Glans (head) girth growth

I remember looking at quite a few studies using extenders suggesting possibility of erect size gains due to stretched length gains but little to no girth gains. Others on here suggested the possibility of base girth gains via extenders or manual stretches (like hanging). Now newer studies suggest that if there is any girth growth via extenders it’s likely to occur in the glans. I think, I may have gained about .125" in glans girth but it’s really hard to tell, unlike my base where I definitely gained in girth. Anyone on here report any glans size gains from manual stretches or extenders?

"These findings were confirmed by another prospective study conducted by Nikoobakht et al, who found a statistically significant increase in length, both for the flaccid and stretched state, after 3 months of use of Golden Erect extender device. This study failed to demonstrate any significant change in penile girth, too, although it suggested the possibility of glans penis enhancement."

Effect of penile-extender device in increasing penile size in men with shortened penis: preliminary results - PubMed

Wow, very interesting. So perhaps the best way to deform the glans tissues for better expansion/girth is to stretch it in the flaccid state? Should we open up a new area of PE in glans stretches? I’m interested. My glans is all that is lacking in my unit at this point.

I think marinera mentioned that constriction of the noose around the glans may impede circulation and resulting lack of oxygenation may trigger growth:

Length exercises….

That idea is very interesting because it suggests you can sorta alter the shape of your unit, depending on where you apply the constriction. Probably at the base (clamping) you might get girth gains more in the shaft, while constriction just below glans may have a greater effect on the glans? I know when I manually stretch, I feel a lot of pressure along the glans-shaft edge, since I use it as a base/fulcrum.

Hmmmm. What is the “filling” of the glans made of? Simply “spongy tissue” with the capacity to hold blood, or smooth muscle also?

It’s been said around here, by Westla for example, that the lack of fibrous tunica layer around the glans limits it’s growth potential since without a rigid “exoskeleton”, the pressures in the glans will always remain relatively low (since the glans surface simply gives way and expands under the slight pressure increase, keeping internal pressure relatively low). Does this lack of potential for internal pressure reduce the growth potential of the blood-holding cells within the glans?

I can see stretching the glans in flaccid state with manual exercises perhaps being of some use in causing growth. Could such a routine could include lateral stretches too, perhaps?

Just a thought so don’t bite my head off lol , but if all thats missing is an “exoskeleton” then can we not give it one in the form of a condom or something similar? This I would think would give something for the glans to get the pressure up against.

As I said just throwing it out there!

Smooth muscle is an essential component of the sinusoids of the glans penis. If you constrict the area just below the glans, the lack of oxygen may lead to metabolite (osmole) accumulation in smooth muscle cells leading to cell swelling and eventually tissue growth of smooth muscle; that is, as metabolites build up inside cells (intracellular hyperosmolarity) due to lack of oxygen, water will tend to move from outside to inside cell (down concentration gradient) causing cell swelling. This has been shown to occur in many cells. So the vascular occlusion and the resulting cell swelling may be seen as a threat to the structural integrity of cell resulting in protein accretion (as a larger cell with more protein would be able to withstand greater internal tension). It might be a possibility and this means it’s not the pressure per se that is the stimulus except with respect to limiting blood/oxygen supply (ischemia).

Those surgical pictures are mind-boggling!

I am very interested in the deoxygenation theory of penis growth. As we know there was the report of penis hypertrophy in a patient with sickle cell anemia. In this condition, the red blood cells essentially clog up the veins(like we would constrict veins with a clamp or noose) and the result is repeated priapism with penis hypertrophy over time. I personally think that deoxygenation is the growth mechanism is clamping. I know we get a lot of pressure buildup from clamping but honestly I think the tunica is a lot tougher than the arteries carrying blood in. So if the pressure got too high I think the first structures that would fail or stretch would be the arteries and not the tunica because it is tougher. Stretching for length I think is pretty straightforward. Girth is more complicated and I think from the reports of deoxygenation causing girth increases in sickle cell and also when using a noose for an extender we can assume that may be the mechanism.

Definitely a good idea I would think. I was actually going to try it a while back to see if I could get my glans “hardness” to an all time high, I suspect I would if clamping with a condom. Although now the question is: is there any benefit to high internal pressures as far as growth is concerned, or does it simply create rigidity?

Do you know anything of the ideal time for the oxygen deprivation? I’d assume slight constriction for long durations would work better than total constriction for relatively short times. Additionally, since we are wanting the built up metabolites to draw water into the cells, would it be ideal to have a blood filled glans at the time, to provide the water for this process? One disadvantage I can see with this is that b having a blood filled glans you are effectively giving the glans tissue cells a lung-full of oxygen to use, so we’d have to hol the constriction for longer in such a case I guess.

