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EDITORIAL COMMENT |
Kinsey Institute for Research in Sex, Gender, and Reproduction, 313 Morrison Hall, University of Indiana, Bloomington, IN 47405
A number of studies have examined endocrine and/or cardiovascular responses during sexual response, mainly in men. Exton and colleagues, in this issue, report the results of a careful study of such responses during both sexual arousal and orgasm in women (1). In reviewing the literature, which focuses predominantly on men, they point out the considerable variability in endocrine response patterns across studies. It remains to be seen whether such variability will also be found in studies of women, but we should in any case consider, as Exton and colleagues do to some extent, the likely sources of such variance.
First, we should not assume consistency when comparing sexual arousal while watching visual erotic stimuli with responses during orgasm in the laboratory, which is usually induced by manual or vibrator stimulation, or responses during coitus, when considerable physical activity may be involved—ie, possible physiological differences related to context. Second, we should be sensitive to the psychological significance of the context; eg, masturbating oneself to orgasm in a laboratory may be associated with a much different emotional response than masturbating to orgasm in the privacy of one’s home or simply watching an erotic film. Issues of embarrassment as well as other aspects of arousal need to be considered. Third, and this is seldom considered in the literature, we should assume, until shown otherwise, that there is individual variability in such response patterns. If that is the case, then, given the small sample sizes that are invariably involved in studies of this kind (often around 10, as in Exton et al.’s study), we should not be surprised to find differences across studies. Such individual differences may also interact with the context so that participation bias may lead to people with a different response pattern volunteering for orgasm studies compared with those who participate in the substantially less emotionally challenging studies of response to visual stimuli.
Exton et al.’s study, although meticulously executed, contains one crucial methodological flaw. By using continuous blood sampling with aliquots collected at 10-minute intervals and by using 10-minute stimulus periods, during the last of which orgasm was induced, they are not able to identify whether changes that occurred during the orgasm time period started before, during, or after orgasm. This is of considerable importance in interpreting the most striking finding in their study, a substantial rise in prolactin that was sustained for a considerable time after orgasm. It is distinctly possible that the prolactin response followed orgasm, in which case it would be of potential theoretical relevance for understanding the postorgasmic state. Change in prolactin in the circulation is difficult to interpret and often has no clear functional significance. However, it may be a useful epiphenomenon acting as a marker of other changes in the neuroendocrine system, as in certain neuroendocrine challenge tests (eg, intravenous l-tryptophan (2)). Central control of prolactin release from the anterior pituitary gland is complex but certainly involves dopaminergic and serotonergic activity. Thus, the increased prolactin in this study could reflect a decrease of hypothalamic dopamine or an increase in hypothalamic serotonin, either or both of which could explain loss of postorgasmic arousability. Interestingly, postorgasmic loss of arousability is generally believed to be less marked in women than in men.
This takes us to another important virtue of Exton et al.’s study: It used a methodology and procedure basically identical to that already reported by this group in a comparable study of men (3). For some reason, no measure of genital response was used in the male study, whereas vaginal pulse amplitude was measured in the female study. Otherwise, the protocols are identical. And, strikingly, a very similar sustained increase in prolactin was found in the men. Clearly, additional studies of this interesting response may shed light on the refractory period in humans.
Generally speaking, these two studies demonstrated similar patterns of response in men and women. Apart from the prolactin change, the most interesting endocrine change was in plasma norepinephrine (NE), which increased around the time of orgasm in both studies. The significance of this pattern is not clear and may be clarified by timing its relationship to orgasm more precisely. Both studies also showed an increase in blood pressure and heart rate, peaking close to orgasm in women and somewhat earlier in men. It is tempting to assume that the NE increase was related to the blood pressure increase, but there is evidence suggesting that, at least in men, the blood pressure increase during sexual response to visual erotic stimuli is related to increased cardiac output rather than increased peripheral resistance, making a NE-mediated effect less likely (4). The authors also consider the possibility that the NE increase may have had an inhibitory effect on sexual response, again contributing to postorgasmic refractoriness. However, the role of NE in sexual response is complex. Whereas peripherally, in the erectile tissue, NE inhibits tumescence, central effects may include sexual arousal. In a study of the effects of intracavernosal prostaglandin E1, men with an apparently psychogenically inhibited response to the injection, quite possibly mediated by increased NE in their erectile tissues (5), had circulating NE levels that were significantly lower than those in the low inhibition group (6). In another study, blood pressure increase in response to visual erotic stimuli was blunted in men with psychogenic erectile dysfunction compared with control subjects. This blunting was normalized by intravenous administration of an alpha-2 antagonist (RS15385) (7), suggesting that the blunted cardiovascular (and erectile) responses in the dysfunctional group were related to an increase in alpha-2 inhibitory tone (and hence a lowering of available NE, at least centrally (8)).
Although there have been a fair number of studies comparing men’s and women’s subjective responses to sexual stimuli (for a meta-analysis of 46 such studies, see Murnen and Stockton (9)), few studies have directly compared male and female physiological response patterns (10–13). Results have been inconsistent and, for various reasons, cannot be considered conclusive.
The issue of whether men and women are the same in these respects is of some theoretical importance. However, what has been lacking is a clear theoretical model that might guide the investigation of such comparisons. In what way, in what situations, and by what mechanisms might we expect men and women to respond differently? For example, a recent theoretical model based on individual differences in the propensity for central inhibition of sexual response in the presence of a threat (14) raises the question of whether men and women differ in inhibition proneness. According to Bjorklund and Kipp (15), women, more predictably than men, show inhibitory patterns of response of various kinds. The combination of a potential gender difference plus the availability of a measure of inhibition proneness would lead to comparative studies in which selection of erotic stimuli (threatening and nonthreatening) and selection of subjects (high and low inhibition proneness in each gender) would result in a design controlling for both context and individual difference, both cited earlier as important causes of variance across studies. Other theoretical models would guide study design and subject selection in a comparable way. With that sort of approach, we may well find comparative studies that are more conclusive as well as informative.
REFERENCES
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