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Classical conditioning of heart rate and electrodermal activity to aversive and non-aversive visual stimuli Wood, Keith 1973

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CLASSICAL CONDITIONING OF HEART RATE AND ELECTRODERMAL ACTIVITY TO AVERSIVE AND NON-AVERSIVE VISUAL STIMULI by KEITH WOOD M.A,, The University of British Columbia, 1967 A THESIS SUBMITTED IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY in the Department of PSYCHOLOGY We accept this thesis as conforming to the required standard THE UNIVERSITY OF BRITISH COLUMBIA FEBRUARY, 1973 In presenting t h i s thesis i n p a r t i a l f u l f i l m e n t of the requirements for an advanced degree at the University of B r i t i s h Columbia, I agree that the Library s h a l l make It f r e e l y available for reference and study. I further agree that permission fo r extensive copying of t h i s thesis for scholarly purposes may be granted by the Head of my Department or by h i s representatives. It i s understood that copying or publication of t h i s thesis for f i n a n c i a l gain s h a l l not be allowed without my written permission. Department The University of B r i t i s h Columbia Vancouver 8, Canada i Chairman: Professor Robert D. Hare ABSTRACT The research reported here was designed to explore the relation-ship between aversive visual stimuli and human physiological activity in a clssical conditioning situation. Specifically, the questions asked were (1) whether homicide pictures were effective stimuli in the classical conditioning of heart rate and electrodermal activity and (2) if condition-ing occurred, what would be the form of the conditioned cardiac response. Thirty-six male undergraduate subjects were randomly assigned to one of three groups; (1) continuous reinforcement, (2) partial reinforcement i and (3) random reinforcement. A differential, delayed, classical conditioning paradigm was utilized with coloured slides of homicide victims and coloured slides of people in ordinary, everyday situations used as the two classes of unconditioned stimuli. A yellow light and a green light were used as the conditioned stimuli. Heart rate, electrodermal activity and respiration were recorded throughout a 10 minute adaptation period, 40 conditioning trials and 20 extinction trials. The results of the experiment clearly indicated that conditioning had occurred with both heart rate and electrodermal activity. Moreover, the use of a differential conditioning procedure demonstrated that conditioning had occurred with the homicide pictures but not with the non-homicide pictures. The form of the conditioned cardiac response to the homicide pictures was heart rate acceleration for the continuous reinforcement group and heart rate acceleration followed by deceleration for the partial reinforcement group. The unconditioned cardiac response was heart rate deceleration. The findings of this experiment were discussed within the framework of the theories of Lacey (1967), Obrist et al (1970a) and Elliott (1969). TABLE OF CONTENTS ABSTRACT i TABLE OF CONTENTS. . i i LIST OF TABLES. iv LIST OF FIGURES vi ACKNOWLEDGEMENT vi CHAPTER I - INTRODUCTION ....1 I. Relationship between HR and environmental events .1 II. The cardiac CR and classical conditioning 7 III. The basis of the present research 26 CHAPTER II - EXPERIMENTAL METHOD 31 I. Subjects 31 II. Apparatus 31 III. Design.... 32 IV. Procedure 34 V. Measurements 35 CHAPTER III- RESULTS 37 I. Electordermal responses 37 II. Heart Rate 53 CHAPTER IV - DISCUSSION 66 BIBLIOGRAPHY 76 APPENDIX - The results of Scoring Heart Rate on a Second-by-Second Basis During the CS Period 81 IV LIST OF TABLES TABLE 1 - Summary of analysis of variance of the unconditioned skin conductance response to UCS-H and UCS-P (Factor B) over three blocks of trials (Factor C) for the three groups (Factor A) during acquisition 39 TABLE 2 - Summary of analysis of variance of the anticipatory skin conductance response to CS-H and CS-P (Factor B) over four blocks of trials (Factor C) for three groups (Factor A) during acquisition .41 TABLE 3 - Summary of analysis of variance of simple effects of anticipatory skin conductance responses for three groups (Factor A) taken over CS-H and CS-P (Factor B) .42 TABLE 4 - Summary of analysis of variance of the anticipatory skin conductance response to CS-H and CS-P (Factor B) over two blocks of trials (Factor C) for three groups (Factor A) during extinction 45 TABLE 5 - Summary of analysis of variance of the skin conductance orienting response to CS-H and CS-P (Factor B) over four blocks of trials (Factor C) for three groups (Factor A) during acquisition 47 TABLE 6 - Summary of analysis of variance of simple effects of the skin conductance orienting response for three groups (Factor A) taken over CS-H and CS-P (Factor B) ...49 TABLE 7 - Summary of analysis of variance of the skin conductance orienting response to CS-H and CS-P (Factor B) over two blocks of trials (Factor C) for three groups (Factor A) during extinction 51 TABLE 8 - Summary of analysis of variance of simple effects of the skin conductance orienting response for three groups (Factor A) taken over CS-H and CS-P (Factor B) .52 TABLE 9 - Summary of analysis of variance of tonic skin conductance for three groups (Factor A) taken as repeated measures at three points in the experiment (Factor B) 55 V TABLE 10 -» Summary of analysis of variance of beat-to-beat (Factor D) heart rate unconditioned response to UCS-H and UCS-P (Factor B) during acquisition over three blocks of trials (Factor C) for three groups (Factor A) 57 TABLE 11 - Summary of analysis of variance of beat-to-beat (Factor D) heart rate to CS-H and CS-P (Factor B) over four blocks of trials (Factor C) for three groups (Factor A) during acquisition 60 TABLE 12 - Summary of analysis of variance of beat-to-beat (Factor D) heart rate to CS-H and CS-P (Factor B) over two blocks of trials (Factor C) for three groups (Factor A) during extinction 63 TABLE 13 - Summary of analysis of variance of tonic heart rate for three groups (Factor A) taken as repeated measures at three points in the experiment (Factor B)...65 TABLE 14 - Summary of analysis of variance of second-by-second (Factor D) heart rate to CS-H and CS-P (Factor B) over four blocks of trials (Factor C) for three groups (Factor A) during acquisition 84 TABLE 15 - Summary of analysis of variance of second-by-second (Factor D) heart rate to CS-H and CS-P (Factor B) over two blocks of trials (Factor C) for three groups (Factor A) during extinction. 86 LIST OF FIGURES vi FIGURE 1 - Electrodermal unconditioned responses to UCS-H and UCS-P over three blocks of trials for each group 38 FIGURE 2 - Electrodermal anticipatory responses to CS-H and CS-P over four blocks of trials for each group during acquisition 40 FIGURE 3 - Electrodermal anticipatory responses to CS-H and CS-P over two blocks of trials for each group during extinction.. 44 FIGURE 4 - Electrodermal orienting responses to CS-H and CS-P over four blocks of trials for each group during acquisition 46 FIGURE 5 - Electrodermal orienting responses to CS-H and CS-P over two blocks of trials for each group during extinction 50 FIGURE 6 - Tonic skin conductance for each group measured at three points during the experiment 54 FIGURE 7 - Beat-to-Beat HR (deviation from pre-stimulus) to UCS-H and UCS-P over three blocks of trials (TB) for three groups during acquisition 56 FIGURE 8 - Conditioned response beat-to-beat heart rate (deviations from pre-stimulus) to CS-H and CS-P for each group during acquisition 59 FIGURE 9 - Conditioned response beat-to-beat heart rate (deviations from pre-stimulus) to CS-H and CS-P over two blocks of trials (TB) for each group during extinction 62 FIGURE 10 - Conditioned response second-by-second heart rate (deviations from pre-stimulus) to CS-H and CS-P for each group during acquisition 83 FIGURE 11 - Conditioned response second-by-second heart rate (deviations from pre stimulus) to CS-H and CS-P over two blocks of trials (TB) for each group during extinction 85 ACKNOWLEDGEMENT Grateful 1 appreciation is extended to Dr. R. D. Hare who directed and supported this research, to Miss J. Frazelle for her assistance in the analysis of the data and to the members of my dissertation committee for their valuable suggestions and assistance. 1 CHAPTER I INTRODUCTION In recent years, research and theoretical developments have demonstrated a considerable growth in interest in cardiac activity and its relationship to both behavioural and psychophysiological processes. Two major areas of research have developed out of this interest. One approach has been concerned with how heart rate (HR) activity influences an organism's interaction with the environment (Lacey, Kagan, Lacey and Moss, 1963; Graham and Clifton, 1966; Lacey, 1967). A second area of interest that has concerned numerous researchers is the investigation of the form of the cardiac conditioned response (CR) and its implications for traditional theories of classical conditioning. RELATIONSHIP BETWEEN HR AND ENVIRONMENTAL EVENTS In a series of studies, Lacey and his associates (Lacey, 1969; Lacey, Kagan, Lacey and Moss, 1963; Lacey, 1967) have proposed a theory of HR activity and its relationship to acceptance or rejection of environmental input. Lacey hypothesizes that cardiac deceleration accompanies and facilitates environmental input. Thus, when Ss were required to attend to and detect environmental events, such as listening to tape recordings or watching flashing lights, such behaviour was accompanied by HR deceleration. Cardiac acceleration, however, facilitates rejection of the environment and is associated with a S attending to internal events such as mental arithmetic, reverse spelling and painful events like the cold pressor test. Neurophysiological Evidence In an extensive review of the neurophysiological literature, Lacey (1967) presents evidence which clearly suggests that HR and blood pressure 2 increases are related to inhibitory processes of higher cortical activity. The aortic arch and carotid sinus are both richly endowed with pressure-sensitive receptors. The nerves from the aortic arch and carotid sinus join the vagus and glossopharyngeal nerves and terminate in the lower brain stem. If blood pressure or HR increase, there is an increase in the rate of discharge of the baroreceptors and subsequent inhibition of cortical activity. Similarly, a decrease in blood pressure or HR results in a decrease in the rate of discharge of the baroreceptors and an increase in cortical arousal. Behavioural Evidence While the findings from neurophysiology are in agreement with Lacey's (1967) hypothesis, he also cites behavioural evidence which supports his position. In a study designed to investigate the relationship between HR and reaction time (RT) it was found that during the period of time between the start of a given trial and the onset of a stimulus requiring a motor response, there was observed a highly significant deceleration of the heart. Moreover, deceleration was accompanied by faster reaction times and acceleration by slower reaction times. Obrist (1963) replicated and extended Lacey's work and confirmed his findings. Ss who were required to attend to environmental events demonstrated HR deceleration, while noxious events and conceptual tasks resulted in cardiac acceleration. HR and Directional Fractionation Within The Autonomic Nervous System In addition to the findings regarding HR and sensory-intake and rejection, Lacey (1967) has argued that the observed cardiac activity is 3 also related to other activity occurring within the autonomic nervous system (ANS). This relationship, however, is not a simple one. He suggeststhat while rejection of the environment results in HR acceleration and increases in skin conductance (SC), attention to the environment results in HR deceleration and increases in SC. The latter type of responding has been referred to by Lacey (1967) as "directional fractionation". Campos and Johnson (1967) and Johnson and Campos (1967) suggest that there is only minimal evidence for directional fractionation. They report that the only time directional fractionation was observed was when Ss viewed unpleasant visual stimuli and were not told in advance that they would be required to give verbal reports on what they saw. When Ss were required to view pleasant visual stimuli there were no significant changes in either HR or SC regardless of instructions to verbalize or not verbalize. It should be noted, however, that their scoring procedures were somewhat crude and may have resulted in an underestimation of the actual responding. Other evidence of directional fractionation has been reported (Hare, Wood, Britain and Shadman, 1970; Hare, Wood, Britain and Frazelle, 1971) in which HR deceleration and increases in SC occurred in Ss who viewed both coloured slides of nude females and unpleasant, coloured slides of homicide victims. Hare (1972) also reported findings consistent with Lacey's (1967) hypothesis of directional fractionation in which viewing unpleasant visual stimuli, without the Ss being told they would be required to make ratings of the stimuli, resulted in HR deceleration and an increase in SC, digital vasoconstriction and cephalic vasodilation. Hare's findings were also in agreement with Campos and Johnson (1967) in that no directional fractionation occurred when Ss were informed ahead 4 of time that they would be required to rate the slides. These manipulations resulted in HR acceleration, digital and cephalic vasoconstriction and increases in SC. These findings would seem to be in agreement, however, with Lacey's (1967) position that when Ss are required to attend to both internal (rating) and external {viewing) tasks, the cardiac deceleration may be reduced, there may be no HR change, or there could be HR acceleration. HR and the Orienting and Defensive Responses Sokolov (1963) reported evidence related to Lacey's (1963) theory which indicated that autonomic changes associated with sensory-intake were also associated with the orienting response (OR) and that changes associated with sensory-rejection were associated with the defensive response (DR). Sokolov (1963) provided a number of criteria for disting-uishing between the OR and the DR. He suggests that the OR occurs in response to stimuli of low or moderate intensity and is associated, along with HR changes with peripheral vasoconstriction and cephalic vasodilation. The DR is characterized by both peripheral and cephalic vasoconstriction. The only conflict between the findings of Sokolov (1963) and Lacey (1963) was Sokolov's suggestion that HR acceleration was associated with the OR rather than deceleration as suggested by Lacey. Graham and Clifton (1966), in a review of the literature, attempted to integrate the findings of Sokolov (1963) and Lacey et al (1963). They suggest that Sokolov presents little evidence that acceleration is the cardiac component of the OR. Graham and Clifton (1966) also point out that when Sokolov's criteria are used to identify an OR, numerous 5 studies provide clear evidence that the cardiac component of the OR is