Electrodermal recordings during human orgasm

Abstract

We tested the hypothesis that palmar sweat glands activation is expressed every time a mass sympathetic activation takes place. We performed 11 palmar electrodermal recordings during sexual intercourse and orgasm of one male and one female student, and 4 palmar electrodermal plus heart rate recordings during sexual intercourse and orgasm of the same couple. High palmar electrodermal activity was recorded during sexual intercourse but low during orgasm. In opposition, the highest value of heart rate was recorded at the moment of orgasm. We concluded that palmar sweat glands activation may not be considered an indiscriminate consequent of sympathetic discharge.

Introduction

The sweating of palms is not controlled by the same thermoregulatory mechanism which activate the sweat glands of the rest of the body skin areas (Kerassidis, 1994). It can accompany fear, anxiety, tension, discomfort, exploratory and sexual behaviour and it can be triggered by novel stimuli, pain, sudden exposure to cold, emotionally loaded words, and every kind of physical or intellectual effort (Edelberg, 1973; Fowles, 1986). Thus, if the electodermal activity (EDA) can accompany almost everything, the Fowles’ (1986) question whether this function is a complex and noisy manifestation of non-specific activity must be considered justified.
If the non-specific activity hypothesis is true, the palmar sweat glands activation must somehow follow the activity of sympathetic nervous system, since sweat glands are innervated only by sympathetic fibers. It is very possible that palmar and plantar sweating is a residue of the evolution and follows mass sympathetic activation at fight and flight reactions (Cannon's theory). Obviously, if the activation of palmar-plantar sweat glands is an indiscriminate consequent of any mass sympathetic discharge, it carries no specific message about inner processes and the question ‘’why is this local sweating expressed?’’ becomes almost meaningless.
We have to clarify that in this work we do not search the capacity for specificity of the sympathetic nervous system. We consider that it has been approved by many works, like the following: (i) the experiments of Lacey (1967) and Miller (1969a, 1969b), (ii) the establishment that autonomic manifestations differ among anxiety disorders (Hoehn-Saric & McLeod, 1988; Ost, Sterner & Lindahl, 1984), or are not correlated; for example Dawson, Schell, Braaten & Catania (1985) found that depressed patients exhibit higher tonic heart rate levels in parallel with lower tonic skin conductance levels, (iii) the recordings during the REM phase of sleep, where EDA was eliminated, in contrast to all other sympathetic functions which remained at the same levels as in awakening (Johnson & Lubin, 1966; Lester, Burch, & Dossett, 1967; Kushniruk, Rustenburg & Ogilvie, 1985), (iv) the intraneural recordings of sympathetic nerve traffic which have shown that "the view of a diffusely acting system led to the term sympathetic tone is not tenable" (Wallin, 1992; Wallin & Elam, 1994).
However, the capacity for specificity of the sympathetic nervous system does not exclude the possibility that the palmoplantar sweating, a residual of evolution function for humans, is nowadays a non-specific response and it follows the mass sympathetic discharges. Chrousos (1992) mentioned that, to a certain threshold, stressors elicit adaptive responses specific to the nature of the stressor; however, once a certain threshold has been exceeded, a systemic reaction takes place. Probably the EDA is noisy and non-specific to the threshold, and follows mass sympathetic discharges, over that threshold. The study of Shih, Wu & Lin (1983) supports the sympathetic activation theory. In this, it is suggested that subjects hyperhidrotic in their palms have an over-functioning of the sympathetic nervous fibres passing through the 2 and 3 thoracic (T2,3) ganglia, which leads to autonomic dysfunction elsewhere.
In order to check whether palmar sweating follows a mass sympathetic activation that takes place when no benefit of palmar wetting exists, we performed recordings of EDA during orgasm. Orgasm could be considered as a mass sympathetic discharge because (i) the neuronal firing in orgasm is initiated within the L1, L2 sympathetic ganglia (Chusid, 1979; Guyton, 1990) which innervate the low extremities, (ii) the augmentation of heart rate that takes place during orgasm, indicates that fibers passing through upper sympathetic ganglia (which innervate the heart and the upper extremities) are also activated and, (iii) the augmentation of blood pressure is an indication of vasoconstrictor activity and/or of elevation of cardiac output that means sympathetic activation also. Additionally, at the moment of orgasm no benefit for the action of palmar wetting exists, because neither friction improvement (Adelman, Taylor, & Meglung, 1975) nor abrasion prevention (Wilcott 1966) of the palms is demanded. This way, if palmar sweat glands activation takes place at the moment of orgasm, it may be considered as a consequent of mass sympathetic discharge.
It must be mentioned, that the choice of orgasm as a mass sympathetic activation was rather inevitable, in spite of the obvious difficulties that implies. The huge emotional interindividual differences, as response to a stimulus, did not permit any certainty that a chosen stimulus could cause high sympathetic activation without causing a reaction in which palmar wetting could be beneficial to the tested subjects.

