Exercise and Sexual Arousal in Women

The Effects of Acute Exercise on Physiological Sexual Arousal in Women

Cindy Meston, Ph.D. & Amelia M. Stanton


Over the past two decades, research has demonstrated a strong link between acute exercise and physiological (i.e., genital) sexual arousal in women. In this chapter we provide a summary of the laboratory studies that have examined the effects of acute exercise on sexual arousal in women, and provide a potential explanation for the mechanisms of action underlying this relationship.  In the latter part of this chapter we provide a discussion of the clinical and treatment implications for the facilitatory effect of exercise on women’s sexual response.

Physiological sexual arousal in women

Physiological sexual arousal results from genital vasocongestion, which occurs with increased blood flow to the genitals. When blood begins to pool in the vaginal walls, the increase in blood volume leads to increased pressure inside the capillaries, which subsequently triggers lubricated plasma to transcend the vaginal epithelium onto the surface of the vagina (Levin, 1980). These platelets form droplets, creating the lubricative film that typically covers the vaginal walls during sexual activity. Increased blood flow also leads the clitoris and the vestibular bulbs to protrude and become engorged (Berman, 2005), and well-oxygenated blood is also supplied to the skin and the breasts (Levin, 2002). In addition to increased blood flow, sexual arousal causes relaxation of the smooth muscles in the vaginal wall, which allows the vagina to lengthen and dilate.

A certain level of arousal is required for orgasm, and that level differs by individual. Stimulation by friction and pressure activates specialized nerve endings in the genitals (Krantz, 1958), which generates impulses to the spinal cord and possibly to the vagus nerve (Komisaruk, Gerdes, & Whipple, 1997). According to Levin (2002), researchers do not fully understand how the signals from the nerve endings are converted into sexual pleasure and ultimately to orgasm, but it is known that the afferent impulses of these nerve endings not only create the spinal reflexes that influence genital blood flow, but they also ascend the spinal cord, via the spinothalamic and spinoreticular tracts, to the brain for processing.

Physiological sexual arousal in women is most commonly measured in laboratory studies using a vaginal photoplethysmograph (Sintchak & Geer, 1975). The vaginal photoplethysmograph is a clear acrylic, tampon-shaped device that contains either an incandescent light source, or an infrared light-emitting diode as a light source, and a photosensitive light detector. The light source illuminates the capillary bed of the vaginal wall, and the phototransistor detects the light that is reflected back from the vaginal wall and the blood circulating within it. The amount of back-scattered light is in direct relation to the transparency of engorged and unengorged tissue and thus serves as an indirect measure of vasoengorgement. Simply stated, the greater the back-scattering signal the more blood is assumed to be in the vessels (Levin, 1992). The vaginal probe was designed to be easily inserted by the participant. A positioning shield can be placed on the probe’s cable in order to standardize the depth of insertion between uses,

There are two components of the signal that can be derived from the photplethysmograph. When the signal is coupled to a Direct Current (DC) amplifier, a measure of vaginal blood volume (VBV) is obtained. VBV is believed to reflect slow changes in the pooling of blood in the vaginal tissue (Hatch, 1979). The DC signal is used at low sensitivity and the standard dependent variable is change from levels of VBV at baseline. Because there is no discernible zero point with VBV, absolute measures of blood volume cannot be detected, hence the need to measure in units of blood volume change. When the signal is AC-coupled (alternating current), a measure of vaginal pulse amplitude (VPA) is obtained. VPA is believed to reflect phasic changes in vaginal engorgement with each heartbeat; higher amplitudes indicate higher levels of blood flow (e.g., Geer, Morokoff, & Greenwood, 1974). The dependent variable typically used is the amplitude of the pulse signal, which is measured from the bottom to the top of the pulse wave. As there is no absolute zero point with VPA, analyses are conducted by either averaging across specific stimulus presentations, across the highest 20-30 seconds of arousal, or across selected time periods. The change in mean genital arousal is typically calculated by subtracting the mean VPA to the neutral film from the mean VPA to the erotic film for each set of films in a given study. These values are then standardized within subjects and compared between stimulus categories.