I have no clue about smooth muscle cells. Maybe someone can look through the literature. I will try when I have some more time and if I find anything, I will post it. For skeletal muscle hypertrophy some protocols used:

One study:
"For the acute study (Experiment 1) and the resistance exercise training protocol (Experiment 2), the contraction bout consisted of bilateral knee extension at 20% of the 1-RM. Subjects performed a set of 30 contractions followed by a 30-sec rest, followed by 3 sets of 15 contractions each with 30-sec rest intervals between sets; a total of 75 contractions requiring about 8 minutes. Individual contraction duration was 4 sec with a 2 sec:2 sec shortening-lengthening contraction duty cycle controlled by a metronome. For the LIT-BFR group, blood flow was restricted by a pressure on both legs during training. On the first day of training (Day 1), the belt pressure was 160 mmHg, and the pressure was increased 20 mmHg each day until a final belt pressure of 220 mmHg (Day 4) was achieved [Abe et al., 2006]. The restriction of muscular blood flow was maintained for the entire exercise session, including the rest periods. The belt pressure was released immediately upon completion of the contraction bout."

Second study:
"Training was conducted twice per day (morning and afternoon sessions, with at least 4 h between sessions), 6 days/wk for 3 wk. Following a warm-up, the subjects performed walking (50 m/min for five 2-min bouts, with a 1-min rest between bouts) on a motor-driven treadmill (Fig. 1). The walking speed and duration
remained constant throughout the training period. Subjects in the Kaatsu-walk group wore pressure belts on both legs during training. Before the Kaatsu-walk training, the subjects were seated on a chair, and the belt air pressure was repeatedly set (30 s) and then released (10 s) from initial (120 mmHg) to final (160 mmHg) pressure (described as acute Kaatsu-walk)."

http://www.jsta ge.jst.go.jp/ar … jktr/4/1/1/_pdf
http://jap.phys iology.org/cgi/ … rint/100/5/1460

Good question and I have no clue but the former is better for safety reasons. One wants stimulus for growth, not cell death.

With skeletal muscle, contraction themselves increase the build up of metabolites. Not sure about smooth muscle? Maybe somebody else knows how to maximize metabolite built-up and hence cell/muscle swelling. Again, there’s a lot of speculative stuff based on studies concerning skeletal muscle hypertrophy and even there the mechanisms are speculative. An interesting quote concerning possible mechanisms for skeletal muscle growth:

"In contrast, it could be hypothesized that the changes muscle CSA/volume are the result of increased muscle water; either in the inter- or intravascular
space or within the muscle itself due to the BFR technique. Indeed, resistance exercise with a cuff belt leads to venous pooling and significan cell/muscle swelling."

One other point. Most of the stuff I looked talking about ischemia, cell swelling and hypertrophy are talking about intra-cellular swelling (within cell swelling) not inter-cellular swelling (between cell swelling) or edema. The two processes appear to lead to quite different adaptations. I’m guessing pumping would have more effect on inter-cellular swelling (edema). This process is not associated with hypertrophy, whereas the former is.

It makes me wonder if creatine supplementation could be used with this to further encourage smooth-muscle cell swelling? *Starts searching for “creatine supplementation smooth-muscle”*

There a few studies that show creatine supplementation will effect smooth muscle. Presumably it could encourage smooth muscle hypertrophy too if we took the right steps to getting it absorbed into the cells(take adequate sodium with hih-dose creatine for example immediately before a PE session, with protein and high-GI sugar immediately after for an insulin spike?).

The following study shows that pyloric smooth muscle reduces in size by up to 50% in dehydrated infants:

http://www.umbj ournal.org/arti … 0524-5/abstract

Assuming a similar effect would be observed in most smooth muscle, maybe this highlights the importance of hydration while PE’ing.

I’m very skeptical about creatine supplementation and hypertrophy on smooth muscle primarily because even in skeletal muscle, hypertrophy isn’t all that significant, I think. But here’s one study looking at creatine supplementation on smooth muscle and connective tissue in lungs of mice. Look at Figure 6. in particular:

"Interestingly, besides exacerbating lung inflammation, creatine supplementation further increased the collagen and elastic fibers deposition in airway walls, the smooth muscle thickness, and also the AHR (airway hyperresponsiveness)."

http://ajrcmb.a tsjournals.org/ … eprint/37/6/660

From a brief read I gather that creatine supplementation over a 1 month period will probably increase the collagen fiber and elastic fiber content of soft tissue, as well as the thickness of smooth muscle? What I’m not sure about is why ovalbumin (egg protein) caused a similar change? For PE purposes, would this heightened rate of elastin and collagen formation hurt or help our efforts?

From experience, and from a lot of experimental data, high dosing creatine as a loading phase causes a lot of muscle-cell swelling/water-retension. As much as 5lb will be gained by most athletes during the few days they load for. Alternatively, there is the low dose method which achieves similar intracellular over 30 days (levels that are achieved within a few days with the loading method), but without the cellular water retention. I use the latter method myself for this very reason.