The biomechanics of erections - understanding the veno-occlusive mechanism

I have previously done a deep-dive into how the biochemistry of erection works - including how this biochemistry can be influenced by PGE5-inhibitors such as Viagra and Cialis - as well as hinted on how the processes in the brain that trigger the erectile response works. It’s high time I take you on a tour of the penile anatomy which enables erections - the so-called “Veno-Occlusive” mechanism. 

“Occlusion” refers to the blockage or closing of a blood vessel or hollow organ, restricting the flow of substances through it. Putting a kink in the shower hose or standing on the garden hose - that’s occlusion. Let’s hang on to that image - standing on the garden hose. It’s an apt analogy for what happens inside the penis. 

Inside the penis, there is a thick membrane or fascia called the Tunica Albuginea (TA). The densely packed collagen fibres make this membrane quite stiff - you can literally dangle kilos of weight from it, and only cause it to stretch a tiny bit, as we all know. Inside this membrane are two much thinner balloons called the Corpora Cavernosa (CC). Blood continuously flows into the CC from the pudendal artery, which divides into penile arteries and from these to the cavernosal arteries. Inside the CC, these arteries branch out and form a network of tiny vessels known as arterioles and capillaries, which permeate the erectile tissue. The blood entering the CC fills the spaces within a spongy framework, composed of smooth muscle, fibrous tissues, veins, and arterial spaces, known as the sinusoids.

As sexual arousal occurs, the nervous system triggers the release of neurotransmitters that lead to the relaxation of the smooth muscles within the arterial walls of the cavernosal arteries. This relaxation allows the arteries to dilate, a process known as vasodilation, increasing the blood flow into the sinusoids of the corpora cavernosa. The filling of these spaces with blood causes the CCs to swell and become rigid.

Side note - I wrote extensively about that process of smooth muscle relaxation in a previous post:
https://fenrirgrowth.com/blogs/fenrir/how-erections-work-and-what-viagra-and-cialis-actually-do

 

Simultaneously, the expansion of the corpora cavernosa presses against the tunica albuginea, compressing the subtunical venules against the tough fibrous tissue of the tunica albuginea. This compression significantly reduces the outflow of blood from the penis. The venous blood, which would normally drain the blood from the penis, is trapped, contributing to the maintenance of an erection by keeping the blood within the corpora cavernosa. This mechanism is referred to as the veno-occlusive mechanism. It’s all about those subtunical venules that get trapped between the CC and the TA, meaning blood flow out of the penis gets very rate limited. Blood does escape, but only a trickle. An erection is a low-flow state. The garden hose trapped between your heel and the ground - that’s the venules trapped between the CC and the TA. 

The rigidity of the erection is supported by the structural characteristics of the tunica albuginea itself. The densely packed collagen fibres of the TA, when stretched during the erectile process, provide a constraining force around the corpora cavernosa. This not only helps to maintain the erection but also ensures that the pressure within the corpora cavernosa is sufficiently high to sustain rigidity. I like to think of it as a football (soccer ball for you hand-egg aficionados - though hand-eggs work the same way as real footballs). There is an internal bladder which is highly elastic (the CC), trapped inside a much more rigid shell (the leather of the football, corresponding to the tunica albuginea). When the bladder is deflated, the leather of the football is very pliable. But inflate the bladder, and the football becomes very rigid indeed. 

What happens in the penis is that the many points of outflow (the subtunical venules) get trapped between the bladder and the leather, so hardly anything gets out, and the whole apparatus remains stiff. To shut off the erection, all you need to do is to squeeze down the arterial inflow, which is what happens after an orgasm, when the brain stops telling the arteries to remain dilated, and instead to constrict inflow. As inflow decreases, the pressure on the trapped venules goes down, allowing them to release more blood, with further decreases pressure, etc - until there is a new equilibrium of inflow and outflow. 

Side note about a common source of erectile dysfunction - being nervous! 

Vasoconstriction kills erections. A sudden splash of cold water, or your mother scaring you by opening the front door just as you are in the act, or a hit of nicotine - these are just some of a plethora of vasoconstriction triggers. Being nervous in general, or in a state of high arousal due to stress, causes your sympathetic tone to be high, meaning there is elevated cortisol, elevated norepinephrine, and therefore peripheral vasoconstriction to increase central blood pressure. This is why some of us have a really hard time getting it up whenever we are with a new partner; perhaps we have previously failed to get it up with someone new, and then we get nervous it will happen again, and the nerves cause vasoconstriction, and… self-fulfilling prophecy. That’s why one or two drinks (not more) can help erection quality for people with “nervous erectile dysfunction”, by helping us relax and lower sympathetic tone, increasing vasodilation. 

 

What about the glans and corpus spongiosum? 

There are some details I have glossed over, which I need to add in order for this to be a complete account of the erection process. The CC and TA only account for the rigidity of the erection - the “hard part” inside the penis. But we all know that there are soft parts that inflate too, right? I recently injected Prostaglandin E-1 for the first time, just because I was curious what a chemically induced erection would feel like, and it was very, very interesting indeed to have an erection where only the interior hard part of the penis was erect, but my glans and spongiosum completely flaccid. 

There is no stiff outer membrane in the glans and corpus spongiosum. Instead, they are encased in a much thinner and more pliable membrane called Buck’s Fascia, which wraps around the whole penis. When arterial blood flow is turned up, they get inflated, but because the outflow is still relatively open, you can easily squeeze blood out of them by pinching them. The glans, by the way, is just a continuation of the spongiosum, anatomically speaking. There is some resistance in Buck’s Fascia, so it does slightly limit the outflow rate in the deep dorsal vein, which is squeezed between the tunica albuginea and Buck’s Fascia - but this venous occlusion is nothing near as restrictive as the one between TA and CC. 

The purpose of the Corpus Spongiosum, by the way, is to keep the passage through the urethra unimpeded during intercourse and ejaculation. It holds it open. This is why we so easily leak pre-cum when fully erect. 

Implication for PE  - and a modest proposal about measuring with cockrings

Because Buck’s Fascia isn’t as stiff as the tunica albuginea, it can quite easily be enlarged by repeated supra-physiological inflation; pumping or clamping. Making one’s glans and spongiosum larger is easier by far, than affecting the tunica albuginea. On the other hand, the slightest squeeze will deflate them, so whether it’s all that useful to make them bigger is a question I leave to my readers to debate.

 

Because there isn’t so much restriction of venous outflow, putting on a single weak cockring can actually be enough to inflate the glans and CS to their maximum proportions, which is why I personally love to wear one when having sex. I also think it’s a perfectly fine thing to report your penis size wearing a cockring to ensure you are at full EQ. Fiddling with a phone to take gains photos can easily make you lose glans- and CS inflation in just seconds, which is why I think many people under-report their actual maximum size. We really should make it a norm to wear one single cockring for both BPEL and MSEG measurements, if we struggle to maintain EQ for documentation. I’m not saying to measure after a clamping session - I’m saying to measure immediately after putting on a c-ring to ensure you’re accurately reporting your max size. 

I hope I have in some way contributed to your understanding of the biomechanics of the erection process, and that this understanding makes you marvel at the inventiveness of mother nature when she solves engineering problems such as how to make an organ that can switch from floppy to hard as diamonds in the course of a few heartbeats.