Effect of acute exercise on physiological sexual response

In a series of laboratory studies, Meston and colleagues examined the direct effects of acute exercise on female sexual function. The first of these studies required sexually functional participants to engage in 20 minutes of intense exercise (stationary cycling) prior to viewing a non-sexual and erotic film sequence (Meston & Gorzalka, 1995). The procedure consisted of an orientation screening and questionnaire session, a 20-minute bicycle ergometer fitness test, and then two counterbalanced experimental sessions (Exercise, No-exercise) that took place on different days. During the fitness test, the experimenters determined each participant’s maximum volume of oxygen uptake so that they could have the participants cycle at a constant 70% of their estimated maximum volume during the exercise session. By ensuring that all participants worked at equivalent levels of their maximum volume of oxygen uptake, differences in physiological responses resulting from variations in fitness levels were minimized. In the exercise experimental session, participants cycled for 20 minutes on the stationary bicycle then after the cessation of exercise they inserted the vaginal photoplethysmograph and watched a non-sexual film followed by an erotic film while their vaginal pulse amplitude was measured. From the cessation of exercise to the onset of the erotic film, approximately 15 minutes had passed. In the no-exercise condition, participants sat for 20 minutes, inserted the vaginal photoplethymograph and viewed a second non-sexual and erotic film sequence. The results revealed that VPA was significantly higher during the presentation of the erotic film after exercise than it was during the erotic film in the no-exercise condition. There were no significant differences between conditions in VPA responses during the non-sexual film indicating that exercise did not simply increase blood flow to the genitals but, rather, it prepared the woman’s body for sexual arousal so that when she was in a sexual context (e.g., viewing the erotic film) her body responded more intensely. This was the first finding to provide support for a facilitatory effect of acute exercise on physiological sexual arousal in women.

In a follow-up study, Meston and Gorzalka (1996) examined the effect of timing on the relationship between exercise and increased sexual arousal in women by measuring physiological arousal in response to erotic films at either 5 minutes, 15 minutes, or 30 minutes post-exercise. Each condition consisted of an experimental exercise session and a no-exercise control session. The results revealed that at both 15 and 30 minutes post-exercise there was a significant increase in genital arousal (VPA) to the erotic films compared to the no-exercise control condition. The finding of a significant facilitatory effect at 15 minutes post-exercise replicated Meston and Goralka’s earlier study (1995). However, in contrast to the facilitation noted at 15 and 30 minutes post-exercise, acute exercise inhibited physiological sexual arousal when measured immediately following exercise. The authors noted that, during and immediately following exercise, a decrease in vascular resistance of the working muscles causes a significant increase in blood flow to those muscles (Christensen & Galbo, 1983). Therefore, blood flow may have shifted away from the genital region to temporarily help restore the working muscles. The finding that exercise inhibited genital arousal immediately following exercise but facilitated at 15 and 30 minutes post-exercise led the authors to speculate an optimal time for sexual activity following exercise.

To further explore whether an optimal level of SNS activation from exercise may exist for facilitating sexual arousal in women, Lorenz and colleagues (Lorenz, Harte, Hamilton, & Meston, 2012) performed a secondary analysis of participants from the control conditions of three previously published studies (Hamilton, Fogle, & Meston, 2008; Harte & Meston, 2008; Harte & Meston, 2007). Sympathetic nervous system activity was assessed using heart rate variability, which refers to the degree of variability in the lengths of time between successive heartbeats, and is a useful index of autonomic activity. The degree of variability in the lengths of time between successive heartbeats (HRV) provides important information about the relative balance of sympathetic and parasympathetic forces acting on the heart (Thayer, Yamamoto, & Brosschot, 2010). Participants in all three studies were sexually healthy women. The methodology of each study involved having the participants watch a non-sexual and erotic film sequence while their VPA responses were recorded. As predicted, the results revealed a curvilinear relationship between SNS activity and women’s physiological sexual arousal. That is, moderate increases in SNS activity were associated with greater physiological sexual arousal responses, while low and high SNS activation were associated with lower physiological sexual arousal. These results provide support for the notion that there is an optimal level of SNS activity from acute exercise for the facilitation of genital sexual arousal in women.

