Which muscles have the most androgen receptors ?

ive experimented a dozen different ways on calves, and even when running aas light weight has never been able to produce mass for me. even when performed for extended sessions, like an hour on just calves. the only pro i get when adding light weight high rep to my calves is they get defined as shit, but even then not an oz of meat is added during the process.

This is a post I made years ago but I still think the routine is close to perfection for guys who aren't genetically gifted with calves, give it a go :)



The calves are, arguably, the most genetically determined of all muscle groups, many people train them hard and still can't develop them properly.
I suspect the main reason for this is due to the location of androgen receptors (AR). AR are what testosterone binds to in order to stimulate protein synthesis. In men their is a higher AR density in the upper body, which is why you see shoulders/traps make huge gains when your on gear. However, the calves have a very, VERY low AR density so testosterone can't exert a strong effect here.

The two main muscles your working on the calf are the gastrocnemius (closer to the knee) and the soleus. The gastro gets worked on straight legged exercises (standing calf raise) while the soleus gets worked on bent knee work (seated calf raises).

The routine I recommend for maximum growth (alongside a caloric surplus obviously) is this:

Straight legged calf raise 5 x 5 with MAX weight
3 minutes rest between sets

For this you want to explode up, take a second to squeeze at the top, and then 3 seconds on the negative.
The gastro is a fast twitch muscle so it responds better to heavy loads & explosive movement, you also want to increase the weight with every set.

Donkey/seated calf raise 3 x 8-10
90 sec rest between sets

Here you want 2 seconds on the positive, 1 second pause, and 2 seconds on the negative (2/1/2).
You will probably have to reduce the weight on each set here because of fatigue, which is fine.
The soleus is a slow twitch muscle so it responds better to slow, long sets (you should feel a strong pump with this exercise).

Do this routine twice a week either on their own or after legs and follow it for around 8 weeks before deloading for 2 weeks.

I've had many people get good growth with this routine, so hope it helps :)
 
Sounds much better than what i'm doing now and i'm getting very slow growth. I'm giving it a shot.

In the end genetics have such a huge role as to how easy it is to get freaky calves. I know a guy with just over 20" calves and lean as hell. Looks like you could cut paper on them without them being flexed. He's worked calves twice now in his life....seriously
 
This is a post I made years ago but I still think the routine is close to perfection for guys who aren't genetically gifted with calves, give it a go :)
me


The calves are, arguably, the most genetically determined of all muscle groups, many people train them hard and still can't develop them properly.
I suspect the main reason for this is due to the location of androgen receptors (AR). AR are what testosterone binds to in order to stimulate protein synthesis. In men their is a higher AR density in the upper body, which is why you see shoulders/traps make huge gains when your on gear. However, the calves have a very, VERY low AR density so testosterone can't exert a strong effect here.

The two main muscles your working on the calf are the gastrocnemius (closer to the knee) and the soleus. The gastro gets worked on straight legged exercises (standing calf raise) while the soleus gets worked on bent knee work (seated calf raises).

The routine I recommend for maximum growth (alongside a caloric surplus obviously) is this:

Straight legged calf raise 5 x 5 with MAX weight
3 minutes rest between sets

For this you want to explode up, take a second to squeeze at the top, and then 3 seconds on the negative.
The gastro is a fast twitch muscle so it responds better to heavy loads & explosive movement, you also want to increase the weight with every set.

Donkey/seated calf raise 3 x 8-10
90 sec rest between sets

Here you want 2 seconds on the positive, 1 second pause, and 2 seconds on the negative (2/1/2).
You will probably have to reduce the weight on each set here because of fatigue, which is fine.
The soleus is a slow twitch muscle so it responds better to slow, long sets (you should feel a strong pump with this exercise).

Do this routine twice a week either on their own or after legs and follow it for around 8 weeks before deloading for 2 weeks.

I've had many people get good growth with this routine, so hope it helps :)

awesome post! I'm throwing this in my leg routine starting this week, I will let you know how well it works for me
 
This is a post I made years ago but I still think the routine is close to perfection for guys who aren't genetically gifted with calves, give it a go :)



The calves are, arguably, the most genetically determined of all muscle groups, many people train them hard and still can't develop them properly.
I suspect the main reason for this is due to the location of androgen receptors (AR). AR are what testosterone binds to in order to stimulate protein synthesis. In men their is a higher AR density in the upper body, which is why you see shoulders/traps make huge gains when your on gear. However, the calves have a very, VERY low AR density so testosterone can't exert a strong effect here.

