What do you guys use to bridge ?

[Manski]

Then you should be more specific in what you want to bridge with, you come on to a steroid forum asking what we bridge with then expect to bridge with AAS, if you don't want to bridge with AAS then be specific that you do not want too. Like I mentioned earlier, a peptide would be good IGF-1 through PCT or run some HGH. I still wouldn't even classify that a bridge it is simply running a peptide when off or in PCT. A bridge is bridging a cycle with AAS.

Don't do it right or don't do it at all is where you got on your high horse, not me, it was a simple comment of if you want to bridge my advice would be to do it properly AKA blast cruise or don't do it at all, you either bridge two cycles together or you don't. Again, bridging is using low doses of AAS to link two cycles, theres only one way to do that and it's staying on.

I agree my post and name calling was a little erratic and I apologise, no offence intended, it's one of the sides that happens to me on test unfortunately it doesn't make me mellow, just shortens my fuse quite a lot and blow a little situation up over nothing, again I apologise dude.



250mg Test per week is the most common cruise dose I have seen and would rec. to anyone wanting to blast/cruise. If you wan't medicore levels for a cruise, you may aswell save yourself the trouble and just do a PCT... If your natty levels are shit anyway, maybe TRT should be a consideration, otherwise to cruise on a dose that is mimicking your natural test levels isn't going to do much for you, the whole idea of a cruise IMO is to have your test levels a little bit higher than natural, say 1200-1500ng/dl would be a good cruise level. Don't get me wrong, a cruise dose isn't meant to be a juicing dose and is important in giving your body a break, but like I said, why be technically on TRT when you don't have to if you plan on cruising on a dose of test that will put you the same as your natty production and again if your natty production is that low you should look at TRT.

I know I put this question on this steriod forum, this is where everybody put all their questions on steriod related issues. I know there's other thread but lets be honest, this thread is where most people that have any kind of rel knowledge hang out. I wasent aware that bringing ment low doses of aas. I think it was pretty much whatever you wanted to use I between cycles to help keep your gains. Everybody seems to agree with you so I will agree your right and I've learned something. I must admit I'm a little sensitive as well while on cycle, drives my girl crazy is I apologize ae well. Thank for. The great advice. I have not done end of cycles bloods yet, I'm getting ready to start my pct in bout a week. I'm going to to give IGF 1 a shot and cycle that intone untill my summer cut cycle. Getting back to my natty is very important to me. Thanks again everybody that chipped in.

 

[Manski]

Manski, have you come down from the "blast" yet. i.e. have you stopped cycling long enough to see where your test levels bounce back post-cycle? I'm curious if your test levels are, were, or will be decent. Since you want to preserve it, and nobody can blame you for that, but staunched has a good point, if they go to shit or already are, you could consider TRT(not the first thing i tell people to do, ever) Have you gotten pre and/or post cycle blood work?



Igf-1 makes a lot of sense for PCT, if you can keep the body anabolic while you bring testosterone levels back up, you should be able to retain a lot more of your on cycle gains. Igf-1 is one of the things that makes test(and other andros) and hgh, muscle builders.

Thanks my friend. No end of cycle bloods done. I start pct in bout a week.

 

[Black Beard]

Got it, good luck man. Crossing my fingers for ya.

 

[Manski]

Got it, good luck man. Crossing my fingers for ya.

Thank you bro !

 

[Black Beard]

x

 

[barnzy7]

I hear different things. I hear S4 is supressive at high doses and lower doses, that ostarine is or is not at all. That's why I was asking if anyone has used it. I guess the best thing would be some peptides because it doesn't seem worth the risk of putting a potentially suppressive substance in your body during pct.

Im using GW and Osta as somewhat of a bridge right now...5-6 weeks after I started PCT and I lost 1-2lbs, strength still there. Just my experience

 

[SicVic]

I believe the best bridging compounds are. GW-501516, EPO, Insulin, Peptides and GH. Theres so much shit out there LOL. Its just the cost.

 

[China_Wall]

Bridging = cruising

so low dose test 200-300mg per week is sufficient

 

[DreDay187]

I know peptides like IGF-1/GH are suppressive to endogenous production of IGF-1/GH, but as far as I'm aware they won't affect the HPTA in the sense of disrupting androgen production...This is why they make for a good choice in PCT. Also, IGF-1/GH will bounce back pretty much over a few days unlike androgen production (someone chime in if that's not true, I have always been under the impression that's how it works).