Mechanism of action for the facilitation of physiological sexual arousal with exercise

Acute exercise influences a number of bodily systems that could feasibly impact women’s sexual function. Exercise has been shown to affect a variety of hormones such as cortisol (e.g. Hill et al., 2008), estrogen (e.g. Smith, Phipps, Thomas, Schmitz, & Kurzer, 2013), prolactin (e.g. Rojas Vega, Hollmann, & Strüder, 2012), oxytocin (e.g. Hew-Butler, Noakes, Soldin, & Verbalis, 2008), and testosterone (for a review, see Vingren et al., 2012),  all of which have been linked to sexual arousal in women. In a recent study, high levels of cortisol and chronic stress were related to low levels of genital sexual arousal in women (Hamilton & Meston, 2013). Reductions in estradiol during menopause and lactation have been associated with reduced blood flow, vasocongestion, and subsequently lubrication (e.g., Simon, 2011). With respect to testosterone, some studies have concluded that moderate levels of exercise increase free or total testosterone (e.g., Vingren et al., 2009), while others have found no change in testosterone from pre- to post-exercise (e.g., Linnamo, Pakarinen, Komi, Kraemer, & Hakkinen, 2005). In women, testosterone is most often linked to increased sexual desire, but it may also affect the genital tissues. One study demonstrated that women treated with exogenous androgens exhibited increases in genital arousal (Heard-Davison, Heiman, & Kuffel, 2007). Clinically high levels of prolactin have been associated with sexual arousal dysfunction in women, specifically decreased vaginal lubrication, as well as with other sexual problems, including decreased desire, atrophic vaginitis, and anorgasmia (Smith, 2003). Finally, plasma oxytocin levels have been associated with genital sexual arousal; specifically, plasma oxytocin was significantly correlated with vaginal lubrication during the luteal phase of the menstrual cycle, and there was a trend toward statistical significance during the follicular phase (Salonia et al., 2005).

To examine whether changes in testosterone may, in part, account for the increases in genital arousal with exercise, Hamilton, Fogle, and Meston (2008) assessed salivary measures of testosterone at multiple time points during a no-exercise and exercise experimental session. The study methodology was similar to the exercise studies described earlier, with the exception that testing was done between 2:00pm and 6:00pm on days 5 through 10 of the woman’s menstrual cycle in order to control for diurnal and menstrual cycle fluctuations in testosterone. Saliva samples were taken at the start of each session to provide a baseline sample, again 10 minutes after the 20-minute period of vigorous exercise (during the exercise session) and 10 minutes after the pre-testing rest period of the no-exercise session. The findings indicated that testosterone did not increase in response to either exercise or the erotic film. In fact, testosterone remained stable during both the exercise session and the no-exercise session, and there were no differences in testosterone between the two sessions. This suggests that testosterone is not likely the mechanism of action associated with increased genital arousal post-exercise.

It is feasible that sympathetic nervous system (SNS) activation may be driving the association between acute exercise and increased physiological sexual arousal in women. Biochemical and physiologic research indicates diffuse SNS discharge occurs during the later stages of sexual arousal in women (Jovanovic, 1971) with marked increases in heart rate and blood pressure occurring during orgasm (Fox & Fox, 1969). Increases in plasma noradrenaline, a sensitive index of SNS activity, have also been shown to accompany increases in sexual arousal during intercourse (Wiedeking, Ziegler, & Lake, 1979).

Laboratory research that specifically manipulated SNS activity supports the mechanistic role that it may play in female sexual arousal. In one such study 20 sexually functional women participated in two counterbalanced conditions in which they received either placebo or ephedrine sulfate (50 mg), a sympathomimetic amine that stimulates the adrenergic receptor system by increasing the activity of norepinephrine,a norepinephrine, before viewing a non-sexual and erotic film sequence (Meston & Heiman, 1998). Norepinephrine is considered to be the dominant neurotransmitter through which the SNS exerts its effects. As in the prior studies described, physiological sexual responses to the films were measured using vaginal photoplethysmography (VPA). The results revealed ephedrine significantly increased VPA responses to the erotic film compared to placebo, but there were no differences in VPA responses to the non-sexual film with ephedrine. As was the case with exercise, these results suggest that ephedrine did not simply facilitate physiological responses through a general increase in peripheral resistance, but, rather, it selectively prepared the body for genital response.