Methods
Participants

Obviously, subjects recruitment for recordings of this kind is very difficult. We found only a couple of 1 male and 1 female student. These individuals participated to another work (Kerassidis, Haristou, Kohiadakis, Tzagournissakis & Bitzaraki, 1997), in which they responded to any stimulus (startling, mental, physical) and they were successfully subjected to many clinical and laboratory tests.
We realized that two subjects were very few, but we decided to take the recordings hoping that extended and repeated recordings during sexual intercourse and orgasm would give us the potentiality to compare the moments of high and low EDA with that of orgasm, and that simultaneous recordings of heart rate could reveal whether the moment of orgasm was indeed a moment of high sympathetic activation for the specific individuals or not.
Materials
The first recordings were performed at home with portable recording apparatuses. The chart recorder of Philip-Harris and an Hg battery (E=1.35 V) as an electric source were used. The applied voltage on the students’ fingers was about 0.5-1 V and the current was less than 10 μA cm-2. The electrodes displayed a surface of 1 cm2 and were covered by silver-silver chloride. A cream prepared according to the published recommendations of Fowles, Christie, Edelberg, Grings, Lykken & Venables (1981) based on neutral ointment cream mixed with saline (2:1) was used as the electrolytic media. For simultaneous recordings of EDA and heart rate (HR), a Beckman R 511A was used.
Procedure
Eleven recordings of the EDA of the couple of students were performed in their house, in a long period of time, at different moments of the day. Electrodes were placed on the first phalanxes of the fingers of the left palm of one participant, after cleaning with a cotton immersed to water with alcohol. The person with the recording electrodes lay in bed and held the arm with the electrodes still during the sexual intercourse; she/he removed one out of the two electrodes, as event-marker, after orgasm.
Four additional recordings of palmar EDA and HR, during the sexual intercourse of the same couple, were performed. The HR recording was used as an indicator of the upper sympathetic chain ganglia activity. For these recordings, Beckman recorder was carried in students’ house. The signals for HR recordings were carried through electrodes attached to the left and right forearm and to the chest (ground). At preparatory sessions, it was completely confirmed that no kind of interaction between EDA and HR recordings occurred. The person with the recording electrodes and wires lay in bed and held a passive attitude during the sexual intercourse and gave immediately after orgasm the Beckman's event-marker signal.

