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Psychophysiology, Vol. 18 No.1, pp. 75-81
First_emp81.doc
Effects of Instructions and Contingency of Reinforcement on the Operant
Conditioning of Human Phasic Heart-Rate Change
Diane M. Riley & John J. Furedy, University of Toronto, Toronto, Canada
Address requests for reprints to: Diane M. Riley, Department of Psychology,
University of Toronto, Toronto M5S 1A1, Canada
ABSTRACT
The
aim
of
these
studies
was
to
determine
reinforcement contingency on phasic heart
the
effects
of
rate (HR) change.
instructions
and
In Exp.I, 36 human
subjects were given 20 conditioning trials with a muscle-tensing task which produced a
phasic HR acceleration.
The experimental manipulation produced an elevated baseline
and allowed for the observation of instructed HR change during exercise. A 2 x 2
between subject design varied instructions (to increase or decrease the phasic tensioninduced
HR
contingent
acceleration)
on
or
and
unrelated
to
contingency
HR
change)
(whether
as
the
factors.
verbal
There
reinforcement
was
a
was
significant
instructional effect at the end of conditioning, with increase subjects producing more
HR acceleration and decrease subjects less acceleration relative to pretrials.
The
instructional effect developed over trials and decrease subjects significantly improved
with practice.
There was no difference between contingent and non-contingent groups in
either of the two conditions in ability to change HR in the instructed direction.
This
study shows the usefulness of the elevated baseline technique for cardiac research. A
second experiment demonstrated that, in subjects not instructed to attempt HR change,
the phasic HR response did not change in magnitude over conditioning.
The results of
these studies indicate that subjects are able to control phasic HR during physicalstress induced tension but biofeedback is not relevant for the production of such HR
changes.
DESCRIPTORS:
Heart-rate change, Heart-rate baseline, Biofeedback
The investigation of the role of instructions and of reinforcement in the
operant conditioning of human heart-rate (HR) change has been extensive, but
the
data
pertaining
to
both
variables
unequivocal assessment of their effects.
have
been
insufficient
for
the
Some studies (e.g., Blanchard &
Young, 1972; Blanchard, Young, Scott & Haynes, 1974; Colgan, 1977; Davidson &
Schwartz, 1976; Gatchel, 1974; Lang & Twentyman, 1974; Rupert & Holmes, 1978)
2
have reported an advantage in HR increase performance when reinforcement was
provided over sessions where no reward was given, whereas others (Bell &
Schwartz, 1975; Bergman & Johnson, 1972; Holmes, Solomon & Buchsbaum, 1979;
Levenson, 1976; White, Holmes & Bennett, 1977) have reported no significant
differences
increase.
between
reinforcement
and
no-reinforcement
conditions
for
HR
For HR decrease the results have been somewhat less conflicting,
the data generally indicating no significant effect of reinforcement on HR
change performance (e.g., Blanchard & Young, 1972; Blanchard et al., 1974;
Davidson & Schwartz, 1976; Levenson, 1976; Rupert & Holmes, 1978; Young &
Blanchard, 1974).
The precise role of instructions as to the nature of the target response
(TR)
in
the
production
of
HR
changes
has
likewise
not
been
clearly
established. There is some support for the position that superior tonic HR
changes are produced when the subject is not informed as to the nature of the
TR (Engel & Chism, 1967; Engel & Hansen, 1966).
However, contrary to this
position, instructed subjects have been reported to perform as well at HR
increase and better at HR decrease than non-instructed subjects (Blanchard &
al., 1974).
Substantial differences between HR increase and decrease performance are
often reported, increase being generally much superior to decrease.
differences
may
be
the
result
of
there
being
many
mediators
of
These
reliable
acceleration, such as muscle tension (c.f., Bell & Schwartz, 1975; Belmaker,
Proctor St Feather, 1972; Lynch, Schuri & D’Anna, 1976) and respiration (c.f.,
Colgan, 1977; Obrist, Galosy, Lawler, Gaebelein, Howard & Shanks, 1975), but
few mediators of any HR deceleration of significant magnitude.