The two main muscles your working on the calf are the gastrocnemius (closer to the knee) and the soleus. The gastro gets worked on straight legged exercises (standing calf raise) while the soleus gets worked on bent knee work (seated calf raises).

The routine I recommend for maximum growth (alongside a caloric surplus obviously) is this:

Straight legged calf raise 5 x 5 with MAX weight
3 minutes rest between sets

For this you want to explode up, take a second to squeeze at the top, and then 3 seconds on the negative.
The gastro is a fast twitch muscle so it responds better to heavy loads & explosive movement, you also want to increase the weight with every set.

Donkey/seated calf raise 3 x 8-10
90 sec rest between sets

Here you want 2 seconds on the positive, 1 second pause, and 2 seconds on the negative (2/1/2).
You will probably have to reduce the weight on each set here because of fatigue, which is fine.
The soleus is a slow twitch muscle so it responds better to slow, long sets (you should feel a strong pump with this exercise).

Do this routine twice a week either on their own or after legs and follow it for around 8 weeks before deloading for 2 weeks.

I've had many people get good growth with this routine, so hope it helps :)

i appreciate that! and holyshit that is heavy as hell. i typically stay around the 12-20 range so that routine should definitely give some shock. i have the nicest calves in my gym but i want those dorian yates style calves ya know. genetics blessed me in the forearm category, my forearm to upper arm ratio is the only aspect of my physique ive really nailed. how long do think people spend on calve routines before bouncing to another routine. ill be honest i hit my calve very hard and i do it twice a week and this is the only way ive had any success with them. i also had to go to a similar routine for my traps to get any real response.
 
Some people say you can tell that someone juices if they have "capped" shoulders. I still dont know wtf that even meens. I guess shoulders have high androgen receptors??
 
apparently shoulders , traps and chest have highest concentration of androgen receptors , hence respond very well to aas with proper training . I was also reading on another thread though that the body already produces even naturaly enough testosterone to occupy most receptors . so one cycle what happens to all the extra test that's hasn't been bound ? Apparently the body produces more receptors to support all the extra test which in theory I guess would lead to more protein synthesis = moer gains and getting bigger . id like to hear more about this
 
good read I found interesting if anyone is interested on the matter .
By Jose Antonio PHD

Everybody knows that anabolic steroids, or what most researchers call androgens, promote muscular growth and produce a man's characteristic "maleness": facial hair, body hair, heavy musculature and, for some, aggressive behavior. (Since women have much less circulating androgen, the effects would be much more profound if they used these hormones.) But how do men get so big? Most sport scientists say that the receptor for testosterone (the androgen receptor) is fully saturated at normal physiological levels, which means that the average guy has enough circulating androgen to bind to all of his receptor sites.

Don't let this science jargon scare you. Think of hormones ***8212; in this case testos-
terone ***8212; as a "key." and its receptor as a "lock" to a door. When testosterone binds
to the androgen receptors in skeletal muscle fibers, it's in essence unlocking a door.
When this door is unlocked, certain physiological processes can occur. In the case of
androgen and androgen receptors, the end result is larger muscles.

Now, if enough keys (androgen) exist for every lock (androgen receptor), then giving someone more keys shouldn't unlock any more doors. Or can we possibly make more doors (androgen receptors) for this powerful hormone to open?

Can the Body Manufacture More Androgen Receptors?