I don't understand the fad about SARM's, I would never put them in me, but hey that's me. And Yep they are suppressive, dose dependant I believe. They won't stop recovery during PCT, but they certainly won't be helping in the recovery department. I would run a peptide, IGF-1 would be at the top of the list, during PCT not a SARM.

Got this link in my email...interesting article lol

Q: “How should I incorporate SARMs (selective androgen receptor modulators) into my steroid cycle or into PCT?”

You should not do so.

Various authors in the scientific literature have tried to make it appear that in contrast to anabolic steroids, SARMs somehow will have an improved side effect profile or an increase in dissociation between anabolic and androgenic effects. But other than in the regard of liver toxicity with oral use, where most oral anabolic steroids have an issue and the SARMs do not, the evidence isn’t there. There isn’t even a reasonable argument as to how they might offer an improvement.

In my opinion, the only difference between these compounds and anabolic steroids is in a structural feature that makes no difference to the user but apparently makes a difference to society, namely whether the compound has a steroid skeleton or not.

You could call them politically correct androgens that have had the socially-unacceptable word “steroid” removed from them.

And that’s it.

That really is no reason to include them in an anabolic steroid cycle, nor is there any other reason.

There’s even less reason to include them in PCT, as they are suppressive of LH production.

 

[shiva4]

Shiva-which ones (ghrh/ghrp) specifically? I was looking in to these, and learned that they work synergistically. If I remember correctly, ghrp6 increases your appetite so I presume that's the secretagogue you used. Can you elaborate on your dosing and duration?

Not trying to hijack this thread...I've just noticed a few things of interest and wanted to inquire. Thanks!

I use MOD GRF for the GHRH as far as the GHRP's go I would use GHRP2 upon waking, GHRP6 post workout and IPA before bed. I didnt like the GHRP6 very much, it made me feel a little odd especially if I didnt eat soon enough so I stopped using it. Currently what I like the most is GHRP 2 upon waking and throughout the day and IPA before bed. Im doing 100 mcg of MOD GRF to 100 mcg of which ever GHRP Im dosing, the amount of doses per day is 3-5 times. GHRP6 tends to cause the most hunger but the GHRP2 is really keeping my appetite up just as much.

 

[STAUNCHED427]

I know I put this question on this steriod forum, this is where everybody put all their questions on steriod related issues. I know there's other thread but lets be honest, this thread is where most people that have any kind of rel knowledge hang out. I wasent aware that bringing ment low doses of aas. I think it was pretty much whatever you wanted to use I between cycles to help keep your gains. Everybody seems to agree with you so I will agree your right and I've learned something. I must admit I'm a little sensitive as well while on cycle, drives my girl crazy is I apologize ae well. Thank for. The great advice. I have not done end of cycles bloods yet, I'm getting ready to start my pct in bout a week. I'm going to to give IGF 1 a shot and cycle that intone untill my summer cut cycle. Getting back to my natty is very important to me. Thanks again everybody that chipped in.

I apologise again bro! No point doing your bloods until after you have completed your PCT, that way you can see how well and if you recovered, I'd get them done no earlier than a month after finishing up your PCT. How long do you plan on staying off until you next cycle? And yep, IGF-1 during your PCT should help a lot, let us know how it works for you!

 

[308power]

500 test 300 eq 300 deca

 

[STAUNCHED427]

500 test 300 eq 300 deca

Shit I'd like to see your blast doses

 

[wiggywild]

Got this link in my email...interesting article lol

That article doesn't really make a lot of sense. We know SARMS don't convert to DHT or estrogen so problems with acne, hair follicles, and the prostrate are lessened. And the reasonable argument for how they offer an improvement is called tissue selectivity. SERMS primarily act only in breast tissue as estrogen receptor antagonists, because the receptor binding pocket shape is slightly different due to the presence of tissue specific coactivators and corepressors. Although the ultimate SARMS goal has not yet been realized, it is to design ligands which only activate (agonize) the androgen receptor in is bone, skeletal muscle, and possibly fat tissues. This would thereby prevent HPTA suppression since the SARM would not bind to receptors involved in HPTA suppression.

