The igf-1 would minimise muscular atrophy during PCT, it doen’t help the recovery of HPTA, but you will hold on to your gains a bit better.
Generally IGF-1 will start to lose it’s effect past 4 weeks of continuous usage, by using EOD/3x week protocol, we hope to minimise antibody build up and stretch the effective cycle length to 6 week. Also, LR3 variant have a longer active period in the body, so EOD injection is sufficient. Altought the PCT will be finished in 4 weeks, it doens’t mean that the body is fully recovered, so every bit of anabolic assitance helps.
Also, if you can’t get real IGF-1LR3, then don’t use it. A lot of the generic IGF/MGF on the market is totally useless. Regular IGF-1 is cost prohibitive to use.
Real IGF-1LR3 are manufactured in Australia by Gropep/NovoEnzyme. The chinese stuff is a bit of hit and miss. [/quote]
The reasons that IGF’s results reduce after a certain time are not fully understood AFAIK, but of the factors that do have a role - i have not heard of any ‘antibodies’, what do you mean?
I was under the impression it was likely due to a few factors, with inhibition, satellite cells and possibly IGFBP all playing a role.
Also - the addition of the LR3 was to increase its activity in the body (time), but it didn’t pan out that simply… I mean - Yes, on the one hand it isn’t attaching to the first receptor it meets on injection, but as it cannot be bound by IGFBP, nor is it attaching to a receptor - it is also not having any activity at all until it is freed of the attached protein (i assume LR3 is some peptide based thang).
So the active life is not increased, more delayed.
If it had a pharmacokinetic profile like any regular drug, then it could be dosed accordingly - as we do for Propionate or Enanthate (and most drugs actually)… but it doesn’t really have an effect like that AFAIK, not quite.
May be wrong of course.
This delay IME tends to mean that whether it is used SC or IM it doesn’t matter, the results are more systemic than when ‘base’ IGF-1 is used. It DOES manage to leave the injected muscle and survive in the blood, without binding to the IGFBP.
This makes it free to attach to a receptor ‘later on’… (scientific aren’t i?)
Unlike the original peptide, the LR3 can be injected just once a day and show great results, and it does not have to be bi-laterally nor does it need to be site specific (lagging groups - although IMO it doesn’t hurt and can only help).
The point is, the LR3 addition is NOT like an ester, where it simply delays the release of the drug and therefore increases it’s DURATION of action.
These are just observations of my experience with the drug and of the writings i have read on it - both of scientific studies and personal accounts
AFAIK/IMO - all that polite shit.