It has also
been suggested that a "floor" effect prevents such deceleration, resting HR
levels of subjects in the laboratory being close to their lowest daily waking
levels (c.f., Bell & Schwartz, 1975; Clemens & Shattock, 1979).
One means of
investigating this "baseline-effects" possibility is to elevate the resting
3
level of the subject's HR, thereby lifting them of the "floor", and to then
observe the production of HR change.
The elevation of HR baseline can be
effected through increasing the muscle-tension of the subject.
The present
study investigated the ability of human subjects to change HR when muscletension was kept constant at a very high level.
through
monitoring
and
instructions,
but
no
Breathing was also regulated
attempt
was
made
to
produce
"unmediated" cardiac changes, the aim being to investigate the differential
effects of instructions on HR change in subjects with elevated baselines.
In the present study the response to be modified was a phasic HR increase
produced by a muscle-tensing task. This elicited phasic response was employed
because it has a number of advantages over the spontaneous IBI measure used in
tonic
studies
(cf.,
Furedy,
1979;
Riley
&
Furedy,
1979).
Firstly,
this
elicited increase in HR is reliably produced by experimental manipulations.
Secondly, this phasic HR change appears to be a more meaningful response unit
than
is
the
spontaneous
IBI
because
the
former
has
the
normal
response-
associated properties of onset latency, recruitment, duration and magnitude,
while the latter has only the property of magnitude, i.e., level.
In addition to being an investigation of instructional effects on phasic
HR in subjects in a state of physical stress-induced tension, this study was
also an investigation of the effect of contingency of reinforcement on HR
change. To adequately assess the effect of contingent reinforcement on the HR
response and to thereby determine less equivocally the role of reinforcement
in cardiac conditioning, a non-contingent control is necessary. Non-contingent
control subjects receive the same reinforcement as do experimental subjects,
but
reinforcement
is
independent
of
responding
for
controls.
The
non-
contingent control group used in this study was a modification of the standard
yoked control. Church (1964) has noted that there can be a problem with the
standard
control
reinforcement
qua
if
subjects
stimulus.
The
are
differentially
differences
in
responsive
responsivity
can
to
the
confound
4
comparisons between groups, with subjects in the "master" (contingent) group
being favored.
can
either
There are two possible ways of overcoming this problem.
equate
subjects
on
their
reinforcement given to subjects.
responsivity,
or
one
can
equate
for
observed
reinforcement
effects
are
due
contingency
to
the
In the present study the latter method was
used, the amount of reinforcement, being equated for each subject.
control
One
the
enables
actual
one
to
relationship
ascertain
between
the
Such a
whether
target
response (TR) and the reinforcer, or simply to stimulus properties of the
reinforcing event (cf., Berlyne, 1960; Furedy & Riley, 1979).
EXPERIMENT I
Method
Subjects
Subjects were 36 University of Toronto students who were paid $3 for
participation in the one hour experiment. Ages ranged from 19 to 37 years,
with a mean age of 23 years.
of
the
two
pathological
There were 9 male and 9 female subjects in each
instructional
conditions.
history,
none
and
were
All
under
subjects
were
medication
at
free
the
of
time
cardioof
the
experiment.
Apparatus
HR., respiration and EKG were recorded by an E & M Instruments physiograph, model 4Af with the signals from the silver/silver chloride recording
electrodes through a Narco Biotachometer BT-1200.
from the EKG by a Narco Impedence pneumograph.
Respiration was monitored
Exercise equipment used for
the production of the phasic HR acceleration comprised a 36 kilogram spring
weight clamped in position horizontally at a height of 83 centimetres. A
handle was attached to the end of the spring on which the subject pulled with
both hands.
To ensure constancy of position, the experimenter placed the
subject's back against a backboard, and their foot position was marked on the
5
floor
indicating
to
the
subject
the
point
themselves in order to maintain balance.
at
which
they
must
position
This positioning ensured that the
body weight of the subject was not being used in the movement of the spring
and the task thus produced a substantial increase in tension in the muscles of
the arms, chest, abdomen and back.
