among the subjects tested. If this is the cast. then the magnitude of increases in heart rate during the 5% CO? challenge could be attributed to differences in excessive ventilation that reflect the degree of ventilatory anxiety induced by differences in experimental procedures. While differences in experimental procedures may be a potent source of variability in heart rate during inhalation of 5% CO?, another factor that may contribute to heart rate variability lies in individual differences in the nature and severity of the presenting complaint i.e.. panic disorder appears not to be a unitary phenomenon (Ley. lYX7: Wolpe & Rowan. IYXX). This hypothesis will be discussed in the following answer to the cluestion: *‘What accounts for the absence of heart rate changes in studies in which a significant portion of the subjects are reported to have experienced panic attacks?” Panic Attacks
Heart
Without
Increases
in Heart Rate
palpitations are the most common symptom of the DSM-IIIR list of symptoms of panic attacks (Barlow, Vermilyea, Blanchard, Vermilyea. DiNardo, & Cerny. IYXS; Margraf. Taylor, Ehlers. Roth, & Agras. lYX7). In terms of intensity. Barlow et al. (lY85) reported that palpitations topped the list of I2 symptoms. while Ley (lY8Sb) found
them to be second from the top discounting fear. The intensity ratings of these two independent studies. which correlated highly (I = .77), are consistent with the findings of adventitious panic attacks that occurred during physiological assessments of panic-disorder patients. La&r and Mathews (lY70) reported three cases of adventitious attacks in which heart rate rose from a resting level of X4 b/min to ;I panic peak of 120.7 (i.e. mean increase = 45.7 bimin); and Cohen. Barlow. and Blanchard ( 1085) reported two cases of adventitious panic in which the mean increase in heart rate rose from ;I relaxation level of 64.5 b/min to II panic peak of 108.S b/min (mean increase = 44.S himin). Other studies which describe panic attacks during the course of laboratory experimentation also report large and sudden increases in heart rate. Murgraf. Ehlers, and Roth (lYX7) reported ;I sudden large increase in heart rate of about 5 I b/min following false feedback that heart rate had increased; and Sander-son. Rapee. and Barlow (IYXX) reported ;I smaller but similar sharp increase in heart rate from X6 to IO5 b/min in a patient who believed that she was inhaling a panic-inducing gas. In view of (a) the plethora of retrospective reports of the high frequency of intense heart palpitations during panic attacks, (b) the objectively recorded tachycardia during adventitious panic attacks. and (c) the relatively high frequency of increases in heart rate during panic attacks induced by laboratory challenges, what accounts for the negligible increase in heart rate during attacks reported by Sanderson (lYX7) and the absence of any increase in heart rate reported by Craske and Barlow (lYYO)? An answer may lie in a refinement in the definition
of “panic”.
sonzotic
Ley (IYYO. in press) has proposed that there are three distinct types of panic attacks, all of which meet the criteria of the DSM-IIIR classification of panic. but each of which differs
IION/‘.l.l~
‘700
the others
from
physiological sic)
panic
on five
psychological
variables. attack
is
While the
and five
the Tyl~
I (clas-
blown”
attack
“full
marked by dyspncic-fear (Lcy. 1%-49) and a sharp increase in heart rate (high probability) (c.g. the adventitious panic attacks reported by Cohen ct al.. IW5: La&r M Mathews. 1970: Margraf. Ehlers. CC Roth. 1987). the Type II (anticipatory) panic attack is marked by fear, but no dyspnca. and less intense heart palpita tions (moderate probability) (e.g.. C’02induced panic attacks reported by Woods et al., I9XX). and the Type III (cognitive) panic attack is the pcvit ~YK~~~~L~ attack marked by anxiety, but neither dyspneic-featnor anticipatory fear. and the absence of palpitations (low probability) (e.g. sc‘c symptoms of SubJect 9. Lcy,
I.l‘L
expected
to show
those
fewer
Type
reported
II
et al..
by Woods
those rcportcd
by Sanderson
attacks
than
hut more
than
( IYX7).
In addition to such rcasscssments. ;I conparison of the details of the experimental procedures employed in thcsc studies ncucls to bc
with
made
those
aspects
might
be
special
expected
excessive
to
ventilation
ing of 5%
CO,.
would
based
be
attention
focused
of the experimental elicit
during
The
overhrcathing
(i.e.
ing inhalation
of 5%
that
differcnccs
in
prolongec!
crucial
on
breath-
comparison
minute
here
volume.
hypcrncic
on
methods
Since
ventilation)
dul-an incrcasc in heart rate, differences in the Increase\ in mean minute volume would predict differences in mean increases in heart rate. C~ produces
lOX5a).
in the classification of panic. the negligible increase in heart rate reported by Sanderson ( 1X37) and the conpletc absence of an increase in heart rate Based on this refinement
reported by C’raskc and Barlow ( 1990) might be explained on the basis of differenccs in the types of panic attacks presented bv their respective patients. That is. sine prolonged inhalation of 5% CO2 prevents the full blown symptoms of h~pcrventilatory hypcaipnca. panic attacks during such inhalations are limited to Types II and 111. Since increases in heart
rate are less typical
II attacks.
it follows
the panic attacks
may most.
the
alI.
it’ not
and Barlow
that some
reported
been
have
of
reported
by the patients answer
theoretical
issues
A similar whom their
the
important
raised
et al.
study
would
preponcierancc
of
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vidual to
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ot’ the
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ot
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The data presented hcrc illustrate how ;I relatively large range of heart rates (i.e.. 69-c)O b/min) can be achieved in ;I single subject bq means of voluntary breathing maneuvers ciuring inhalation of 3% CO2 and room ail-. If ;I
to
procedures (e.g.
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gas through
of
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Differences
in research positions
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research yield the
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findings
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theoretical differences
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