HR deceleration. Moreover, it would appear that HR acceleration is, in fact, a component of the DR. Graham and Clifton (1966) further suggested that cardiac changes and vasomotor responses occur together in such a way as to demonstrate the OR and the DR. To date, however, there has been only minimal empirical evidence which supports this position. Raskin, Kotses and Bever (1969) attempted to demonstrate an OR and a DR to an 80 db tone and a 120 db tone respectively. Although deceleration was observed with the 80 db tone and acceleration with the 120 db tone, the cephalic vasomotor data were equivocal. Hare (1972), in a reanalysis of earlier studies (Hare et al, 1970; Hare et al, 1971) found that different Ss responded differently to the same stimuli. Some Ss responded to unpleasant visual stimuli with HR acceleration and cephalic vasoconstriction while others responded with HR deceleration and cephalic vasodilation. While Hare's (1972) findings are consistent with Graham and Clifton's (1966) position regarding the relationship between cardiac and vasomotor changes and the OR and DR, it is suggested that the results are only preliminary to further research. Interestingly, the fact that these results were observed in Ss exposed to the same experimental procedure would indicate that the type of responding would depend on individual factors. Moreover, not all Ss responded with the complete pattern of cardiac and vasomotor activity associated with the OR and DR. Hare (1972) makes the point that there is a good possibility that with each S there is an individual response stereotypy present at the level of the OR and DR. Electrodermal Activity and the OR Other research has shown that electrodermal activity also reflects 6 OR activity. Stewart, Stern, Winokur and Fredman (1961) argue that the electrodermal OR is often mistaken for the anticipatory response (AR) in classical conditioning experiments. The authors demonstrated in a classical conditioning paradigm using a 6.5 sec delay and a shock unconditioned stimulus (UCS) that the electrodermal OR occurs between 1 and 4 sec after conditioned stimulus (CS) onset whereas the electrodermal AR occurs between 4 sec after CS onset and UCS onset. Gale and Stern (1967) suggest that conditioning of the electrodermal OR can best be demonstrated by using a long delay, differential classical conditioning paradigm. A long delay allows for clear discrimination between the OR and AR and the differential procedure provides good control for sensitiza-tion effects. By using this paradigm with a 7.8 sec delay and shock UCS, Gale and Stern (1967) were able to demonstrate conditioning of the electrodermal OR to a reinforced CS whereas the OR to a nonreinforced CS adapted over trials. Furthermore, during extinction, the OR was found to be resistant to extinction for the reinforced CS but not for the nonreinforced CS. Ohman (1971) argues that in a classical conditioning situation there is a two stage process involved in the development of the OR and the AR. The first stage is the development of the association between the CS and the UCS and the second stage involves the development of the AR. Thus, the initial response to CS onset and UCS onset is in fact an OR. It is only when the CS operates as a signal for the UCS that the AR appears. 7 THE CARDIAC CR AND CLASSICAL CONDITIONING In studies concerned with the classical conditioning of human HR, the form of the cardiac CR has been a matter of considerable controversy. Notterman, Schoenfeld and Bersh (1952) attempted to determine whether the human HR demonstrated conditioning using procedures designed to produce experimental anxiety. Using a 1 sec tone, a 6 sec trace interval and a 6 sec shock UCS the authors reported significant cardiac deceleration between pre-CS HR and the HR measured over the last two beats prior to UCS onset. The unconditioned response (UCR) to the shock was reported as a significant acceleration of HR. Zeaman, Deane and Wegner (1954), however, reported that by using the same procedure as Notterman et al (1952) but measuring HR on a beat-to-beat basis, a biphasic cardiac CR was revealed -- acceleration followed by deceleration. Moreover, the form of the UCR also was found to be biphasic. The authors argue that the predominantly decelerative CR could be explained on the basis of drive reduction. That is, the heart was decelerating at the time of maximum drive reduction --when the 6 sec shock terminated. Thus, the form of the CR could be expected to be predominantly decelerative. In a test of this position, Zeaman and Wegner (1954) used the same procedure as Zeaman et al (1954) but reduced shock duration to 2 sec. With a 2 sec shock duration HR is accelerating at the time the shock is terminated. Thus, drive reduction theory would predict an accelerative cardiac CR. The results of this study supported the drive reduction hypothesis. In a further test of the drive reduction approach Zeaman and Wegner (1957) used shock durations of 0.1 sec and 15 sec paired with a tone CS 8 of 1 sec duration and a trace interval of 6 sec. The expectation was that with very short durations of shock (0.1 sec) the HR has had no time to change before the point of maximum drive reduction (shock offset). Similarly, with a 15 sec shock, HR would have returned to its pre-CS level by the time the shock terminated. Under these conditions, there would be an absence of cardiac conditioning according to the predictions from drive reduction theory. Contrary to predictions, however, conditioning occurred with both shock durations. In a further study, Wegner and Zeaman 0958) used a range of shock durations (0.1, 2, 6, and 15 sec) and found no relationship between the conditioned HR response magnitude and the range of shock durations. The authors suggest that the data from the last two studies reported do not support a drive reduction position and that contiguity theory is better able to account for the findings. Moreover, the possibility that respiratory activity could have influenced the findings was suggested (Zeaman and Wegner, 1957) but no systematic observations were reported. The Effects of Respiration on the Cardiac CR The relationship between respiratory activity and HR is a well known phenomenon. Young adults not engaged in physical exercise very often demonstrate sinus arrhythmia where variations in HR are directly related to respiration. Westcott and Huttenlocher (1961) report findings from an unpublished study in which respiration changes were observed along with changes in cardiac rate. Presentations of a CS paired with a shock UCS were frequently accompanied by sharp inspirations and when such trials were eliminated from the analyses no evidence was found for conditioned cardiac acceleration. Moreover, Westcott and Huttenlocher 9 (1961) reported they found that under neutral conditions a sudden inspiration produced cardiac activity similar to the biphasic response observed in earlier studies (Wegner and Zeaman, 1958; Zeaman et al, 1954; Zeaman and Wegner, 1954, 1957), and that increases and decreases in HR were found to be directly related to increases and decreases in depth of respiration. In the second phase of the study (Westcott and Huttenlocher, 1961) respiration was controlled by having the Ss breath shall owly at a constant rate of 46 cycles/minute (paced by the clicking of a metronome) during the 7 sec CS interval. With respiration controlled, the CR to the tone CS was cardiac acceleration. When these findings are compared with the results of Wegner and Zeaman (1958), Zeaman et al (1954), Zeaman and Wegner (1954, 1957), it would appear that the decelerative phase of the biphasic response occurs only when respiration is not controlled. Westcott and Huttenlocher's (1961) findings are inconsistent with those of Notterman, Schoenfeld and Bersh (1952) who found only HR deceleration as the cardiac CR. It should be noted, however,that a breathing rate of 46 cycles/ minutes actually constitutes hyperventilation. It would be expected, therefore, that such a procedure would, independently of the experimental manipulations, produce HR acceleration. Such a procedure does not constitute an adequate control for the effects of respiration. The Effects of the Sympathetic and Parasympathetic Divisions of the ANS on the Cardiac CR While a complex relationship has been shown to exist between respiration and HR, Dykman and Gantt (1959) pointed out further complexities in a study designed to investigate the roles of the sympathetic and the 10 parasympathetic divisions of the ANS in cardiac conditioning. Changes in HR in the resting adult can occur through increases in sympathetic activity or through decreases in vagal tonus (a decrease in parasympathetic activity), both of which produce cardiac acceleration. Conversly, increases in vagal tonus produce HR deceleration (Manzotti, 1958). Dykman and Gantt (1959) found the HR component of both the OR and the CR to be the result of both sympathetic and parasympathetic activity. In this study the authors used atropine to block vagal (parasympathetic) activity in dogs. When the vagus nerve was blocked by atropine, the cardiac acceleration produced by sympathetic activity had a long latency (between 5 and 10 sec) and small amplitude. In the intact animal, however, the cardiac acceler-ation had a latency between 0 and 5 sec and a much greater amplitude. The indication here, of course, is that the acceleration observed in the cardiac CR is largely dependent on a decrease in vagal tonus resulting from a decrease in parasympathetic activity. Wood and Obrist (1964) while recognizing the importance of sympathetic and parasympathetic activity as well as respiration, undertook a study designed to investigate the effects of controlled and uncontrolled respiration on the cardiac CR in human male Ss. Using a trace condition-ing procedure with a 1 sec tone, a CS-UCS interval of 7 sec and a 6 sec shock UCS, Wood and Obrist (1964) observed a biphasic cardiac CR when respiration was not controlled. When respiration was controlled by training the Ss to breath at their normal resting respiration rate and depth the same conditioning procedure resulted in a cardiac CR consisting only of HR deceleration. The authors (Wood and Obrist, 1964) state that HR acceleration can 11 be influenced by increases in sympathetic activity and decreases in vagal tonus as well as by respiratory activity. They point out that since there was no HR acceleration when respiration was controlled, it would appear that no sympathetic activity occurred. This, however, was unlikely since sympathetic activity was observed in the galvanic skin response (GSR) and vasomotor recordings. Wood and Obrist (1964) suggest that the probable mechanism here is the blocking of sympathetic activity by increases in vagal tonus (Samaan, 1934-35). Such increases in vagal activity could result from conditioned vasomotor responses which trigger increased vagal tonus via the baroreceptors. In a test of these hypotheses, Obrist, Wood and Perez-Reyes (1965) completed two experiments using a trace conditioning procedure similar to that reported by Wood and Obrist (1964). The first study made use of four groups of human male Ss, two groups having the vagus blocked by atropine sulfate and the other two without vagal blockade. Two levels of shock intensity (high and low shock UCS) were used under both conditions. Under vagal blockade with the high intensity UCS an acceleratory conditioned cardiac response was observed, whereas with the low-intensity UCS only a small deceleration occurred. The suggestion here is that with a low intensity UCS there is little sympathetic involvement as far as the heart is concerned. Without vagal blockade a biphasic cardiac response of initial acceleration followed by deceleration was observed. This acceleration was interpreted as reflecting an initial decrease in vagal restraint rather than an increase in sympathetic activity. Such an interpretation was supported by the fact that the acceleration had a short latency and peaked much sooner than the sympathetic activity 12 o b s e r v e d under v a g a l b l o c k a d e and as r e p o r t e d by o t h e r s (Samaan, 1934; Dykman and G a n t t , 1959). The aim o f t h e second s t u d y was t o d e t e r m i n e whether o r not t h e d e c e l e r a t o r y c a r d i a c CR c o u l d be due t o p r e s s o r r e s p o n s e s r e s u l t i n g from vasomotor a c t i v i t y . U s i n g a low i n t e n s i t y shock i t was found t h a t t h e r e were no d i f f e r e n c e s i n t h e f o r m o f t h e d e c e l e r a t o r y CR under c o n d i t i o n s o f a d r e n e r g i c b l o c k a d e o f vasomotor a c t i v i t y as compared t o no b l o c k a d e . Thus, i t would appear t h a t t h e HR d e c e l e r a t i o n o b s e r v e d by O b r i s t e t a l (1965).was due t o a c o n d i t i o n e d i n c r e a s e i n v a g a l r e s t r a i n t r a t h e r t h a n t o p r e s s o r r e s p o n s e s o f vasomotor o r i g i n . A l t h o u g h t h e s e f i n d i n g s p r o v i d e i n s i g h t i n t o t h e p h y s i o l o g i c a l bases g o v e r n i n g t h e CR, H a s t i n g s and O b r i s t (1967) were i n t e r e s t e d i n d e t e r m i n i n g how t h e CR was d e v e l o p e d i n a c l a s s i c a l c o n d i t i o n i n g paradigm. The a u t h o r s s u g g e s t t h a t t h e CR c o u l d r e s u l t from CS-UCS p a i r i n g s , c o u l d be an OR t o t h e CS, o r c o u l d be m e d i a t e d t h r o u g h a n t i c i p a t i o n o f t h e UCS. H a s t i n g s and O b r i s t (1967) used a d i s c r i m i n a t i v e , c l a s s i c a l c o n d i t i o n i n g paradigm w i t h t h r e e groups o f male Ss. The I S I was d i f f e r e n t f o r each group w i t h a shock UCS o c c u r r i n g a f t e r a 0.8, 7, o r 13 sec l i g h t CS. The f i n d i n g s s u p p o r t e d t h e a n t i c i p a t i o n h y p o t h e s i s w i t h o n l y a s m a l l and e a r l y d e c e l e r a t i v e CR w i t h t h e 0.8 sec I S I and p r o g r e s s i v e l y l a t e r and more pronounced CRs w i t h t h e 7 sec I S I and t h e 13 sec I S I . In a somewhat d i f f e r e n t a p p r o a c h , D r o n s e j k o (1972) i n v e s t i g a t e d t h e form o f t h e c a r d i a c AR t o a shock UCS u s i n g d i f f e r e n t l e n g t h I S I s s t a r t i n g w i t h 4 sec and i n c r e a s i n g o v e r t r i a l s t o 12 s e c . D r o n s e j k o found t h a t w i t h 4, 5 and 6 sec I S I s t h e c a r d i a c r e s p o n s e was a c c e l e r a t i o n . 