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Psychomotor Performance And Change In Cardiac Rate In Subjects Behaviorally Predisposed To Coronary Heart Disease

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Psychomotor Performance And Change In Cardiac Rate In Subjects Behaviorally Predisposed To Coronary Heart Disease

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University Microfilms
300 N orth Z e e b R oad
Ann A rbor, M ichigan 48106
A X erox E d u catio n C om pany
74-21,452
A B R A H A M S , Joel Peter, 1944-
PSYCHCMTrOR PERFORMANCE AND CHANGE IN CARDIAC
RATE IN SUBJECTS BEHAVTORALLY PREDISPOSED TO
CORONARY HEART D ISEASE.
University of Southern California, Ph.D., 1974
Psychology, experimental
|
I University Microfilms, A X ER O X Com pany, Ann Arbor, Michigan
© 1973
GERONTOLOGICAL SOCIETY
ALL RIGHTS RESERVED
THIS DISSERTATION HAS BEEN MICROFILMED EXACTLY AS RECEIVED.
PSYCHOM OTOR PERFORM ANCE A N D CH A N G E IN CARDIAC
R A TE IN SUBJECTS BEHAVIORALLY PREDISPOSED
TO CO RO N A RY H EART DISEASE
b y
Joel Peter Abrahams
A D issertation Presented to the
FACULTY OF THE G RA D U A TE SCH O O L
UNIVERSITY OF SOUTHERN CALIFORNIA
In Partial Fulfillment of the
Requirements for the Degree
DO CTO R OF PHILOSOPHY
(Psychology)
January 1974
UNIVERSITY O F S O U T H E R N CA LIFO RN IA
THE GRADUATE SCHOOL
UNIVERSITY PARK
LOS ANGELES, CALIFORNIA 9 0 0 0 7
This dissertation, •written by
Joel Peter Abrahams
under the direction of Dissertation Com
mittee, and approved by 'all its members, has
been presented to and accepted by The Graduate
School, in partial fulfillment of requirements of
the degree of
D O C T O R OF P H I L O S O P H Y
Dean
DISSERTATION COMMITTEE
Chairman
ACKNOW LEDGEMENTS
This dissertation was conducted while the author was supported
by NICHD Training Grant H D 00157. There are many persons whose
contributions and encouragement deserve recognition.
F irs t, I would like to thank my dissertation committee chairman,
Dr. James E. Birren, not only for his guidance in this d isse rta tio n ,
but also for his encouragement and tutelage over the past three
years.
I would also like to express my thanks to the rest of my
d issertatio n and guidance committee Dr. James Walker, Dr. Gary
Galbraith, and Dr. Vern Bengtson fo r th eir contributions to this
d isserta tio n . Also, to Dr. James Kahan and Mr. Garst Reese, m y
thanks for th e ir assistance in the data analysis.
I would like to thank Dr. J. S. Felton, Medical Director of
Los Angeles County Occupational Health Service, and his s ta f f for
th e ir great help in recruiting volunteers to serve as subjects for
th is study and for supplying necessary space, equipment, and
technical advice.
M y thanks also to Dr. Ray Rosenman of the Harold Brunn
In s titu te , Mt. Zion Hospital and Medical Center, San Francisco
fo r his instruction in the interview method used for id en tificatio n
of coronary-prone subjects.
I wish also to express my thanks to the la te Dr. Jacek Szafran
for his many and lasting contributions to my graduate education.
Finally, I wish to thank my wife Karen, for her encouragement
and support during my years as a graduate student. I t is to her
th a t th is work is dedicated.
TABLE OF CONTENTS
Page
ACKN O W LED G EM EN TS ..................................................................................... 11
INTRODUCTION ...................................................................................... 1
Hypotheses to be t e s t e d ........................................................... 13
M ETHODS ....................................................................................................... 14
Subjects .......................................................................................... 14
Classification of behavior type .......................................... 14
A p p a r a t u s .......................................................................................... 14
P r o c e d u r e .......................................................................................... 15
Design .............................................................................................. 16
RESULTS ....................................................................................................... 13
Reaction time: Hypothesis I .............................................. 18
Reaction time: Hypothesis II .............................................. 20
Heart rate change: Hypothesis III .................................. 21
RT/Age regression analysis ................................................... 22
DISCUSSION ....................................................................................... 26
Psychomotor slowness in coronary-prone subjects . 26
Equivalent cardiac deceleration .......................................... 32
Nonlinear relationship between RT and age . . . . 37
Future research ......................................................................... 40
SU M M A R Y A N D CONCLUSIONS .................................................................... 44
REFERENCES........................................................................ 48
iv
L i s t o f T a b le s and F ig u re s
Table Page
1. Means and Standard Deviations of Ages and
Reaction Times ........................................................................ 18
2. Univariate Analyses of Variance fo r Zero
C o v a r i a t e s ................................................................................. 19
3. Univariate Analyses of Variance fo r One
Covariate, A g e ........................................................................ 20
4. Means and Standard Deviations of Heart Rate
Change Ratios ........................................................................ 21
5. Regression A n a l y s e s ................................ 23
6. Age/Reaction Time Correlation Ratios ........................ 25
Figure
1. Plot of Reaction Times by Age D e c a d e s ........................ 43
v
CHAPTER I
INTRODUCTION
In te re s t in the psychological variables associated with
coronary heart disease {CHD) dates back several decades, but i t
has only been during the past 10 years th at studies on a large
scale have been conducted. Current research on the psycho-etiology
of CHD has basically taken three forms: (1) id en tificatio n of
personality factors d if f e r e n tia lly associated with c e rta in of the
clinical forms of CHD; (2) delineation of those psycho-social and
sociological variables which places an individual at high risk for
CH D ; and (3) id en tificatio n and elaboration of personality and
behavioral t r a it s which seem to predispose one to CHD. For the
purposes of th is investigation only the l a s t i s of in te r e s t.
The current approach to the epidemiology of C H D involves the
identificatio n of individuals who have early stage or "pre-clinical"
disease, or disease-free persons who are lik e ly to develop CHD.
Hopefully, then, through early detection, the natural course of the
disease can be altered . Potential coronary victims are identified
by searching for certa in risk f a c to rs . Risk factors are character
i s t i c s , signs, or symptoms in a CHD-free individual which are
s t a t i s t i c a l l y associated with an increased incidence of subsequent
C H D . The primary ris k factors have been hypercholesterolemia,
hypertension, smoking, obesity, electrocardiographic abnorm alities,
and lipoprotein electrophoresis abnormality. However, more
recently personality, behavioral, and social factors have been
added to the l i s t .
The question of risk factors associated with C H D is one of
logic. With the exception of personality, behavioral, and social
factors, and smoking (which is more than likely a reflection of
personality), risk factors or clinical pre-cursors are also signs
or actual symptoms of the disease state. On the one hand,
hypercholesterolemia, hypertension, EC G abnormalities, etc. are
considered pre-clinical risk factors in coronary disease; on the
other hand, these same variables are also relied on in the diagnosis
of C H D before the actual myocardial infarction occurs. The logical
issue of th is approach to risk factors reduces to the question:
W hen does a risk factor become a symptom? (Abrahams, 1972)
On the intuitive level, behavior has long been considered to
be in some manner associated with CHD. This, in addition to the
need to identify a true risk factor independent of disease sympto
matology, has led researchers to study psychosocial and behavioral
factors. Indeed, i t has been shown that behavioral and psycho
social variables are able to identify high risk individuals even in
the absence of traditional biomedical pre-cursor signs (Friedman,
1969; Shekelle, Ostfeld, and Paul, 1969).
