Journal of Abnormal Psychology 1977, Vol. 86, No. 1, 65-74
A Test of Reciprocal Inhibition: Are Anxiety and Sexual Arousal in Women Mutually Inhibitory? Peter W. Hoon, John P. Wincze, and Emily Franck Hoon Dalhousie University Halifax, Nova Scotia, Canada The purpose of this investigation was to test Wolpe's prediction that autonomic sexual and anxiety arousal states are mutually inhibitory. Using a new physiological measure of female sexual arousal (vaginal blood volume), changes were compared during erotic video stimulation following anxiety and control stimulus preexposure and during anxiety and control stimulation following erotic stimulus preexposure. Consistent with reciprocal inhibition theory, when women were sexually aroused by erotic preexposure, anxiety arousal inhibited sexual arousal more rapidly than did an attention control stimulus. However, contrary to reciprocal inhibition theory, women became more rapidly aroused sexually following anxiety preexposure than following neutral preexposure. In the case of heart rate, changes were compared during erotic and neutral stimulation following anxiety preexposure and during anxiety arousal following erotic and neutral preexposure. Consistent with the literature to date, there were no heart rate changes that could be attributed to differential preexposure. Taken together, the results do not support Wolpe's reciprocal inhibition theory but do suggest a context interpretation: The way in which sexual and anxiety arousal states interact with each other may depend on the context in which subjects perceive the stimuli that generate these respective arousal states. The clinical implications of the findings were discussed. so that it is accompanied by a complete or partial suppression of the anxiety responses, the bond between the stimuli and the anxiety responses will be weakened, (p. 71)
To provide the context for the experiment to be described, let us briefly review Wolpe's original definition of reciprocal inhibition and his use of the construct in clinical applications. Wolpe (1958) defined reciprocal inhibition as follows:
This definition was based on Wolpe's work with cats, which was aimed at determining ways anxiety and avoidance behavior might be reduced. Cats were originally conditioned via shock to display intense fear behavior in an experimental cage. When they were fed in this cage, Wolpe observed that the behavioral correlates of anxiety decreased. Drawing on Hull (1943), Wolpe reasoned that the ensuing reduction of the hunger drive created a measure of conditioned inhibition of the anxiety response and a subsequent weakening of the habit of responding with anxiety to the original cues. When Wolpe (1958) went on to apply the reciprocal inhibition construct to his innovative clinical systematic desensitization procedure, he began to conceptualize reciprocal inhibition as a construct that was operative
If a response antagonistic to anxiety can be made to occur in the presence of anxiety-provoking cues
This work was made possible by grants from the Canada National Research Council and from Carl Abbott of the Dalhousie Medical School. John Wincze is currently at the Department of Psychiatry, Brown University School of Medicine, and at the Veterans Administration Hospital, Providence, Rhode Island. Emily Franck Hoon is currently at the Psychology Department, Nova Scotia Hospital, Dartmouth, Nova Scotia, Canada. The authors wish to express their appreciation to Frances Moriarity, Mary Lynch, Sandy Hodson, and Brenda Van Zoost, who assisted with data reduction and manuscript preparation. Requests for reprints should be sent to Peter Hoon, Psychological Services Center, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4J2.
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P. HOON, J. WINCZE, AND E. HOON
in both behavioral and autonomic dimensions. He proposed that several human emotional states, characterized by parasympathetic arousal (sexual arousal, relaxation, assertion), had associated with them behavior that would inhibit anxiety in the same way food consumption did in his cat experiments. Here Wolpe seems to be acknowledging the behavioral paradigm drawn from Hull (1943), in which the behavioral correlates of these parasympathetic arousal states produce conditioned inhibition over repeated pairings with original anxiety cues. But, in further discussion, Wolpe (1958) alluded to reciprocal inhibition as a process that was simultaneously operative at a neural or autonomic level. Here parasympathetic arousal was said to interfere with sympathetic arousal produced by the anxiety state. That is, parasympathetic arousal competed with sympathetic arousal and diminished it. Though not explicitly stated, it would seem that this conceptualization of reciprocal inhibition paralleled the Pavlovian construct of "irradiation of inhibition" (Hilgard & Bower, 1966, p. 56). It is interesting that Pavlov was never able to provide data in support of this and other neurologically based learning processes (Hilgard & Bower, 1966, p. 59). Wolpe (1958) cited only two sets of observations that seemed to support his notion that parasympathetic and sympathetic arousal states are mutually inhibitory at an autonomic or neural level. One observation was his own unpublished report that during relaxation training, his patients showed pulse rate, respiration, and perspiration decreases (Wolpe, 1958). The other, published observations by Jacobsen (1939, 1940) showed that pulse rate and blood pressure decreases accompanied relaxation training. Although these findings are suggestive, several assumptions underlying Wolpe's theory can be seriously challenged: 1. Failure to clearly link sympathetic and parasympathetic arousal to specified emotional states. Wolpe merely hypothesized that patients' reports of decreased anxiety during relaxation training signified lowered sympathetic arousal. Indeed, important recent studies summarized by Rimm and Masters
(1974, pp. 76-78) seriously question Wolpe's (1958) assumption that sympathetic and parasympathetic arousal states, respectively, are mediated by anxiety and stress on one hand and by sexual arousal, humor, and assertion on the other. 2. Failure to precisely define sympathetic and parasympathetic arousal with physiological measures. Wolpe assumed that when a patient reported being anxious, heart rate and blood pressure would be elevated, and conversely, that when blood pressure and pulse were elevated, a patient was subjectively experiencing a state of anxiety. Recent studies by Leitenberg, Agras, Butz, and Wincze (1971) and Hoon, Wincze, and Hoon (1976) show that these physiological changes may not accompany moderate levels of subjectively reported anxiety. 3. Failure to show that sympathetic and parasympathetic arousal are mutually inhibitory. Assuming for the moment that relaxation procedures do innervate parasympathetic arousal and that sympathetic arousal is simultaneously diminished (as indicated by lowered pulse), Wolpe can at best argue that parasympathetic arousal inhibits sympathetic arousal. If the theory of reciprocal inhibition is truly generalizable, it remains to be shown that sympathetic and parasympathetic arousal are mutually inhibitory regardless of the order in which they occur; that is, whether sympathetic arousal precedes parasympathetic arousal or the reverse. Taking our cue from Mathews (1971) and Paul (1969), we undertook a precise test with physiological measures of the reciprocal inhibition hypothesis in humans. We limited a test of the reciprocal inhibition hypothesis to the context of two arousal states, namely, anxiety and sexual arousal. Furthermore, since the constructs sympathetic and parasympathetic are unsupported generalizations and are unnecessary in testing the reciprocal inhibition hypothesis in the context of anxiety and sexual arousal, they will not be stressed in further portions of this article. To test for reciprocal inhibition within the context of anxiety and sexual arousal, we monitored vaginal blood volume (VBV), a physiological correlate of sexual arousal, and
RECIPROCAL INHIBITION
a second physiological measure (heart rate), which may be differentially innervated by both anxiety and sexual arousal (Obrist, Lawler, and Gaebelein, 1974, pp. 311-334) during the subsequent presentation of an anxiety-evoking and sexually arousing stimulus. We chose sexual arousal as the competing arousal state for two reasons: (a) it makes possible precise, instantaneous, and continuous physiological measurement of female sexual arousal (Geer, Morokoff, & Greenwood, 1974; Wincze, Hoon, & Hoon, in press); and (b) as clinicians, we wanted to determine if reciprocal inhibition might be the operative mechanism underlying the systematic desensitization treatment of female sexual arousal dysfunction (cf. Wincze & Caird, 1976). Four predictions emerge if Wolpe's (1958) theory of reciprocal inhibition holds at the neural or autonomic level: 1. When women are sexually aroused by preexposure to an erotic video sequence, a subsequent anxiety video sequence will produce a lower level and more rapid decline in sexual arousal than a neutral sequence following a similar erotic preexposure. 2. When women are aroused by anxiety preexposure, they will show a lower level and less rapid increase in sexual arousal during subsequent presentation of an erotic sequence than during a similar erotic sequence preceded by neutral preexposure. 3. When women are aroused by anxiety preexposure, sexual arousal produced by subsequent viewing of an erotic sequence will produce a lower level and more rapid decline in heart rate than a neutral stimulation following a similar anxiety preexposure. 4. When women are sexually aroused by erotic preexposure, they will show a lower level and less rapid increase in heart rate during subsequent viewing of an anxiety sequence than during a similar sequence preceded by neutral preexposure. Method Subjects Seven women volunteered and were paid $10 for participation in this investigation. One subject was separated from her spouse, two were single, two
67
were unmarried but living with partners, and two were married. Subjects were sexually experienced. The mean Bentler Heterosexual Experience Scale score (Bentler, 1968) was 18, and reported coital frequencies ranged between 1.6 and 3.2 times per week. All women reported satisfactory sexual functioning. The mean age was 27, and subjects were typically college educated and involved in professional careers.