13 Beyond 6 sec, however, the response changed to acceleration followed by deceleration with the largest deceleration occurring during the 10 sec ISI. The author suggests that her findings are consistent with the position of Lacey (1967) and Sokolov (1963) in as much as the initial acceleration reflects a DR because the CS acquires warning properties about forthcoming shock. As the ISI is increased the opportunity is available for the deceleratory component of the response to develop and such deceleration is viewed by Dronsejko (1972) as an effective mechanism for coping with stress. Thus, she argues, the deceleration observed with a long ISI reflects a homeostatic mechanism of "vagal rebound". Cardiac Conditioning and Somatic-Motor Activity Obrist and Webb (1967) were concerned with carrying out further investigations into the nature of the cardiac CR and UCR and focused their attention on the relationship between HR and somatic-motor activity during conditioning. While it has long been recognized that HR can be affected by psychological states, the authors were interested in determining the extent to which HR was influenced by somatic-motor activity within the conditioning situation. The primary concern in this study was to determine the respective influence of central events and somatic-motor events on cardiac activity. Obrist and Webb (1967) performed two classical conditioning experiments using dogs as Ss. The first used a delayed conditioning paradigm with a 7 sec light CS followed by a 6 sec shock UCS and was intended to evaluate the relationship between somatic-motor events and HR. The authors found that during the anticipatory period there was an increase in HR, gross body movements (GBM) and depth of respiration. Moreover, the magnitude of the HR acceleration and somatic-motor responses were directly proportional. Finally, it was found that the latency of the cardiac and somatic-motor responses were very similar. The important finding here, of course, was the significant inter-dependence of cardiac activity and somatic-motor changes. Further conditioning trials were carried out in which the sympathetic, innervations of the heart were pharmacologically blocked to determine whether or not the acceleration was mediated by sympathetic activity. The results of this procedure revealed no change in the size of the anticipatory cardiac acceleration as a result of pharmacologically blocking the heart's sympathetic innervations. The findings suggest that in this study the anticipatory HR acceleration was due to a decrease in vagal inhibition. The second experiment used food ?s the UCS and food plus shock (experimental conflict) in order to manipulate the affective impact of the UCS. The dogs were first exposed to a conditioning procedure (same as Experiment 1) using food as the UCS. After training the Ss were introduced to the conflict situation consisting of shock whenever the anim attempted to eat the food. The results demonstrated that HR activity and somatic-motor activity were interrelated and that this relationship was not altered by experimental conflict. With food as the UCS all the Ss demonstrated an UCR of HR acceleration whereas the AR was acceleration for three of the Ss and no change or deceleration for the remaining three Ss. When compared to shock (Experiment 1 ) , the food UCS resulted in fewer correlations between HR and somatic-motor activity. 15 In the conflict situation, the AR for all Ss was acceleration. Under these conditions the relationship between HR and somatic-motor activity was more pronounced than with the food UCS but smaller than that observed with shock alone. In general, the conflict situation did not result in any overall indication of greater independence of HR and somatic-motor activity. The findings of Obrist and Webb (1967) clearly indicate a relation-ship between HR activity and somatic-motor activity. The authors suggest that their findings have a number of implications for behavioural processes. "The results suggest that the influence which processes like emotion or motivation may have on heart rate is to some extent mediated via the effect these processes have on somatic-motor activity, That is, the cardiac response in anticipation of some relevant stimulus, aversive, or otherwise, will in part be determined by whether the organism initiates some of somatic-motor activity in preparation for the stimulus. This, it is ventured, occurs because the somatic and cardiovascular systems are intimately coupled neurophysiologically, both centrally and peri-pherally. In turn, this coupling serves a very basic biological function, namely the rapid and efficient adjustment of the cardio-vascular system to the metabolic needs of the working muscles." (Obrist and Webb, 1967, p. 28). With these findings in mind the authors point out that the nature of the coupling between cardiac and somatic-motor events can be viewed in a number of ways. For example, the cardiac and somatic-motor activity could be seen as two peripheral aspects of the same central response. A possible alternative to this position is that the observed cardiac activity could be due to somatic-motor changes which occur during conditioning but which are not initiated by some central process. The authors also point out that while there does appear to be a coupling between cardiac and somatic-motor activity there is also the possibility that HR can be controlled by processes other than those already suggested. 16 Their results point to the possibility that HR changes can occur without corresponding somatic-motor changes and would appear to be related to emotional processes. From the preceding discussion it is clear that when shock is used as the UCS, the UCR is HR acceleration and is accompanied by increases in both respiration and somatic-motor activity. The AR is deceleration and is not accompanied by respiratory or somatic-motor changes. Wood and Obrist (1968) therefore predicted that a sensory UCS which resulted in a UCR of HR deceleration would be accompanied by an AR which would also be HR deceleration. However, should the UCS require attention to cognitive activity with no associated somatic-motor or respiratory changes then the response to both the CS and UCS would be HR acceleration. Wood and Obrist (1968) used 22 Ss in two groups in a classical conditioning situation. The first group was exposed to a UCS consisting of pictures of nude females. The second group was briefly exposed to a UCS requiring considerable cognitive activity. The hypothesis was not confirmed since with both types of stimuli the AR was cardiac deceleration as was the UCR to the nude UCS, whereas the UCS requiring cognitive activity resulted in a UCR of cardiac acceleration. Since stimulus typing with respect to the AR did not occur, the authors performed a second experiment which attempted to increase motiva-tion in Ss looking at the nude UCS. The Ss were told they would be required to answer questions related to what they saw at the end of the experimental session and that a monetary reward would be involved. Although there were no significant overall differences between the nude UCS groups in both experiments it was found that there was a biphasic 17 deceleration-acceleration response following the UCS presentation. Since the task in the second experiment required both stimulus intake and attention to cognitive activity, the biphasic response to the UCS was thought to reflect this activity and that stimulus typing had occurred. A third experiment used physical activity as the UCS since this type of activity results in marked cardiac acceleration. The purpose here was to test for the generality of the deceleratory effect which has been shown to occur in anticipation to a number of different kinds of UCS. The authors predicted that since physical exercise produces marked acceleration and since it has such a considerable effect on the whole cardiovascular system then acceleration should be easily demonstrated as the AR. Again, it was found that anticipatory HR changes were predominantly deceleration. The overall findings thus suggest that anticipation of any UCS will result in deceleration and that stimulus typing responses only occur to the UCS. Obrist (1968) conducted a series of experiments in order to determine whether or not the anticipatory HR changes observed during classical conditioning were related to changes in somatic-motor activity. The author hypothesized that the HR deceleration observed during antici-patory periods of more than 4 sec would occur concomitantly with a reduction in striate muscle activity. Also, the HR acceleration observed on test trails with an ISI of 1 sec (Hastings and Obrist, 1967) would be con-comitant with an increase in striate muscle activity. In the first experiment, Obrist (1968) used a trace conditioning procedure with a 2 sec CS and a 6 sec shock and found cardiac deceleration during a 7 sec ISI occurring concomitantly with, an i n h i b i t i o n of bursts of muscle activity (EMG) recorded from the chin. This attenuation of EMG activity peaked at the point where the UCS occurred during reinforced trials. Since these findings provided support for the hypothesis that cardiac deceleration during the anticipatory period prior to an aversive stimulus was part of an inhibitory process which included a reduction in somatic-motor activity, Obrist (1968) hypothesized that there should be a similar relationship between HR and EMG activity in periods other than the anticipatory period. The author measured HR and EMG during periods when the Ss had been instructed to make no unnecessary movements and these included a 10 minute rest period at the start of the experiment and during intertrial intervals. In virtually all of the 261 instances that were evaluated, HR was found to accelerate during burst of EMG activity. In the second experiment, Obrist used a 1.0 sec ISI to determine whether or not the acceleration reported by Hastings and Obrist (1967) was related to an increase in striate muscle activity. The results supported the hypothesis. Bursts of EMG activity were found to parallel very closely the activity of the heart with increasing amounts of EMG activity corresponding to increases in HR. The third experiment was designed to determine whether or not the relationship between HR and striate activity could be accentuated by increasing base levels of somatic-motor activity. In the previous two experiments the Ss had been requested to keep movements to a minimum. By eliminating these instructions and all attempts to control respiration 19 it was thought that restraint on striate activity would be reduced. Using the same procedure as used in Experiment 1 an increase in basal EMG was observed and although the results replicated those of Experiment 1 the effects were not as consistent nor were they more pronounced as had been predicted. Obrist found that the HR deceleration observed in this experiment was greater than that in Experiment 1 although with a number of Ss it was found that deceleration occurred without a decrease in EMG activity. These findings suggest that there exists the possibility that (1) deceleration effects and EMG effects are unrelated or (2) that there is a relationship but cardiac activity is also related to other events which were not factors in Experiment 1. Further analysis of the data from the above experiment indicated a concomitant relationship between HR and somatic-motor activity. However, it was also clear that events other than somatic-motor activity could influence HR. Respiration appeared to be related to cardiac changes although other studies have not demonstrated a consistent relationship (Smith, 1966; Wood and Obrist, 1964) while some evidence (Hastings, 1966; Obrist et al, 1965; Hastings and Obrist, 1967) suggests that HR deceleration can occur independently of changes in respiration. In an attempt to understand the relationship between cardiac deceleration and somatic-motor activity, Obrist, Webb and Sutterer (1969) performed four experiments in which a number of variables were manipulated. It was pointed out that deceleration did not result from respiratory activity nor from pressor-responses caused by barorecptor activity (Wood and Obrist, 1964). Furthermore, deceleration has been shown to result from increases in vagal restraint which masks sympathetic activity (Obrist et al, 1965). Other research has demonstrated that deceleration is part of the response which involves the inhibition of somatic-motor activity (Obrist, 1968; Obrist and Webb, 1967). The purpose of the four experiments was to explore further the deceleratory effect through the study of somatic-motor activity. The first experiment (Obrist et al, 1969) was concerned with determining whether the decrease in somatic-motor activity which ocurred in anticipation of noxious stimuli would also occur in anticipation of non-aversive stimuli known to produce HR deceleration. A simple RT task with a fixed foreperiod of 5 sec was used as the experimental procedu Analysis of the data revealed a decrease in EMG bursts from the chin and neck muscles and HR deceleration just before and during the second the response was made. Moreoever, the magnitude of the somatic-motor decrease and HR deceleration were directly correlated and occurred concomitantly, and were directly correlated with RT. The second experiment was designed to determine whether the somatic-motor activity from the chin and neck were actually related to more extensive motor acts such as postural adjustments. The Ss were instructed to make a number of different specific motor acts once every 20 seconds during which time EMG recordings were made from the chin and neck muscles. It was found that bursts of EMG activity accompanied the movements the Ss were instructed to make. It was felt that these findings pointed to the possibility that chin EMGs may reflect somatic-motor activity in other parts of the body. Moreover, decreases in chin EMGs in anticipation of some stimulus or a RT task could reflect diffuse inhibition of spontanious or irrelevant motor activity. 