The verbal reinforcement was delivered to
the subject by the experimenter through a microphone that transmitted to the
Koss
Pro
4A
headphones
worn
by
the
subject.
White
noise
was
delivered
continually to the subject in order to mask any cues from the clicking of the
physiograph.
Procedure
On arrival at the laboratory the subjects were randomly allocated to one
of 4 groups, with allocation being initially restricted to one of the 2
experimental
groups,
since
control
subjects
were
yoked
to
experimental
partners. Subjects were given instructions on the experiment as they were
placed in the spring-pulling position and electrodes were attached.
Following
placement, the position to which the subject would be required to pull the
spring was determined by calculating 80% of the maximum point at which the
subject could hold the spring steady for 10 seconds following a smooth pull.
The position calculated was marked on the spring calibration for the subject.
The
subject
was
instructed
to
relax,
then
instructions
were
delivered
regarding pretrials. After 3 successful practice trials and 2 pretrials, on
which the subject carried out the muscle-tensing task without attempting to
change the phasic HR acceleration produced by it, subjects were instructed as
to the nature of their task on the 20 conditioning trials.
Subjects in the
increase condition were instructed to attempt to increase HR when they pulled
and during each 10 second spring-pull trial, while decrease condition subjects
were instructed to decrease HR in this period.
The response to be modified
was the HR acceleration elicited by the pull, occurring 2-3 seconds after
6
trial onset.
of
A pilot study had shown that 10 seconds was the minimum duration
spring-pull
effective
for
maintaining
a
sufficiently
elevated
baseline
throughout the session. Subjects were consequently required to hold the spring
for a full 10 seconds.
The reinforcement was then explained to the subject. Verbal reinforcement
was administered following a shaping procedure with a shifting performancedependent criterion.
The size of the phasic HR change occurring 2-3 seconds
after trial onset was read from the physiograph record by the experimenter,
who calculated reinforcement and delivered it immediately.
Reinforcement was
thus delivered approximately 4-5 seconds after trial onset, being contingent
upon the phasic HR acceleration produced by experimental subjects commencing
the muscle-tensing task.
positive
reinforcement
If the subject failed to meet the criterion for
on
a
particular
trial
then
no
verbal
reward
was
delivered.
One half of the subjects in each condition received reinforcement
contingent
upon
the
correct
response.
For
the
increase
condition
this
response was larger HR acceleration relative to the previous trial, while for
the
decrease
condition
it
was
smaller
acceleration.
reinforced according to a shifting criterion.
HR
responses
were
The "amount" of reinforcement
for each trial for increase subjects was determined as follows:
"good", "very
good", and "excellent" was said if, respectively, relative to the immediate
trial there was an increase of 2-4, 4-6, and 6 or more bpm.
For decrease
subjects, reinforcement was calculated on the basis of less strict criteria,
decrease being less reliably produced than increase (see introduction). A l
bpm decrease in magnitude of phasic acceleration over the previous trial was
reinforced with "good", 2 bpm with "very good", and 3 bpm with "excellent".
The control subjects received the same reinforcement as their experimental
partners, delivered at the same time during the trial, but for controls this
reinforcement was non-contingent on the nature of their response.
To overcome
the statistical problems associated with variable amounts of reinforcement for
7
subjects
due
to
their
different
HR
labilities,
the
reinforcement
was
determined in advance as being delivered on approximately 80% of trials.
There were 20 conditioning trials, with intertrial intervals (ITIs) of
40,
45,
or
Following
written
50
the
seconds.
During
conditioning
trials
questionnaire.
This
conditioning
the
subjects
questionnaire
trials
were
were
asked
pertained
to
not
to
the
blocked.
complete
a
subject's
cognitions, strategies and awareness of HR during the experiment and also
asked the subject whether or not he had perceived the reinforcement as being
dependent on his response i.e., contingent.
Results
HR was sampled second by second from 2 seconds prior to task onset to 3
seconds following onset, the first 3 seconds being the baseline and the last 3
the phasic HR response that was to be modified.