Experimental Design Each subject was presented, in random order, six videotaped cassette stimulus sequences on a Sony VP-1000 cassette videoplayer. Each sequence included a 1-minute segment during which the word relax was displayed, followed by a 1-minute orientation-stimulus travelogue. Following the orientation stimulus, a preexposure stimulus was presented, followed in turn by the experimental stimulus. Preexposure and experimental stimuli consisted of all possible pairs of three different stimuli: a 2-minute anxiety sequence that depicted in vivid detail the aftermath of several tragic automobile accidents, including occupants' death cries; a 2-minute neutral sequence that depicted a travelogue of Nova Scotia; and a 2-minute erotic sequence that showed a nude couple engaging in foreplay leading up to but not including intercourse. Changeover from preexposure to experimental stimulus was immediate. The content of the anxiety, erotic, and neutral sequences was similar across exposures, but the scenes differed to avoid repetition. The focus of the investigation was on VBV and heart rate changes that took place during the 120 sec of experimental stimulus. The VBV and heart rate data during the last 80 sec of preexposure stimuli were also examined to determine if counterbalancing had been effective prior to the introduction of the experimental stimuli. Changes in sexual arousal (in VBV) during the 80 sec of preexposure and 120 sec of experimental stimuli were examined in four pairs of preexposure and experimental stimuli: (a) erotic to anxiety, (b) erotic to neutral, (c) anxiety to erotic, and (d) neutral to erotic. Sexual arousal changes (in VBV) were compared during the anxiety and neutral sequences after erotic arousal (a and b) and during the erotic sequences after arousal by the neutral and anxiety stimuli (c and d). Since heart rate may be differentially innervated by both anxiety and sexual arousal, a different set of sequences was examined to maximize the sensitivity of a test for reciprocal inhibition with this physiological measure. Heart rate changes were compared at the same times in the following four pairs of preexposure and experimental stimuli: (a) anxiety to erotic, (b) anxiety to neutral, (c) erotic to anxiety, and (d) neutral to anxiety. Here, heart rate changes were compared during erotic and neutral sequences after anxiety preexposure (the first two items above) and during the anxiety
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P. HOON, J. WINCZE, AND E. BOON
sequence following erotic and neutral preexposure (the last two items above).
Apparatus Measurement of sexual arousal was achieved by having subjects insert into their vaginas an acrylic probe similar to that described by Sintchak and Geer (1975), but with improvements. An infrared light-emitting diode (LED) and phototransistor were used in place of an incandescent light source and selenium photocell, respectively. The use of an LED and phototransistor eliminated potential artifacts associated with blood oxygenation level (Weinman, 1967, pp. 185-217) as well as the hysteresis and light history effects frequently associated with selenium detectors (Novelly, Berone, & Ax, 1973). The acrylic vaginal probe measure was shown to be a valid indicator of female sexual arousal in two earlier investigations (Geer et al., 1974; Wincze et al., in press). The relative amount of current passing through the phototransistor depended on the amount of infrared light returning from the vaginal barrel. This reflected light, in turn, depended on the relative degree of vaginal capillary engorgement that was present. Solid-state voltage-regulated circuitry provided a constant current to the LED and amplified the direct-current signal from the phototransistor. Heart rate was recorded by placing each subject's right forefinger inside a Grass PTT1 photoelectric transducer. The resultant alternate current signal was processed by a Grass 7P4-D preamplifier. Both the direct-current signal from the phototransistor and the alternate current heart rate signals were further amplified by Grass 7DAE driver amplifiers. The signals provided pen deflection analogs of sexual arousal and heart rate on two channels of a Grass 79B-8P physiograph. Chart speed was 5 mm/sec.
Procedure Subjects participated singly. They were told that the purpose of the investigation was to learn more about human emotions during exposure to different kinds of videotapes. Subjects inserted the vaginal probe in privacy at the Clinical Research Center at Dalhousie University with the aid of diagrammed instructions. The probe was washed with pHisoDan soap and sterilized with Cidex between uses. A Sony CVM-192U TV monitor was placed on a high table so that subjects could comfortably recline on a couch with a full view of the monitor screen. Subjects were covered with a light cloth blanket and room temperature was kept at a constant 21.7 °C. Subjects lay quietly for about 10 minutes for adaptation before the onset of the experiment and were instructed to remain as still as possible during the session. Two female research assistants conducted the experiment.
Sampling and Data Reduction Subjects' VBV was sampled once per sec in millimeters of deviation from a reference level taken for each subject at the instant of changeover from preexposure to experimental stimulus. Data were taken during the last 80 sec of preexposure stimulus and during the entire 120 sec of experimental stimulus. These data were averaged for each subject separately across 4-sec blocks. Heart rate was determined first in analog form as the distance to the nearest .005 cm between 10 successive photoplethysmographic peaks in accordance with the methodology described by Lockhart (1973). The accuracy of this method was typically within ±.07 beats per minute. Heart rate was sampled every 10 sec during the last 80 sec of preexposure stimulus and during 110 sec of experimental stimulus. Since it was not possible to obtain a 10beat sample for every subject during the last 10 sec of experimental stimulus, heart rate measures were analyzed for 11 10-sec periods. Heart rate analogs were converted to beats per minute prior to statistical analysis.
Results Check on Sources of Internal Invalidity A repeated measures design was used in this investigation in which each subject observed all possible pairs of preexposure and experimental stimuli. It was assumed that a random order of preexposure and experimental stimulus pairs would prevent subjects from being exposed to certain pairs of stimuli sooner than other pairs. This assumption was checked in the following manner: A number between 1 and 6 was assigned to a given sequence depending on the order in which it actually occurred for each subject. Four correlated t tests were computed between these scores for the following four pairs of preexposure and experimental stimuli: (a) erotic followed by anxiety versus erotic followed by neutral, t ( 6 ) = —.76, p > .05; (b) anxiety followed by erotic versus neutral followed by erotic, t ( 6 ) = — .56, p > .05; (c) erotic followed by anxiety versus neutral followed by anxiety, t ( 6 ) = .92, p > .05; (d) anxiety followed by erotic versus anxiety followed by neutral, t ( 6 ) = .61, p > .05. None of these t values reached statistical significance and therefore
RECIPROCAL INHIBITION
there does not appear to have been any accidental sequence effects. Since each subject was exposed to all possible pairs of preexposure and experimental stimuli, a second important assumption was that each subject's level of vaginal capillary engorgement relative to the onset of the experiment was the same at the instant of changeover from the preexposure stimulus to the experimental stimulus. To check this assumption, the polygraph pen was set at 0 just prior to the onset of the relax segment of the first video sequence. Each subject was given a score in millimeters of deviation from this zero point at the four points of changeover from preexposure to experimental stimulus. Correlated t tests were computed between the two pairs of preexposure and experimental stimuli: (a) erotic followed by anxiety versus
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erotic followed by neutral, .OS; and (b) anxiety followed by erotic versus neutral followed by erotic, t ( 6 ) = — 1.51, p > .05. Apparently there were no differences in levels of vaginal capillary engorgement relative to the onset of the experiment at the instant of changeover from preexposure to experimental stimuli. Since conclusions in this experiment are based on many repeated measures across time, the statistical assumption of equality and symmetry of variance-covariance matrixes is in greater danger of being violated than in an experiment using a fewer number of timeunrelated repeated measures (Kirk, 1968). To avoid possible F-test bias, F ratios of time and the Stimulus X Time interaction are based on a conservative degrees of freedom estimate (Geisser & Greenhouse, 1958).