21 The third experiment concentrated on determining whether decreases in somatic-motor activity and HR deceleration ocurring in anticipation of an aversive stimulus were generalized to other somatic-motor acts such as eye-movements and blinks. Furthermore, would there be inhibition of a motor act which was imposed on the S (finger-tapping) but which had no relevance to the CS, the UCS or the relationship between them? The authors used a simple trace conditioning procedure (2 sec CS and a 7 sec ISI) with a 6 sec shock UCS. It was found that somatic-motor activity decreased and HR deceleration occurred concomitantly with decreases in eye-movements and blinking. With tapping, however, there was a small but significant increase in intensity at the time the UCS was expected. Obrist and his co-workers suggest that the increase in intensity of finger tapping does not necessarily contradict their hypothesis that decreases in somatic-motor activity accompany HR deceleration. They point out that tapping is not an extensive motor task and that the observed increases are very small. . The authors also suggest that the cessation or inhibition of somatic-motor acts may be specific to events which are spontaneous rather than imposed even though imposed events may be irrelevant to the task. The fourth experiment was a further investigation of the relationship between respiration and HR. The authors noted that in previous experiments respiration was related to cardiac change. That is, respiration amplitude and frequency tend to decrease during HR deceleration. When respiration rate and depth were controlled (Obrist, 1968; Wood and Obrist, 1964) HR deceleration was still observed. The hypothesis here is that respiration and deceleration are two peripheral responses having common mediation with-22 in the central nervous system (CNS). It was also noted, however, that when respiration was controlled by suspending respiration during the CS-UCS interval (Smith, 1966; Zeaman and Smith, 1965) only HR acceleration was observed. The fourth experiment was designed to investigate both methods of respiration control. The same conditioning paradigm as used in Experiment 3 was used to investigate the effect of normal respiration as compared to suspended respiration on HR activity. Contrary to the findings of Smith (1966) and Zeaman and Smith (1965), the HR deceleration accompanying suspended respiration was slightly larger than that with normal respiration and was coupled with greater cessation of eye-movements and blinks and, to a lesser degree, with greater reduction in EMG bursts. Obrist et al (1969) suggest that the results of the foregoing experiments support the hypothesis that HR and somatic-motor activity are different peripheral aspects of the same central response process. This position differs from that of Lacey (1967) who views the HR response as an instrumental act which can facilitate behavioural processes. The authors point out, however, that the two hypotheses may in fact be complementary. Obrist et al suggest that the inhibition of irrelevant or non-essential somatic-motor activity may set in motion HR deceleration and thus facilitate excitatory processes relative to performance. Such a position does not contradict the proposition by Lacey (1967) that HR deceleration, via an afferent feedback system, may further act to modify the CNS in such a way as to facilitate relevant behavioural events. Obrist, Webb, Sutterer, and Howard (1970b) performed a further experiment to test these two hypotheses. They argue that if the cardiac response is primarily a manifestation of efferent processes associated 23 with the inhibition of ongoing, task irrelevant somatic activity, then atropine blockade should result in no performance decrement. If, however, the cardiac deceleratory response is part of an afferent feedback mechanism which facilitates performance then atropine blockade should result in a decrement in task performance. The authors used the data and procedure from an earlier experiment (Webb and Obrist, 1970) in which different preparatory intervals (PI) were used with a RT task. Webb and Obrist (1970) using human male Ss, had shown that with different Pis there were significant differences in HR deceleration. That is, with a 2 sec PI there was significantly less HR deceleration than that observed with longer Pis. Specifically, it was hypothesized by Obrist et al (1970b) that if HR deceleration facilitates performance through afferent feedback then there would be the greatest facilitation at longer Pis when the HR deceleration is not blocked by atropine and that a greater performance decrement would be found with the longer Pis than with the short Pis when deceleration is blocked pharmacologically. The results indicated no differences in performance of the RT task between the Ss with vagal blockade and Ss without blockade. The RT was essentially the same for both groups for each of the four Pis (2,4,8 and 16 sec). Differences between groups were obtained, however, in HR activity. With no vagal blockade there were small but significant decreases in HR with a 2 sec PI and a larger decrease in HR (also significant) with an 8 sec PI. With vagal blockade, however, the HR for the 2 sec PI was not different from the base HR and with the 8 sec PI there was a small but non-significant decrease in HR. The authors were also able to show that the faster RTs were reliably associated 24 w i t h g r e a t e r d e c r e a s e s i n s o m a t i c and c a r d i a c e v e n t s . M o r e o v e r , i t was found t h a t the s l o w e r RTs a s s o c i a t e d w i t h t h e 2 s e c PI were a l s o a s s o c i a t e d w i t h a f a i l u r e t o i n h i b i t o n g o i n g s o m a t i c a c t i v i t y . O b r i s t , Webb, S u t t e r e r , and Howard (1970a) s u g g e s t t h a t the f i n d i n g s o f t h e f o r e g o i n g s t u d y p r e s e n t some d i f f i c u l t y f o r L a c e y ' s (1967) p o s i t i o n t h a t HR d e c e l e r a t i o n i s an i n s t r u m e n t a l a c t n e c e s s a r y f o r t h e f a c i l i t a t i o n o f p e r f o r m a n c e o f a t a s k . They s u g g e s t t h a t the most p a r s i m o n i o u s e x p l a n a t i o n o f t h e r e s u l t s i s t h a t t h e HR d e c e l e r a t i o n i s p a r t o f a c e n t r a l e f f e r e n t p r o c e s s , w h i c h i n v o l v e s t h e i n h i b i t i o n o f o n g o i n g , t a s k - i r r e l e v a n t s o m a t i c a c t i v i t y , d e m o n s t r a t i n g t h e m e t a b o l i c a l l y r e l e v a n t r e l a t i o n s h i p between c a r d i a c and s o m a t i c e v e n t s . In a c r i t i q u e o f L a c e y ' s (1967) h y p o t h e s i s c o n c e r n i n g the e f f e c t s o f c a r d i o v a s c u l a r f e e d b a c k on a t t e n t i o n , E l l i o t t (1972) s u g g e s t s t h a t t h e r e i s o n l y e q u i v o c a l s u p p o r t f o r the t h e o r y . He f u r t h e r s u g g e s t s t h a t t h e work o f O b r i s t (1970b) has l e d t o t h e d e v e l o p m e n t o f a more p a r s i m o n i o u s h y p o t h e s i s w h i c h can be more r e a d i l y t e s t e d . E l l i o t t (1972) p o i n t s o u t , h o w e v e r , t h a t O b r i s t ' s (1970b) work has d e a l t o n l y w i t h p h a s i c HR changes and t h a t any t h e o r y o f HR a c t i v i t y s h o u l d c o n s i d e r t o n i c HR (HR measured o v e r p e r i o d s o f 30 s e c o r more) changes a l s o . W h i l e O b r i s t ' s ( O b r i s t e t a l , 1970b) f i n d i n g s c l e a r l y d e m o n s t r a t e c a r d i a c -s o m a t i c r e l a t i o n s h i p s w i t h r e s p e c t t o p h a s i c HR c h a n g e s , E l l i o t t (1972) s u g g e s t s t h a t t h e c a r d i a c - s o m a t i c f o r m u l a t i o n does n o t a p p e a r to a p p l y t o e x i s t i n g t o n i c HR d a t a ( E l l i o t t , 1964, 1966 , 1969 ) . F o r example E l l i o t t ( 1964 , 1 9 6 6 , 1969) had d e m o n s t r a t e d t h a t i n c r e a s e s i n i n c e n t i v e r e s u l t i n i n c r e a s e s i n t o n i c HR wh ich a r e a c c o m p a n i e d by d e c r e a s e s i n motor a c t i v i t y . E l l i o t t (1972) h y p o t h e s i z e s , however , t h a t i n c r e a s e s i n 25 tonic HR may be related to increases in muscle tension, resulting from increases in incentive, or that tonic and phasic HR changes may reflect different processes altogether. Jennings, Averill, Opton and Lazarus (1971) reported a study, the results of which, they suggest, are in opposition to both the Lacey and Obrist hypotheses. The authors used a modified RT task in order to determine the degree to which HR was influenced by (1) perceptual tasks, (2) combined perceptual and motor tasks and (3) motor tasks alone. The RT task utilized a ready signal followed 10 sec later by a discriminative signal requiring one of two possible responses. The go signal either followed the discriminative signal by 10 sec (perceptual discrimination) or occurred simultaneously with the signal (perceptual discrimination and motor task). A third condition was employed in which Ss were confronted with a simple RT task (motor task). In different sessions the discriminative signal was paired with shock on 0%, 33% or 100% of the trials in order to investigate the influence of noxiousness and uncertainty on HR. The pattern of HR change was the same for all conditions and was characterized by HR acceleration to the ready signal followed by deceleration just prior to the discriminative and go signals. It was also found, however, that the least deceleration and fastest RTs occurred with the go signal alone. The authors point out that this finding is contradictory to the hypotheses of both Lacey (1967) and Obrist (1970a). The authors hypothesize that any factors which produce or increase attention will also tend to produce HR deceleration, whereas any task which is accompanied by increases in metabolic activity during the 26 preparation for or execution of the task, or any response involving increases in sympathetic activity will result in less cardiac deceleration or even acceleration, THE BASIS OF THE PRESENT RESEARCH Research investigating autonomic responding to different types of visual stimuli has demonstrated that coloured slides of homicide victims produced significantly greater and more sustained cardiac decelera-tion than slides of nude females (Hare et al, 1970; Hare et al, 1971; also see Davis and Buchwald, 1957). Although the studies by Hare et al were briefly discussed earlier it should be pointed out that the observed HR deceleration to the homicide pictures was unexpected. It was felt that these stimuli, which the Ss reported as being gruesome and very disturbing, would result in the HR acceleration thought to be associated with the DR (Sokolov, 1963) and "rejection of the environment" (Lacey, 1967). The fact that the presentation of different homicide scenes on successive trials (Hare, Wood, Britain, and Shadman, 1971) was found to be a potent stimulus in terms of physiological activity, it was felt that these stimuli would be highly effective UCS for conditioning studies involving cardiac and electrodermal events. The effectiveness of such stimuli in the classical conditioning of electrodermal activity had already been shown by Geer (1968). In this study, Geer used a 5 sec presentation of coloured slides of victims of violent death as the UCS, and a 9 sec tone as the CS in a forward, backward and random conditioning paradigm. The author found that the electrodermal UCR was approximately the same in all groups and that, unlike the findings of Hare et al (1971), there was habituation of the 27 response over trials. An electrodermal AR was demonstrated in both the forward and random group but not in the backward conditioning group. In fact, during conditioning there were no significant differences between the forward and random groups in the electrodermal OR to the CS, the AR, or in the UCR to the pictures. Geer took the position that there was a high level of arousal in the random group since the Ss were not provided with warning signals about forthcoming aversive events. He argues that such warnings either allow the S to make preparatory reponses which reduce the impact of the aversive UCS (Kimmel, 1966) or, since the S cannot predict when or which stimulus will occur, the S will become generally aroused and may react to all stimuli with sensitized responding (Seligman, 1969). Since sensitized responding is usually elicited by stimulus onset (Kimble, 1961, p. 64) and since Geer defined any response between 1 and 5 sec after CS onset as an OR, it is difficult to see how a response occuring between 5 and 10 sec after CS onset (the CR) could be due to sensitization. It also should be noted, however, that the random conditioning group was not truly random since the CS and UCS were always separated by at least 5 sec. According to Rescorla (1967) such a procedure could allow CS-UCS contingencies to become established and, if this were the case, could account for the appearance of a CR in a supposedly random conditioning group. It is evident from the foregoing review of the literature that there are three theoretical positions regarding HR activity and its relationship to behavioural and psychophysiological processes. Lacey (1967) views HR acceleration and deceleration as instrumental acts which facilitate 28 sensory-intake or rejection. Obrist et al (1970a) consider HR change a peripheral aspect of a central efferent process related to the metabolic needs of the working muscles. Jennings et al (1971) argue for a position which incorporates aspects of the theories of both Lacey and Obrist. Basically, they state that increases in attention produce cardiac deceleration whereas increases in metabolic activity or sympathetic activity produce less deceleration or even acceleration. Other evidence (Lacey, 1967; Hare et al, 1970; Hare et al, 1971; Hare, 1972) suggest, however, that when cardiac activity is considered as part pf an overall response pattern which includes other measures of physiological activity (i.e. electrodermal, vasomotor, etc.) no simple relationship between measures can be found. Evidence is now accumulating supporting such phenomena as directional fractionation and response stereotypy. Moreover, the pattern of responding exhibited by any particular S may be related to how that S evaluates the stimulus (Hare, 1972). As was noted earlier different Ss responded to homicide pictures with different patterns of autonomic activity. Some Ss demonstrated physiological activity characteristic of the OR while others demonstrated DR patterns of activity. In evaluating such findings it would appear that some Ss found homicide pictures to be attention provoking while others may have found them to be disturbing and unpleasant. Thus, a case can be made for the position that both cognition and affect will influence how a S responds to this particular class of stimuli. The fact that homicides pictures proved to be potent stimuli raised the question as to their effectiveness in a conditioning situation. Geer (1968) had demonstrated that pictures of victims of violent death 29 were effective in conditioning the electrodermal response. There was no data available, however, as to their effectiveness in cardiac conditioning. Earlier studies (Hare et al, 1970, Hare et al, 1971) have shown that Ss consistently report homicide pictures to be aversive, yet the UCR demonstrated by these Ss has been opposite (decelerative) to what is usually found with other types of aversive stimuli (i.e. shock). The Lacey (1967) and the Jennings et al (1971) hypotheses would suggest that even though the homicide class of stimuli are aversive they are attention provoking and result in considerable cardiac deceleration facilitating sensory-intake. Obrist et al (1970a) would explain these findings as indicating a general reduction in somatic activity of which the cardiac deceleration is but a part. Moreover, assuming that these stimuli were effective in cardiac conditioning, the form of the cardiac CR could not be predicted with any certainty on the basis of present theoretical alternatives. Thus, the research to be reported here is concerned with two major issues; (1) to determine the effectiveness of pictures of homicide victims as stimuli for the conditioning of HR and (2) to determine the form of the cardiac CR should conditioning occur. This study uses three groups of Ss in a differential, delayed classical conditioning paradigm. The two classes of UCS are (1) coloured slides of homicide victims and (2) coloured slides of people in ordinary, everyday situations. A different schedule of reinforcement was maintained with each group, the first group receiving continuous reinforcement, the second group, partial reinforcement (70%) and the third group, random reinforcement (Rescorla, 1967). The schedule of partial reinforcement was included in order to 30 provide procedures comparable to those used in other studies in which electric shock had been used as the UCS. In these studies (see Zeaman and Smith, 1965; Obrist et al, 1969), schedules of partial reinforce-ment were used since test (non-reinforced) were interspersed among conditioning trials throughout acquisition. The two dependent variables in this study are electrodermal and cardiac activity. 