This is a short article I wrote on site injection
Ok this is a topic that has a huge division as far as whether site specific gains occur or not. When in fact the answer to this question is such a simple one. Not to insult anyone intelligence though, but it is a very easy concept when you have all the right infomation available to you.
Steroids/AAS/Testosterone are regulated in the body by binding proteins much like IGF. So at any given time only about 2% of the testosterone in your body is free to act on the androgen receptors. The remaining 98% is bound to SHBG (sex hormone binding globulin) and albumin. This bound testosterone is not biologically active. IGF-I has binding proteins that regulate ti as well but the LR3 is much les likly to bcome bound to the the IGF binding proteins.
So lets think of the way we administer these drugs. They are IM injections that go into the blood stream from the injection site. In the case of water based substances like IGF move much faster than oil based AAS but the principle here is going to be the same. The area exposed to the greatest free biologically active compound is going to be the inj site istelf. The further you get from the inj site the lower the blood concentration will be not only b/c its futher from the source and has been dilute further but b/c it has had a change to be bound to binding proteins, degrade, or have already bound to a receptor. So you see you can't deny a site specific effect if you think in terms of receptor saturation. The inj site receptors are going to be far more saturated than those far from it.
All of these drugs are systemic and travel through the blood and effect the entire body but the fact remains the greatest blood concetration is at the inj site. If you inject your left bicep only you right bicep will never expereince the same level of active hormone that the left does. While in the case of water based inj this time period may be more breif the effect is still their reguardless. You must take into account that the quick hitting high concentration of IGF at the inj site is really going to shock the receptors there and this will be way before the body can release more IGFBPs that will be present in the blood in the rest of the body.
On thing to account though is f you keep inkecting the same site day after day, that is going to increase the receptor downregulation significantly more than the rest of the body so you may actaully lose your site specific effect and have an inhibitory effect if proper cycling is not used.
So not to quote VIKI from I-ROBOT. But my logic is undeniable lol. No matter how you look at it site specific activity is un-avoidable. The reason some people may not think they see it is you must remember you only have so many receptors, so you can only saturate so much. In the case of androgen receptors though, there would be a higher site specific upregulation in response to AAS administration for about 6 weeks site specific effects would increase. There are other limiting factors still with satellite cells, gorwth factors etc to consider as well that may make it harder to see. But most likely if one were to make a direct comparison of site inj vs an equally mass/trained muscle you would see a significat effect over the course of 3-6 weeks.
In conclusions, site specifc results are a undenaible reality. How significant is a variable form user to user and conditioned base, but it exist non the less.
here is a link showing some AR binding/active sites. http://www.ebi.ac.uk/thornton-srv/da...t01_01&pdf=YES
So activity depends on the compound and placement of the ester.
Either way though esters can be removed once its in the body by enzymes in the blood, some more rapidly than others depending on how protected the binding site is.
And here is an example of how the cholesterol esterases work to naturally cleave esters from cholesterol to make steroids from scratch in the body.
Ok this is a topic that has a huge division as far as whether site specific gains occur or not. When in fact the answer to this question is such a simple one. Not to insult anyone intelligence though, but it is a very easy concept when you have all the right infomation available to you.
Steroids/AAS/Testosterone are regulated in the body by binding proteins much like IGF. So at any given time only about 2% of the testosterone in your body is free to act on the androgen receptors. The remaining 98% is bound to SHBG (sex hormone binding globulin) and albumin. This bound testosterone is not biologically active. IGF-I has binding proteins that regulate ti as well but the LR3 is much les likly to bcome bound to the the IGF binding proteins.
So lets think of the way we administer these drugs. They are IM injections that go into the blood stream from the injection site. In the case of water based substances like IGF move much faster than oil based AAS but the principle here is going to be the same. The area exposed to the greatest free biologically active compound is going to be the inj site istelf. The further you get from the inj site the lower the blood concentration will be not only b/c its futher from the source and has been dilute further but b/c it has had a change to be bound to binding proteins, degrade, or have already bound to a receptor. So you see you can't deny a site specific effect if you think in terms of receptor saturation. The inj site receptors are going to be far more saturated than those far from it.
All of these drugs are systemic and travel through the blood and effect the entire body but the fact remains the greatest blood concetration is at the inj site. If you inject your left bicep only you right bicep will never expereince the same level of active hormone that the left does. While in the case of water based inj this time period may be more breif the effect is still their reguardless. You must take into account that the quick hitting high concentration of IGF at the inj site is really going to shock the receptors there and this will be way before the body can release more IGFBPs that will be present in the blood in the rest of the body.
On thing to account though is f you keep inkecting the same site day after day, that is going to increase the receptor downregulation significantly more than the rest of the body so you may actaully lose your site specific effect and have an inhibitory effect if proper cycling is not used.
So not to quote VIKI from I-ROBOT. But my logic is undeniable lol. No matter how you look at it site specific activity is un-avoidable. The reason some people may not think they see it is you must remember you only have so many receptors, so you can only saturate so much. In the case of androgen receptors though, there would be a higher site specific upregulation in response to AAS administration for about 6 weeks site specific effects would increase. There are other limiting factors still with satellite cells, gorwth factors etc to consider as well that may make it harder to see. But most likely if one were to make a direct comparison of site inj vs an equally mass/trained muscle you would see a significat effect over the course of 3-6 weeks.
In conclusions, site specifc results are a undenaible reality. How significant is a variable form user to user and conditioned base, but it exist non the less.
here is a link showing some AR binding/active sites. http://www.ebi.ac.uk/thornton-srv/da...t01_01&pdf=YES
So activity depends on the compound and placement of the ester.
Either way though esters can be removed once its in the body by enzymes in the blood, some more rapidly than others depending on how protected the binding site is.
And here is an example of how the cholesterol esterases work to naturally cleave esters from cholesterol to make steroids from scratch in the body.