Table 1 Preexposure and Experimental Comparisons for All Sequence Pairs Sequence pairs Dependent measure
Preexposure comparison
Experimental comparison
Time F(l, 12.6) Interaction F(l, 12.6)
2.83 ( d f = l , 90)
< 1.00
< 1.00 (df = 1, 12.9)
< 1.00
< 1.00 (df = 1, 12.9)
1.08
Time F(l, 12.2) Interaction F(l, 12.2) * p < .05. ** p < .005. *** p < .001,
32.74***
37.20***
(df = I , 90)
Anxiety —> erotic, neutral —> erotic Vaginal blood volume Stimulus F(l, 354)
Experimental comparison
Anxiety —» erotic, anxiety —> neutral
Erotic —* anxiety, neutral —> anxiety Heart rate Stimulus F(l, 126)
Preexposure comparison
< 1.00 (df = 1, 12.9)
< 1.00
< 1.00 (df = 1, 12.9)
< 1.00
Erotic —» anxiety, erotic —> neutral
2.81 ( d f = l , 234)
81.89***
3.17 (df-1, 234)
110,42***
< 1.00 (df = 1, 12.3)
6.57*
2.24 (df = 1, 12.3)
12.40**
< 1.00 (df = 1, 12.3)
1.02
< 1.00 (df = 1, 12.3)
< 1.00
P. HOON, J. WINCZE, AND E. HOON
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EXPERIMENTAL
P R E - EXPOSURE STIMULUS
STIMULUS
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Figure 1. Mean vaginal blood volume (VBV) deviation in millimeters (mm) from basal levels across 4-sec blocks during four sequences of stimulus exposure.
A 2 X 20 analysis of variance (ANOVA), Stimuli X 4-Sec Time Block Means, with repeated measures on both factors (Kirk, 1968, p. 237), was computed separately for two pairs of preexposure stimuli in the case of VBV data: (a) the anxiety versus neutral stimulus preceding the erotic experimental stimulus, and (b) the erotic stimulus preceding anxiety versus the erotic stimulus preceding neutral. The purpose of these analyses was to test the assumption that subjects were at similar levels of vaginal capillary engorgement across the last 80 sec of preexposure relative to changeover basal levels. Since F values in Table 1 relevant to this point were not significant, the assumption can be supported. Visual inspection of Figure 1 verifies these statistically based conclusions. In the case of heart rate data, 2 X 7 ANOVAs were computed for the following two pairs of preexposure stimuli: (a) erotic versus neutral stimuli preceding the anxiety experimental stimulus, and (b) the anxiety preexposure stimulus preceding erotic versus the anxiety preexposure stimulus preceding neutral. The purpose of these analyses was to determine whether subjects were at similar heart rate levels across the last 80 sec of pre-
exposure prior to the introduction of the experimental stimuli. Table 1 shows that for (b) only, preexposure differences were highly significant. Unfortunately, due to the law of initial values (Wilder, 1957), this significant preexposure difference precludes a heart rate change score analysis during the experimental stimulus taken from a basal level during preexposure. Also, interpretation of the effects of the experimental stimuli in the case of (b) will have to include the fact that subjects were at different heart rate levels prior to the introduction of the experimental stimuli. Visual inspection of Figure 2 verifies these statistical findings. Analysis of Experimental
Effects
A 2 X 30 ANOVA (Stimuli X 4-Sec Time Block Means) with repeated measures on both variables was computed separately for two- pairs of experimental stimuli in the case of VBV data: (a) anxiety following erotic versus neutral following erotic, and (b) erotic following anxiety versus erotic following neutral. The purpose of this analysis was to determine if anxiety arousal produced greater inhibition of sexual arousal, regardless of
RECIPROCAL INHIBITION
which of these arousal states was present initially. In the case of the above pairs of stimuli, Table 1 shows that stimulus effects were highly significant and that changes across time were consistent with trends in Figure 1. The results in Table 1 and Figure 1 show that when women were sexually aroused by erotic preexposure, subsequent anxiety arousal produced a lower level and more rapid decline in sexual arousal than a neutral, attentioncontrol stimulus. However, women showed a higher level and more rapid increase in sexual arousal following anxiety arousal than following a neutral attention-control stimulus. In the case of heart rate data, a 2 X 11 repeated measures ANOVA was computed for the following two pairs of experimental stimuli: (a) anxiety following erotic versus anxiety following neutral, and (b) erotic following anxiety versus neutral following anxiety.
We assumed that heart rate increases might reflect an anxiety arousal produced by anxiety stimulation and that heart rate decreases might reflect a sexual arousal produced by erotic stimulation (cf. Obrist et al., 1974). The purpose of this analysis, then, was to determine if anxiety and sexual arousal were mutually inhibitory, regardless of which of these arousal states occurred first. The 2 X 7 ANOVA (Stimuli X 10-Sec Time Blocks) of heart rate data for stimulus, time, and Stimulus X Time interaction effects was not significant in the case of the first stimuli pair (a). Erotic preexposure failed to differentially inhibit both heart rate level and acceleration during subsequent anxiety stimulation (see Table 1 and Figure 2). The experimental stimulus effect in a 2 X 7 ANOVA of heart rate data in the case of the second pair (b) was highly significant. Time and Stimulus X Time interaction effects were
EXPERIMENTAL STIMULUS
PRE - EXPOSURE STIMULUS 79 u, 77 t— - 75
«--• Erotic stimulus followed by anxiety stimulus 0-—o Neutral stimulus followed by anxiety stimulus
E 73 1/1
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m
z
*-—* Anxiety stimulus followed by erotic stimulus
82 *
°-—f> Anxiety stimulus followed by neutral stimulus
*
« 80 z 5 78 £
/ \. V
76 74 .a~a-o°
72 70
4
6
8
10 1
3
5
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71
9 11
10 S E C O N D B L O C K S Figure 2. Mean heart rate (HR) across 10-sec blocks during four sequences of stimulus exposure.
P. HOON, J. WINCZE, AND E. HOON
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not significant (see Table 1). It is important to note that the effects of the experimental stimulus must be considered within the context of any preexisting differences during preexposure stimulation. For reasons that are not obvious, counterbalancing during anxiety stimulation prior to experimental stimulation was not effective. Inspection of Figure 2 indicates that the differences between erotic and neutral stimulation following anxiety preexposure are due to the fact that similar differences existed during preexposure. The drop in heart rate during erotic stimulus after anxiety preexposure (see Figure 2) can easily be attributed to the law of initial values, or regression toward the mean. Also, the topography of the heart rate decrease in this instance is erratic, not smooth (see Figure 2). Therefore, the heart rate data show no evidence for an inhibitory effect when erotic arousal follows anxiety arousal. Discussion Psychophysiological Implications Heart rate. The finding that heart rate was not changed by anxiety stimulation is in accord with the conclusions of Obrist et al. (1974). These investigators put forth the view that sympathetic influences on heart rate are normally minimal and that heart rate increases can only be evoked by intense stress. In this investigation, subjects reported in debriefing that the anxiety sequences had been very vivid and anxiety arousing, but other subjects' Likert ratings of similar tapes in comparative investigations imply that both anxiety and sexual arousal were probably present at only moderate levels. Such an interpretation would be consistent with the findings of Klorman, Wiesenfeld, and Austin (1975); Lang (1969, pp. 160-191); and others, who have observed heart rate increases in phobic patients during presentation of feared stimuli. Here, anxiety levels seem to be high enough to produce heart rate increases. Heart rate measurement could be useful in further research aimed at testing for the inhibition effects of relaxation on anxiety arousal, but only if high levels of anxiety are produced.