If SNS activation increases sexual arousal, as suggested by the previous study, it is likely that drugs that decrease SNS activity would also decrease sexual arousal. Moreover, if exercise increases genital arousal via SNS activation, then blocking SNS arousal during exercise would be expected to diminish the enhancing influence of exercise on VPA responses. To test this hypothesis, Meston and colleagues (1997) administered either 0.2mg of clonidine or placebo to 30 sexually functional women in two counterbalanced sessions where they viewed a non-sexual and erotic film sequence. The researchers chose the antihypertensive medication clonidine because it acts centrally as a norepinephrine antagonist and peripherally as an inhibitor of sympathetic outflow. Before viewing the experimental films, half of the participants engaged in 20 minutes of exercise in order to elicit significant SNS activation, and the other half did not exercise. Following heightened SNS activation (via acute exercise), there was a significant decrease in VPA responses to the erotic film in the clonidine compared to placebo condition. Among the participants who did not engage in exercise prior to viewing the film sequence, clonidine showed a non-significant trend toward decreasing VPA responses compared with placebo. Because clonidine has both central and peripheral properties, it is unclear at which level clonidine acted to influence sexual responding (Meston et al., 1997). Centrally, clonidine may have suppressed sexual responses indirectly via changes in neurohypophyseal hormone release, or directly by activating central sites that are responsible for the inhibition of sexual reflexes (Riley, 1995). Peripherally, clonidine may have suppressed sexual arousal by direct inhibition of sympathetic outflow. Support for the latter explanation is provided by the finding that clonidine significantly inhibited sexual responding only when participants were in a state of heightened SNS activity. The fact that clonidine has been reported to significantly inhibit SNS, but not hormonal, responses to exercise (Engelman et al., 1989) is consistent with the suggestion that clonidine acted to inhibit sexual responding via suppressed SNS activity.

Research on sexual function in women following spinal cord injury provides additional support for the relationship between SNS activation and physiological sexual arousal in women. In one study, Sipski and colleagues (2001) assessed the impact of spinal cord injury on genital sexual arousal in women by comparing premenopausal women with spinal cord injuries to able-bodied, age-matched controls. They found that preservation of sensory function in the T11-L2 level of the spinal cord was associated with genital sexual arousal. As sympathetic pathways controlling genital function originate at this level of the spinal cord (Hancock & Peveto, 1979; Nadelhaft & McKenna, 1987; Neuhber, 1982), the authors noted that their findings were consistent with those of Meston and colleagues, who showed that activation of the SNS via exercise (Meston & Gorzalka, 1995, 1996) and ephedrine (Meston & Heiman, 1998) led to increases in genital sexual arousal. Building upon their findings, Sipski and colleagues (2004) assessed the effects of sympathetic stimulation on sexual arousal in women with spinal cord injuries. Because of the physical limitations of the population, the authors used anxiety-eliciting videos, which have been shown to increase genital arousal in sexually dysfunctional women (Palace & Gorzalka, 1990), instead of exercise in order to elicit sympathetic arousal. In women with greater sensory function in the T11-L2 level of the spinal cord, where the sympathetic nerve fibers to the genitals arise, there was a significant effect of the anxiety-inducing film on genital responsiveness; this was not the case for women with low sensory function at the T11-L2 level. The authors interpreted their findings as further evidence for the role of the sympathetic nervous system in the regulation of genital vasocongestion.

Clinical implications of the relationship between SNS activation and female sexual function

    Exercise and sexual arousal in women with a history of childhood sexual abuse

Several clinical populations of women may be directly affected by the observed relationship between acute exercise and increased physiological sexual arousal. One such population is women with histories of childhood sexual abuse (CSA), specifically those who meet diagnostic criteria for posttraumatic stress disorder (PTSD). Individuals with both CSA histories and PTSD diagnoses have increased levels of baseline SNS activity (e.g.,Yehuda, 2003). Given the evidence that there may be an optimal level of SNS activity for the facilitation of sexual arousal in women, Rellini and Meston (2006) investigated the possibility that activating the SNS before sexual arousal in women with a history of CSA and PTSD, who already have high baseline SNS activity, may have a negative impact on their physiological sexual arousal response. The same methodology used in the earlier exercise studies was applied to three groups of women: women with both a CSA history and a PTSD diagnosis, women with a CSA history and no PTSD diagnosis, and a control group of women with no history of CSA or PTSD. As in previous studies (e.g. Meston & Gorzalka, 1995b, 1996), exercise had a significant facilitatory effect on physiological sexual arousal in the control group of women with no history of CSA. However, this effect did not hold for the women who had histories of CSA either with or without coexistent PTSD. In these women, there was no additional increase in physiological sexual arousal to the erotic videos during the exercise visit; to the contrary, there was a non-significant inhibition of sexual arousal responding. The authors speculated that, given these women had elevated baseline SNS activity, increasing SNS activity further, as was the case with exercise, may have put them beyond the optimal level of SNS activation for the facilitation of sexual arousal.  The authors suggested that women with a history of CSA and/or PTSD who are experiencing problems with physiological sexual arousal may benefit from treatment that focuses on decreasing, rather than increasing, SNS activity during sexual activity. This might entail engaging in relaxation exercises prior to engaging in sexual activity.   