Muscle obviously responds to androgens. Some scientists believe that the differences in muscle mass between the sexes is related to levels of the androgen receptor. Men have more and should therefore be sensitized to circulating androgen. It has been postulated that the shoulder (deltoids, trapezius) and pectoral muscles exhibit higher androgen receptor levels in males than in females, which might explain some of the differences in upper-body size between men and women.
A number of researchers believe that if the androgen receptor is saturated at normal physiological amounts, then any excess androgen would only down-regulate (decrease the number or affinity of) the receptor. But androgens don't have the same response in all tissues. For example, a down-regulation of androgen receptors in the penis takes place in response to androgen. It makes sense that as circulating androgens rise in a developing animal, the level of androgen receptors in the penis would decrease along with androgen-induced growth. As the penis reaches adult size, it consequently becomes insensitive to the anabolic effects of androgen.
But is this what occurs in muscle tissue? Probably not. Androgens seem to exert their anabolic effects through multiple mechanisms. One possibility is that if you take exogenous androgen (that is, oral or injectable anabolic steroids), you may actually increase the level of androgen receptors present in skeletal muscle. If you have more receptors, you'd have an enhanced anabolic effect as a result of steroid use.
In some of my rat subjects, the androgen receptor levels are decreased in certain skeletal muscles ***8212; when you take away almost all of the animals' normal circulating lestos-terone, they end up with fewer receptors. So guess what happens when you give these rats androgens? They up-regulate, or increase the number of androgen receptors.
Big deal, you say. This is just a bunch of chemistry gob-bledygook. Well, if you've been paying attention, you'll see how this scenario might explain why taking greater and greater doses of androgens produces larger and more muscular bodybuilders. A plateauing effect of androgens doesn't seem to occur: The more you take, the more receptors you make, the more sensitized your muscles become and the bigger you get. It becomes a constant anabolic cycle.
Although not proven scientifically, this may explain some of the profound effects seen with steroid use among bodybuilders.

The Abortion Pill: an Anabolic Agent?

Androgens can bind to other receptors, too. Think of this process as being like having a key that fits really well in one door, but if you jiggle and wiggle it a little you can open other locks as well. For instance, androgens may actually bind with receptor sites for glucoconicoids, which would then have an anticatabolic effect. RU486 (the French abortion pill) has been shown to block the glucocorticoid receptor and have anticatabolic properties in skeletal muscle. In fact, some scientists believe this blocking of anticatabolic receptors to be the most important way in which steroids affect muscle. If that's true you'd think the use of RU486 would be prevalent among serious athletes and bodybuilders, but it isn't.
The bottom line is that androgens may act physiologically through many avenues to produce potent anabolic effects. Given their effects on androgen receptors and their ability to block the effects of muscle-wasting hormones via the glucocorticoid receptor, you're dealing with a very powerful hormone. Just look at today's elite bodybuilders and you'll see what I mean.
 
But is this what occurs in muscle tissue? Probably not. Androgens seem to exert their anabolic effects through multiple mechanisms. One possibility is that if you take exogenous androgen (that is, oral or injectable anabolic steroids), you may actually increase the level of androgen receptors present in skeletal muscle. If you have more receptors, you'd have an enhanced anabolic effect as a result of steroid use.
In some of my rat subjects, the androgen receptor levels are decreased in certain skeletal muscles ***8212; when you take away almost all of the animals' normal circulating lestos-terone, they end up with fewer receptors. So guess what happens when you give these rats androgens? They up-regulate, or increase the number of androgen receptors.
Big deal, you say. This is just a bunch of chemistry gob-bledygook. Well, if you've been paying attention, you'll see how this scenario might explain why taking greater and greater doses of androgens produces larger and more muscular bodybuilders. A plateauing effect of androgens doesn't seem to occur: The more you take, the more receptors you make, the more sensitized your muscles become and the bigger you get. It becomes a constant anabolic cycle.
Although not proven scientifically, this may explain some of the profound effects seen with steroid use among bodybuilders.

I would ignore all this "aas creates more androgen receptors" and receptors get "downregulated" bullshit.
Rat studies dont mean a thing.
The guy also admits that none of this has been scientifically proven.

All interesting theories, all are non-applicable in real life :)
 
I would ignore all this "aas creates more androgen receptors" and receptors get "downregulated" bullshit.
Rat studies dont mean a thing.
The guy also admits that none of this has been scientifically proven.

All interesting theories, all are non-applicable in real life :)

I agree. Id pay more attention to something like this that proves that in the presence of excess androgens the androgen receptor half life doubles as does the rate of production of new androgen receptors. People seem to be under the mistaken belief that there are androgen receptors and they are just there forever etc. The fact is they are constantly replaced. Anyway this pretty much disproves any down regulation nonsense as well as supports an increase in both AR receptors as well as their life span in the presence of excess androgen. So in spite of the lack of scientific evidence the gentleman we both agree that does not properly support his contentions is in fact pretty much correct.