Our failure to observe heart rate decreases during erotic arousal in this investigation was in accord with our findings in two earlier studies with women (Hoon et al., 1976; Wincze et al., in press) and in accord with conclusions reached by Zuckerman (1971) based on male studies. Assuming for the moment that parasympathetic arousal predominates in initial stages of erotic arousal in women (Kaplan, 1974), we fail to find support for the view of Obrist et al. (1974) that parasympathetic restraining influences on heart rate may be more salient than sympathetic accelerative influences. To summarize, data in this investigation indicated that heart rate was not an adequate correlate of moderate levels of either anxiety or sexual arousal. The topography of heart rate changes also failed to match the smooth topography of VBV changes. Therefore, heart rate did not provide an adequate basis for testing the reciprocal inhibition hypothesis put forth by Wolpe (19S8). The VBV data. The results show that if anxiety arousal is initially present the effect is catalytic, and higher levels of sexual arousal subsequently result. This finding is not consistent with predictions of reciprocal inhibition theory. However, it may be consistent with subjective reports by some men and women that a certain amount of anxiety or tension heightens subsequent enjoyment of sexual activity. Along similar lines, Bancroft (1970) has reported that anxiety can heighten erection in males. On the other hand, if sexual arousal is initially present, subsequent anxiety arousal inhibits it more rapidly than does an attentioncontrol stimulus. This outcome is consistent with reciprocal inhibition and also consistent with subjective reports by men and women that anxiety during sex play can inhibit arousal and subsequent enjoyment of sex. When VBV data are considered in total, they seem to support a theory of context rather than a theory of reciprocal inhibition. When women are erotically aroused, by contrast, they perceive the anxiety stimulus as more aversive and therefore more detrimental to sexual arousal than the neutral stimulus. By the same token, when anxiety levels are
RECIPROCAL INHIBITION
initially increased by exposure to videotapes of traffic accidents, the subsequent erotic stimulus seems more erotic by contrast than when subjects are preexposed to a neutral stimulus. Hence, the way in which anxiety and erotic arousal interact with each other may depend on the context in which subjects perceive the stimuli that generate these arousal states. Alternatively, the findings of this investigation could be interpreted in a more parsimonious manner as the direct interaction between two autonomic arousal states, regardless of the context in which they are generated. If anxiety arousal precedes sexual arousal, subsequent sexual arousal is catalyzed; in the case where sexual arousal precedes anxiety arousal, the effect of subsequent anxiety arousal is to inhibit sexual arousal. Future research may determine whether the context in which arousal states occur is important. Clinical Implications In a recent investigation that examined the efficacy of video and traditional imaginal desensitization, Wincze and Caird (1976) concluded that both methods reduce heterosexual anxiety in women that is associated with coitus and sexual activity in general. These investigators did not propose a specific mechanism. Data from this investigation would suggest that a reciprocal inhibition explanation is not adequate, since subjects in the present investigation, once their anxiety is aroused, become more sexually aroused subsequently. Alternatively, moderate and transitory levels of anxiety arousal (characteristic of normal subjects viewing traffic accidents) may catalyze subsequent sexual arousal, but high levels of anxiety with a lengthy history (typical of clinical patients being exposed to sexual cues) may inhibit sexual arousal. Summary and Conclusions Due to the failure of neutral, anxiety, and erotic stimulation to differentially activate heart rate, this measure failed to provide an adequate basis for testing the reciprocal inhibition hypothesis put forth by Wolpe (1958). On the other hand, vaginal capillary engorgement changed in smooth and consist-
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ent ways when erotic arousal was present and appeared to be a good correlate of sexual arousal. Focusing on the vaginal blood volume findings, if erotic arousal was initially present then subsequent anxiety arousal inhibited it. This outcome was consistent with Wolpe's (19S8) reciprocal inhibition prediction. On the other hand, if anxiety arousal was present initially, the effect was catalytic, and higher levels of erotic arousal were the subsequent result. This outcome was in opposition to the reciprocal inhibition theory prediction. Further research is necessary to determine whether anxiety and relaxation (or assertion) arousal states interact in a similar manner. In any case, the VBV data here cast doubt on Wolpe's implication that anxiety and erotic arousal states are reciprocally inhibitory regardless of the order in which they occur. Actually, the VBV data suggest that the context in which subjects perceive stimuli that generate anxiety and erotic arousal is the important determinant of how these respective arousal states will interact with each other. References Bancroft, J. Disorders of sexual potency. In 0. Hill (Ed.), Modern trends in psychosomatic medicine. New York: Appleton-Century-Crofts, 1970. Bentler, P. Heterosexual behavior assessment: II. Females. Behavior Research and Therapy, 1968, 6, 27-30. Geer, J., Morokoff, P., & Greenwood, P. Sexual arousal in women: The development of a measurement device for vaginal blood volume. Archives oj Sexual Behavior, 1974, 3, 559-564. Geisser, S., & Greenhouse, S. An extension of Box's results on the use of the F distribution in multivariate analysis. Annals of Mathematical Statistics, 1958, 29, 885-891. Hilgard, E., & Bower, G. Theories of learning. New York: Appleton-Century-Crofts, 1966. Hoon, P., Wincze, J., & Hoon, E. Physiological assessment of sexual arousal in women. Psychophysiology, 1976, 13, 196-208. Hull, C. Principles of behavior. New York: Appleton-Century-Crofts, 1943. Jacobsen, E. Variation of blood pressure with skeletal muscle tension and relaxation. Annals of International Medicine, 1939, 12, 1194. Jacobsen, E. Variation of blood pressure with skeletal muscle tension and relaxation. Annals oj InterNational Medicine, 1940, 13, 1619. Kaplan, H. The new sex therapy. New York: Brunner/Mazel, 1974.
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Kirk, R. Experimental design: Procedures for the behavioral sciences. Belmont, Calif.: Brooks/Cole, 1968. Klorman, R., Wiesenfeld, A., & Austin, M. Autonomic responses to affective visual stimuli. Psychophysiology, 1975, 12, 553-560. Lang, P. The mechanics of desensitization and the laboratory study of human fear. In C. M. Franks (Ed.), Behavior therapy: Appraisal and status. New York: McGraw-Hill, 1969. Leitenberg, H., Agras, S., Butz, R., & Wincze, J. Relationship between heart rate and behavioral change during treatment of phobias. Journal of Abnormal Psychology, 1971, 78, 59-68. Lockhart, R. A simple and accurate measurement device for hand scoring of interbeat intervals of the electrocardiogram. Psycho physiology, 1973, 9, 402-411. Mathews, A. Psychophysiological approaches to the investigation of desensitization and related procedures. Psychological Bulletin, 1971, 76, 73-91. Novelly, R., Berone, P., & Ax, A. Photoplethysmography: System calibration and light history effects. Psycho physiology, 1973, 10, 67-73. Obrist, P., Lawler, J., & Gaebelein, C. A psychophysiological perspective on the cardiovascular system. In L. Dicara (Ed.), Limbic and aulonomic nervous systems research. New York: Plenum Press, 1974. Paul, G. Outcome of systematic desensitization. II: Controlled investigations of individual treatment,
technique variations, and current status. In C. M. Franks (Ed.), Behavior therapy: Appraisal and status. New York: McGraw-Hill, 1969. Rimm, D., & Masters, J. Behavior therapy: Techniques and empirical findings. New York: Academic Press, 1974. Sintchak, G., & Geer, J. A vaginal plethysmograph system. Psychophysiology, 1975, 12, 113-115. Weinman, J. Photoyplethysmography. In P. Venables & I. Martin (Eds.), A manual of psychophysiological methods. New York: Wiley, 1967. Wilder, J. The law of initial value in neurology and psychiatry. Journal of Nervous and Mental Disease, 1957, 125, 73-86. Wincze, J., & Caird, W. The effects of systematic desensitization and video desensitization in the treatment of essential sexual dysfunction in women. Behavior Therapy, 1976, 7, 155-166. Wincze, J., Hoon, E., & Hoon, P. A comparison of the physiological responsivity of normal and sexually dysfunctional women during exposure to an erotic stimulus. Journal of Psychosomatic Research, in press. Wolpe, J. Psychotherapy by reciprocal inhibition. Stanford, Calif.: Stanford University Press, 1958. Zuckerman, M. Physiological measures of sexual arousal in the human. Psychological Bulletin, 1971, 75, 347-356.
