Number 28, 2005
Sex and the Heart

The hemodynamics of sex

Back to the Summary

Ian Eardley
St James University Hospital, Leeds, Yorks, UK
Correspondence: Dr Ian Eardley, Department of Urology, St James University Hospital, Beckett Street, Leeds LS9 7TF, UK.
Tel: +44 (0) 113 2066994, fax: +44 (0) 113 2064920

Introduction
A penile erection is a vascular event in which the degree of tumescence depends upon the balance between arterial inflow and venous outflow, such that when inflow is low and outflow balances it, the penis is flaccid, but when inflow increases and outflow decreases, tumescence occurs. An erection can be initiated in a number of ways. Some form of erotic stimulus, be it visual, auditory, olfactory, or imaginative, can initiate a process that acts via the hypothalamus to initiate descending parasympathetic activity. An alternative neural pathway involves tactile stimulation of the genitals, with afferent impulses traveling via the pelvic nerves to the spinal cord. The efferent nerves that produce an erection are parasympathetic and arise from the 2nd, 3rd, and 4th segments of the sacral spinal cord. They pass forward around the rectum to the pelvic plexus at the base of the bladder. From there, cavernous nerves pass posterolateral to the prostate before leaving the pelvis beneath the pubic arch, where they penetrate the corpora cavernosa of the penis. They then spread out to innervate the smooth muscle, blood vessels, and endothelium of the penis.
When the parasympathetic nerves are activated, they release a cocktail of neurotransmitters that lead to smooth muscle relaxation within the penis [1]. These include acetylcholine, vasoactive intestinal polypeptide, and nitric oxide, of which the last is by far the most important. In addition to this neural release of nitric oxide, during an erection there is also release of nitric oxide from the vascular endothelium surrounding the sinusoidal spaces. The nitric oxide penetrates the smooth muscle cell, where it stimulates the enzyme guanylate cyclase to produce cyclic guanosine 3′5′-monophosphate (cGMP), which is the active second messenger within the cell. The production of cGMP ultimately leads to smooth muscle relaxation.
While the parasympathetic nerves are pro-erectile, the sympathetic nervous system provides the primary anti-erectile innervation, with the main stimulator of smooth muscle contraction within the penis being norepinephrine. In this respect, the actions of the sympathetic and parasympathetic nervous systems are reciprocal.

Vascular changes during erection
The penis is a vascular organ consisting of three tubes, one of which serves primarily to transmit urine, while the other two (the corpora cavernosa) have the primary erectile function. They are anchored to the pelvis, so that they are stable when erect, and they have a tough fibrous outer layer (called the tunica albuginea). They are filled with spongy tissue within which are vascular spaces (sinusoids) surrounded by walls (trabeculae) containing smooth muscle. The sinusoids are lined with endothelium. The main arterial inflow comes via the central penile arteries, which give off several helicine arterioles, which in turn feed the sinusoidal spaces. Venous blood drains from the sinusoidal spaces via a plexus that lies beneath the tunica albuginea, and from which efferent veins penetrate out to the superficial venous system. Passive closure of these venous channels (emissary veins) by the expanding sinusoidal tissue is a crucial part of normal erectile physiology.
When the penis is flaccid, the sympathetic nervous system is dominant in keeping the arterioles constricted and the cavernosal smooth muscle contracted. Blood flow through the penis is low. Erection is brought about under the influence of parasympathetic stimulation, which leads to arteriolar dilatation and trabecular smooth muscle relaxation. Eight separate phases of erection have been identified [2]:

• Phase 0: The flaccid phase – Sympathetic tone predominates. The arterial inflow is low and the trabecular smooth muscle is contracted. The sinusoids are relatively empty at this stage.
• Phase 1: The filling phase – Parasympathetic stimulation leads to arteriolar dilatation, with a massive increase in arterial flow. Trabecular relaxation leads to sinusoidal filling, without any significant increase in intracavernosal pressure.
• Phase 2: The tumescent phase – Parasympathetic stimulation is maintained. As blood continues to pool in the sinusoids, the sinusoidal pressure increases, resulting in a decrease in the arterial inflow. As the pressure increases above diastolic blood pressure, flow continues only during the systolic phase. Furthermore, as the sinusoids expand there is compression of the subtunical venous plexus.
• Phase 3: The full erection phase – The intracavernosal pressure continues to increase to around 90% of systolic blood pressure. The arterial flow into the penis decreases further, but is still greater than during the flaccid phase. The expanding sinusoids compress the subtunical venous plexuses, which results in reduced flow into the emissary veins. The mechanism by which the venous outflow from the penis ceases is called the “veno-occlusive mechanism”.
• Phase 4: The rigid erection phase – Under the influence of the pudendal nerve, the ischiocavernosus muscle contracts, squeezing the crura and increasing the intracavernosal pressure above systolic blood pressure. The penis becomes fully rigid and erect. Arterial inflow ceases and the emissary veins are completely closed, such that the penis acts as a closed space. As the skeletal muscle fatigues, there is a decrease in the intracavernosal pressure back to those values seen during the full erection phase, allowing circulation to return to the cavernosal tissue.
• Phase 5: The initial detumescence phase – There is a small transient increase in intracavernosal pressure, probably induced by sympathetic stimulation against a closed venous outflow.
• Phase 6: The slow detumescence phase – The trabecular smooth muscle contracts, the penile arterioles constrict, and the intracavernosal pressure decreases, leading to reduced compression of the subtunical veins and increased venous outflow.
• Phase 7: The fast detumescence phase – Sympathetic stimulation leads to a rapid decrease in both arterial inflow and intracavernosal pressure, with an increase in venous outflow and rapid detumescence.

Cardiovascular effects of sexual activity
Coitus is physical activity, and there are changes in the blood pressure, heart rate, and cardiac output which reflect this and which have been recognized for some years [3]. Both heart rate and blood pressure increase with foreplay, stimulation, and orgasm and, in general, coital activity produces larger changes than does masturbation. The changes reach a peak during orgasm, but then rapidly return to normal (Table I). There are relatively minor differences relating to the position of the partners during intercourse.

Table I. Cardiovascular consequences of sexual activity (data from [3])

Conclusion
Penile erection is a vascular event under neural control. Parasympathetic stimulation leads to smooth muscle relaxation that results in an active increase in arterial inflow, active relaxation of the cavernosal sinusoids, and a passive reduction in venous outflow (the veno-occlusive mechanism). Sexual activity is accompanied by a modest increase in heart rate and blood pressure, and can be thought of as being “mild” exercise, within the capacity of almost all men.

REFERENCES