S4 was not so good in this selectivity, but it is said ostarine is less suppressive by this method. However, to date I am unaware of a large enough study with blood work to show this. And I have seen blood work posted by individuals using lower doses of ostarine in PCT who recovered, but a few random posts do not an experiment make, so I can draw no conclusions.

 

[STAUNCHED427]

That article doesn't really make a lot of sense. We know SARMS don't convert to DHT or estrogen so problems with acne, hair follicles, and the prostrate are lessened. And the reasonable argument for how they offer an improvement is called tissue selectivity. SERMS primarily act only in breast tissue as estrogen receptor antagonists, because the receptor binding pocket shape is slightly different due to the presence of tissue specific coactivators and corepressors. Although the ultimate SARMS goal has not yet been realized, it is to design ligands which only activate (agonize) the androgen receptor in is bone, skeletal muscle, and possibly fat tissues. This would thereby prevent HPTA suppression since the SARM would not bind to receptors involved in HPTA suppression.

S4 was not so good in this selectivity, but it is said ostarine is less suppressive by this method. However, to date I am unaware of a large enough study with blood work to show this. And I have seen blood work posted by individuals using lower doses of ostarine in PCT who recovered, but a few random posts do not an experiment make, so I can draw no conclusions.

If only. And I am pretty sure, someone correct me if I am wrong that even if such a ligand did exist, it would still be suppressive to some extent.

 

[DreDay187]

That article doesn't really make a lot of sense. We know SARMS don't convert to DHT or estrogen so problems with acne, hair follicles, and the prostrate are lessened. And the reasonable argument for how they offer an improvement is called tissue selectivity. SERMS primarily act only in breast tissue as estrogen receptor antagonists, because the receptor binding pocket shape is slightly different due to the presence of tissue specific coactivators and corepressors. Although the ultimate SARMS goal has not yet been realized, it is to design ligands which only activate (agonize) the androgen receptor in is bone, skeletal muscle, and possibly fat tissues. This would thereby prevent HPTA suppression since the SARM would not bind to receptors involved in HPTA suppression.

S4 was not so good in this selectivity, but it is said ostarine is less suppressive by this method. However, to date I am unaware of a large enough study with blood work to show this. And I have seen blood work posted by individuals using lower doses of ostarine in PCT who recovered, but a few random posts do not an experiment make, so I can draw no conclusions.

The article isn't mine just thought it interesting to see what comments it gets. I personally have no interest in SARMs and don't see what the fuss is about but I will admit I have not looked into them as much as other compounds so I may not know everything about them.

I agree the 'ultimate goal' for SARMs might be something to look into but does that mean these inferior versions we have now are worth spending money on, worth including in a cycle, etc? I'm not sold.

The argument isn't that ostarine or a suppressive agent will make recovery impossible but that no suppressive agent be used during a period of recovery for obvious reasons. One being it interferes with your recovery which if you're running a PCT is a priority for you. If I was to run a suppressive compound during recovery why choose a weak/current SARM when I have the option of Tbol, var, dbol, HCG, low dose test, etc?

As to SERMs I'm not sure I agree unless you're specifically talking about males I guess. Tamoxifen is primarily an antagonist in breast tissue, it does affect the hypothalamus as well, but not all SERMs are. Clomid is an antagonist at the hypothalamus moreso than breast. In fact it's an extremely weak antagonist at the breast ER. Other SERMs we don't typically use such as ormeloxifene, lasofoxifene, ospemifene, and raloxifene all act as antagonists at the uterus as well.

 

[SHIFTY]

I use the Golden Gate to Oakland cause the ferry takes too long and I'm usually in a rush.

 

[STAUNCHED427]

In fact it's an extremely weak antagonist at the breast ER.

Yes, I agree. I was getting itchy nipples and devloped gyno whilst using a Clomid only PCT @ 50mg.

 

[DreDay187]

Yes, I agree. I was getting itchy nipples and devloped gyno whilst using a Clomid only PCT @ 50mg.

They've done studies on gyno reversal using clomid and while some reults were favorable, nolva and ralox were far superior.

 

[STAUNCHED427]

Seemed to only aggravate the problem in my case. I will post up how ralox works for these two unwelcome lumps of mine, hope to get in the next few days.