Received April 22, 1976 Revision received November 3, 1976 •
A Test of Reciprocal Inhibition: Are Anxiety and Sexual Arousal in Women Mutually Inhibitory? Peter W. Hoon, John P. Wincze, and Emily Franck Hoon Dalhousie University Halifax, Nova Scotia, Canada The purpose of this investigation was to test Wolpe's prediction that autonomic sexual and anxiety arousal states are mutually inhibitory. Using a new physiological measure of female sexual arousal (vaginal blood volume), changes were compared during erotic video stimulation following anxiety and control stimulus preexposure and during anxiety and control stimulation following erotic stimulus preexposure. Consistent with reciprocal inhibition theory, when women were sexually aroused by erotic preexposure, anxiety arousal inhibited sexual arousal more rapidly than did an attention control stimulus. However, contrary to reciprocal inhibition theory, women became more rapidly aroused sexually following anxiety preexposure than following neutral preexposure. In the case of heart rate, changes were compared during erotic and neutral stimulation following anxiety preexposure and during anxiety arousal following erotic and neutral preexposure. Consistent with the literature to date, there were no heart rate changes that could be attributed to differential preexposure. Taken together, the results do not support Wolpe's reciprocal inhibition theory but do suggest a context interpretation: The way in which sexual and anxiety arousal states interact with each other may depend on the context in which subjects perceive the stimuli that generate these respective arousal states. The clinical implications of the findings were discussed. so that it is accompanied by a complete or partial suppression of the anxiety responses, the bond between the stimuli and the anxiety responses will be weakened, (p. 71)
To provide the context for the experiment to be described, let us briefly review Wolpe's original definition of reciprocal inhibition and his use of the construct in clinical applications. Wolpe (1958) defined reciprocal inhibition as follows:
This definition was based on Wolpe's work with cats, which was aimed at determining ways anxiety and avoidance behavior might be reduced. Cats were originally conditioned via shock to display intense fear behavior in an experimental cage. When they were fed in this cage, Wolpe observed that the behavioral correlates of anxiety decreased. Drawing on Hull (1943), Wolpe reasoned that the ensuing reduction of the hunger drive created a measure of conditioned inhibition of the anxiety response and a subsequent weakening of the habit of responding with anxiety to the original cues. When Wolpe (1958) went on to apply the reciprocal inhibition construct to his innovative clinical systematic desensitization procedure, he began to conceptualize reciprocal inhibition as a construct that was operative
If a response antagonistic to anxiety can be made to occur in the presence of anxiety-provoking cues
This work was made possible by grants from the Canada National Research Council and from Carl Abbott of the Dalhousie Medical School. John Wincze is currently at the Department of Psychiatry, Brown University School of Medicine, and at the Veterans Administration Hospital, Providence, Rhode Island. Emily Franck Hoon is currently at the Psychology Department, Nova Scotia Hospital, Dartmouth, Nova Scotia, Canada. The authors wish to express their appreciation to Frances Moriarity, Mary Lynch, Sandy Hodson, and Brenda Van Zoost, who assisted with data reduction and manuscript preparation. Requests for reprints should be sent to Peter Hoon, Psychological Services Center, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4J2.
65
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P. HOON, J. WINCZE, AND E. HOON
in both behavioral and autonomic dimensions. He proposed that several human emotional states, characterized by parasympathetic arousal (sexual arousal, relaxation, assertion), had associated with them behavior that would inhibit anxiety in the same way food consumption did in his cat experiments. Here Wolpe seems to be acknowledging the behavioral paradigm drawn from Hull (1943), in which the behavioral correlates of these parasympathetic arousal states produce conditioned inhibition over repeated pairings with original anxiety cues. But, in further discussion, Wolpe (1958) alluded to reciprocal inhibition as a process that was simultaneously operative at a neural or autonomic level. Here parasympathetic arousal was said to interfere with sympathetic arousal produced by the anxiety state. That is, parasympathetic arousal competed with sympathetic arousal and diminished it. Though not explicitly stated, it would seem that this conceptualization of reciprocal inhibition paralleled the Pavlovian construct of "irradiation of inhibition" (Hilgard & Bower, 1966, p. 56). It is interesting that Pavlov was never able to provide data in support of this and other neurologically based learning processes (Hilgard & Bower, 1966, p. 59). Wolpe (1958) cited only two sets of observations that seemed to support his notion that parasympathetic and sympathetic arousal states are mutually inhibitory at an autonomic or neural level. One observation was his own unpublished report that during relaxation training, his patients showed pulse rate, respiration, and perspiration decreases (Wolpe, 1958). The other, published observations by Jacobsen (1939, 1940) showed that pulse rate and blood pressure decreases accompanied relaxation training. Although these findings are suggestive, several assumptions underlying Wolpe's theory can be seriously challenged: 1. Failure to clearly link sympathetic and parasympathetic arousal to specified emotional states. Wolpe merely hypothesized that patients' reports of decreased anxiety during relaxation training signified lowered sympathetic arousal. Indeed, important recent studies summarized by Rimm and Masters
(1974, pp. 76-78) seriously question Wolpe's (1958) assumption that sympathetic and parasympathetic arousal states, respectively, are mediated by anxiety and stress on one hand and by sexual arousal, humor, and assertion on the other. 2. Failure to precisely define sympathetic and parasympathetic arousal with physiological measures. Wolpe assumed that when a patient reported being anxious, heart rate and blood pressure would be elevated, and conversely, that when blood pressure and pulse were elevated, a patient was subjectively experiencing a state of anxiety. Recent studies by Leitenberg, Agras, Butz, and Wincze (1971) and Hoon, Wincze, and Hoon (1976) show that these physiological changes may not accompany moderate levels of subjectively reported anxiety. 3. Failure to show that sympathetic and parasympathetic arousal are mutually inhibitory. Assuming for the moment that relaxation procedures do innervate parasympathetic arousal and that sympathetic arousal is simultaneously diminished (as indicated by lowered pulse), Wolpe can at best argue that parasympathetic arousal inhibits sympathetic arousal. If the theory of reciprocal inhibition is truly generalizable, it remains to be shown that sympathetic and parasympathetic arousal are mutually inhibitory regardless of the order in which they occur; that is, whether sympathetic arousal precedes parasympathetic arousal or the reverse. Taking our cue from Mathews (1971) and Paul (1969), we undertook a precise test with physiological measures of the reciprocal inhibition hypothesis in humans. We limited a test of the reciprocal inhibition hypothesis to the context of two arousal states, namely, anxiety and sexual arousal. Furthermore, since the constructs sympathetic and parasympathetic are unsupported generalizations and are unnecessary in testing the reciprocal inhibition hypothesis in the context of anxiety and sexual arousal, they will not be stressed in further portions of this article. To test for reciprocal inhibition within the context of anxiety and sexual arousal, we monitored vaginal blood volume (VBV), a physiological correlate of sexual arousal, and
RECIPROCAL INHIBITION