Henry and Cassel (1969) have presented epidemiological and
animal experimental evidence which allows for greater emphasis to
be placed on the etiologic role of psychosocial stimulation,
early experience, and environmental stress in essential hypertension
and coronary disease. They cite evidence to indicate that chronic
arousal of the defense alarm response may be a c r itic a l factor in
3
the occurrance o f essential hypertension, coronary disease, and
cerebrovascular disease.
The defense alarm response (DAR) is an alerting response to
stimulation of the la teral hypothalamus. This hypothalamic
activation can re su lt from downward disinhabition from the cortex
or from direct ennervation from the subthalamic sensory receiving
centers. The DAR puts the organism in a s ta te appropriate for e ith er
attack o r flig h t. There is a syndrome o f hormonal and neurogenic
cardiovascular changes typical of the defense alarm s ta te . These
include an elevation of a rte ria l pressure, increased heart rate
and often cardiac output, and increased blood flow to the muscles
while the flow through the gastro in testin al tra c t and kidneys is
rad ically reduced. Perhaps of equal significance to this pattern of
autonomic arousal is the increased catecholamine discharge and the
reported increase in levels of 17 hydroxycorticosteroids (17 OHCS)
which also accompany the stim ulation of the DAR. Additionally,
Brod, ejt (1959) have shown that the DAR can be induced by
symbolic stim uli. The importance of the D A R and i t s possible role
in the etiology o f coronary-prone behavior and eventual CH D is
detailed elsewhere (Abrahams, 1972).
The chronic activation of the D A R is a central feature of the
developmental/multivariate theory of the psycho-etiology of CH D as
formulated by Abrahams (1972). This is especially so as i t relates
to the manifestations of coronary-prone behavior. A basic tenet of
this theory is th a t stre ss which the coronary-prone individual
encounters as a re su lt of goals, coping strategy, and motivation,
in the presence of a personality not allowing of stress dissipation
or which places one in chronic stressful situations yields chronic
physiological arousal over many years. In fa c t, Rosenman and
Friedman, e t al_ (1966) have shown th at when compared to non-coronary
prone males, coronary-prone males of the same age show greater mean
serum lipid concentrations of both triglycerides and cholesterol
and higher urinary excretion of catecholamines. The lipid
differences are highly significant in the 39-47 year age group.
The most extensive program of research attempting to link
behavioral variables to coronary disease has been undertaken by
Friedman, Rosenman, and th e ir associates (Friedman, 1969). These
investigators have designated the coronary-prone behavior pattern
as Type A, and have defined i t as a "characteristic action-emotion
complex which is exhibited by those individuals who are engaged in
a relatively chronic struggle to obtain an unlimited number of
poorly defined things from their environment in the shortest period
of time, and i f necessary, against the opposing efforts of other
things or persons in this same environment." (Friedman, 1969)
Individuals exhibiting the Type A behavior pattern are highly
competitive, seem to be involved in multiple a c tiv itie s having time
restrictio n s or deadlines. They appear to be extraordinarily
a le rt, and like to set th e ir own work pace. Persons exhibiting
Type A behavior tend to be impatient with slowness, even to the
point of hurrying conversations or supplying words for persons with
whom they are speaking.
Beginning in 1960-61 Friedman, Rosenman, and th e ir associates
embarked upon the Western Collaborative Group Study(WCGS) of over
3500 men aged 39-59 and free of c lin ic a l CHD. Almost 50% of the
sample were judged as exhibiting behavior Pattern A. Approximately
70-80% of the to ta l group' of subjects exhibited the incompletely
developed form of e ith e r Type A or i t s an tith esis Type B. Type
B is the absence o f the manifestations of Type A.
Thus fa r, Friedman, Rosenmen, e t al_, have reported associations
between Pattern A behavior and an increased incidence of clinical
CHD; elevations in total serum cholesterol, tr ig ly s e r id e s , and Beta
lipoproteins; decreased whole blood clotting time; elevated daytime
excretion of catecholamines, and cap illary ischemia in conjunctival
tissu e . Additionally, they report the incidence of new C H D to be
three times higher in Pattern A subjects as compared to Pattern B
subjects (Friedman, 1968; Rosenman, et^ al_, 1966).
Recently Rosenman, e t al^ (1970) have reported on the current
statu s of the W C G S and the present findings merit summary.
Cumulative data from the W CG S showed a sig n ific a n tly increased
incidence of CH D to be associated with Type A behavior, parental
history of CHD, elevated sy sto lic or d ia sto lic blood pressure,
cig arette smoking, higher serum level of cholesterol, trig ly c e rid e s,
and Beta lipoproteins. A dditionally, the association of Type A
behavior with a sig n ific a n tly increased risk of CH D was not found to
be ascribable to an association of the behavior pattern with other
risk factors. Even when all other risk factors were s t a t i s t i c a l l y
co ntrolled, i . e . , held constant in a multiple regression analysis,
6
the Type A subjects had over twice the C H D risk as compared to
the Type B subjects.
The actual incidence rates for the Type A and Type B subjects
were: 8.9/1000 and 4.0/1000 respectively in the 39-49 age group;
and 18.7/1000 and 13.2/1000 respectively in the 50-59 age group.
This compares with the following rates of f i r s t events of disabling
C H D among Bell System men age 30-59 as reported by Hinkle, e t al
(1968): executives, 1.85/1000; general area managers, 2.85/1000;
local area managers, 3.91/1000; supervisors, 3.91/1000; foremen,
4.52/1000; and workmen, 4.33/1000. These morbidity data from
Hinkle, e t a]_ (1968) include only a small proportion of episodes of
angina pectoris and of asymptomatic CHD which often does not
cause d isa b ility and may not be recognized or reported.
Thus there are clear physiological as well as pathological
consequences of manifesting coronary-prone behavior. On an
intuitive level one would suspect th at there should be some cognitive
psychological or psychomotor performance consequences or correlates
as a r e s u lt of possessing Type A behavior. At present i t is not
known whether or not such js the case. However, research in parallel
areas of in te re st point to certain p o s s ib ilitie s .
Birren, trt a/L (1963) intensively studied 47 relatively
healthy men over the age of 65. When the subjects were divided
into two groups, those regarded as in optimal health and those
having subclinical signs of disease, there were significant
differences in the verbal intelligence scores o f the two groups.
The investigators in te rp re t the re su lts as suggesting that physiolo-
ical changes, especially those related to cerebral c irc u la tio n ,
pace cognitive regression. However, unlike verbal te s ts , measure
ments of psychomotor speed showed sim ilar re su lts for the two
groups. Both v/ere s ig n ific a n tly slower than young adults. The
authors feel th at these re su lts indicate th at there may be age-
related increments and decrements in mental a b i l i t i e s as well as
disease-paced decrements.
Spieth (1964) studied the psychological performances of more
than 600 men age 23-59 years. Subjects, who were all aviation p ilo ts
and a ir t r a f f i c control s p e c ia lis ts , were divided into six groups
based upon cardiovascular health statu s: (la) S t r i c t l y healthy;
(lb) "False positive" subjects who had been referred to the Federal
Aviation Administration c lin ic a l research i n s titu te due to mistaken
findings of coronary pathology; (2) Mild rheumatic or congenital
cardiovascular disease; (3a) Somatic a r te rio s c le ro tic or coronary
h eart disease; (4a) Hypertension or hypertensive cardiovascular
disease in mild or moderate degree; (5) Subjects presenting history
or c lin ic a l symptoms of cerebrovascular disease.