Exercise and sexual arousal in women who have undergone hysterectomy

Hysterectomy is the most frequently performed gynecological surgery in many world nations. In the United States, 80% of hysterectomies are intended to treat benign conditions (Merrill, 2008). Reports of positive outcomes of hysterectomies include the cessation of abnormal uterine bleeding, relief from menstrual symptoms and pelvic pain, and decreases in depression and anxiety (for review, see Farquhar & Steiner, 2002). However, some women experience negative symptoms post-hysterectomy, including depression, fatigue, urinary incontinence, constipation, early ovarian failure, and sexual dysfunction (e.g., Thakar, Ayers, Clarkson, Stanton, & Manyonda, 2002). Up to 40% of women report a decrease in their sex life following the surgery (e.g., Dennerstein, Wood, & Burrows, 1977), including lack of vaginal lubrication, loss of libido, and sexual pain. The uterine supporting ligaments contain sympathetic, parasympathetic, sensory, and sensory-motor nerve types and are considered a major pathway for autonomic nerves to the pelvic organs. It is feasible that the negative sexual outcomes following a hysterectomy are a result of the pelvic autonomic nervous being affected through excision of the cervix and separation of the uterus from the cardinal and uterosacral ligaments (Thakar, Manyonda, Stanton, Clarkson, & Robinson, 1997).

If sexual arousal processes are negatively impacted by hysterectomy, and this is associated with autonomic innervation, differences between women who have and have not undergone hysterectomy may emerge under conditions of heightened autonomic arousal. To test this hypothesis, Meston (2002) examined subjective and physiological sexual arousal processes in women with a history of benign uterine fibroids who had or had not undergone hysterectomy using the same study methodology as in the prior exercise studies. Based on research that the uterine supporting ligaments are transected in hysterectomy (Butler-Manuel, Buttery, A’Hern, Polak, & Barton, 2002) and on research indicating that autonomic innervation is important for physiological sexual arousal (Giuliano et al., 2001), Meston (2004) expected that women who have undergone hysterectomy would have an impaired vasocongestive response to erotic stimuli, and that this would be most apparent during the exercise condition. The results revealed that, contrary to Meston’s (2002) hypothesis, exercise significantly increased VPA responses in women who had undergone hysterectomy. Meston (2002) suggested that epinephrine and/or norepinephrine may have been responsible for the findings. Epinephrine and norepinephrine are released from the adrenal medulla during exercise, and they could have feasibly facilitated physiological arousal. Exercise could also have induced changes in endocrine factors, neuromediators, or substances released by endothelial cells (Guiliano et al., 2002). Regardless of the mechanisms that may have been involved, it is clinically relevant that exercise facilitated physiological sexual arousal in women who had undergone hysterectomy. As such, exercise may serve as a non-invasive way to enhance sexual responding in women who experience sexual arousal difficulties post-hysterectomy.

Exercise and sexual arousal in women experiencing antidepressant-induced sexual dysfunction

Women compared to men are at twice the risk for mood and anxiety disorders, and are twice as likely to be prescribed antidepressants for their complaints (Thiels, Linden, Grieger, & Leonard, 2005). In the US, an estimated one in six women has been prescribed an antidepressant (Paulose-Ram, Safran, Jones, Gu, & Orwig, 2007), the most commonly prescribed antidepressants being selective serotonin reuptake inhibitors (SSRIs) and selective norepinephrine reuptake inhibitors (SNRIs). The vast majority of women taking antidepressants (96%) report at least one sexual side effect (Clayton, Keller, & McGarvey, 2006), most commonly decreased desire, decreased arousal, and impaired orgasm. Both SSRIs and SNRIs are associated with these sexual problems, though SNRIs have been shown to have lower rates of arousal and orgasm side effects compared to SSRIs (Serretti & Chiesa, 2009).