31 CHAPTER II METHOD Subjects Thirty-six undergraduate male, paid volunteers from the University of British Columbia Summer School Session were used as subjects (Ss) in this study. The Ss ranged in age from 18 to 32 years with a mean age of 22.7 years. Apparatus A Beckman Type R Dynograph was used to simultaneously record heart rate (HR), skin resistance, respiration and stimulus events. Beckman biopotential electrodes were used to record HR and skin resistance. The standard lead II configuration was used for HR recording (Venables and Martin, 1967), with the HR read-out being expressed directly in beats per minute (BPM). Skin resistance electrodes were attached to the third phalange of the first and third fingers of the right hand. Current p density for the skin resistance electrodes was 9 microamps/cm (Venables and Martin, 1967). Respiration was measured by a strain belt around the lower part of the chest. The conditioned stimuli were 12 volt D.C. lights, yellow and green, mounted three feet above the floor and directly underneath the projection screen approximately seven feet away from the S. Both lights were one-half inch in diameter, mounted horizontally and 3.5 inches apart. The unconditioned stimuli were (1) 20 different coloured slides of homicide victims and (2) 20 different coloured slides of people in ordinary, everyday situations. The pictures of homicide victims showed people who had met sudden and violent death. The pictues were taken by the police 32 at the scene of the crime or after the body had been placed in the morgue. The slides were projected through a Kodak Carousal 850 automatic focus projector with the image on the screen measuring 3 feet by 4 feet. The Ss were seated in a reclining chair in a sound dampened, electro-magnetically shielded, air-conditioned room. The UCS were projected from the adjoining polygraph room through a 12 inch by 18 inch window approximately two feet above the Ss head. The presentation of stimuli was controlled by an Ohr-Tronics 8 channel punched papertape reader with each stimulus event recorded through one channel of the Dynograph. Recorded white noise was introduced to each S through earphones for the duration of each experimental session in order to prevent the S hearing equipment noise from the polygraph room. The Ss communicated with the experimenter (E) through a Fannon two-station intercom system mounted on the wall next to the S. The level of white noise was sufficient to prevent the S from hearing noise from the polygraph room but not sufficient to prevent communication with E. Design Two CS and two classes of UCS were used in a discriminative, delayed classical conditioning paradigm. Each S was randomly assigned to one of three groups. Group 1 received continuous reinforcement (CRF), group 2 partial (70%) reinforcement (PRF), and group 3 random presentation of the UCS in relation to the CS (Rescorla, 1967). The CRF group received 20 conditioning trials with homicide pictures as one UCS (UCS-H) and twenty trials with the non-homicide pictures (UCS-P) as the other UCS. The UCS-H were presented in random order over the 40 conditioning trials with the limitation that no more than two slides 33 in one category could occur in a row. Each UCS was presented for 20 seconds and was preceded by a 10 second CS (a yellow light or a green light). The offset of the CS and the onset of the UCS occurred simultan-eously. The inter-trial interval was varied randomly between 15 and 45 seconds with a mean of 30 seconds. Half of the Ss in groups CRF and PRF had the yellow light paired with the UCS-H and the green light with the UCS-P. The remaining Cs received a reversed pairing. The presentation of lights was also counterbalanced in the random group. The sequence of slides within both categories (UCS-H and UCS-P) was randomized but was the same for all three groups. To control for sequence effects within a category of slides, six different sequences were used within each group. The PRF group was treated in exactly the same manner as the CRF group with the exception that only 70% of the CS for homicide slides (CS-H) and 70% of the 20 CS for non-homicide slides (CS-P) were actually followed by their respective UCS. The ramining 6 CS-H and 6 CS-P were followed by no UCS. The random group retained the same orderings and intervals for the CS-H and CS-P as occurred in the CRF and PRF groups. The presentation of the UCS was made on a random basis without regard for the occurrence of CS-H and CS-P. Thus, a CS could occur before, during or after the presentation of UCS. All three groups were given 40 trials. This acquisition phase was followed by 20 extinction trials in which there were 10 presentations of CS-H and 10 presentations of CS-P without further exposure to UCS. 34 Procedure Upon arrival at the experimental room each S was asked to wash his hands with soap and warm water. The S was then led into the shielded room and asked to be seated in a reclining chair. The following statement was then made: The purpose of this experiment is to measure people's physio-logical responses to various visual stimuli. The stimuli consist of lights and pictures. The lights are the green and yellow ones you see at the bottom of the screen. The pictures consists of slides of people in ordinary, everyday situations and slides of homicide victims - people who have met sudden and violent death. The first thing I want to know is whether or not you have any objections to looking at these types of slides. If the S objected the session was terminated at this point. (Three Ss refused to continue and were dropped from the sample.) If the S had no objections then the following instructions were given: Since you don't object, just let me add that if at any time during the course of the experiment you don't want to continue just let me know by speaking into the intercom on the wall. One S in the CRF group completed 24 conditioning trials and then asked to be released from the experiment. This S was dropped from the sample. When the hook-up procedure was completed the S was asked to make himself comfortable and to try to avoid moving during the course of the experiment. The Ss were further instructed to pay attention to the stimulus events and to attempt to look at each slide without closing his eyes or looking away. E then left the room and a 10 minute period was allowed to elapse in order for the S to adapt to the experimental setting. The S was given a two minute warning before the experiment started. 35 Measurements (a) Skin Resistance All skin resistance values were converted to skin conductance (SC) before any analyses were undertaken. Three measures of electrodermal activity were scored. Theie were the orienting response (OR), the anticipatory response (AR), and the unconditioned response (UCR). An OR was defined as any reponse initiated between one and four seconds after CS onset, and the AR as any response initiated between four and eleven seconds after CS onset, and the UCR as any response initiated between one and four seconds after UCS onset (Lockhart, 1966; Stewart, Stern, Winokur, and Fredman, 1961). Tonic skin conductance was measured at three points during the experiment. The first was measured immediately prior to the two minute warning, the second measure was taken after the 40 acquisition trials but before extinction began, and the third measure was after extinction. Since skin conductance can be markedly affected by bodily movements, sudden changes in respiration, and similar causes, any responses associated with such activity were not included in the analyses. (b) Heart Rate Heart rate (HR) was scored on a beat-to-beat basis for three periods during each trial. Five beats prior to CS onset composed the prestimulus period, the first 10 beats during the CS presentation formed the CS period and the first 20 beats after UCS onset the UCS period. These data were obtained over all Ss for 40 acquisition trials except for the PRF group where the 20 beats for the UCS period were not scored on the non-reinforced trials. Only the pre CS period and CS period data were scored during extinction. Three measures of tonic HR were obtained by taking a mean HR over 15 seconds prior to the two minute warning, between acquisition and extinction and after extinction. As with skin conductance, any changes in HR that were attributable to movements, sudden respiration changes, etc. were not included in the data. 37 CHAPTER I I I RESULTS E lec t rodermal Responses 1. Uncond i t ioned Responses The mean e lec t roderma l UCR e l i c i t e d by each type of s t imu lus was computed f o r each t r i a l . However, s i n c e the PRF group rece i ved on ly 14 p resen ta t i ons of each UCS, equal N was ach ieved by us ing on ly the cor respond ing t r i a l s i n the CRF and random groups . The r e s u l t s are presented i n F igu re 1, and the a n a l y s i s of va r i ance summarized i n Table 1. I t was found tha t the e lec t roderma l UCRs to the homicide s l i d e s were s i g n i f i c a n t l y g r e a t e r than those to the non-homicide s l i d e s . The ampl i tude of the UCR g e n e r a l l y decreased (hab i tua ted) w i th repeated s t imu lus p re -s e n t a t i o n s , w i th the r a t e o f h a b i t u a t i o n being un re la ted to the type of s t imu lus or the group i n v o l v e d . 2 . A n t i c i p a t o r y Responses The mean e lec t roderma l ARs to the two cond i t i oned s t i m u l i are p l o t t e d s e p a r a t e l y f o r each group i n F igu re 2 . The s i g n i f i c a n t main e f f e c t f o r s t i m u l i (see Table 2) i n d i c a t e s tha t the ARs to the CS preceding the homicide s l i d e s (CS-H) were s i g n i f i c a n t l y l a r g e r than those preceding the non-homicide s l i d e s ( C S - P ) . I t i s apparent from i n s p e c t i o n of F igu re 2 tha t the s i g n i f i c a n t Groups x S t i m u l i i n t e r a c t i o n r e f l e c t s the f a c t tha t the ARs to the CS-H were l a r g e r than those to the CS-P on l y i n groups CRF and PRF. An a n a l y s i s o f the s imple e f f e c t s of t h i s i n t e r a c t i o n , presented i n Table 3 , f u r t h e r suppor ts t h i s f i n d i n g . Wi th in the random group, the d i f f e r e n c e s between CS-H and CS-P were not s i g n i f i c a n t . F u r t h e r , the th ree 1.3 1.2 -1.1 • LO-CI.9 _ 0.8 0.7 CO o S 0.6 S 0,5 S 0.4H " 0.3 -I 0.2 -1 0.1 1 2 TRIAL BLOCKS CRF GROUP \ TRIAL BLOCKS PRF GROUP UCS-H UCS-P —r-3 TRIAL BLOCKS RANDOM GROUP Figure 1. Electrodermal unconditioned responses to UCS-H and UCS-P over 3 blocks of trials for each group 00 CO Table 1 Summary of analysis of variance of the unconditioned skin conductance response to UCS-H and UCS-P (Factor B) over three blocks of trials (Factor C) for three groups (Factor A) during acquisition. Source df MS F P Between Subjects 35 Groups (A) 2 1.3457 0.45 _ Subjects Within Groups 33 2.9695 Within Subjects 180 Stimuli (B) 1 12.3980 28.54 < .001 AB 2 0.3476 0.80 -B x Subjects Within Groups 33 0.4344 Trials (C) 2 2.4435 12.83 < .001 AC 4 0.2440 1.28 -C x Subjects Within Groups 66 0.1904 BC 2 0.1935 2.24 _ ABC 4 0.0898 1.04 -BC x Subjects Within Groups 66 0.0862 0.5 0.4-o o o 0.3-• . CS-H A A CS-P c_> I — o ZD Q 2 : o o oo 0.2-0.1' / 1 1 2 3 TRIAL BLOCKS CRF GROUP 4 T-3 4 TRIAL BLOCKS PRF GROUP TRIAL BLOCKS RANDOM GROUP Figure 2. Electrodermal anticipatory responses to CS-H and CS-P over 4 blocks of trials for each group during acquisition. o 41 Table 2 Summary of analysis of variance of the anticipatory skin conductance response to CS-H and CS-P (Factor B) over four blocks of trials (Factor C) for three groups (Factor A) during acquisition. Source df MS F P Between Subjects 35 Groups (A) 2 0.5958 1.31 Subjects Within Groups 33 0.4537 Within Subjects 252 Stimuli ; 1 0.8944 8.13 <.01 AB 2 0.5423 4.93 <.02 B x Subjects Within Groups 33 0.1100 Trials (C) 3 0.0928 2.89 <.04 AC 6 0.0795 2.48 <.03 C x Subjects Within Groups 99 0.0321 BC 3 0.1154 3.04 <.04 ABC 6 0.0277 0.73 -BC x Subjects Within Groups 99 0.0380 Table 3 Summary of analysis of variance of simple effects of anticipatory skin conductance responses for three groups (Factor A) taken over CS-H and CS-P (Factor B). Source df MS A for CS-H 2 1.1373 10.3390 .01 A for CS-P 2 0.0006 0.0054 B for Group 1 1 B for Group 2 1 B for Group 3 1 B x Subjects Within Groups 33 0. 0. 0. 9725 9145 0926 0.1100 8.8409 8.3136 0.8418 .01 .01 groups differed in the mean amplitude of the AR to the CS-H, but not to the CS-P. Considered along with Figure 2 , these results indicate that differentiation between CS-H and CS-P occurred only for groups CRF and PRF. This differentiation developed within the first few trial blocks, with the AR to the CS-H then decreasing in amplitude during the last two blocks, while the AR to the CS-P remained more or less constant. It is worth noting that conditioned differentiation was possible because the homicide slides were far more potent unconditioned stimuli than were the non-homicide slides. Not only did the former elicit larger electrodermal UCRs, they were also the only UCS associated with the development of appreciable electrodermal ARs. As Figure 2 indicates, the ARs to the CS-H were larger in the two conditioning groups than in the random group, while there were no differences between groups in the ARs to the CS-P. The mean amplitude of ARs during the extinction phase of the experiment is shown in Figure 3. There was a significant effect due to stimuli (see Table 4), incidating that the AR to the CS-H was generally greater than that to the CS-P. It is of interest that the response amplitudes to both stimuli of group PRF were generally larger than those of the other groups although the differences between groups were not significant. 3. Orienting Responses The mean amplitude of the electrodermal OR to both conditioned stimuli for each group is plotted in Figure 4. An analysis of variance of the OR, summarized in Table 5, revealed a significant Groups x Stimuli interaction but no main effects for either of these factors. It Figure 3. Electrodermal anticipatory responses to CS-H and CS-P over 2 blocks of trials for each group during extinction. Table 4 Summary of analysis of variance of the anticipatory skin conductance response to CS-H and CS-P (Factor B) over two blocks of trials (Factor C) for three groups (Factor A) during extinction. Source df MS F P Between Subjects 35 Groups (A) 2 0.4444 1.76 -Subjects Within Groups 33 0.2531 Within Subjects 108 CS-H, CS-P (B) 1 0.2312 4.45 <.05 AB 2 0.0493 0.95 -B x Subjects Within Groups 33 0.0519 0.88 -Trials (C) 1 0.7211 9.54 <.01 AC 2 0.0749 0.99 -C x Subjects Within Groups 33 0.0756 BC 1 0.3034 5.15 <.03 ABC 2 0.0038 0.06 -B x Subjects Within Groups 33 0.0588 " I 1 1 1 1 1 1 I ! 