a second physiological measure (heart rate), which may be differentially innervated by both anxiety and sexual arousal (Obrist, Lawler, and Gaebelein, 1974, pp. 311-334) during the subsequent presentation of an anxiety-evoking and sexually arousing stimulus. We chose sexual arousal as the competing arousal state for two reasons: (a) it makes possible precise, instantaneous, and continuous physiological measurement of female sexual arousal (Geer, Morokoff, & Greenwood, 1974; Wincze, Hoon, & Hoon, in press); and (b) as clinicians, we wanted to determine if reciprocal inhibition might be the operative mechanism underlying the systematic desensitization treatment of female sexual arousal dysfunction (cf. Wincze & Caird, 1976). Four predictions emerge if Wolpe's (1958) theory of reciprocal inhibition holds at the neural or autonomic level: 1. When women are sexually aroused by preexposure to an erotic video sequence, a subsequent anxiety video sequence will produce a lower level and more rapid decline in sexual arousal than a neutral sequence following a similar erotic preexposure. 2. When women are aroused by anxiety preexposure, they will show a lower level and less rapid increase in sexual arousal during subsequent presentation of an erotic sequence than during a similar erotic sequence preceded by neutral preexposure. 3. When women are aroused by anxiety preexposure, sexual arousal produced by subsequent viewing of an erotic sequence will produce a lower level and more rapid decline in heart rate than a neutral stimulation following a similar anxiety preexposure. 4. When women are sexually aroused by erotic preexposure, they will show a lower level and less rapid increase in heart rate during subsequent viewing of an anxiety sequence than during a similar sequence preceded by neutral preexposure. Method Subjects Seven women volunteered and were paid $10 for participation in this investigation. One subject was separated from her spouse, two were single, two
67
were unmarried but living with partners, and two were married. Subjects were sexually experienced. The mean Bentler Heterosexual Experience Scale score (Bentler, 1968) was 18, and reported coital frequencies ranged between 1.6 and 3.2 times per week. All women reported satisfactory sexual functioning. The mean age was 27, and subjects were typically college educated and involved in professional careers.
Experimental Design Each subject was presented, in random order, six videotaped cassette stimulus sequences on a Sony VP-1000 cassette videoplayer. Each sequence included a 1-minute segment during which the word relax was displayed, followed by a 1-minute orientation-stimulus travelogue. Following the orientation stimulus, a preexposure stimulus was presented, followed in turn by the experimental stimulus. Preexposure and experimental stimuli consisted of all possible pairs of three different stimuli: a 2-minute anxiety sequence that depicted in vivid detail the aftermath of several tragic automobile accidents, including occupants' death cries; a 2-minute neutral sequence that depicted a travelogue of Nova Scotia; and a 2-minute erotic sequence that showed a nude couple engaging in foreplay leading up to but not including intercourse. Changeover from preexposure to experimental stimulus was immediate. The content of the anxiety, erotic, and neutral sequences was similar across exposures, but the scenes differed to avoid repetition. The focus of the investigation was on VBV and heart rate changes that took place during the 120 sec of experimental stimulus. The VBV and heart rate data during the last 80 sec of preexposure stimuli were also examined to determine if counterbalancing had been effective prior to the introduction of the experimental stimuli. Changes in sexual arousal (in VBV) during the 80 sec of preexposure and 120 sec of experimental stimuli were examined in four pairs of preexposure and experimental stimuli: (a) erotic to anxiety, (b) erotic to neutral, (c) anxiety to erotic, and (d) neutral to erotic. Sexual arousal changes (in VBV) were compared during the anxiety and neutral sequences after erotic arousal (a and b) and during the erotic sequences after arousal by the neutral and anxiety stimuli (c and d). Since heart rate may be differentially innervated by both anxiety and sexual arousal, a different set of sequences was examined to maximize the sensitivity of a test for reciprocal inhibition with this physiological measure. Heart rate changes were compared at the same times in the following four pairs of preexposure and experimental stimuli: (a) anxiety to erotic, (b) anxiety to neutral, (c) erotic to anxiety, and (d) neutral to anxiety. Here, heart rate changes were compared during erotic and neutral sequences after anxiety preexposure (the first two items above) and during the anxiety
68
P. HOON, J. WINCZE, AND E. BOON
sequence following erotic and neutral preexposure (the last two items above).
Apparatus Measurement of sexual arousal was achieved by having subjects insert into their vaginas an acrylic probe similar to that described by Sintchak and Geer (1975), but with improvements. An infrared light-emitting diode (LED) and phototransistor were used in place of an incandescent light source and selenium photocell, respectively. The use of an LED and phototransistor eliminated potential artifacts associated with blood oxygenation level (Weinman, 1967, pp. 185-217) as well as the hysteresis and light history effects frequently associated with selenium detectors (Novelly, Berone, & Ax, 1973). The acrylic vaginal probe measure was shown to be a valid indicator of female sexual arousal in two earlier investigations (Geer et al., 1974; Wincze et al., in press). The relative amount of current passing through the phototransistor depended on the amount of infrared light returning from the vaginal barrel. This reflected light, in turn, depended on the relative degree of vaginal capillary engorgement that was present. Solid-state voltage-regulated circuitry provided a constant current to the LED and amplified the direct-current signal from the phototransistor. Heart rate was recorded by placing each subject's right forefinger inside a Grass PTT1 photoelectric transducer. The resultant alternate current signal was processed by a Grass 7P4-D preamplifier. Both the direct-current signal from the phototransistor and the alternate current heart rate signals were further amplified by Grass 7DAE driver amplifiers. The signals provided pen deflection analogs of sexual arousal and heart rate on two channels of a Grass 79B-8P physiograph. Chart speed was 5 mm/sec.
Procedure Subjects participated singly. They were told that the purpose of the investigation was to learn more about human emotions during exposure to different kinds of videotapes. Subjects inserted the vaginal probe in privacy at the Clinical Research Center at Dalhousie University with the aid of diagrammed instructions. The probe was washed with pHisoDan soap and sterilized with Cidex between uses. A Sony CVM-192U TV monitor was placed on a high table so that subjects could comfortably recline on a couch with a full view of the monitor screen. Subjects were covered with a light cloth blanket and room temperature was kept at a constant 21.7 °C. Subjects lay quietly for about 10 minutes for adaptation before the onset of the experiment and were instructed to remain as still as possible during the session. Two female research assistants conducted the experiment.
Sampling and Data Reduction Subjects' VBV was sampled once per sec in millimeters of deviation from a reference level taken for each subject at the instant of changeover from preexposure to experimental stimulus. Data were taken during the last 80 sec of preexposure stimulus and during the entire 120 sec of experimental stimulus. These data were averaged for each subject separately across 4-sec blocks. Heart rate was determined first in analog form as the distance to the nearest .005 cm between 10 successive photoplethysmographic peaks in accordance with the methodology described by Lockhart (1973). The accuracy of this method was typically within ±.07 beats per minute. Heart rate was sampled every 10 sec during the last 80 sec of preexposure stimulus and during 110 sec of experimental stimulus. Since it was not possible to obtain a 10beat sample for every subject during the last 10 sec of experimental stimulus, heart rate measures were analyzed for 11 10-sec periods. Heart rate analogs were converted to beats per minute prior to statistical analysis.