Spieth reports th a t the resu lts o f his investigation "demon
strated quite conclusively th a t subjects suffering a rte rio s c le ro tic
coronary heart disease or who show evidence of old myocardial
in fa rc tio n s, and those with essential hypertension, will perform
more poorly than reasonably well matched healthy subjects on a
wide variety of self-paced tasks in which sheer physical e f f o r t is
minimal; and that th is is tru e of those who are recovered from
8
acute symptoms and who have the diseases in re la tiv e ly moderate
degree." (Spieth, 1964) The hypothesis that these results were
due merely to more cautious self-pacing on the p a rt of the cardio
vascular disease subjects is not tenable. The CVD groups were
somewhat poorer in th e ir performance on the-untimed recall task
(Halstead Tactual Performance Task) which was free of any speed
e ffe c ts. In the psychomotor performance battery there was a
sig n ifican t health-group by subtest-complexity interaction of
reaction times. The differences between the reaction times of the
healthy and C V D groups increased as the complexity of the performance
task increased.
According to Spieth, most of the slowness in performance of
the CVD subjects on the more complex tasks was not in the actual
movement phase of the response, but rather in the decision phase
of the reaction process. Additionally, Spieth points out that a set
toward slowness would not seem to explain the findings of Simonson
and Enzer (1941) of a subnormal flick e r fusion threshold in subjects
with coronary heart disease. Other indirect evidence concerns
Anderson's (1963) finding th at C H D subjects not only performed
more slowly than healthy controls, but also made more errors in a
one-hour speed te s t of solving simple but tricky arithmetic problems.
The major import of the Birren, e t a l and o f the Spieth
studies is that substantial parts of the mean age differences
found in cross-sectional studies of psychological performance
might be better attributed to "disease processes which are not
inexorably bound up with age, but are positively correlated with
age, than to age i t s e l f . " (S pieth, 1964) I t is also extremely
important to consider th a t Spieth found th a t the s tr i c t l y healthy
subjects also showed decrements in performance with age. Thus,
there appear to be both decrements in the speed and time of
behavior associated with age and decrements in the speed and timing
of behavior due to the e ffe c ts o f cardiovascular disease regardless
of age.
With regard to the differences in performance between the
healthy, pathological, and aged groups on reaction time ta sk s,
two possible explanations may be offered. The f i r s t is th a t the
observed differences are due to disease-changes and age-changes
in the central nervous system. The second is related to the
condition o f the cardiovascular feedback mechanism.
Lacey and Lacey (1971) have described the cardiovascular
feedback mechanism and i t s possible e ffe c ts on behavior in
gating environmental inputs and behavioral motor outputs into and
out of the CNS. These investigators feel that elevations in blood
pressure and heart ra te may produce, under appropriate circumstances
a stimulus b a rrie r and th at decreases in heart rate and blood
pressure may produce a more permeable stimulus barrier.
The Laceys feel th a t a rein te rp re ta tio n of cardiovascular
responses to stimuli are in order. According to them, "The
temporary hypertension and tachycardia observable in acute emotional
sta te s and in aroused behaviors of all sorts may not be the d ire ct
index of so-called arousal or activation they are so often considered
to be. Instead they may be a sign of the attempt of the organism
instrum entally to constrain, to lim its and to terminate the turmoil
produced inside the body by appropriate stimulating circumstances.
I f increases in blood pressure and heart ra te signal a physiolog
ical attempt to re stra in excitatory processes, then i t seems
lik e ly that th e ir diminution, absence, or conversion to blood
pressure and heart ra te decrease signify an absence of this
restrain in g process, and therefore, a net increase in excitation:
a lowering of threshold, a prolongation of the impact of stim uli,
and increase in spontaneous a c tiv ity , e c t." (Lacey and Lacey, 1971)
Lacey and others (Lacey, 1959; Lacey, Kagan, Lacey, and Moss,
1963; Qbrist, 1963) have demonstrated th a t heart rate changes
in psychological performance tasks vary according to the nature of
the task. Those tasks which require internal cognitive elaboration
of a problem-solving s o rt, or exposure to noxious stimuli produce
cardiac acceleration, both in minimum and maximum ra te s , and also in
v a ria b ility . Also there is an increase in other arousal responses.
However, in those tasks in which only simple environmental reception
is required, there occurs cardiac deceleration, decreases in
v a r ia b ility , but also increases in other indices of arousal. Thus
th ere is b i-d ire c tio n a lity of h e a rt rate changes which are dependent
upon the nature of the task.
The Laceys have reported on a series of reaction time
experiments in which heart rate was monitored. They report
beat-by-beat deceleration during fixed preparatory intervals of
4, 9, and 10 seconds. This e ffe c t was seen both e a rly and la te in
the experiment. The cardiac response to the preparatory signal
was generally accelerativ e in nature and then there was massive
deceleration 3 or 4 beats before the imperative stim ulus. An
in tere stin g r e s u l t of these studies was th a t there was a p o sitiv e
correlation between the amount of deceleratio n and the speed of
reaction time. That i s , the g re a te r the amount of cardiac d ecel
e ratio n , the f a s t e r the reaction time. This was shown both on an
in te r- and in tra -s u b je c t basis.
Given the re su lts of the s tu d ie s by Lacey and Lacey, and others,
and the general theory of the cardiovascular feedback mechanism,
a second possible explanation fo r th e slower reaction times found
in unmedicated hypertensives and persons su ffering from CHD may
be offered. In periods of increased a ro u sa l, as occurs during
reaction time performance task s, an individual who is e ith e r
developing hypertension or already su fferin g from i t or CHD may
possess a cortex which sends a suboptimum pattern of information to
the hypothalamic area and other subcorttcal centers and a d iffe re n t
pattern of input could occur via dysfunctioning cardiovascular
feedback mechanism which i s improperly gating environmental inputs
to the cortex. Other possible mechanisms causing th is alte re d
input p attern are the hypothalamic and ascending r e t ic u la r a c t i
vating system and/or endocrine controlled events in the r e s t of
the organism.
As Tall and (1968) has pointed out, the processes involved
in the performance of even simple reaction time tasks are sufficiently
complex to be susceptible to many influences. These influences
can effect events anywhere along the chain from readiness for the
signal to the execution of the proscribed movement. I t has been
discussed that both age and disease states influence reaction time
processes, resu ltin g in greater latency of response. Talland has
also confirmed the finding that time to respond increases even
in a middle age group.
The question now arises as to whether there e x ist increased
response latencies in healthy adults who, by v irtue of manifesting
Type A behavior, are considered to be at high risk for coronary
disease. I t must be remembered th a t persons recovered from acute
symptoms of CHD do indeed show increased reaction times when compared
to healthy controls. The basic issue is whether or not those
performance d e f i c i ts found in disease-state individuals will also
be found in coronary-prone but pathology-free persons.
The hypotheses being tested in this investigation are based
upon both the lite ra tu re previously reviewed and the necessity of
f illin g an empirical void in the area of psychological performance
consequences (or correlates) to pre-pathological disease sta te s.
Behavior of a ll types is the re su lt of h isto rical antecedents
upon the organism. These antecedents may be biogenic, intra-personal,
psycho-social, environmental, etc. There are eventual consequences
of cardiovascular health upon psychological performance. I t is
important to assess if there are any psychological performance
consequences as a resu lt of behavioral predisposition to a disease
s ta te .
The hypotheses of th is investig atio n can be lis te d as follows:
1. Coronary-prone, Pattern A subjects will show greater
response latencies in a simple visual reaction time performance
task than will Pattern B co ntrols.
2. The response laten cies of the Pattern A group will
be disproportionately longer in a complex, three-choice reaction
time ta sk , when compared to Pattern B controls.
3. Pattern A subjects will show a pattern of lessened cardiac
deceleration in response to a warning signal than will Pattern
B controls.
CHAPTER II
M ETHODS
Subjects
Forty-eight males between 25-59 years of age served as subjects
in th is investigation. Mean age was 40.187 years. The Ss were
all civil service employees of Los Angeles County and held e ith er
blue c o lla r (building maintainance) or managerial/executive
(foreman, department head)positions. All Ss^were screened by the
physicians of the Occupational Health Service of Los Angeles County
for coronary statu s. Only those Stewho (1) had sy sto lic blood
pressure levels considered within the normotensive range (between
100mm Hg and 150mm Hg), and (2) were free of clinical CH D were used.