1 I I I 1 2 3 4 1 2 3 4 1 2 3 4 TRIAL BLOCKS TRIAL BLOCKS TRIAL BLOCKS CRF GROUP PRF GROUP RANDOM GROUP Figure 4. Electrodermal or ient ing responses to CS-H and CS-P over 4 blocks of t r i a l s for each group during acqu is i t i on . C T l Table 5 Summary of analysis of variance of the skin conductance orienting response to CS-H and CS-P (Factor B) over four blocks of trials (Factor C) for three groups (Factor A) during acquisition. Source df MS F P Between Subjects 35 Groups (A) 2 2.3549 1.18 -Subjects Within Groups 33 2.0018 Within Subjects 252 CS-H, CS-P (B) 1 0.7150 3.01 _ AB 2 0.9133 3.85 <.04 B x Subjects Within Groups 33 0.2372 Trials (C) 3 1.1963 6.25 < .001 AC 6 0.3032 1.58 -C x Subjects Within Groups 99 0.1913 BC 3 0.3310 3.23 <.03 ABC 6 0.0548 0.53 -B x C x Subjects Within Groups 99 0.1024 48 is apparent from Figure 4, and confirmed by an analysis of simple effects (see Table 6) that the interaction could be accounted for by the signifi-cant differences which occurred between the OR to CS-H and the OR to CS-P in the PRF group. In this group the amplitude of the OR to CS-H increased significantly from trial block 1 to -trial block 2, indicating the acqusition of a conditioned OR, and was significantly higher than the OR to CS-P for the last three trial blocks. It is interesting to note that there were no differences in the amplitude of the OR to CS-H and CS-P for the CRF and random groups nor were there any differences between these groups. The repeated presentation of the conditioned stimuli resulted in the habituation of the OR and a significant main effect for trials. The Stimuli x Trials interaction was due to a significant increase in the amplitude of the OR to CS-H on trial block 2. An analysis of variance of the OR during extinction (see Table 7) revealed overall differences in responding to the two conditioned stimuli with the OR to CS-H being significantly larger than the OR to CS-P. The mean amplitude of the ORs to both conditioned stimuli for each group are plotted in Figure 5. It is evident from this figure that the significant Groups x Stimuli interaction was due to the large ORs elicited by CS-H for the PRF group. An analysis of simple effects of the interaction, reported in Table 8, further revealed that the OR to CS-H was not only different from the OR to CS-P in the PRF group but also significantly different from the OR to CS-H and CS-P in the CRF and random groups. Thus, it is apparent that the conditioning of electrodermal ORs using partial reinforcement renders that response highly resistant to Table 6 Summary of analysis of variance of simple effects of the skin conductance orienting response for three groups (Factor A) taken over CS-H and CS-P (Factor B). Source df MS F P A for CS-H 2 3.0925 13.0375 <.01 A for CS-P 2 0.1754 0.7394 -B for Group 1 1 0.1617 0.6817 _ B for Group 2 1 2.2019 9.2828 <.01 B for Group 3 1 0.1779 0.7500 -B x Subjects Within Groups 33 0.2372 1.0 0.9 • 0.8 -3 0.7 -I s: ^ 0.6 LU o =| 0.5 i 0.4 H o 0.3 -\ 0.2 0.1 1 J TRIAL BLOCKS CRF GROUP • — 1 2 TRIAL BLOCKS PRF GROUP • • CS-H A CS-P 1 2 TRIAL BLOCKS RANDOM GROUP F i g u r e 5. E l e c t r o d e r m a l o r i e n t i n g r e s p o n s e s t o CS-H and CS-P o v e r 2 b l o c k s o f t r i a l s f o r each group d u r i n g e x t i n c t i o n o 51 Table 7 Summary of analysis of variance of the skin conductance orienting response to CS-H and CS-P (Factor B) over two blocks of trials (Factor C) for three groups (Factor A) during extinction. Source df MS F P Between Subjects 35 Groups (A) 2 1.9880 1.44 _ Subjects Within Groups 33 1.3812 Within Subjects 108 CS-H, CS-P (B) 1 1.8678 11.68 <.005 AB 2 0.7266 4.54 <.02 B x Subjects Within Groups 33 0.1599 Trials (C) 1 0.2162 0.60 AC 2 0.0893 0.25 -C x Subjects Within Groups 33 0.3590 BC 1 0.1237 0.72 _ ABC 2 0.0732 0.43 BC x Subjects Within Groups 33 0.1723 52 Table 8 Summary of analysis of variance of simple effects of the skin conductance orienting response for 3 groups [Factor A) taken over CS-H and CS-P (Factor B). Source df MS F P A for CS-H 2 2.4421 15.2671 <.01 A for CS-P 2 0.2719 1.7002 -B for Group 1 1 0.2396 1.4979 _ B for Group 2 1 3.0652 19.1619 <.01 B for Group 3 1 0.0421 0.2629 -B x Subjects Within Groups 33 0.1599 53 extinction. 4. Tonic Skin Conductance Tonic skin conductance was measured at three points during the experiment; before the two minute warning signal, after the acquisition phase but before extinction, and after extinction. The tonic SC at each of these points was plotted for each group in Figure 6. An analysis of variance, summarized in Table 9 , revealed a significant main effect for conductance with the tonic level increasing significantly during acquisition and remaining at this high level throughout extinction. It is interesting to note that the PRF group showed a significantly greater increase in tonic SC than either the CRF or the random group and that this accounted for the significant Groups x Conductance interaction. Heart Rate 1. Unconditioned Responses The unconditioned HR response to both types of stimuli was calculated by taking beat-to-beat HR for the first 20 beats after UCS onset. As with the electrodermal UCR, the trials used from the CRF and random groups were limited to those corresponding to the reinforced trials from the PRF group. The results are plotted in Figure 7. The analysis of variance, summarized in Table 10 , indicated no main effects for groups, stimuli or trials but did reveal a signficant main effect for beats. This effect was one of cardiac deceleration. The significant Stimuli x Trials interaction resulted from differential cardiac UCRs to the two types of stimuli. That is, while both UCS produce cardiac Figure 6. Tonic skin conductance for each group measured at three points during the experiment. on Table 9 Summary of analysis of variance of tonic skin conductance for three groups (Factor A) taken as repeated measures at three points in the experiment (Factor B). Source df MS F P Between Groups 35 Groups (A) 2 77.3106 1.44 _ Subjects Within Groups 33 53.4639 Within Groups 72 Conductance (B) 2 141.5779 45.12 <.01 AB 4 8.8977 2.84 <.05 B x Subjects Within Groups 66 3.1380 a. 23 3 cu :D o as u PL. C i a* o OS CJ o x i CO u =1 I' OQ u 3 I CO C_) 3 I co u 3 ORDINAL BEATS (1 TO 20) Figure 7. Beat-to-beat HR (deviations from pre-stimulus) to UCS-H and UCS-P over three blocks of trials • (TB) for three groups during acquisition, Table 10 Summary of analysis of variance of beat-to-beat (Factor D) heart rate unconditioned response to UCS-41 and UCS-P (Factor B) during acquisition over three blocks of trials (Factor C) for three groups (Factor A). Source df MS F P Between Subjects 35 Groups (A) 2 255.74 1.22 _ A x Subjects Within Groups 33 208.99 Within Subjects 4284 UCS-H, UCS-P (B) 1 850.67 3.29 _ AB 2 117.52 0.45 -B x Subjects Within Groups 33 258.34 Trials (C) 2 172.41 1 .22 AC 4 65.21 0.46 -C x Subjects Within Groups 66 141.01 Beats (D) 19 20.45 1.91 <.02 AD 38 14.17 1.33 -D x Subjects Within Groups 627 10.69 BC 2 404.60 3.23 <.05 ABC 4 137.23 1 .10 -BC x Subjects Within Groups 66 125.00 BD 19 24.31 2.65 < .001 ABD 38 10.16 1.11 -BD x Subjects Within Groups 627 9.16 CD 38 6.04 0.77 — ACD 76 6.09 0.77 -CD x Subjects Within Groups 1254 7.88 BCD 38 7.03 0.92 ABCD 76 9.94 1.30 <.05 BCD x Subjects Within Groups 1254 7.66 58 deceleration, the amount of deceleration to UCS-P gradually diminished over trials whereas there was progressively greater deceleration to UCS-H over trials. The Stimuli x Beats interaction was produced by greater cardiac deceleration across beats to UCS-H than UCS-P. The complex Groups x Stimuli x Trials x Beats interaction can best be understood through inspection of Figure 7. In all three groups the amount of cardiac deceleration to UCS-H was related to the number of presentations of the stimulus, with more deceleration on trial block 3 than on trial block 1 and 2. The same pattern of responding also occurred to UCS-P in the PRF group. For the CRF and random groups, however, repeated presentation of the UCS-P resulted in the habituation of the cardiac response. It is of interest that the decelerative response to UCS-H not only increased over trials but also began to occur earlier in the UCS period. Thus, it is apparent that, as with the electrodermal UCR, the two types of stimuli produced differential HR responding. 2. Conditioned Responses The response to both CS for all groups was measured by taking beat-to-beat HR for the first 10 beats after the CS onset. The results are plotted in Figure 8 and the analysis of variance summarized in Table 11. As with the UCR, the only significant main effect was for beats, but unlike the UCR the response was one of cardiac acceleration rather than deceleration. The Beats x Groups interaction resulted from the fact that the greatest amount of cardiac acceleration came from the CRF group and that an elevated HR was maintained to the end of the sampling period. The PRF and random groups showed initial acceleration followed by deceleration by the sixth beat. It was also found that the cardiac acceleration to the 59 ORDINAL BEATS (1 TO 10) Figure 8. Conditioned response beat-to-beat heart rate (deviations from pre-stimulus) to CS-H and CS-P for each group during acquisition. Table 11 Summary of analysis of variance of beat-to-beat (Factor D) heart rate to CS-H and CS-P (Factor B) over four blocks of trials (Factor C) for three groups (Factor A) during acquisition. Source df MS F P Between Subjects 35 Groups (A) 2 94.974 1.60 A x Subjects Within Groups 33 59.411 Within Subjects 2844 CS-H, CS-P (B) 1 125.830 1.76 _ AB 2 27.735 0.39 -B x Subjects Within Groups 33 71.563 Trials (C) 3 46.136 1.23 _ AC 6 22.581 0.60 -C x Subjects Within Groups 99 37.631 Beats (D) 9 85.743 15.89 < .001 AD 18 10.484 1.94 <.02 D x Subjects Within Groups 297 5.394 BC 3 76.939 1 .97 _ ABC 6 18.059 0.46 -BC x Subjects Within Groups 99 38.973 BD 9 10.294 2.13 <.03 ABD 18 2.091 0.43 -BD x Subjects Within Groups 297 4.834 CD 27 5.879 1.24 _ ACD 54 3.055 0.65 -CD x Subjects Within Groups 891 4.728 BCD 27 3.934 0.79 ABCD 54 6.437 1.29 -BCD x Subjects Within Groups 891 4.978 61 CS-H was significantly greater than that to the CS-P and thus accounted for the Stimuli x Beats interaction. The mean beat-to-beat HR to both CS during extinction is plotted for each group over trials in Figure 9. The analysis of variance (see Table 12) revealed a significant main effect for beats due to cardiac acceleration to both CS. The Groups x Beats interaction resulted from the PRF group producing the largest and most persistant amount of acceleration while the random group produced no significant changes across beats. While there was no significant main effect for trials the Groups x Stimuli x Trials interaction resulted from a significant increase in HR to CS-P from trial block 1 to trial block 2 for the CRF group. The typical response over trials to the CS in the remaining groups was a gradual reduction in the amount of cardiac acceleration. The Stimuli x Beats interaction was accounted for by greater and more persistant cardiac acceleration across beats to CS-P than to CS-H. The Groups x Stimuli x Trials x Beats interaction can best be understood by referring to Figure 9. In the CRF group there was a large increase in HR to CS-P between trial block 1 and trial block 2 whereas there was evidence of extinction of the response to CS-H. For the PRF group, the CS-P on trial block 1 produced the largest and most persistant cardiac acceleration followed by extinction of this response by trial block 2. There were no differences over trial blocks in the cardiac response to CS-H for the PRF group, nor were there any differences in cardiac respond-ing either between stimuli or over trials for the random group. -2 ORDINAL BEATS (1 TO 10) Figure 9. Conditioned response beat-to-beat heart rate (deviations from pre-stimulus) to CS-H and CS-P over 2 blocks of trials (TB) for each group during extinction. Table 12 Summary of analysis of variance of beat-to-beat (Factor D) heart rate to CS-H and CS-P (Factor B) over two blocks of trials (Factor C) for three groups (Factor A) during extinction. Source df MS F P Between Subjects 35 Groups (A) 2 26.213 0.49 _ A x Subjects Within Groups 33 54.022 Within Subjects 1404 CS-H, CS-P (B) 1 13.709 0.29 _ AB 2 105.190 2.22 -B x Subjects Within Groups 33 47.283 Trials (C) 1 4.958 0.14 _ AC 2 39.426 1.08 -C x Subjects Within Groups 33 36.370 Beats (D) 9 52.665 9.99 < .001 AD 18 10.869 2.06 < .01 D x Subjects Within Groups 297 5.272 BC 1 31.005 0.96 _ ABC 2 187.770 5.80 <.01 BC x Subjects Within Groups 33 32.371 BD 9 7.600 1.08 <.04 ABD 18 5.781 1.58 -BD x Subjects Within Groups 297 3.661 CD 9 2.713 0.65 _ ACD 18 4.822 1.16 -CD x Subjects Within Groups 297 4.171 1.09 -BCD 9 3.184 0.83 _ ABCD 18 10.709 2.79 <.005 BCD x Subjects Within Groups 297 3.841 64 3, Tonic Heart The tonic HR for each group was taken at three points during the experiment. The mean HR over all groups for each of these points was 79.5, 75.0 and 73.0 BPM respectively. An anlysis of variance, summarized in Table 13, revealed no differences between groups but did indicate a significant decrease in HR between the beginning and the end of the experiment. It should be noted that scoring HR data on a beat-to-beat basis has the effect, depending on the tonic HR, of sampling different amounts of the stimulus period. Although the differences in tonic HR between groups were not significant, it was found that approximately the last 1.5 sec of the CS period was not sampled for the PRF group and 1.0 sec for the CRF group. It was not felt, however, that these differences were of sufficient proportion to materially affect the results. Moreover, a second-by-second analysis of HR also results in problems of scoring. Often, with such a method, arbitrary decisions have to be made with regard to which of a pair of HR scores E will assign to a particular 1 sec period and often to which 1 sec period a particular score will be assigned. Libby, Lacey and Lacey (in press) report having used both methods of scoring HR data and that both methods produced the same results. In order to compare the two methods, HR during the CS period was scored on a second-by-second basis and the results are included in the Appendix. Table 13 Summary of analysis of variance of tonic heart rate for three groups (Factor A) taken as repeated measures at three points in the experiment (Factor B). Source df MS F P Between Subjects 35 Groups (A) Subjects Within Groups 2 33 1303.6944 505.2407 2.58 -Within Subjects 72 Heart Rate (B) AB B x Subjects Within Groups 2 4 66 403.5277 12.5972 21.5134 18.75 0.59 <.01 66 CHAPTER IV DISCUSSION The results of this experiment provide adequate support for the position that pictures of homicide victims are potent stimuli in the conditioning of both cardiac and electrodermal activity. Although there is clear evidence for the conditioning of electrodermal activity the findings from the HR data are considerably more complex. The findings replicated the Hare et al studies, (1970, 1971), in as much as the UCR to UCS-H was differentiated from the UCR to UCS-P for both the HR and electrodermal measures. The electrodermal UCR to both stimuli, with the exception of the UCR to