Results Check on Sources of Internal Invalidity A repeated measures design was used in this investigation in which each subject observed all possible pairs of preexposure and experimental stimuli. It was assumed that a random order of preexposure and experimental stimulus pairs would prevent subjects from being exposed to certain pairs of stimuli sooner than other pairs. This assumption was checked in the following manner: A number between 1 and 6 was assigned to a given sequence depending on the order in which it actually occurred for each subject. Four correlated t tests were computed between these scores for the following four pairs of preexposure and experimental stimuli: (a) erotic followed by anxiety versus erotic followed by neutral, t ( 6 ) = —.76, p > .05; (b) anxiety followed by erotic versus neutral followed by erotic, t ( 6 ) = — .56, p > .05; (c) erotic followed by anxiety versus neutral followed by anxiety, t ( 6 ) = .92, p > .05; (d) anxiety followed by erotic versus anxiety followed by neutral, t ( 6 ) = .61, p > .05. None of these t values reached statistical significance and therefore
RECIPROCAL INHIBITION
there does not appear to have been any accidental sequence effects. Since each subject was exposed to all possible pairs of preexposure and experimental stimuli, a second important assumption was that each subject's level of vaginal capillary engorgement relative to the onset of the experiment was the same at the instant of changeover from the preexposure stimulus to the experimental stimulus. To check this assumption, the polygraph pen was set at 0 just prior to the onset of the relax segment of the first video sequence. Each subject was given a score in millimeters of deviation from this zero point at the four points of changeover from preexposure to experimental stimulus. Correlated t tests were computed between the two pairs of preexposure and experimental stimuli: (a) erotic followed by anxiety versus
69
erotic followed by neutral, .OS; and (b) anxiety followed by erotic versus neutral followed by erotic, t ( 6 ) = — 1.51, p > .05. Apparently there were no differences in levels of vaginal capillary engorgement relative to the onset of the experiment at the instant of changeover from preexposure to experimental stimuli. Since conclusions in this experiment are based on many repeated measures across time, the statistical assumption of equality and symmetry of variance-covariance matrixes is in greater danger of being violated than in an experiment using a fewer number of timeunrelated repeated measures (Kirk, 1968). To avoid possible F-test bias, F ratios of time and the Stimulus X Time interaction are based on a conservative degrees of freedom estimate (Geisser & Greenhouse, 1958).
Table 1 Preexposure and Experimental Comparisons for All Sequence Pairs Sequence pairs Dependent measure
Preexposure comparison
Experimental comparison
Time F(l, 12.6) Interaction F(l, 12.6)
2.83 ( d f = l , 90)
< 1.00
< 1.00 (df = 1, 12.9)
< 1.00
< 1.00 (df = 1, 12.9)
1.08
Time F(l, 12.2) Interaction F(l, 12.2) * p < .05. ** p < .005. *** p < .001,
32.74***
37.20***
(df = I , 90)
Anxiety —> erotic, neutral —> erotic Vaginal blood volume Stimulus F(l, 354)
Experimental comparison
Anxiety —» erotic, anxiety —> neutral
Erotic —* anxiety, neutral —> anxiety Heart rate Stimulus F(l, 126)
Preexposure comparison
< 1.00 (df = 1, 12.9)
< 1.00
< 1.00 (df = 1, 12.9)
< 1.00
Erotic —» anxiety, erotic —> neutral
2.81 ( d f = l , 234)
81.89***
3.17 (df-1, 234)
110,42***
< 1.00 (df = 1, 12.3)
6.57*
2.24 (df = 1, 12.3)
12.40**
< 1.00 (df = 1, 12.3)
1.02
< 1.00 (df = 1, 12.3)
< 1.00
P. HOON, J. WINCZE, AND E. HOON
70
EXPERIMENTAL
P R E - EXPOSURE STIMULUS
STIMULUS
A...* Anxiety stimulus followed by erotic
stimulus
A
stimulus
A Neutral stimulus followed by erotic
i—i Erotic stimulus followed by anxiety stimulus o o Erotic stimulus followed by neutral stimulus
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Figure 1. Mean vaginal blood volume (VBV) deviation in millimeters (mm) from basal levels across 4-sec blocks during four sequences of stimulus exposure.
A 2 X 20 analysis of variance (ANOVA), Stimuli X 4-Sec Time Block Means, with repeated measures on both factors (Kirk, 1968, p. 237), was computed separately for two pairs of preexposure stimuli in the case of VBV data: (a) the anxiety versus neutral stimulus preceding the erotic experimental stimulus, and (b) the erotic stimulus preceding anxiety versus the erotic stimulus preceding neutral. The purpose of these analyses was to test the assumption that subjects were at similar levels of vaginal capillary engorgement across the last 80 sec of preexposure relative to changeover basal levels. Since F values in Table 1 relevant to this point were not significant, the assumption can be supported. Visual inspection of Figure 1 verifies these statistically based conclusions. In the case of heart rate data, 2 X 7 ANOVAs were computed for the following two pairs of preexposure stimuli: (a) erotic versus neutral stimuli preceding the anxiety experimental stimulus, and (b) the anxiety preexposure stimulus preceding erotic versus the anxiety preexposure stimulus preceding neutral. The purpose of these analyses was to determine whether subjects were at similar heart rate levels across the last 80 sec of pre-
exposure prior to the introduction of the experimental stimuli. Table 1 shows that for (b) only, preexposure differences were highly significant. Unfortunately, due to the law of initial values (Wilder, 1957), this significant preexposure difference precludes a heart rate change score analysis during the experimental stimulus taken from a basal level during preexposure. Also, interpretation of the effects of the experimental stimuli in the case of (b) will have to include the fact that subjects were at different heart rate levels prior to the introduction of the experimental stimuli. Visual inspection of Figure 2 verifies these statistical findings. Analysis of Experimental
Effects
A 2 X 30 ANOVA (Stimuli X 4-Sec Time Block Means) with repeated measures on both variables was computed separately for two- pairs of experimental stimuli in the case of VBV data: (a) anxiety following erotic versus neutral following erotic, and (b) erotic following anxiety versus erotic following neutral. The purpose of this analysis was to determine if anxiety arousal produced greater inhibition of sexual arousal, regardless of
RECIPROCAL INHIBITION
which of these arousal states was present initially. In the case of the above pairs of stimuli, Table 1 shows that stimulus effects were highly significant and that changes across time were consistent with trends in Figure 1. The results in Table 1 and Figure 1 show that when women were sexually aroused by erotic preexposure, subsequent anxiety arousal produced a lower level and more rapid decline in sexual arousal than a neutral, attentioncontrol stimulus. However, women showed a higher level and more rapid increase in sexual arousal following anxiety arousal than following a neutral attention-control stimulus. In the case of heart rate data, a 2 X 11 repeated measures ANOVA was computed for the following two pairs of experimental stimuli: (a) anxiety following erotic versus anxiety following neutral, and (b) erotic following anxiety versus neutral following anxiety.
We assumed that heart rate increases might reflect an anxiety arousal produced by anxiety stimulation and that heart rate decreases might reflect a sexual arousal produced by erotic stimulation (cf. Obrist et al., 1974). The purpose of this analysis, then, was to determine if anxiety and sexual arousal were mutually inhibitory, regardless of which of these arousal states occurred first. The 2 X 7 ANOVA (Stimuli X 10-Sec Time Blocks) of heart rate data for stimulus, time, and Stimulus X Time interaction effects was not significant in the case of the first stimuli pair (a). Erotic preexposure failed to differentially inhibit both heart rate level and acceleration during subsequent anxiety stimulation (see Table 1 and Figure 2). The experimental stimulus effect in a 2 X 7 ANOVA of heart rate data in the case of the second pair (b) was highly significant. Time and Stimulus X Time interaction effects were
EXPERIMENTAL STIMULUS
PRE - EXPOSURE STIMULUS 79 u, 77 t— - 75
«--• Erotic stimulus followed by anxiety stimulus 0-—o Neutral stimulus followed by anxiety stimulus
E 73 1/1
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m
z
*-—* Anxiety stimulus followed by erotic stimulus
82 *
°-—f> Anxiety stimulus followed by neutral stimulus
*
« 80 z 5 78 £
/ \. V
76 74 .a~a-o°
72 70
4
6
8
10 1
3
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9 11
10 S E C O N D B L O C K S Figure 2. Mean heart rate (HR) across 10-sec blocks during four sequences of stimulus exposure.