J Biol Chem. 1985 Jan 10;260(1):455-61.
Mechanism of androgen-receptor augmentation. Analysis of receptor synthesis and degradation by the density-shift technique.
Syms AJ, Norris JS, Panko WB, Smith RG.
The ductus deferens smooth muscle tumor cell line (DDT1MF-2) contains receptors for, and is stimulated by, androgens. Cells cultured in the absence of androgens maintain a basal level of androgen receptors. Following incubation with various concentrations of the synthetic androgen methyltrienolone (R1881) for 1-6 h, the concentration of these receptors increased from 6.0 to 12.2 fmol/micrograms of DNA, while the equilibrium dissociation constant (Kd) of 0.5 nM for this steroid remained unchanged. The steroid-induced increase in androgen receptor levels was specific for androgens and dependent upon protein synthesis. The mechanism of receptor augmentation was examined by utilization of isotopically dense amino acids to determine rates of receptor appearance and degradation in the presence or absence of [3H]R1881. In the absence of androgens, the half-life of the androgen receptor was 3.1 h, with a rate constant (kD) of 0.22/h. In the presence of 1 nM [3H]R1881, however, the half-life was 6.6 h, with kD = 0.11/h. The rate constant for receptor synthesis (ks) in the absence or presence of [3H]R1881 was calculated to be 1.35 and 2.23 fmol/micrograms of DNA/h, respectively. Thus, androgen-induced androgen-receptor augmentation is explained by an increase both in receptor half-life and in rates of receptor synthesis.
 
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I agree. Id pay more attention to something like this that proves that in the presence of excess androgens the androgen receptor half life doubles as does the rate of production of new androgen receptors. People seem to be under the mistaken belief that there are androgen receptors and they are just there forever etc. The fact is they are constantly replaced. Anyway this pretty much disproves any down regulation nonsense as well as supports an increase in both AR receptors as well as their life span in the presence of excess androgen. So in spite of the lack of scientific evidence the gentleman we both agree that does not properly support his contentions is in fact pretty much correct.

J Biol Chem. 1985 Jan 10;260(1):455-61.
Mechanism of androgen-receptor augmentation. Analysis of receptor synthesis and degradation by the density-shift technique.
Syms AJ, Norris JS, Panko WB, Smith RG.
The ductus deferens smooth muscle tumor cell line (DDT1MF-2) contains receptors for, and is stimulated by, androgens. Cells cultured in the absence of androgens maintain a basal level of androgen receptors. Following incubation with various concentrations of the synthetic androgen methyltrienolone (R1881) for 1-6 h, the concentration of these receptors increased from 6.0 to 12.2 fmol/micrograms of DNA, while the equilibrium dissociation constant (Kd) of 0.5 nM for this steroid remained unchanged. The steroid-induced increase in androgen receptor levels was specific for androgens and dependent upon protein synthesis. The mechanism of receptor augmentation was examined by utilization of isotopically dense amino acids to determine rates of receptor appearance and degradation in the presence or absence of [3H]R1881. In the absence of androgens, the half-life of the androgen receptor was 3.1 h, with a rate constant (kD) of 0.22/h. In the presence of 1 nM [3H]R1881, however, the half-life was 6.6 h, with kD = 0.11/h. The rate constant for receptor synthesis (ks) in the absence or presence of [3H]R1881 was calculated to be 1.35 and 2.23 fmol/micrograms of DNA/h, respectively. Thus, androgen-induced androgen-receptor augmentation is explained by an increase both in receptor half-life and in rates of receptor synthesis.

That's more like it :)
Although I'm not aware of those results being replicated in vivo, so we're assuming it will still be the same.

So if we accept that it is possible to increase androgen receptors, and that any sort of "downregulation" is a myth, is it possible to apply this in a selective manner?
So rather than increase androgen receptors in general, can we increase them in select areas like the calves or other lagging bodyparts?

I'm pretty sure there are no definitive answers to these questions but am always interested in your views Jimi.
 
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Some people say you can tell that someone juices if they have "capped" shoulders. I still dont know wtf that even meens. I guess shoulders have high androgen receptors??

man I agree with everyone about certain areas showing more evidence than others, but genetics, and smart training play a huge part in shoulders and shoulder caps. show me someone with good shoulders and nice caps and I'll show you someone who trains good form and never skips lateral raises on shoulder day. 2cnts. :)
 
What about quads and the rest of our leg since they are predisposed to being some of the most active muscles in our body?
 
That's more like it :)
Although I'm not aware of those results being replicated in vivo, so we're assuming it will still be the same.