A series of ANOVAs on the HR
data revealed no group differences in either tonic or phasic HR on pretrials,
and
there
v/ere
no
tonic-level
differences
between
groups
over
the
conditioning trials, which were blocked into 4 blocks of 5 trials. For phasic
HR, expressed in the ANOVAs as the Seconds (1-6) factor, the ANOVA with Trials
(Pre vs Block 1) and Instruction Direction (Increase vs Decrease) did not
yield a significant Seconds x Instruction Direction x Trials interaction.
That is, the introduction of instructions immediately following the pretrials
but preceding Block 1 did not differentially affect phasic HR acceleration.
However, a significant Trials x Seconds interaction, (F(5,170) = 4.712, p<
.001), indicated that the instructions generally (independently of direction)
produced an increase in the phasic HR acceleratory response, as shown in
Figure 1.
An ANOVA on Block 1 data revealed that phasic HR did not change
over the 5 trials (F<1), indicating that the observed difference from the 2
pretrials was not simply due to there being relatively more HR acceleration in
the later 3 trials of Block 1.
8
Fig. 1: Phasic HR change on pretrials and on four blocks of five
conditioning trials.
With respect to changes in phasic HR over conditioning, an ANOVA revealed
no
significant
main
effect
significant
interactions
significant
Seconds
x
for
contingency
involving
of
contingency.
Instruction-Direction
x
reinforcement,
A
breakdown
Trial-Block
nor
any
of
the
interaction
(F(15,480) = 1.763, p<.O5), revealed by this analysis of conditioning data
showed that there was a significant change in phasic HR over blocks for the
decrease condition (F(15,240) = 2.904, p< .001).
There was no such change for
the increase condition, HR increase subjects showing no further change in the
magnitude of phasic HR acceleration over that produced on the first block of
conditioning.
Inspection of the concomitantly monitored HR and respiration recordings
indicated
that
subjects
complied
with
instructions
requesting
regular
breathing even during the task, and that the observed changes in phasic HR
9
acceleration were not due to gross changes in respiratory rate or depth.
Since, as indicated above, this study was not designed to produce cardiac
changes that were independent of respiratory variations it is quite possible
that subtle changes in respiration contributed to the observed phasic HR
changes.
The responses to the post-experimental questionnaire items on subjectivestate during the task on HR change trials indicated distinctly different
patterns of cognition and affect for increase and decrease subjects. All of
the 18 increase-condition subjects reported having concentrated on exciting or
frightening thoughts or images while all of the 18 decrease-condition subjects
reported
relaxing
thoughts
or
images.
With
regard
to
the
contingency
of
reinforcement received by the subject, 30 of the 36 subjects stated that they
had considered the reinforcement given to them to be dependent upon the nature
of their response. Those subjects expressing doubt as to the genuine nature of
reinforcement (6 subjects) were equally from contingent (3) and non-contingent
(3) groups.
awareness
Questions as to the subject's awareness of his HR indicated that
had
not
increased
over
the
session,
pre-
ratings of subjects not being significantly different.
and
post-experimental
All subjects, however,
did express being aware of the HR acceleration produced by the muscle-tensing
task.
An analysis of the actual mean percentage reinforcement delivered to each
of the 4 groups showed that the amount of reinforcement for subjects in each
group did not differ significantly (F<1), thus indicating that any differences
in responding between groups could not be attributed to variability in amount
of reinforcement. In order to determine the amount of contingent reinforcement
delivered
to
subjects,
the
relationship
between
reinforcement
actually
delivered and HR response on each trial was calculated for every subject.
The
mean number of trials with response-contingent (correct) reinforcement for
contingent subjects was 18 (18.5 for increase, 18 for decrease).
The mean
10
number
with
response-contingent
(adventitious)
reinforcement
for
the
non-
contingent subjects was 6 (6.3 for increase, 6.3 for decrease). An ANOVA on
this
received
reinforcement
revealed
a
significant
contingency
(1,32) = 857, (p<.01), but no instructional effect (£<1).
effect
(F
The absence of a
contingency-of-reinforcement effect in this study could, therefore, not be
simply
due
to
a
failure
to
establish
contingent
versus
non-contingent
reinforcement schedules. Conversely, since there was no difference in the
amount of contingent reinforcement received by increase and decrease groups,
the
obtained
instructional
effects
could
not
be
due
to
reinforcement-
contingency differences.