C lassification of behavior type
All S^ in th is study were given the Standard Situation In te r
view for Pattern A Behavior. This interview technique has been
developed by Friedman and Rosenman (Friedman, 1969) and is considered
to be the best and most re lia b le method of classifying S£ as e ith e r
Pattern A or Pattern B. A lengthy discussion of this method is
availabe elsewhere (Abrahams, 1972).
Apparatus
Heart rate was monitored using a multi-channel E and M
Instruments Physiograph Six with event marker. An E and M
Biotelemetry tran sm itter, Model FM-1100-E2 and an E and M
14
15
Biotelemetry receiver, Model FM-1100-7 were employed and heart rate
was recorded on rec tilin e a r paper a t the speed of 0.5 cm/sec.
Reaction time was recorded to the nearest 0.005 second using
a Lafayette timer. Duration of the warning signal was determined
by a Lafayette interval timer. The reaction time equipment i t s e l f
was a Lafayette Model 63011 Multi-choice reaction time apparatus.
The apparatus consists of a control unit, stimulus unit,;and res
ponse keyboard. The stimulus unit consists of three colored
lights (red, blue, and green) which are projected on a common
surface and a set of auxiliary pin jacks. The response keyboard
consists of three heavy duty telegraph keys mounted on a fiberesin
board. The control unit contains the stimulus selector, pre-level
selector control, and an in itia te switch. This apparatus has a
1 second ready signal which may be presented a t variable delay
intervals from 1 to 10 seconds prior to the onset of the stimulus.
Procedure
There were two levels of complexity to the reaction time
experiment. In both, the Ss_were seated in front of the response
keys and Stimulus box in a well-lighted room. A restraining line
12 inches from the edge of the table and 11 inches in front of the
response keys was employed. The stimulus box was placed eight
inches to the rear of the response keyboard. The were instructed
to keep th eir hands on the restraining line until the imperative
stimulus was presented. In both levelSc of the reaction time task
a preparatory signal was presented. This was a white warning light
16
of 1 second duration. This was followed by a preparatory interval
of 4 seconds. At the end of the PI the imperative stimulus was
presented.
The signal-to-respond for Level I was the presentation of the
RED stimulus lig h t. The Ss were instructed to respond, as f a s t as
possible, by depressing the key which corresponded to the red
stimulus lig h t.
The signal-to-respond for Level II was the presentation of
e ith e r the BLUE, or the RED, or the GREEN stimulus lig h t. The
Ss_were instructed to respond to the stimulus by depressing, as
fa s t as possible, the response key which corresponded to the presented
stimulus lig h t. The order of presentation of the colored lights
was randomized for each S _ .
I n te r- tria l intervals in both levels was 5 seconds. Each
!S received 5 warm-up t r i a l s in Level I and 5 warm-up t r i a l s a t each
color condition in Level II. All S£ received 50 t r i a l s a t each
level of complexity, making a to ta l of 100 t r i a l s . Heart rate was
continuously monitored throughout the t r i a l s .
Design
The over-all design of th is investigation was a two-way
c la ssific a tio n m ultivariate analysis of variance with repeated
measurements on each S ^. The two independent variables were behavior
type: Pattern A and Pattern B. The two dependent variables were
simple and choice reaction time. Additionally, there were 50
observations per :S for each dependent variable.
The design of the analysis of the heart rate data is basically
the same as th at for the analysis of the reaction time data.
The two independent variables were behavior type. For the purpose
of s ta tis tic a l evaluation, a single measure of heart rate change
during the reaction time tria ls was used; R-S: the change in rate
from the beat during which the warning signal occurred (R) to the
beat during which the imperative stimulus occurred (S). This
paradigm for the analysis of heart rate change data is similar to
that utilized by Morris and Thompson (1969) and by Lacey and Lacey
(1965). The heart rate change data in this investigation took the
form of an R/S ratio . The specific dependent variables for the
heart rate analysis were the R/S ratios for the ten fa ste st reaction
time tria ls and the ten slowest reaction time tria ls for both simple
and choice conditions. Thus, the s ta tis tic a l technique used to te st
the heart rate changes was a two-way classification multivariate
analysis of variance with repeated measurements on each subject.
CHAPTER III
RESULTS
Reaction Time: Hypothesis I
The resu lts of th is experiment demonstrate the subjects
displaying the coronary-prone behavior, Pattern A have greater
response latencies than non-coronary-prone, Pattern B subjects,
in both simple and choice RT performance tasks. The means and
standard deviations of simple and choice RT fo r both behavior
pattern groups are shown in Table 1. A m ultivariate analysis of
variance was run between the two behavior groups and a sig n ifican t
F-ratio was found for simple and choice RT ^ , 4 5 = 9.727). The
univariate ANOVAs for both simple RT and choice RT were sig n ifican t
(F],46 = 14.25 and 19.8 respectively).
TABLE 1
M EA N S A N D STANDARD DEVIATIONS OF AGES A N D REACTION TIMES
A GE SIMPLE RT CHOICE RT
PATTERN A
M 39.71 0.535 0.719
SD 11.08 0.058 0.087
PATTERN B
M 40.67 0.472 0.618
SD 9.83 0.059 0.070
18
19
A n analysis of covariance showed th at age was a significant
covariate in the RT data (F-j, 44 = 3.78). The R T data was reanalyzed
with one covariate, age. The results of this analysis s t i l l showed
significant differences between the two groups for both simple and
choice R T (F-j, 45 = 37.99 and 15.41 respectively). The univariate
F-tests of the RT data for zero covariates is shown in Table 2.
The univariate F-tests of the RT data for one covariate is shown
in Table 3. These results support hypothesis I.
TABLE 2
UNIVARIATE A NOVAs FO R ZERO COVARIATES
SIMPLE REACTION TIM E
Source SS df M S F
Treatment 46937.53 1 46937.53 14.25**
Error 151443.95 46 3293.26
Total 293813.48 47
CHOICE REACTION TIM E
Source SS df M S F
Treatment 122614.08 1 122614.71 19.80**
Error
Total
284857.83
407471.91
46 6192.56
**p 0.01
20
TABLE 3
UNIVARIATE ANOVAs FOR O N E COVARIATE, A G E
SIMPLE REACTION TIME
Source SS df M S F W 2
Treatment 98310.15 1 98310.15 37.99** .43
Error 116647.50 45 2592.17
Total 214957.65
W 2 (omega-squared) =.43
CHOICE REACTION TIME
Source SS df M S F W 2
Treatment 69471.69 1 69471.69 15.41** .24
Error
Total
202829.07
272300.76
45 4409.33
W 2 (omega-squared) =.24
**p 0.01
Reaction Time: Hypothesis III
The means of the RT data for each in both groups was
converted to a ra tio of simple/choice. A t - t e s t for independent
groups was run between the two behavior type groups and a
sig n ific a n t t - r a t i o was found (t^g = 7 .5 9 ). A ra tio of simple/
21
choice was chosen as the datum for significance testing rather than
a simple-minus-choice difference because a ratio would more
accurately re fle c t any performance difference between the two groups.
These results support hypothesis II.
Heart Rate Change: Hypothesis III
The means and standard deviations of the heart rate change
ratios for the ten fastest and the ten slowest simple and choice
R T times are shown in Table 4. When a multivariate analysis of
variance was run between the two groups the only significant F-ratio
was that found between the heart rate change ratio which occurred
during the ten fa ste st and the ten slowest simple reaction times
/
(f-j, 46 = 49.12). This was within-subjects difference; no between
groups differences were found on heart rate change data in either
condition.