So if we accept that it is possible to increase androgen receptors, and that any sort of "downregulation" is a myth, is it possible to apply this in a selective manner?
So rather than increase androgen receptors in general, can we increase them in select areas like the calves or other lagging bodyparts?


I'm pretty sure there are no definitive answers to these questions but am always interested in your views Jimi.

If this was the case site injections of androgens would lead to increases in actual muscle in the muscle where the injection was administered. As anecdotal as it is I think and size increase due to site injections is more from oil volume and inflammation as opposed to actual AR # and life being increased so my opinion on that would be no, we cannot selectively increase the numbers and lifespan in a site specific fashion.
The thing is this as well, the activation of the AR is not a merely site specific phenomenon. The effects are systemic in many ways so AR # in certain muscle groups is not necessarily the sole or defining reason for muscle hypertrophy or the ease or difficulty of muscle hypertrophy in certain muscle groups. It also has to do with the type of muscle fibers that make up those muscle groups as we know the response to resistance training (or HOW we train, ie: heavy, lower reps, lighter , higher reps) also plays a role in hypertrophy in those muscle groups.

ps- An interesting tie in. If IGF does in fact induce muscle cell hyerplasia, can one increase the number of ar's in specific muscles by using site injections of igf? We could chew on that one for a while as well!
 
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ill tell you one thing . when I first started training , I learnt on my own . never knew about diet and much . but I remember always training in whatever way I needed to in order to get DOMS the next . Still to this day that's the sign I used to tell me I got an effective workout . its a sign u broke down the muscle and that's how it builds back and repairs stronger . seems to have always worked for me and seems a sure sign . of course over time the DOMS fade and aren't as noticeable , but u can still tell a bit , especially in certain muscle groups like legs . anyone have any input in this ?
 
What about quads and the rest of our leg since they are predisposed to being some of the most active muscles in our body?

Legs fall in the middle as far as androgen receptors go - depending on exactly what part we're talking about (its not just quads, hams, glutes as some believe).

There is a large degree of slow twitch fibres in your legs (quads in particular) so, in general, they respond better to high rep until failure style training vs low rep heavy weight stuff IME.

If this was the case site injections of androgens would lead to increases in actual muscle in the muscle where the injection was administered. As anecdotal as it is I think and size increase due to site injections is more from oil volume and inflammation as opposed to actual AR # and life being increased so my opinion on that would be no, we cannot selectively increase the numbers and lifespan in a site specific fashion.
The thing is this as well, the activation of the AR is not a merely site specific phenomenon. The effects are systemic in many ways so AR # in certain muscle groups is not necessarily the sole or defining reason for muscle hypertrophy or the ease or difficulty of muscle hypertrophy in certain muscle groups. It also has to do with the type of muscle fibers that make up those muscle groups as we know the response to resistance training (or HOW we train, ie: heavy, lower reps, lighter , higher reps) also plays a role in hypertrophy in those muscle groups.

ps- An interesting tie in. If IGF does in fact induce muscle cell hyerplasia, can one increase the number of ar's in specific muscles by using site injections of igf? We could chew on that one for a while as well!

This confirms my fears that site specific stimulation wasn't possible.
It also confirms my initial view that training becomes more important for areas containing less receptors such as forearms, calves, etc.

There is evidence showing that slow twitch muscles (forearms, lower half of calves, parts of the leg, etc) tend to respond less well to aas muscle growth.
I think this is where training comes in - high reps, maximum time under tension (due to the low range of motion) until failure works better for these areas.
In general guys need to be prioritizing their weak points anyway but the research also shows that their really is no need to specialise in the high androgen receptor areas like chest/shoulders - basically you do NOT need to have separate chest/shoulder days, etc.

Your IGF question links up nicely to the idea that androgen receptors aren't the whole story, so trying to adapt everything in a programme according to AR density is probably the wrong solution.
I think the influence of IGF, ARs etc is all secondary to DNA & genetics & this is confirmed by most studies.

My advice, prioritise your weak areas on cycle - simple route everyone can understand & apply :)
 
androgen receptors aren't the whole story, so trying to adapt everything in a programme according to AR density is probably the wrong solution.
I think the influence of IGF, ARs etc is all secondary to DNA & genetics & this is confirmed by most studies.

My advice, prioritise your weak areas on cycle - simple route everyone can understand & apply :)

Spot on IMO as well.....
 
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