UCS-H inthe PRF group, habituated over trials whereas there was little habituation to the UCS-H in Hare's et al findings. The observed habituation in this and Geer's (1968) study lend support to Kimmel's (1966) position that the CS has an inhibitory effect on the UCR resulting in response decrement over trials. In the Hare studies, stimuli were presented to Ss without the occurrence of a CS and thus no inhibitory effect was observed. The electrodermal habituation to the UCS was not, however, carried over to the cardiac UCR for the UCS-H. In all groups the cardiac deceleration to UCS-H became more pronounced over trials. In classical conditioning it is usually the CR which demonstrates build-up rather than the UCR which is normally a full-blown response whenever the UCS is presented (Kimble, 1961). Obviously, the CS does not have the same inhibitory effect on the cardiac UCR as on the electrodermal UCR. Instead, the repeated presentation of UCS-H appears to have a facilatory effect on the cardiac UCR. One possible explanation is that the build-up of 67 cardiac deceleration over trials results from decreases in sympathetic activity as observed in the electrodermal UCR. Obrist, Wood and Perez-Reyes (1965) noted that cardiac acceleration and deceleration resulted from changes in vagal tonus rather than from changes in sympathetic activity. It would follow then that the observed HR deceleration in this study resulted from similar increases in vagal activity. Moreover, Obrist et al (1965) have demonstrated that the sympathetic activity observed in electrodermal responding does not usually result in HR acceleration because of masking by increases in vagal restraint. It would be expected, however, that sympathetic activity does have an inhibitory effect on the more dominant deceleration produced by increases in vagal tone. Successive decreases in sympathetic activity, however, will have successively less of an inhibitory effect on vagal responding and should result in an increase in HR deceleration over trials. Another possible explanation for increases in HR deceleration over trials as compared to the reduction of electrodermal responding is that cardiac and electrodermal activity are response systems which reflect different aspects of the conditioning process. For example, cognitive activity and sensory-intake and sensory-rejection have been shown to produce different types of cardiac activity (Lacey, 1967, Obrist et al, 1970a) but not different types of electrodermal activity. The implication here is that the homicide pictures may initially result in cognitive activity, in as much as the S may spend some time attempting to cope with the nature of the stimulus. Only after the S has had some exposure to the pictures does he begin to demonstrate greater cardiac deceleration indicative of sensory-intake. The habituation of the deceleration observed in the UCR to UCS-P would indicate that the stimuli have little signficance 68 for the S and that there is a gradual reduction of sensory-intake to what are essentially innocuous stimuli. The only condition which did not produce habituation of the HR deceleration to UCS-P was the PRF procedure. An examination of the results of the PRF procedure reveals marked differences between PRF and CRF groups. As noted above, the electro-dermal UCR to UCS-H did not demonstrate the habituation observed in the other groups. There was a significant increase in the electrodermal UCR between trial block 1 and trial block 2, and the decrease in respond-ing between trial block 2 and trial block 3 did not bring the UCR down to the level of the other groups. Similar patterns of responding were demonstrated for the electrodermal AR and OR during acquisition. This higher level of responding was also observed during extinction although not to the same extent for the AR as for the OR. The fact that a partial reinforcement procedure produces noteworthy results, at least as far as electrodermal activity is concerned, is further supported by the tonic SC data. For all groups there was a significant increase in tonic SC between the start and the end of acquisi-tion which was maintained throughout extinction. In the PRF group, however, this increase was significantly greater that that observed in either the CRF or the random groups. Such a finding would indicate a higher level of arousal for the Ss in the PRF group than in either of the other groups (Sternbach, 1966). This high level of arousal could be due to an element of uncertainty introduced by the schedule of reinforcement. In the CRF group the S knows, after a few trials, that each CS is followed by a UCS. Moreover, it is clear from the results that the S also learns 69 which type of UCS follows a particular CS. In the random group, the occurrence of a UCS is unpredictable and the S's only task is to follow events in whatever order they occur. In the PRF group, however, the S quickly learns that there are times when the anticipated event fails to occur. Thus, a S in this group is concerned with two events. The first, as with the CRF groups, is the aversive stimulus itself, while the second is whether or not the stimulus will appear. Previous studies (Hare et al, 1970; Hare et al, 1971) have demonstrated that the viewing of homicide pictures is an aversive, unpleasant experience for many Ss. For example, Hare et al (1970) had Ss rate homicide pictures on a 7 point scale (1 = very unpleasant; 7 = very pleasant) and obtained a mean rating of 1.9. This rating was significantly different from the mean ratings for pictures of simple objects (4.1) and pictures of nude females (5.6). It would follow, therefore, that a S anticipating an aversive event would engage in cognitive activity related to that event, especially since each homicide picture was different. If the anticipation of an aversive event results in increased arousal then an additional factor of uncertainty would tend to increase that arousal. Such a hypothesis would be in accord with the findings of Hare (1972) who reported increases in SC when a S switched from the simple viewing of homicide pictures to a cognitive task which involved evaluating the stimuli. Similarly, Lacey and Lacey (1970) suggest that tasks requiring attention to the environment, attention to both the environment and internal activity, or attention only to internal events can produce different patterns of physiological activity associated with each task. Unlike the findings of Geer (1968), the random group was not 70 characterized by sensitized responding. There was little evidence of pseudoconditioning or sensitization for either the OR or AR during acquisition and extinction. These finds are contrary to Seligman's (1969) position that the use of a random reinforcement group as a control results in high levels of arousal and subsequent sensitization. It should be noted, however, that the procedure followed by Geer (1968) was not truly random since at least 5 sec always separated the CS and UCS. The consistent findings of other conditioning studies (see Lacey, 1967; Obrist et al, 1970a) of a decelerative cardiac AR to both aversive and non-aversive UCS was not replicated in the present study. The fact that the cardiac AR was acceleration for the CRF group and acceleration followed by deceleration for the PRF group presents problems for some of the current theories of HR activity. Obrist's et al (1970a) hypothesis that HR activity is a peripheral component of a central process would suggest that the acceleration observed in the CRF group in this study would have to be associated with increases in somatic activity. While this is a possibility, there is no explanation of why the same activity is not indicated in the PRF group. It should be noted that Obrist's procedures have usually employed test trials interspersed with reinforced trials and such a method is, in effect, a schedule of partial reinforcement. Moreover, his findings have often been much the same as those observed with the PRF group in this study - acceleration followed by deceleration. The question arises as to whether the results from a continuous reinforce-ment schedule using Obrist's procedure would be the same as observed in this study. Lacey's (1967) theory that HR activity is an instrumental act which 71 facilitates sensory intake or rejection only partially accounts for the findings of this study. It would be understandable for a S in the CRF group to respond to the CS with apprehension and distaste. He may be actively attempting to reject the stimulus or he may be engaging in considerable cognitive activity related to the nature of the stimulus. In either case the response would be the observed acceleration. The question as to why the UCR is deceleration could be accounted for by the compelling nature of the stimulus and the subsequent attention to a very novel although disturbing picture. The biphasic response observed with the PRF groups is somewhat more difficult to account for. It has already been shown that this group demonstrates considerably more arousal than the CRF group as indicated by the sympathetic electrodermal activity. It is possible, however, that the uncertainty about the occurrence of the stimulus could result in a reduction in cognitive activity and increased attention towards the end of the CS period to see if the stimulus was presented or not. Such activity would result in a biphasic response. The biphasic response of the PRF group closely approximates the predictions of Dronsejko (1972) that the anticipatory response to an aversive stimulus with a 10 sec ISI is acceleration followed by deceleration. She hypothesized that the deceleratory phase was a mechanism for coping with stress produced by the anticipation of a noxious event. If this were the case then a similar response would be expected with the CRF group. Jennings et al (1971), on the basis of their research, have developed a hypothesis which includes aspects of both Obrist's (1970a) theory and that of Lacey (1967). They suggest that attention produces 72 deceleration whereas tasks requiring increases in metabolic activity or increases in sympathetic activity will produce less deceleration or even acceleration. While this theory might account for the acceleration of the CRF group by way of increases in sympathetic activity it cannot account for the biphasic response observed in the PRF group. The electrodermal activity in the PRF group is considerably greater than that in the CRF group and neither group is faced with a task requiring increases in metabolic activity. The discussion to this point has considered electrodermal and cardiac events as separate issues. When considered together, a number of inconsistencies, especially with the PRF group, become apparant. As has already been discussed, there is greater sympathetic (electrodermal) arousal associated with the PRF group than with either of the other groups. This arousal, if associated with attention to internal activity, does not, however, appear to be reflected in the HR data for the group. Obrist et al (1970a) points out, however, that a considerable amount of evidence now indicates that HR activity is under vagal control rather than sympathetic control as has been assumed for so long. Since this is the case then it would appear to be unwarranted to attempt to integrate the electrodermal and HR data into theories which cannot handle them. Such a position requires that we view the electrodermal activity in terms of sympathetic activity which is unrelated to the HR data. The anticipatory HR acceleration observed with the CRF group most likely reflects a sustained decrease in vagal inhibition rather than a marked increase in sympathetic activity (Obrist et al, 1965). The biphasic anticipatory cardiac response in the PRF group would reflect a decrease followed by an increase in vagal restraint. 73 The possibility that electrodermal and HR activity should be viewed as representing different processes is clearly suggested by the findings of Lacey (1967) and Hare (1972) regarding response stereotypy and directional fractionation. Both Lacey and Hare have demonstrated directional fractionation with regard to HR and electrodermal activity. Moreover, Hare (1972) has also observed this phenomenon with vasomotor activity. Cephalic vasodilation and digital vasoconstriction were observed to occur simultaniously within the same Ss. In the present study, directional fractionation was demonstrated by increases in SC with corresponding decreases in HR. Obviously, these findings provide additional support to the foregoing position. Elliott (1969, 1972) and Elliott, Bankart and Light (1970) have proposed the hypothesis that HR and SC activity actually reflect different processes. Specifically, the authors propose that there are factors which are distinctively effective in causing increases in SC. Such factors have been called collative by Berlyne (1960) and include pro-perties such as novelty, complexity, surprisingness, uncertainty and so on. Increases in HR on the other hand, are viewed as being under the control of other factors, principally instigation, anticipation and initiation of responses. The term "arousal" has been used by Elliott (1969) to apply to these collative factors while "activation" has been used to apply to the response instigation-anticipation-initiation factors. Elliott's formulations, although derived from his work with tonic HR, demonstrate considerable agreement with the findings of the present study. The significant decrease in tonic HR observed in all groups in this study would be predicted by Elliott since there are no activation factors included in the experimental design. Phasic HR changes can be 74 best accounted for, according to Elliott (1972), by viewing them as part of a peripheral process involving the cardiac-somatic relationship (Obrist et al, 1970a). In the same way, collative (arousal) factors can account for many of the SC findings. For example, if it can be assumed that uncertainty, novelty and similar factors are included in the present design, then the significant increases in tonic SC can be accounted for. Moreover, the significantly greater increase in tonic SC observed in the PRF group can be explained on the basis of greater uncertainty for this group than for either the CRF or the random groups. While Elliott's (1969) hypothesis regarding HR change and "activation" are applied only to tonic HR changes, i t would seem that the "arousal" hypothesis concerning SC can be applied to both tonic and phasic changes. This is not meant to imply, however, that other factors cannot result." in increases and decreases in SC. It is a well accepted phenomenon, for example, that increases in SC occur to many stimuli, as with the OR, which have no apparent collative or "arousal" factors. It is quite possible, however, that the addition of collative factors could result in increases in the magnitude of SC responses. Thus, the assumption that there were more collative factors operating in the PRF group than in either of the other two groups provides an explanation for the significantly greater electrodermal OR to CS-H for the PRF group. It should be noted that the findings from the present study may reflect the use of different procedures, particularly with respect to the work of Obrist and his associates. The acceleratory cardiac CR to the homicide pictures may have resulted from the use of a CRF procedure which Obrist has not typically employed. A replication of the present study would be necessary to confirm the present fidings, and such a replication should utilize both the present procedure plus those employed by other researchers. Such procedures would include the use of test trials and the quantification of HR on a sec-by-sec rather than beat-to-beat basis. In addition, information obtained from cephalic and digital vasomotor activity would be useful in determining whether or not the cardiac acceleratory CR was a DR elicited by the CS prior to the aversive homicide picture. Finally, some attempt should be made to determine whether the changes in HR observed in this experiment might not reflect concurrent changes in the Ss somatic-motor activity. 