TABLE 4
M EA N S A N D STAN D A RD DEVIATIONS OF HEART RATE CH A N G E RATIOS
SIMPLE REACTION TIME
M SD
10 FASTEST RT TRIALS 0.907 0.017
10 SLOW EST RT TRIALS 0.924 0.014
CHOICE REACTION TIME
M SD
10 FASTEST RT TRIALS 0.916 0.017
10 SLOW EST RT TRIALS 0.918 0.014
2 2 j
The w ithin-subjects difference in heart rate change was
expected based upon the research of Lacey and Lacey and others.
This attempt to extend the observation was not successful.
An analysis of covariance using Wilkes lambda c rite rio n showed
that age was not a sig n ifican t covariate in the heart rate change
data. These results do not support hypothesis III.
RT/Age Regression Analysis
Regression analyses of age on reaction time were run for both
groups under both RT conditions. All four t e s t for lin e a rity of
regression and for deviations from lin e a rity were sig n ifican t.
The null hypothesis th a t the regression coefficient for simple RT
for the Type A group was equal to the regression co efficien t for
simple RT for the Type B group was supported. A sim ilar conclusion
was reached with regard to the pair of coefficients for choice RT.
That i s , bSRT^ = bgRyg; and bQRT^ = b ^ y g . Table 5 contains the
source data for the regression analyses and the computed coefficients.
Correlation ratio s (eta-squared) were computed between age and
RT-condition for the two groups of subjects; these are presented in
Table 6. The correlation ra tio is a descriptive index of total
relationship in a given set of data. I t applies only to a sample,
and is usually discussed only when both variables are numerical.
23
TABLE 5
REGRESSION ANALYSES
SIMPLE RT/AGE: PATTERN A ___________________
Source SS df M S F
Between groups 4033232.3 23
- -
Linear reg. 2553048.2 1 2553048.2 599.4**
Dev. from Tin. 1480184.1 22 67281.09 15.7**
Error 5008798.9 1176 4259.2
Totals 9042031.2 1199
CHOICE RT/AGE: PATTERN A
Source SS df M S F
Between groups 8514721.8 23
- -
Linear reg. 5741513.1 1 5741513.7 4220.4**
Dev. from lin . 2773208.7 22 126054.1 9.3**
Error
Totals
1600311.2
10115043.0
1176
1199
1360.4
**p O.01
REGRESSION COEFFICIENTS
Beta
Simple RT/age Type A 0.0997
Simple RT/age Type B 0.1477
Choice RT/age Type A 0.1671
Choice RT/age Type B 0.1716
24
TABLE 5
REGRESSION ANALYSES
SIMPLE RT/AGE: PATTERN B ___________________
Source SS df M S F
Between groups 4236208.0 23 - -
Linear reg. 3466018.5 1 3466018.5 1433.6**
Dev. from lin. 770189.5 22 35008.6 14.5**
Error 2842565.6 1176 2417.6
Totals 7078773.6 1199
CHOICE RT/AGE: PATTERN B
Source SS df M S F
Between groups 5649903.04 23
Linear reg. 5279251.3 1 5279251.3 578.1**
Dev. from lin 370651.74 22 16847.8 1.84*
Error 10739258 1176 9132.02
Totals 16389161.04 1199
**p O.Ol
*p 0.025
TABLE 6
AGE/RT-CONDITION CORRELATION RATIOS (ETA-SQUARE)
Type B
.598*
.344*
*p 0.05
Type A
Simple RT/age .446
Choice RT/age .841
CHAPTER IV
DISCUSSION
Ps.ychomotor Slowness in Coronary-Prone Subjects
Hypotheses I and II were supported by the data in this
investigation. The coronary-prone, Pattern A subjects showed
greater response latencies in both simple and choice visual reaction
time performance tasks than did non-coronary-prone, Pattern B
subjects. Additionally, the data showed th at the response latencies
of the Type A group were disproportionately longer in a three-choice
RT task when compared to Type B subjects.
Thus, i t was shown th a t in the absence of c lin ical signs of
pathology, Type A subjects exhibit psychomotor characteristics
sim ilar to those found in persons already suffering from coronary
heart disease. The resu lts of this study demonstrate th a t the
observed psychomotor performance ch aracteristics of a disease state
may have actually preceded the onset of the disease, rath er than
have resulted from the acute event. Additionally, the data suggest
that the psychoiiiotor slowing may be the re su lt of the prepathological
biochemical and behavioral factors which eventually produce the
disease, rather than from the disease i t s e l f .
A possible causal explanation for the observed re su lts is
couched in activation theory. One of the basic tenets of activation
theory is th a t there is a curvilinear relationship between behavioral
efficiency and measures of physiological arousal. Neuroanatomically,
activation theory places emphasis on the ascending re tic u la r
26
27
activating system. According to Lindsley (1958), i t is this
structure which is the primary source of excitation to the cortex
and is responsible for maintaining arousal or activation.
The activation theory originally rested on the following
facts: (1) the EEG in emotion is characterized by a desynchronization
or activation pattern; (2) alpha blocking or activation pattern
of the EEG can be induced in animals by electrical stimulation of
various sense modalities; (3) interruption of the ascending RAS
by lesion abolishes activation of the EEG and restores synchrony.
More recently, several additional points in support of the general
thesis that the descending and ascending RASs together play a
significant role not only in the mechanisms underlying emotion-
motivational behavior, but also in relation to alertin g , attention,
vigilance, and the regulation and control of sensory input have been
delineated.
The re tic u la r formation can be activated not only through
colaterals from specific sensory afferen ts, but also through
connections with the cortex. This makes i t possible to conceive
of internal states such as thoughts, worries, and apprehensions
generating arousal a ctiv ity in the re tic u la r formation. Through
descending pathways there can be modification of visceral and
somatosensory activ ity . Through ascending pathways affecting
cortical e x c ita b ility and inhibitory control there can be arousal,
alertin g , and enhanced or suppressed perceptual effects.
(Lindsley, 1971) The functioning of the RAS would appear to be a
28
necessary feature of the defense alarm response.
A minimum background of general arousal is necessary for
specific sensory information processing by the central nervous
system. The basic processes of perception, learning, and coordin
ated motor performance will not occur as readily without th is
general level of arousal. At optimal levels of co rtic al arousal
such behavioral dimensions as speed, correctedness, and learning
a b ility are most e ffic ie n t. Deviations in e ith e r direction from
th is optimal level of arousal produce less e f fic ie n t behavior.
This relatio n sh ip between arousal and performance can be described
by an inverted U-shaped curve.
Research conducted by S.joberg (1968); Pinneo (1961); Freeman
(1948); and Fuster (1958) have all demonstrated th is inverted-U
functional relatio n sh ip between measures of arousal and performance.
Sjoberg (1968) found a curv ilin ear relatio n sh ip between reaction
time and muscle tension as a measure of arousal. Pinneo (1961)
showed th a t performance on an auditory tracking task was s ig n if i
cantly improved under conditions of induced muscle tension. In
a repeated measures, within subjects design, Freeman (1948) found
th a t the f a s te s t reaction times occurred with moderate as opposed
to e ith e r smaller or larger GSR responses. Fuster (1958) demonst
rated the inverted U-shaped relatio n sh ip between arousal and both
speed and proficiency of behavior in his study using d ire c t e le c t
ric a l stim ulation of the brainstem of monkeys.
Lansing, Schwartz, and Lindsley (1959) studied reaction time
as a function of changes in the EEG pattern under two d iffe re n t
29
conditions. Under one condition a warning signal preceeded the
imperative stimulus, while under the other condition no preparatory
signal was given prior to the imperative stimulus. Within the
non-alerted condition, RT was found unrelated to the sta te of the
EEG pattern. However, under the alerted condition, the degree of
alpha blocking in the EEG pattern was positively related to both
speed of RT and length of the preparatory interval. The largest
blocking of the EEG coincided with the longest PI. The authors
feel that these results suggest th at the preparatory signal functioned
as an alerting mechanism and this yielded fa ste r RTs and greater
alpha blocking.