Results

The first 11 recordings of sexual intercourse showed that during orgasm, of both participants, the EDA was small or negligible, the skin conductance level (SCL) of the palm was decreased, and when a skin conductance response (SCR) occurred, it was small in relation to the great SCRs during sexual intercourse. In the case shown in Fig.1, for example, during orgasm the SCR is 0,2 μS, but during sexual intercourse, many SCRs, up to 0,6 μS, were recorded. In the case shown in Fig. 2, huge SCRs were recorded at moments of discomfort due to real life problems, while no SCR was recorded during orgasm.
The finding that EDA during orgasm was small in relation to EDA of other moments during sexual intercourse was very important. However, it could not undoubtedly be interpreted as a demonstration that EDA does not indiscriminately follow mass sympathetic activity, because the moments during sexual intercourse of higher recorded EDA could be of higher sympathetic activity in relation to the moment of orgasm. This way, the EDA during orgasm could have been masked.
The simultaneous recording of EDA and HR, of the same couple during sexual intercourse and orgasm, confirmed the previous findings that the EDA during orgasm was small or negligible. However, the value of HR recorded at the moment of orgasm was the highest. In the recordings of the male student, the HR was elevated to 125 pulses min-1 during orgasm (both times) but his EDA was negligible. In the recordings of the female student the HR was elevated to about 100 pulses min-1 during orgasm (both times). The HR of both students was varied (about 60-83 pulses min-1 for the female, and 60-100 pulses min-1 for the male), during sexual intercourse.

Discussion

From the first recordings during sexual intercourse and orgasm it was found that the palmar sweat glands activation was weak during orgasm, for both male and female students, but it was strong, especially at moments of discomfort, during sexual intercourse. The recordings of EDA plus HR during sexual intercourse and orgasm confirmed that the sweat glands activation was weak during orgasm and showed that the recorded HR was maximum at that time.
In general, findings deriving from only two subjects are not rightfully considered enough to sustain a conclusion. The idiosyncrasy of any kind is avoided only by large and representative number of subjects. But in the case of sexual intercourse and orgasm the recruitment of a large number of subjects is very difficult. Of course, the difficulty does not justify the violation of the rule of the large numbers. However, we think that the performed recordings have not brought to light any idiosyncrasy. Everybody can observe that the palms and soles do not sweat at the moments of orgasm as it happens at the moments of discomfort in real life. In addition, the HR recordings showed that the individuals of the present work presented a high sympathetic activation at the moment of orgasm, normally, and as it was theoretically expected. These individuals were subjected to tests like general hematological, blood glucose concentration as well as levels of thyroid hormones (FT3, FT4, TSH) and electrolytes (Na, K, P, Ca, Mg), and neurological examination, and no abnormality was revealed. In addition, as it was mentioned above, they responded to all kind of stimuli that normally cause EDA. It is reasonable to accept that they normally did not present a significant EDA during orgasm, and unjustified that they did not. In the second case, we must explain why especially in these individuals the verified high sympathetic activity during orgasm was not followed by EDA.
The simple and reasonable explanation of the findings is that the mass sympathetic activation which indeed took place at the moment of orgasm did not activate the sweat glands of the palm. Undoubtedly, the sympathetic nervous system may act as a unit: faster heart rate, vasoconstriction, increased blood sugar, discharge of adrenaline, erection of the hairs, sweat glands activation, in ‘’fight’’ and ‘’flight’’ reactions (Cannon’s theory). The capability of mass activation may be the reason of its anatomical unity. But the findings show that the sympathetic nervous system has also the capability of specificity (probably, a later creation of the evolution). As Wallin (1992) mentioned "... the degree of sympathetic differentiation is even greater than previously known; it occurs not only between different tissues but may also occur between different regions of the same tissue. Probably such differences may originate both at spinal and supraspinal levels." In the palmar sweat glands activation, structures of all the levels of the central nervous system are involved (Ladpli & Wang, 1960; Isamat, 1961; Wilcott, 1969; Wilcott & Bradley, 1970; Venables & Christie, 1973; Edelberg, 1973; Delerm, Delsaut & Roy, 1982; Fowles, 1986; Sato, Kang, Saga & Sato, 1989; Weitkunat, Buhrer & Sparrer, 1990; Venables, 1991; Turkstra, 1995). Probably, the highest centers control the palmar sweat glands activation unless otherwise prevented (Venables, 1991) and the whole expression of the function is more complicate than the simple scheme of the general sympathetic arousal view implies.
The recordings showed that the mass and high sympathetic discharge, which takes place in orgasm, did not activate the sweat glands of the palm, and we conclude that palmar EDA may not be considered as an indiscriminate consequent of sympathetic discharge.

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