The sexual side effects of SSRIs are most likely linked to peripheral nervous system adrenergic pathways (Montejo & Rico-Villademoros, 2008), particularly to changes in SNS activity (Serretti & Chiesa, 2009). Antidepressants, specifically SSRIs, inhibit serotonin (5HT) reuptake via antagonism of the serotonin transporter, which increases synaptic serotonin (Stahl, 1998). It is generally accepted that serotonin diminishes sexual function (e.g., Stahl, 2001), likely due to its inhibitory effect on norepinephrine (Millan, Lejeune, & Gobert, 2000), which is associated with sympathetically-controlled blood vessels (Gothert et al., 1995) and other peripheral nervous system outputs (e.g., Hull, Muschamp, & Sato, 2004). In other words, SSRIs likely suppress SNS activity through norepinephrine release (Shores, Pascualy, Lewis, Flatness, & Veith, 2001) and through sympathetic muscle and vascular nerve firing (Barton et al., 2007). Unlike SSRIs, SNRIs may counter the inhibition of norepinephrine, which occurs due to increased serotonin, by facilitating an increase in the availability of norepinephrine (Licht, Penninx, & De Geus, 2009). Given that moderate SNS activity, compared to very high or very low SNS activity, is associated with increased genital arousal, it follows that SNRIs, which suppress SNS activity less than SSRIs, are associated with lower rates of genital arousal problems than are SSRIs. Though there may be other mechanisms that contribute to the association between SSRIs and negative sexual side effects, SNS activity seems to play a strong role and may therefore be an important intervention target for this population. In addition, interventions that facilitate increased SNS activation affect the peripheral nervous system, so they are less likely to interfere with the central nervous system mechanisms that are presumably responsible for the antidepressants’ beneficial therapeutic effects.

There are few treatment options for women who experience antidepressant-induced sexual dysfunction. Options including adding a drug to try to counteract the side effect, have the patient switch antidepressants in the hopes that a different antidepressant will not have the same side effect, or encourage the patient to take a “drug holiday,” a structured interruption in treatment for a period of time, typically a few days. However, with respect to depression, drug holidays make little pharmacological sense, as they risk withdrawal symptoms, and they may lead to illness relapse (Baldwin & Foong, 2013).

Given the lack of strong treatment options for women with antidepressant-induced sexual problems, acute exercise is a viable intervention. As described earlier, acute exercise activates the SNS, which has been shown to play a mechanistic role in the relationship between antidepressants and adverse sexual side effects (Serretti & Chiesa, 2009). Recently, Lorenz and Meston (2012) examined the effect of acute exercise on genital arousal in women taking either SSRIs or SNRIs. The women participated in three counterbalanced experimental sessions, where they watched an erotic film while their genital sexual arousal (VPA) and their SNS activity was measured. During two of the three sessions, participants exercised for 20 minutes and viewed the non-sexual and erotic film sequence at either 5 minutes post-exercise or 15 minutes post-exercise. One session acted as a control, as women were simply asked to watch the film sequence without exercising. The authors hypothesized that the women who were on SSRIs were more likely to have increased SNS tone compared to their counterparts on SNRIs; therefore, their genital arousal would be greater 5 minutes post-exercise compared to 15 minutes post-exercise. Similarly, they expected that the women who were taking SNRIs would experience some of the benefits of the exercise intervention with respect to genital arousal, but to a lesser extent than those taking SSRIs. They also suggested that women who reported higher levels of impairment in genital arousal would experience the largest gains from the exercise intervention. The results showed that, as the authors hypothesized, SSRIs decrease SNS activity and genital arousal more so than SNRIs. That is, during the no-exercise control session, women taking SSRIs had lower genital arousal and SNS response to sexual stimuli than those taking SNRIs. More importantly, the authors found that, as anticipated, exercise-induced increases in genital arousal were greatest for those women reporting the lowest sexual arousal functioning.