Discussion
A significant instructional effect emerged clearly in this study,
as
reflected in the significant differences between pretrial and conditioningtrial performance for increase- and decrease-condition subjects. The results
indicate that there was no difference in magnitude of HR acceleration for the
two conditions on the first block of conditioning, all subjects showing a
significant increase in the magnitude of phasic HR acceleration as compared to
pretrials.
This increase may be interpreted as a general instructional effect
which is due to the subject directing attention to the experimental task, and
may be related to the initial anxiety of the subject.
Over conditioning/
however, a significant differential instructional effect did emerge, with the
increase
condition
performance,
and
maintaining
the
decrease
increased
condition
acceleration
producing
smaller
relative to pretrials and the first stage of conditioning.
conditioning
there
was
a
significant
difference
in
over
the
pretrial
acceleration
By the end of
magnitude
of
HR
acceleration between the two conditions.
One possible interpretation of this differential instructional effect is
that subjects are habituating to the muscle-tensing task and increase subjects
11
are simply accelerating against this habituation.
In order to assess this
possibility that the instructional effect was entirely due to acceleration in
the increase groups and not to any deceleration in the decrease groups, a
second experiment was conducted in which subjects were not instructed to
change HR.
EXPERIMENT II
To determine whether the phasic HR acceleration to the muscle-tensing
task did habituate, subjects were run who were not instructed to attempt to
change HR.
Subjects
The 9 subjects, 4 males and 5 females, were from the University of
Toronto. Their ages ranged from 18 to 32 years, with a mean age of 23, and
they were each paid $3 for participation.
Apparatus
The apparatus was the same as described for Exp. I.
Procedure
The procedure was the same as that used in Exp. I, except that the
instructions given to the subject after pretrials were modified. ; Rather than
being
instructed
to
attempt
either
HR
increase
or
decrease
after
the
pretrials, subjects were told to pull back on the spring rapidly and smoothly,
as they had been instructed at the beginning of the session.
Results
As in Exp. I, the concomitant monitoring of HR and respiration indicated
that subjects complied with instructions requesting regular breathing at all
times,
and
the
absence
respiratory activity.
of
a
systematic
relationship
between
cardiac
and
HR was sampled as for Exp. I.
An ANOVA on the phasic HR data revealed that there was a significant
increase in HR over seconds 1-6 (F(5,40) = 6.803, p<.01), indicating that
12
there was a phasic response to the task.
This response was found not to
change over conditioning (F<1), the mean HR responses from baseline to the
third second following trial onset being 4.72 bpm for pretrials and 5.13,
5.36, 5.15 and 5.27 bpm for each of the four blocks of five conditioning
trials.
GENERAL DISCUSSION
The results of the second experiment indicate that with no instructions
to change HR the magnitude of the phasic HR response did not change over
conditioning.
This makes it improbable that the differential instructional
effect in Exp. I was simply the result of the increase-condition subjects
producing acceleration against a background of habituation.
at
the
end
of
conditioning
for
the
second
study
was
Further, the mean
5.3
bpm,
which
is
comparable to the 6 bpm of the increase-instructed groups, suggesting that
decrease rather than increase was improved.
To precisely access the degree of
acceleration and deceleration that is due to instruction, however, it would be
necessary to run a no-treatment control group within the same experiment.1
These findings of an instructional effect on HR increase performance are
in accord with results of other cardiac conditioning studies (e.g., Bergman &
Johnson, 1972; Blanchard & Young, 1972; Blanchard et al., 1974; Colgan, 1977;
Davidson & Schwartz, 1976; Gatchel, 1974; Lang & Twentyman, 1974; Schwartz,
Young & Volger, 1976; Shapiro, Tursky & Schwartz, 1970; Sirota, Schwartz &
Shapiro, 1974, 1976).