P. HOON, J. WINCZE, AND E. HOON
72
not significant (see Table 1). It is important to note that the effects of the experimental stimulus must be considered within the context of any preexisting differences during preexposure stimulation. For reasons that are not obvious, counterbalancing during anxiety stimulation prior to experimental stimulation was not effective. Inspection of Figure 2 indicates that the differences between erotic and neutral stimulation following anxiety preexposure are due to the fact that similar differences existed during preexposure. The drop in heart rate during erotic stimulus after anxiety preexposure (see Figure 2) can easily be attributed to the law of initial values, or regression toward the mean. Also, the topography of the heart rate decrease in this instance is erratic, not smooth (see Figure 2). Therefore, the heart rate data show no evidence for an inhibitory effect when erotic arousal follows anxiety arousal. Discussion Psychophysiological Implications Heart rate. The finding that heart rate was not changed by anxiety stimulation is in accord with the conclusions of Obrist et al. (1974). These investigators put forth the view that sympathetic influences on heart rate are normally minimal and that heart rate increases can only be evoked by intense stress. In this investigation, subjects reported in debriefing that the anxiety sequences had been very vivid and anxiety arousing, but other subjects' Likert ratings of similar tapes in comparative investigations imply that both anxiety and sexual arousal were probably present at only moderate levels. Such an interpretation would be consistent with the findings of Klorman, Wiesenfeld, and Austin (1975); Lang (1969, pp. 160-191); and others, who have observed heart rate increases in phobic patients during presentation of feared stimuli. Here, anxiety levels seem to be high enough to produce heart rate increases. Heart rate measurement could be useful in further research aimed at testing for the inhibition effects of relaxation on anxiety arousal, but only if high levels of anxiety are produced.
Our failure to observe heart rate decreases during erotic arousal in this investigation was in accord with our findings in two earlier studies with women (Hoon et al., 1976; Wincze et al., in press) and in accord with conclusions reached by Zuckerman (1971) based on male studies. Assuming for the moment that parasympathetic arousal predominates in initial stages of erotic arousal in women (Kaplan, 1974), we fail to find support for the view of Obrist et al. (1974) that parasympathetic restraining influences on heart rate may be more salient than sympathetic accelerative influences. To summarize, data in this investigation indicated that heart rate was not an adequate correlate of moderate levels of either anxiety or sexual arousal. The topography of heart rate changes also failed to match the smooth topography of VBV changes. Therefore, heart rate did not provide an adequate basis for testing the reciprocal inhibition hypothesis put forth by Wolpe (19S8). The VBV data. The results show that if anxiety arousal is initially present the effect is catalytic, and higher levels of sexual arousal subsequently result. This finding is not consistent with predictions of reciprocal inhibition theory. However, it may be consistent with subjective reports by some men and women that a certain amount of anxiety or tension heightens subsequent enjoyment of sexual activity. Along similar lines, Bancroft (1970) has reported that anxiety can heighten erection in males. On the other hand, if sexual arousal is initially present, subsequent anxiety arousal inhibits it more rapidly than does an attentioncontrol stimulus. This outcome is consistent with reciprocal inhibition and also consistent with subjective reports by men and women that anxiety during sex play can inhibit arousal and subsequent enjoyment of sex. When VBV data are considered in total, they seem to support a theory of context rather than a theory of reciprocal inhibition. When women are erotically aroused, by contrast, they perceive the anxiety stimulus as more aversive and therefore more detrimental to sexual arousal than the neutral stimulus. By the same token, when anxiety levels are
RECIPROCAL INHIBITION
initially increased by exposure to videotapes of traffic accidents, the subsequent erotic stimulus seems more erotic by contrast than when subjects are preexposed to a neutral stimulus. Hence, the way in which anxiety and erotic arousal interact with each other may depend on the context in which subjects perceive the stimuli that generate these arousal states. Alternatively, the findings of this investigation could be interpreted in a more parsimonious manner as the direct interaction between two autonomic arousal states, regardless of the context in which they are generated. If anxiety arousal precedes sexual arousal, subsequent sexual arousal is catalyzed; in the case where sexual arousal precedes anxiety arousal, the effect of subsequent anxiety arousal is to inhibit sexual arousal. Future research may determine whether the context in which arousal states occur is important. Clinical Implications In a recent investigation that examined the efficacy of video and traditional imaginal desensitization, Wincze and Caird (1976) concluded that both methods reduce heterosexual anxiety in women that is associated with coitus and sexual activity in general. These investigators did not propose a specific mechanism. Data from this investigation would suggest that a reciprocal inhibition explanation is not adequate, since subjects in the present investigation, once their anxiety is aroused, become more sexually aroused subsequently. Alternatively, moderate and transitory levels of anxiety arousal (characteristic of normal subjects viewing traffic accidents) may catalyze subsequent sexual arousal, but high levels of anxiety with a lengthy history (typical of clinical patients being exposed to sexual cues) may inhibit sexual arousal. Summary and Conclusions Due to the failure of neutral, anxiety, and erotic stimulation to differentially activate heart rate, this measure failed to provide an adequate basis for testing the reciprocal inhibition hypothesis put forth by Wolpe (1958). On the other hand, vaginal capillary engorgement changed in smooth and consist-
73
ent ways when erotic arousal was present and appeared to be a good correlate of sexual arousal. Focusing on the vaginal blood volume findings, if erotic arousal was initially present then subsequent anxiety arousal inhibited it. This outcome was consistent with Wolpe's (19S8) reciprocal inhibition prediction. On the other hand, if anxiety arousal was present initially, the effect was catalytic, and higher levels of erotic arousal were the subsequent result. This outcome was in opposition to the reciprocal inhibition theory prediction. Further research is necessary to determine whether anxiety and relaxation (or assertion) arousal states interact in a similar manner. In any case, the VBV data here cast doubt on Wolpe's implication that anxiety and erotic arousal states are reciprocally inhibitory regardless of the order in which they occur. Actually, the VBV data suggest that the context in which subjects perceive stimuli that generate anxiety and erotic arousal is the important determinant of how these respective arousal states will interact with each other. References Bancroft, J. Disorders of sexual potency. In 0. Hill (Ed.), Modern trends in psychosomatic medicine. New York: Appleton-Century-Crofts, 1970. Bentler, P. Heterosexual behavior assessment: II. Females. Behavior Research and Therapy, 1968, 6, 27-30. Geer, J., Morokoff, P., & Greenwood, P. Sexual arousal in women: The development of a measurement device for vaginal blood volume. Archives oj Sexual Behavior, 1974, 3, 559-564. Geisser, S., & Greenhouse, S. An extension of Box's results on the use of the F distribution in multivariate analysis. Annals of Mathematical Statistics, 1958, 29, 885-891. Hilgard, E., & Bower, G. Theories of learning. New York: Appleton-Century-Crofts, 1966. Hoon, P., Wincze, J., & Hoon, E. Physiological assessment of sexual arousal in women. Psychophysiology, 1976, 13, 196-208. Hull, C. Principles of behavior. New York: Appleton-Century-Crofts, 1943. Jacobsen, E. Variation of blood pressure with skeletal muscle tension and relaxation. Annals of International Medicine, 1939, 12, 1194. Jacobsen, E. Variation of blood pressure with skeletal muscle tension and relaxation. Annals oj InterNational Medicine, 1940, 13, 1619. Kaplan, H. The new sex therapy. New York: Brunner/Mazel, 1974.
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Received April 22, 1976 Revision received November 3, 1976 •