76 BIBLIOGRAPHY Berlyne, D.E. Conflict and arousal. Scientific American, 1966, 215, 82-87. Brown, CC. (Ed.), Methods in Psychophysiology. Baltimore: Williams and Wilkins, 1967. Campos, J.J. and Johnson, H.J. Affect, verbalization, and directional fractionation of autonomic responses. Psychophysiology, 1967, _3, 285-290. Chase, W.G., Graham, F.K. and Graham, D.T. Components of the heart rate response in anticipation of reaction time and exercise tasks. Journal of Experimental Psychology, 1968, 76_, 642-648. Craig, K.D. and Wood, K. Autonomic components of observer's reponses to pictures of homicide victims and nude females. Journal of  Experimental Research in Personality, 1971, 5^, 304-309. Davis, R.C. and Buchwald, A.M. An exploration of somatic response patterns: Stimulus and sex differences. Journal of Comparative  and Physiological Psychology, 1957, 50, 44-52. Dronsejko, K. Effects of CS duration and instructional set on cardiac anticipatory responses to stress in field dependent and independent subjects. Psychophysiology, 1972, 9^, 1-13. Dykman, R.A. and Gantt, W.H. The parasympathetic component of unlearned and acquired cardiac responses. Journal of Comparative and  Physiological Psychology, 1959, 52, 163-167. Elliott, R. Physiological activity and performance: A comparison of kindergarten children with young adults. Psychological  Monographs, 1964, 78 (10, Whole No. 587). Elliott, R. Effects of uncertainty about the nature and advent of a noxious stimulus (shock) upon heart rate. Journal of Personal i ty  and Social Psychology, 1966, 3, 353-356. Elliott, R. Tonic heart rate: Experiments on the effects of collative variables lead to a hypothesis abouts its motivational significance. Journal of Personality and Social Psychology, 1969, 1_2, 211-228. Elliott, R. The significance of heart rate for behavior: A critique of Lacey's hypothesis. Journal of Personality and Social Psychology, 1972, 22, 398-409. Elliott, R., Bankart, B. and Light, T. Differences in the motivational significance of heart rate and palmer conductance: Two tests of a hypothesis. Journal of Personality and Social Psychology, 1970, 14, 1966-197?: 77 Gale, E.N. and Stern, J.A. Conditioning of the electrodermal orienting response. Psychophysiology, 1967, 3_, 291-301. Geer, J.H. A test of the classical conditioning model of emotion: The use of non-painful aversive stimuli as UCS in a conditioning procedure. Journal of Personality and Social Psychology, 1968, J_0, 148-156. Graham, F.K. and Clifton, R.K. Heart rate change as a component of the orienting response. Psychological Bulletin, 1966, 6_5, 305-320. Hare, R. D. Response requirements and directional fractionation of autonomic responses. Psychophysiology, 1972, £, 419-427. Hare, R.D. Cardiovascular components of orienting and defensive responses. Psychophysiology, 1972, 9_, 606-614. Hare, R.D., Wood, K., Britain, S., and Frazelle, J. Autonomic responses to affective visual stimulation: Sex differences. Journal of Experimental  Research in Personality, 1971, 5_, 14-22. Hare, R.D., Wood, K., Britain, S., and Shadman, J. Autonomic responses to affective visual stimulation. Psychophysiology, 1970, 7_, 408-417. Hastings, S.E. Heart rate during conditioning in humans: Effect of varying the interstimulus (CS-UCS) interval. Masters thesis, University of North Carolina, Chapel Hill, 1966. Hastings, S.E. and Obrist, P.A. Heart rate during conditioning in humans: Effect of varying the interstimulus (CS-UCS) interval. Journal of  Experimental Psychology, 1967, 74. 431-442. Jennings, J.R., Averill, J.R., Opton, E.M., and Lazarus, R.S. Some parameters of heart rate change: Perceptual versus motor task require-ments, noxiousness and uncertainty. Psychophysiology, 1971, _7, 194-212. Johnson, H.J. and Campos, J.J. The effect of cognitive tasks and verbalization instructions on heart rate and skin conductance. Psychophysiology, 1967, 4, 143-150. Kimble, G.A. Hilgard and Marquis' Conditioning and Learning. New York: Appleton-Century-Crofts, Inc., 1961. Kimmel, H.D. Inhibition of the unconditioned response in classical conditioning. Psychological Review, 1966, _73, 232-240. Lacey, J. Somatic response patterning and stress: Some revisions of activation theory. In M. Appley and R. Trumbell (Eds.), Psychological  Stress: Issues in Research New York: Appleton-Century-Crofts, 1967. Pp. 14-42. 78 Lacey, J.I., Kagan, J., Lacey, B.C., and Moss, H.A. The visceral level: Situational determinants and behavioral correlates of autonomic response patterns. In P. Knapp (Ed.), Expressions of  the emotions in man. New York: International Universities Press, 1962. Pp. 161-196. Lacey, J., and Lacey, B. Some autonomic-central nervous system inter-relationships. In P. Black, (Ed.), Physiological correlates of  emotion. New York, Academic Press, 1970. Pp. 205-227. Lang, P.J. and Hnatiow, M. Stimulus repetition and the heart rate response. Journal of Comparative and Physiological Psychology, 1962, 55, 781-785. Lockhart, R.A. Comments regarding multiple response phenomena in long interstimulus interval conditioning. Psychophysiology, 1966, 33 108-114. Manzotti, M. The effect of some respiratory manoeuvers on the heart rate. Journal of Physiology, 1958, 144, 541-557. Notterman, J.M., Schoenfeld, W.N., and Bersh, P.J. Conditioned heart rate response in human beings during experimental anxiety. Journal  of Comparative and Physiological Psychology, 1952, 45_, 1-8. Obrist, P.A. Cardiovascular differentiation of sensory stimuli. Psychosomatic Medicine, 1963, 25_, 450-458. Obrist, P.A. Heart rate and somatic-motor coupling during classical aversive conditioning in humans. Journal of Experimental Psychology, 1968, 77, 189-193. Obrist, P.A. and Webb, R.A. Heart rate during conditioning in dogs: Relationship to somatic-motor activity. Psychophysiology, 1967, 4_. Obrist, P.A., Webb, R.A., and Sutterer, J.R. Heart rate and somatic changes during aversive conditioning and a simple reaction time task. Psychophysiology, 1969, 5_, 696-723. Obrist, P.A., Webb, R.A., Sutterer, J.R. and Howard, J.L. The cardiac-somatic relationship: Some reformulations. Psychophysiology, 1970, 6, 569-587. (a) Obrist, P.A., Webb, R.A., Sutterer, J.R., and Howard, J.L. Cardiac deceleration and reaction time: An evaluation of two hypotheses. Psychophysiology, 1970, 6_, 695-706. (b) Obrist, P.A., Wood, D.M., and Perez-Reyes, M. Heart rate during conditioning in humans: Effects of UCS intensity, vagal blockade, and adrenergic block of vasomotor activity. Journal of Experimental  Psychology, 1965, 70, 32-42. 79 Ohman, A. Differentiation of conditioned and orienting response components in electrodermal conditioning. Psychophysiology, 1971, 8, 7-22. Raskin, D., Kotses, H., and Bever, J. Cephalic vasomotor and heart rate measures of orienting and defensive reflexes. Psychophysiology, 1969, 6, 149-159. Rescorla, R.A. Pavlovian conditioning and its proper control procedures. Psychological Review, 1967, 74, 71-80. Samaan, A. The antagonistic cardiac nerves and heart rate. Journal of  Physiology, 1934-35, 83, 332-340. (a). Samaan, A. Muscular work in dogs submitted to different conditions of cardiac and splanchnic innervations. Journal of Physiology, 1934-35, 85, 313-331. (b) Seligman, M.E.P. Control group and conditioning: A comment on operation-ism. Psychological Review, 1969, 76, 484-491. Smith, R. W. Discriminative heart rate conditioning with sustained inspiration as respiratory control. Journal of Comparative and  Physiological Psychology, 1966, 61_, 221-226. Sokolov, E.N. Perception and the Conditioned Reflex. New York: Macmillan, 1963. Sternbach, R.A. Principles of psychophysiology. New York: Academic Press, 1966. Stewart, M.A., Stern, J.A., Winokur, G. and Fredman, S. An analysis of GSR conditioning. Psychological Review, 1961 , 68^  60-67. Venables, P.H., and Martin, I., (Eds). A manual of psychophysiological  methods. New York: John Wiley and Sons, 1967. Webb, R.A. and Obrist, P.A. Physiological concomitants of reaction time performance as a function of preparatory interval. Psychophysiology, 1970, 6, 389-403. Wegner, N. and Zeaman, D. Strength of cardiac conditioned responses with varying unconditioned stimulus durations. Psychological Review, 1958, 65, 238-241. Westcott, M.R. and Huttenlocher, J. Cardiac conditioning: The effects and implications of controlled and uncontrolled respiration. Journal  of Experimental Psychology, 1961, 61, 353-359. Wilder, J.F. Stimulus and response: The law of initial value. Bristol: Wright, 1967. 80 Winer, B. Statistical Principles in experimental design. New York: McGraw-Hill, 1962. Wood, D.M. and Obrist, P.A. Effects of controlled and uncontrolled respiration on the conditioned heart rate response in humans. Journal of Experimental Psychology, 1964, 68, 221-229. Wood, D.M. and Obrist, P.A. Minimal and maximal sensory intake and exercise as unconditioned stimuli in human heart-rate conditioning. Journal of Experimental Psychology, 1968, 76_, 254-262. Zeaman, D., Deane, G., and Wegner, N. Amplitude and latency characteristics of the conditioned heart response. Journal of Psychology, 1954, 38, 235-250. ~ Zeaman, D., and Smith, R.W. Human cardiac conditioning. In W.F. Prokasy (Ed.), Classical conditioning: A symposium. New York: Appleton-Century-Crofts, 1965. Pp. 378-418. Zeaman, D. and Wegner, N. The role of drive reduction in the classical conditioning of an autonomically mediated response. Journal of  Experimental Psychology, 1954, 48, 349-354. Zeaman, D., and Wegner, N. A further test of the role of drive reduction in human cardiac conditioning. Journal of Psychology, 1957, 43, 125-133. APPEND LX THE RESULTS OF SCORING HEART RATE ON A SECOND-BY-SECOND BASIS DURING THE CS PERIOD 82 APPENDIX THE RESULTS OF SCORING HEART RATE ON A SECOND-BY-SECOND BASIS DURING THE CS PERIOD Since beat-to-beat HR for the entire CS period had already been scored and recorded on computer cards, a computer program was written which transformed the beat-by-beat data to second-by-second. This was achieved by converting the rate for each heart beat back to a time interval and then having the computer sample HR on each second of the 10 sec CS period. As with the beat-to-beat method, the five beats prior to the CS period composed the prestimulus period. Results The second-by-second HR responding to both CS for all groups during acquisition is plotted in Figure 10 and the analysis of variance is summarized in Table 14. The only significant finding produced by the second-by-second scoring procedure was for beats and resulted from a response of acceleration followed by decelera-tion. HR responding to both CS during extinction is plotted over two blocks of trials for each group in Figure 11. An analysis of var-iance summarized in Table 15, revealed a significant main effect for beats, again due to a response of acceleration followed by de-celeration. As with the beat-to-beat HR analysis, the Groups x Stimuli x Trials interaction resulted from the significant in-crease in HR for CS^ P from trial block 1 to trial block 2 for the CRF group. 83 ORDINAL SECONDS (1 TO 10] Figure 10. Conditioned response second-by-second heart rate (deviations from pre-stimulus) to CS-H and CS-P for each group during acquisition. TABLE 14 Summary of analysis of variance of second by second (Factor D) heart rate to CS-H and CS-P (Factor B) over four blocks of trials (Factor C) for three groups (Factor A) during acquisition. Source df MS F P Between Subjects 35 Groups (A) 2 60.133 1 .143 _ A x Subjects Within Groups 33 52.624 Within Subjects 2844 CS-H, CS-P (B) 1 136.194 1.983 _ AB 2 38.818 0.565 -B x Subjects Within Groups 33 68.681 Trials (C) 3 47.672 1 .081 AC 6 20.548 0.466 -C x Subjects Within Groups 99 44.106 Beats (D) 9 57.388 7.403 .01 AD 18 10.726 1.384 -D x Subjects Within Groups 297 7.752 BC 3 103.688 2.586 _ ABC 6 15.675 0.391 -BC x Subjects Within Groups 99 40.096 BD 9 7.623 1.724 _ ABD 18 3.203 0.724 -BD x Subjects Within Groups -297 4.421 CD 27 6.439 1 .309 _ ACD 54 4.892 0.791 -CD x Subjects Within Groups 891 4.920 BCD 27 5.287 0.962 ABCD 54 6.564 1.194 -BCD x Subjects With Groups 891 5.496 85 +3 -i +2 H § o CD Di ° -1 -2 J • •CS-H, TB 1 • •CS-P, TB 1 o oCS-H, TB 2 o - ^ C S - P , TB 2 ORDINAL SECOND (1 to 10) Figure 11 - Conditioned response second-by-second heart rate (deviations from pre-stimulus) to CS-H and CS-P over two blocks of t r i a ls (TB) for eacn group during extinction TABLE 15 86 Summary of analysis of variance of second by second (Factor D) heart rate to CS-H and CS-P (Factor B) over two blocks of trials (Factor C for three groups (Factor A) during extinction. Source df MS F P. Between Subjects 35 Group (A) 2 29.919 0.586 -A x Subjects Within Groups 33 51.080 -Within Subjects 1404 CS-H, CS-P (B) 1 41.453 0.940 -AB 2 94.656 2.145 . -B x Subjects Within Groups 33 44.120 Trials (C) 1 0.294 0.009 -AC 2 25.621 0.807 -C x Subjects Within Groups 33 31.736 Beats (D) 9 47.255 7.071 .01 AD 18 5.081 0.760 -D x Subjects Within Groups 297 6.683 BC 1 65.227 1 .684 ABC 2 256.663 6.627 .01 BC x Subjects Within Groups 33 38.730 BD 9 3.002 0.660 -ABD 18 5.862 1.288 -BD x Subjects Within Groups 297 4.552 CD 9 3.226 0.670 -ACD 18 3.611 0.750 -CD x Subjects Within Groups 297 4.813 BCD 9 1 .927 0.557 -ABCD 18 4.034 1 .165 -BCD x Subjects Within Groups 297 3.461 It is clearly evident from both summaries of analysis of var-iance that the second-by-second method of quantifying data is con-siderably less sensitive than the beat-to-beat method for both the acquisition and extinction procedures. In comparing beat-to-beat HR with second-by-second HR it is obvious that there are short-comings with both methods. Often, the beat-to-beat analysis fails to include all the data within the CS period due to differences between Ss in tonic heart rate. On the other hand, a second-by-second analysis often fails to sample some beats during the CS period. That is, some beats during the CS period are not sampled because they may occur between two sampl-ing points. Moreover, if a beat lasts for more than one second it may be sampled twice. Thus, the second-by-second method of scoring tends to maximize the contribution of slow HR to the data and to minimize the contribution of fast HR. 

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