The fact that the performance of decrease subjects
improved significantly over conditioning is not consistent with the majority
of
earlier
findings
of
tonic
HR
decrease
where,
after
correction
for
HR
decrease due to general relaxation, no improvements are found (e.g., Bell &
Schwartz, 1975; Bouchard & Granger, 1977; Gatchel, 1974; Lang & Twentyman,
1974, 1976). The main differences between these studies and the present one
are that the present study employed a phasic response and the baseline against
13
which change was to be demonstrated was an elevated one.
Clemens and Shattock
(1979) and Holmes, Frost and Bennett (1977) have reported significant tonic HR
decrease over training with an elevated baseline.
change
as
the
TR,
other
researchers
have
With respect to phasic HR
noted
that
significant
phasic
decelerations can be produced with training (e.g., Gatchel & Proctor, 1976;
Schwartz
et
al.,
1976;
Sirota
et
al.,
1974,
1976).
These
tonic/phasic
indicates that the contingently reinforced subjects had no advantage over
their non-contingently reinforced partners in the production of phasic HR
change.
On a strict or ‘narrow’ definition of biofeedback, we have argued
elsewhere that a contingency-of-reinforcement effect is necessary for it to be
said that the biofeedback phenomenon has occurred (cf., Furedy, 1979; Furedy &
Riley, 1979), biofeedback being due to the relationship between the TR and the
reinforcer, or to the information conveyed to the subject.
cardiac
conditioning
conditions
which
have
studies
not
to
date,
allowed
for
however,
the
have
evaluation
The majority of
employed
of
control
contingency-of-
reinforcement effects and consequently the present findings of no such effect
cannot be meaningfully compared to earlier findings. Most other studies have
employed controls in which the reinforcement is totally removed rather than,
as in the present study, the relationship between the reinforcer and the TR
being manipulated.
By removing reinforcement totally one may also be removing
a stimulus which is producing the observed HR change through some property
which
is
totally
Berlyne, 1960).
independent
of
its
relationship
to
the
response
(cf.,
One may, for example, be also removing a stimulus which is
functioning as a general motivator for the subject, and as a consequence of
its total removal one cannot unequivocally say that any observed effect is due
to the contingency of the reinforcement.
The
instructional
and
experimental
manipulations
used
in
this
study
controlled only for gross physiological changes, and the changes in HR that
were found may have been mediated by a variety of subtle physiological changes
14
such as those in muscle tension, respiration and general activity. The results
of the post-experimental questionnaire indicate that psychological processes
may also have been contributing to the instructional effect obtained. The very
different patterns of cognition and affect noted in the two conditions is of
particular interest, and in line with the findings of other researchers (e.g.,
Engel & Chism, 1967; Engel & Hansen, 1966; Stephens et al., 1975). Subjects in
the increase condition consistently reported exciting or frightening thoughts,
those in the decrease condition relaxing ones.
It would thus appear that the
cognitive and affective state of the subject is related to the direction of HR
change, but as to whether such states are causally efficacious or merely
epiphenomena remains to be determined through further systematic experimental
observations.
What is clear from the present study is that significant differential
instructional
effects
on
phasic
HR
can
be
obtained
in
subjects
during
exercise, and that contingent reinforcement is irrelevant to this effect.
This
finding
of
there
being
no
effect
on
HR
other
than
that
due
to
instructions is in line with a number of other studies which have controlled
for the effects of instructions alone (e.g., Holmes et al., 1977, 1979; White
et al., 1977). With regard to the development of procedures for changing
cardiac responses, it has been suggested elsewhere (cf., Johnston, 1977; Lang,
1977), that the feedback methodology is not an efficient one.
The failure of
any contingency-of-reinforcement or a narrowly defined 'biofeedback1 effect to
emerge in the present study could also be seen to indicate that biofeedback
may not be one of the processes necessary for the production of HR change.
Footnote
We wish to acknowledge
suggestions on this issue
Kirk
Blankstein
and
the
journal's
referees
for
15
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