Building upon these findings, a follow up study compared the effects of acute exercise immediately before sexual activity to exercise separate from sexual activity (Lorenz & Meston, 2014). Given that laboratory-based psychophysiological measures of female sexual arousal may not directly map on to reports of sexual function outside of the laboratory, Lorenz and Meston (2014) sought to examine potential differences between the effects of SNS activation on sexual responding (e.g. increased genital blood flow following acute exercise) and the general benefits of exercise on sexuality. Women who were experiencing antidepressant-induced sexual problems were entered into a 9-week trial. For the first 3 weeks, baseline levels of sexual activity were recorded. Participants were then randomized to either 3 weeks of exercise, 3 times a week, immediately prior to sexual activity or 3 weeks of exercise, also 3 times a week, at a time unrelated to sexual activity (at least 6 hours between exercise and sexual activity). The women in this study were provided with a 30-minute strength and cardio exercise video as well as a set of resistance bands in order to standardize the type of exercise across all participants.  Exercise involved … At the end of 3 weeks, participants crossed over to the other exercise condition.

Results revealed that, overall, exercise improved sexual desire, and for women who were experiencing clinically relevant sexual dysfunction at baseline, exercise improved overall sexual function. There was some evidence to suggest that exercise immediately before sexual activity was more beneficial than exercise in general. Overall, the results of this study indicate that exercise improves sexual function in women who report sexual problems due to antidepressant medication use, and there may be an additional benefit to exercising immediately prior to sexual activity.

Summary and Conclusions

The studies presented in this chapter strongly suggest that acute exercise increases physiological sexual arousal in women with normal or low levels of resting SNS activity. The most likely mechanism of action associated with the facilitatory effect of exercise on sexual arousal is SNS activation, although the roles of hormonal and other potential changes that occur with exercise cannot be ruled out. There appears to be an optimal level of SNS activation for the enhancement of genital arousal in women. Specifically, moderate increases in SNS activity have been associated with high physiological sexual arousal responses, while both very low and very high SNS activation are associated with lower physiological sexual arousal.

These findings have important clinical implications. For women who have normal baseline SNS levels and who are having problems becoming sexually aroused, as little as 20 minutes of acute exercise before sexual activity could help improve genital arousal. Acute exercise may also facilitate increased genital arousal in women who may have suppressed sympathetic activation due to hysterectomy, or antidepressant medication use, particularly SSRIs.  As most of the treatment options for women with antidepressant-induced sexual dysfunction are pharmacologic in nature, acute exercise may be a valuable alternative for women seeking to increase their physiological sexual arousal without taking medication.

Drawing on the finding that high levels of SNS activation inhibited blood flow to the genitals, acute exercise prior to sexual activity may not be beneficial for women with high baseline SNS arousal. High SNS arousal is typical of women with high sexual anxiety, posttraumatic stress disorder, and childhood sexual abuse. For these women, treatments that decrease baseline SNS activity and SNS activity during sexual activity may prove more beneficial.

Sexual arousal in women consists of both a genital (i.e. physiological) and psychological (i.e. the experience of being mentally “turned on”) component, and both are important to a woman’s overall sexual experience. This review focused exclusively on genital sexual arousal because the studies presented were almost all conducted within a laboratory setting and the accurate measurement of psychological arousal is difficult to obtain in a contrived laboratory setting.  Although laboratory studies often show a low concordance between physiological and psychological sexual arousal in women (for a review, see Chivers, Seto, Lalumière, Laan, & Grimbos, 2010), we would expected that in a real life sexual scenario feedback from increased genital arousal post-exercise would serve to also enhance the psychological experience of arousal for most women.

It should also be noted that this reviewed focused exclusively on the effects of acute exercise on women’s sexual arousal response. The long-term, chronic effects of exercise on a woman’s sexualityality are also noteworthy. It is widely accepted that constructs such as self-esteem, body image, and body satisfaction are related to women’s sexuality and overall sexual well-being. Exercise has been associated with improvements in self-esteem in both adolescents (e.g., Ekeland, Heian, & Hagen, 2005) and adults (e.g., McAuley, Mihalko, & Bane, 1997). Among healthy individuals, increased exercise has beneficial effects on body image (e.g., Adame & Johnson, 1989), and in women, researchers have noted a significant negative relationship between amount of exercise and body satisfaction (Tiggemann & Williamson, 2000). Exercise has also been linked to increased energy and decreased fatigue (for a review, see (Berger & Motl, 2001), which also play an important role in women’s sexuality.


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