Lacey and Lacey (1959) studied the spontaneous beat-by-beat
fluctuations in the resting level of heart rate as a measure of
activation. They differentiated two groups of subjects on the
basis of the extent of this spontaneous v a ria b ility . Those
individuals whose resting heart rate varied considerably were
labeled "Labile," while those whose heart rate varied less were
call "Stabile." The authors studied the R T performances of these
two differentiated groups in relation to preparatory intervals of
3, 4, and 5 seconds. The "stabile" group was found to be not only
slower over all Pis, but were disproportionately slower under the
5 second PI.condition. Although Lacey and Lacey explain th e ir
resu lts on the basis of d iffic u lty in maintaining a set to respond,
the data supports the notion th a t RT is related to differences in
levels of activation.
Past research has indicated that persons manifesting Pattern
30
A behavior may be more physiologically aroused than th e ir Pattern B
cohorts. Observationally, Type A subjects display marked impatience,
appear to be e x trao rd in arily a l e r t , and show excessive gross motor
features such as facial grimaces, fist-c le n c h in g , and an in a b ility
to remain seated without movement. On a biochemical le v e l, coronary-
prone persons have shown to have a higher daytime excretion level
of catecholamines, and higher mean serum lip id concentrations of
both trig ly cerid es and cholesterol than Pattern B cohorts.
(Rosenman, e t a j, 1966)
Thus, both observational and biochemical data seem to lend
support to the hypothesis th a t Type A subjects have a higher back
ground level of activation or arousal than Type B subjects. This
being so, coronary-prone subjects would be placed higher on the
inverted U-shaped curve than would be non-coronary-prone subjects.
Even the mildly arousing nature of the RT task might then push the
Type A subjects over the apex of the inverted U curve. This would
then re s u lt in less e f f ic ie n t performance than the more optimally
aroused Type B subjects. Add to th is the fu rth er arousal necessitated
by the contingencies of the choice RT task and yet less e f f ic ie n t
performance on the part of Type A subjects is the re su lt.
The fa c t th a t age was a sig n ific a n t covariate with RT was
expected on the basis of re su lts obtained by Birren and Botwinick
(1955), Obrist (1953), Talland (1968), Welford (1959), and many
others. But th a t the variable of behavioral predisposition to
coronary disease was s t i l l a sig n ific a n t fa c to r in RT even when the
data analysis was adjusted fo r the covariate of age, leaves no
doubt th a t hypothesis I is supported.
A s tr i c t l y biological alternative explanation for the results
of this study may be offered. Type A subjects, by virtue of th eir
predisposition to coronary disease, may already be suffering
central nervous system circulatory insufficiencies as a re su lt of
cardiovascular dysfunctioning. The insufficiencies are then behavior-
ally manifested by slowed RT performance. This argument does not
seem tenable in lig h t of the medical condition of the subjects. It
must be remembered that all participants in this investigation were
screened by physicians for coronary health statu s. All subjects
were considered to be in reasonably good health, free of clinical
signs of coronary disease, and normotensive. I t should be noted
however, th at the medical records of these subjects date back as
far as 12 months.
Additionally, the heart rate change data seem to indicate that
a t least su p erficially , there is normal cardiovascular functioning
in Type A subjects. Furthermore, the p o ssib ility of an advanced
atherosclerotic process, while not altogether discounted, can be
minimized as an antecedent to the observed psychomotor slowing in
view of the normal blood pressures of the Type A subjects. While
Rosenman has reported that the mean systolic and d ia sto lic blood
pressure levels of Type A subjects are higher than th at of Type B
subjects, this difference is neither s ta tis tic a lly sig n ifican t nor
medically meaningful. The mean blood pressures of the subjects in
the W C G S are as follows: 39-47 year age group, 81.8 m m Hg
32
d ia s to lic and 128.4 m m Hg sy sto lic fo r Type A and 81.6 m m Hg d ia s t
o lic and 126.5 m m Hg s y sto lic for Type B; 50-59 year age group: 84.1
m m Hg d ia s to lic and 132.5 m m Hg s y sto lic for Type A and 83.2 m m Hg
d ia sto lic and 131.0 m m Hg s y sto lic fo r Type B (Rosenman, e t a l, 1966).
Another possible explanation for the re su lts of this study is
th a t the central nervous system of the coronary-prone subjects mimics
the functioning of the CNS o f the aging adult. The results obtained
here are sim ilar to those found in studies which compare the
performance o f groups of young and aged subjects. Not only has age
been associated with psychomotor slowing, but the response latencies
become disproportionately longer with increasing task complexity.
I t may be th a t one of the consequences, or more precisely
the physiological concomitants, of coronary-prone behavior is
gero-mimetic functioning of a t le a s t some portion of the CNS.
The mode of operation could be through more rapid wear and te a r of
the central nervous system due to the accumulated effects of increa
sed blood pressure, higher serum lip id concentrations, and greater
daytime excretion of catecholamines. Via th is route could re su lt
less e f f ic ie n t systemic integration due to dysfunctioning afferen t
feedback. Improper systemic afferen t feedback has been cited as
a possible fa c to r in the contradictory findings regarding the state
of arousal in the eld erly autonomic nervous system (Thompson and
Marsh, 1973).
Equivalent Cardiac Deceleration in Behavior Pattern Groups
Hypothesis III was not supported by the data in th is investiga-
tion. Coronary-prone subjects did not show a pattern of lessened
cardiac deceleration in response to the warning signal than did
the non-coronary-prone subjects. In neither the simple nor the
choice RT conditions were the cardiac rate change ratios of the two
behavior pattern groups sig n ifican tly different. The results do
support the findings of other investigators which found that there
was a sig n ifican t positive correlation between the amount of
deceleration and the speed of response. The data in this study
showed th at there was a greater amount of cardiac deceleration
occurring on the ten f a s te s t simple reaction times than there was
occurring on the ten slowest simple RT times. This resu lt was not
seen for the choice reaction time condition.
The fa c t that age was not a significant covariate in the
cardiac range data is somewhat surprising in the light of the
results of Morris and Thompson (1969). In th e ir study of RT arid
cardiac rate change in both young and old subjects, the authors
found th at although the deceleration phenomenon was demonstrated
in the aged sample, i t was not as pronounced as in the younger
sample. One possible explanation for the current finding is the
re stric tio n in age of the subjects. The oldest subject was only
59 years old. This may not have been sufficient to demonstrate a
covariance with age. Additionally, the Type B group must be
considered to be less prone to cardiovascular disease and thus less
prone to any possible cardio-feedback mechanism dysfunction than
the Type A subjects.
34
The fa ilu re of the data to support hypothesis III can be viewed
in several ways. The most parsimonious explanation is simply th a t
cardiac deceleration differences between the two groups are not
meaningful. I t may be th a t in the absence of gross c lin ical
cardiopathology feedback mechanism is unaffected by the consequences
of behavioral predisposition to CHD.
Research by Surwillo (1971) and Nowlin, Eisdorfer, Whalen, and
Troyer (1970) strongly support the conclusion th a t background
heart rate level is not an important determinant of reaction time.
These studies showed th a t RT performance appears to be re la tiv e ly
independent of endogenous and exogenous changes in heart rate.
The re su lts of the current investigation which show that
cardiac deceleration is related to speed of RT cannot be taken as
support for the cardiovascular feedback mechanism position of
Lacey, nof. can i t be taken as evidence against the position of
Surwillo, and of Nowlin, e t aJL The form in which the data was
analyzed was such as to favor a r e s u lt consonant with Lacey's
position. Had the cardiac rate change data been taken over a ll RT
t r i a l s rath er than the ten f a s te s t and ten slowest observations,
the re su lts could quite possibly have been d iffe re n t.
O brist, Webb, S u tte re r, and Howard (1970) conducted an
investigation which evaluated two hypotheses concerning the
basis of the association between performance on a simple RT task
and the deceleration of heart ra te found as the subject responds.
Two groups were used. To determine i f the occurrence of the cardiac
response f a c ilita te d performance through an afferen t feedback
35
mechanism the cardiac response was blocked with a pharmacological
agent atropine. Two aspects of somatic a ctiv ity were also assessed
to determine i f the cardiac deceleration and the associated behavioral
f a c ilita tiv e effects were linked to a common mediating process
involving cardiac rate change and the inhibition of on-going,
task -irrelevant somatic a c tiv itie s . The la tte r hypothesis was
consistently supported. Blocking the cardiac response did not
significantly influence performance. However, a within-subject
analysis revealed a profound d ire c t relationship between RT and the
magnitude of the inhibition of the somatic effects and the magnitude
of the cardiac deceleration when the la t t e r was not blocked. Data
indicated that heart rate deceleration may not be significantly
involved in an afferent mechanism but rather is more understandable
as a peripheral manifestation of central processess.
Buck, et al_ (1970) investigated directional cardiac rate change
in response to an environmental rejection task, an environmental
acceptance task, and a task involving attention to bodily events.
They found th a t both the rejection task and the body monitoring
task were not associated with significant cardiac rate change. The
environmental intake task was associated with cardiac deceleration,
but only during the f i r s t 60 seconds. The authors feel that certain
external influences such as verbalization and distraction can have
effects which override the heart rate deceleration.
The results of Kalafat's (1971) study of the relationship
between signal detection and magnitude of heart rate deceleration
also raises some doubts as to the generality of Lacey's hypothesis
concerning the f a c ilia to r y e ffe c t of cardiac deceleration in atten-
tional processes. Finally Proges (1971) found th a t when the prepara
tory interval was of fixed duration heart ra te v a r ia b ility was not
correlated with performance.
The re su lts of the O brist, e ta l_ study ra ise the question as to
how accurately peripheral responses r e fle c t central processes,
esp ecially with regard to changes in cardiac r a te . The re s u lts of
the studies conducted by Surwillo and the others even question the
efficacy of the cardiac deceleration phenomenon. Results of
studies measuring th is variable seem to be related to the contingen
cies of the experimental s itu a tio n .
Finally, the current study d iffe rs methodologically from the
others. The mode of stimulus presentation in the vast m ajority
of other investigations was auditory. This study u tiliz e d visual
stim u li. Also, to the au thor's knowledge th is study represented
the f i r s t attempt to extend the cardiac deceleration phenomenon to
a choice RT condition. What e ffects i f any these methodological
differences had on the outcome of the experiment is unknown.
The f a ilu r e of the data to find any s ig n ific a n t differences
between the cardiac ra te changes during the ten f a s te s t and the ten
slowest choice RT t r i a l s may not only be due to the questionable
f a c i l i t a t i v e effe c ts of cardiac deceleration but also the contingen
cies of the experimental situ a tio n . The decision which the subjects
were required to make in the simple RT condition was whether or
not the imperative stimulus appeared. In the choice RT condition
however, the decision to be made was not only one of the presence
37
or absence of the imperative stimulus, but also one of which signal
actually appeared and which response key had then to be pressed.
Thus whatever fa c ilita tiv e effects might have resulted from cardiac
deceleration coCild have been overrided by the increased decision
time necessitated by the experiment situ atio n .
Nonlinear Relationship Between RT and Age.
Significant linear and curvilinear regressions were found
between age and RT condition for both groups at both conditions.
The regression coefficients themselves were quite modest: Simple
RT/age Type A, 0.0997; Simple RT/age Type B, 0.1477; Choice RT/age
Type AjO.1671; and Choice RT/age Type B, 0.1716.
This data appear to disagree with Szafran (1968) in that
although the slope characteristic of the equation shows that there
is a rather unimpressive tendency of RT to increase with age, the
te s t for regression was significant. Additionally, age was a
significant covariate in the RT performances of both groups. Thus
age definitely contributes to the RT variances within the groups.
I t has been Szafran's position that those investigations which
reported slowing of response with age as an increase in the slope
must have inadvertantly included Ss with subclinical cardiovascular
disorders. To the extent th at the interview technique correctly
identifies persons predisposed to CHD, and to the extent that the
Type A subject is already manifesting decremental performance
ch aracteristics, and that these characteristics are not seen in
the Type B group, the problem of Type B Ss with disease or predisease
states effecting the RT performance is minimized.
38
Figure 1 is a graphic representation of the p lo t of reaction
times by decade. The Ss in each group were blocked by decade and
the mean RT for the represented decades were p lotted. I t must be
noted that the plotted decade means are based upon a very small
number Ss a t each point and th a t the mean age within each decade
is d iffe re n t fo r the two groups. Any analysis of means presented
in th is manner would not be meaningful due to the problem of
collapsing the ages in to decades.
One must also look at the intercepts of the regression
equations as being of importance in contributing to the differences
between Type A and Type B Ss. The d iffe re n t in tercep ts of the four
regression lines demonstrated th a t the SRT^ and CRj^ lines were
of a higher general level than the SRTB and CRTB lin e s. This la s t
point demonstrates the differences in simple and choice RT between
coronary-prone and non-coronary-prone Ss.
The sig n ific a n t cu rv ilin ea r component found in the regression
equations of the Type A Ss might be explained on the basis of
survivorship, or ra th e r, sele ctiv e dropout. At a given point in
time an individual is a survivor of a ll possible members of his
cohort. While th is is true of any person, i t is especially so of
coronary-prone Ss. That i s , a cohort of Type A Ss a t 50 years of
age represents the survivors of th at same cohort a t 40 years of age.
As a ris k fa c to r for CHD Type A behavior is most potent in the
35-49 year age range. After age 50 the behavioral c o n ste llatio n is
not as important as a risk factor independent of biochemical v ariables.
Thus, between ages 35-49 one could p red ict th a t over time there
would be an increasing a ttr itio n of cohort membership due to death
in the Type A group. Thus the survivors would certainly have
characteristics which d iff e r from the nonsurvivors.
The curvilinear component, would then be made up of all Type A
Ss who manifest psychomotor slowing a t all ages as well as the
not-yet-deceased Type A Ss between 35-49 years of age who display
even greater slowing. After age 50, due to the selective dropout
of the less f i t Type A Ss, only the relativ e ly more f i t survivors
are available for inclusion in any sample. The RTs of the cohort
survivors would then be less effected by the presence of severely
deteriorated members than was true at an e a rlie r point in time.
The significant curvilinear component in the regression
equations of the Type B Ss does not readily lend i t s e l f to a
satisfactory explanation. There is a p o ssib ility that a process
analogous to th at described for Type A Ss is at work in the Type
B Ss, but to a lesser extent. Also, i t is quite possible th at the
medical screening procedures and the excerise regimen to which
these subjects were subjected selectively removed from the potential
subject pool those persons with subclinical cardiovascular and/or
cerebrovascular diseases. Thus the effects due to subclinical
disease states would be minimized, especially in an older cohort of
the sample. I f this situ atio n were true for the Type B Ss i t would
also be true of the Type A Ss, thus placing even greater emphasis
on the psychomotor differences found between the two groups.
40
FUTURE RESEARCH
The resu lts of this investigation open up several broad areas
of research necessitated by questions raised by th is study. The
f i r s t area of future research regards the implications of the
cu rv ilin e a rity of the Type A regression equations. The proposed
explanation for th i s re su lts was predicated on the cross-sectional
methodology employed in th is study. The im plications for future
research regarding th is observed cu rv ilin ea r re la tio n between age and
RT in coronary-prone £s seem apparent. The possible consequences
of individual differences in the RTs o f Type A Ss of the same
cohort must be examined longitudinally. The p o s sib ility remains
th a t these inter-in d iv id u al differences in RT within the same cohort
can be used as a predictor variable fo r survival.
A second area fo r future research concerns the usefulness of the
activation theory position and the gero-mimetic hypothesis as process-
oriented explanatory concepts. Studies centering upon the activ atio n
theory position would require a se rie s of d ire c t and in d ire c t physio
logic measures of activ atio n or arousal. This would include
monitoring such EEG measures as alpha a c tiv ity and the contingent
negative v ariatio n . Also GSR, forearm blood flow, and d ia s to lic and
sy sto lic blood pressure v a ria b ility would be monitored.
Studies concerning the a p p lic a b ility of the gero-mimetic
hypothesis would focus upon a broad array of variables which have
tra d itio n a lly been associated with age differences. This would
involve monitoring some of the same physiologic variables indicated
above. Careful atten tio n would be paid to percent-time and frequency
of alpha a c tiv ity , and to GSR habituation in conditioning situations. ■
In addition to physiologic variables, assessment of psychological
performance would be made. Those psychological variables which
would be of in te re st include among others, measures of verbal and
nonverbal intelligence, forward and mirror-reversal of a pursuit
rotor task, and c ritic a l flic k e r fusion threshold.
I t is interesting to note that the gero-mimetic hypothesis and
the activation theory position are at once antithetical and
complimentary. On the one hand, as an explanatory concept for the
results of this study, the activation theory position suggests that
the Type A Ss have a higher background level of CNS arousal than do
the Type B Ss. On the other hand, the psychophysiological lite ra tu re
in gerontology suggests that the CNS of elderly Ss may be under
aroused.
However, a current controversy in the psychophysiology of
aging concerns whether the ANS of elderly Ss is under- or overaroused.
A partial resolution of th is problem is contained in the position
that in the elderly the trad itio n al measures of autonomic activity
no longer accurately re fle c t the extent of A N S arousal.
The gero-mimetic hypthesis is an attempt to describe the
observed RT differences between coronary-prone and non-coronary-
prone Ss without recourse to the identification of the process
involved. The activation theory position and the gero-mimetic
hypothesis are complimentary to the extent that the parallel between
the results of th is study and the documented age changes in psycho
logic and psychophysiologic functioning are sim ilar consequents
which are due to d issim ila r processes.
43
FIGURE 1
PLOT OF REACTION TIMES GROUPED B Y DECADES
Reaction Time
800
msec
700
msec CRT 713
CR T, 646 649
606 600
msec
SRT 527 522
500
msec 511 499
487 SRT,
470
400
msec
381
300
msec
40-49 50-59 30-39 Age 20-29
CHAPTER V
SU M M A R Y A N D CONCLUSIONS
Coronary-prone and non-coronary-prone subjects were compared on
both simple and choice visual RT tasks using a fixed preparatory
interval. The purpose of the experiment was to te s t whether the
coronary-rpone subjects exhibited slower psychomotor performance than
the non-coronary-prone subjects. This investigation marked the f i r s t
attempt to assess i f any psychological performance consequences exist
as the resu lt of behavioral predisposition to coronary disease.
Twenty-four coronary-prone, Type A, subjects and twenty-four
non-coronary-prone, Type B subjects were given 50 simple and 50
choice visual RT t r i a l s . Heart rate was continuously monitored
throughout the experiment. The preparatory interval was a constant
4 seconds.
The results indicated th at the Type A subjects exhibited
psychomotor slowing in both the simple and choice conditions.
Additionally, the Type A subjects were disporportionately slower
than the Type B subjects in the choice RT condition. No differences
in cardiac deceleration prior to the imperative stimulus were seen
between the two groups in e ith er stimulus condition. The only
significance found in the heart rate change data was that both groups
had significantly greater amounts of deceleration occurring during
the ten fa ste st simple RT t r i a l s than occurring during the ten
slowest RT t r i a l s . This was not true for the choice RT condition.
44
45
The resu lts of this investigation also show th a t age was a
s ig n ific a n t covariate in the RT data. Age however, was not a
sig n ific a n t covariate in the heart rate change data.
The psychomotor slowing exhibited by the coronary-prone subjects
was interpreted in terms of activation theory. Activation theory
hypothesizes th at there is an inverted U-shaped relationship between
amount of activation or arousal and performance. On the basis of
biochemical and behavioral data from other investigations Type A
subjects could be thought of as maintaining higher background levels
of activation or arousal then Type B subjects. Thus, in the presence
of the added arousal brought about by the conditions of the experiment,
the i n i t i a l l y more activated Type A subjects would be at a function
disadvantage when compared to the more optimally activated Type B
su b jects.
Other possible explanations fo r the observed psychomotor slowing
in Type A subjects was offered. A biological interpretation posited
*
the existence of subclinical C N S circulatory insufficiency. This
was held untenable in lig h t of the medical screening procedure. A
gero-mimetic in terp retatio n offered the p o ssib ility th a t the physiolo
gical consequences or concommitants of behavioral predisposition to
CH D resulted in more rapid wear and tear in the CN S of the Type A
subjects. Possible tests of these hypotheses were suggested.
The equivalence of the two groups on the heart ra te change ra tio
data was interpreted in several ways. The most important of these
p o s s ib ilitie s had to do with the efficacy of the f a c i l it a t i v e effect
of cardiac deceleration in RT tasks. Empirical re su lts for and
46
against the concept of performance f a c ilita tio n resulting from
cardiac deceleration was discussed. Finally, the po ssib ility that
the fa ilu re of the cardiac rate change data to support hypothesis
III was due to methodological differences between the present
investigation and past studies was discussed.
Regression analyses of age upon RT were run for both groups,
under both conditions. The four te sts for lin earity and curvilin
earity were significant. Additionally, the regression coefficients
were not significantly different from each other. These results
were discussed in terms of possible effects survivorship upon the
av ailability of Type A Ss for inclusion as potential subjects.
The following conclusions may be drawn from th is experiment
regarding differences in the psychomotor performance of Type A
and Type B Ss:
1. Healthy males, behaviorally predisposed to CHD, have
significantly longer response latencies in a simple visual RT
performance task than do non-coronary-prone males of the same age.
2. The response latencies of the coronary-prone Ss are
disproportionately longer in a three-choice RT task.
3. In the absence of any clinical signs of disease, Type A
subjects display psychomotor characteristics similar to those found
in Ss already suffering from coronary heart disease.
4. I t is most probable that the psychomotor slowing exhibited
by subjects suffering from C H D are not the result of the disease
state i t s e l f , but rather are the consequences of psychophysiological
antecendents of CHD.
5. The observed psychomotor performance c h aracteristics of
the Type A subjects cannot be regarded as the re su lt of a
dysfunctioning cardiovascular feedback mechanism.
6. There is a p o ssib ility that the relationship between age
and RT in Type A subjects is a curvilinear one due to delective
dropout due to death of potential subjects in the Type A group.
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Asset Metadata

Creator Abrahams, Joel Peter (author)

Core Title Psychomotor Performance And Change In Cardiac Rate In Subjects Behaviorally Predisposed To Coronary Heart Disease

Degree Doctor of Philosophy

Degree Program Psychology

Publisher University of Southern California (original), University of Southern California. Libraries (digital)

Tag OAI-PMH Harvest,psychology, experimental

Language English

Contributor Digitized by ProQuest (provenance)

Advisor Birren, James E. (committee chair), Bengtson, Vern L. (committee member), Galbraith, Gary C. (committee member), Walker, James Paul (committee member)

Permanent Link (DOI) https://doi.org/10.25549/usctheses-c18-835748

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