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SubQ VS IM (estrogen)

Is not true, try this inject 10 mg SQ and have the test 11 to 12 hours after injection, then inject IM and have the blood test agent, also inject 10mg or 20mg and have blood test 12 hours after, then same day 16 hours and one after 24 hours. Then we can talk.
I'm confused about your proposed method:

Is it that, the subject is to, on day 1, inject 10 mg testosterone enanthate subcutaneously (0 hr), then measure serum E2 +12 h, then the following day (day 2) +12 h (so 24 h post-10 mg TE i.m.), inject 10 mg testosterone enanthate intramuscularly, then measure serum E2 +12 h, +4 h, +8 h (day 3)?

So, EX: 7 pm, inject 10 mg TE s.c., then measure serum E2 at 7 am, then 8 pm second evening, inject 10 mg TE i.m., then measure serum E2 at 7 am then measure serum E2 at 7 pm (+12 h), and again at 11 pm (+4 h), and
again at 7 am on the third day?

Honestly, I've been trying various permutations of times for this to be done during normal business hours, but cannot find any permutation that would work under that constraint.

Is this correct, that this is what you propose?
 
I'm confused about your proposed method:

Is it that, the subject is to, on day 1, inject 10 mg testosterone enanthate subcutaneously (0 hr), then measure serum E2 +12 h, then the following day (day 2) +12 h (so 24 h post-10 mg TE i.m.), inject 10 mg testosterone enanthate intramuscularly, then measure serum E2 +12 h, +4 h, +8 h (day 3)?

So, EX: 7 pm, inject 10 mg TE s.c., then measure serum E2 at 7 am, then 8 pm second evening, inject 10 mg TE i.m., then measure serum E2 at 7 am then measure serum E2 at 7 pm (+12 h), and again at 11 pm (+4 h), and
again at 7 am on the third day?

Honestly, I've been trying various permutations of times for this to be done during normal business hours, but cannot find any permutation that would work under that constraint.

Is this correct, that this is what you propose?
Sorry, definitely fucked that up, tried to go back and edit.

Is this what you propose, EX: 7 pm, inject 10 mg TE s.c., then measure serum E2 the following day at 7 am; then, inject 10 mg TE at 7 pm day 2, then the following day (day 3), measure serum E2 at 7 am, again at 11 am, and again at 7 pm?
 
Sorry, definitely fucked that up, tried to go back and edit.

Is this what you propose, EX: 7 pm, inject 10 mg TE s.c., then measure serum E2 the following day at 7 am; then, inject 10 mg TE at 7 pm day 2, then the following day (day 3), measure serum E2 at 7 am, again at 11 am, and again at 7 pm?
Yes, you fucked that up, but this was already pretty fucked up from the start. 😂

Still waiting to see someone post those 6 date-stamped hormone panels for consideration.
 
I don't disagree with any of this... Were you agreeing with what I wrote? Were you disagreeing with something that I wrote? I certainly never wrote that injected s.c. T is never absorbed, or that it evaporates or?
I was just adding on to what you said. Some people get excited about peak levels i think total amount available and utilized matters more. In the end from just the testosterone point of view i doubt how it is injected will make no noticeable difference on muscle growth. From an estrogen point there may be a difference. Most of the studies i have seen seem to show it works out about the same. Daily sub-q mine E levels are higher then once a week with the same dose. Which is different then many report. But i am also years older so that can be a factor as well as pathways change as a person gets older.
 
Sweet. Post them up. That's a lot of bloodwork. At least 4 male hormone panels in 2 days. My every two month panel shows no abnormalities. Estrogen is high but so is Free and Total T. So the ratio is good. And it's stable. I don't need a AI or SERM at the moment.

Sorry, definitely fucked that up, tried to go back and edit.

Is this what you propose, EX: 7 pm, inject 10 mg TE s.c., then measure serum E2 the following day at 7 am; then, inject 10 mg TE at 7 pm day 2, then the following day (day 3), measure serum E2 at 7 am, again at 11 am, and again at 7 pm?
The lab opens at 8 AM in my City, if your lab open at 7 then yes inject 7PM have your blood test at 7 AM not later, then go back 4 hours later and have on other test, then next day morning at 7 one more test, this way you will see how fast your test levels drops, and you will understand why is the best way to inject daily.
 
I was just adding on to what you said. Some people get excited about peak levels i think total amount available and utilized matters more. In the end from just the testosterone point of view i doubt how it is injected will make no noticeable difference on muscle growth. From an estrogen point there may be a difference. Most of the studies i have seen seem to show it works out about the same. Daily sub-q mine E levels are higher then once a week with the same dose. Which is different then many report. But i am also years older so that can be a factor as well as pathways change as a person gets older.
Got it now, thanks for clarifying. Yes, I agree. Peak T, while commonly understood to be associated with strength/performance (ergogenic), this is not strongly supported by anything particularly persuasive. An analogy would be reports or anecdotes that 17AAs like oxymetholone or oxandrolone pre- training leads to increased strength. It's quite possible, as this use has just never been the subject of rigorous study (insofar as I am aware), however. I'd be interested to see, if you're able to dig anything up, what studies you might be referring to that support the null hypothesis (peak T does not affect strength), as I cannot recall anything on the subject. Conversely, peak T is associated with the increase to hematocrit/hemoglobin, and too frequent intramuscular pinning (e.g., at ~ every t1/2) can lead to the need for phlebotomy that would not otherwise be required, for example. Whereas daily subcutaneous pinning would lead to dramatically reduced peak T (reducing the hematopoietic effects of T).
 
Got it now, thanks for clarifying. Yes, I agree. Peak T, while commonly understood to be associated with strength/performance (ergogenic), this is not strongly supported by anything particularly persuasive. An analogy would be reports or anecdotes that 17AAs like oxymetholone or oxandrolone pre- training leads to increased strength. It's quite possible, as this use has just never been the subject of rigorous study (insofar as I am aware), however. I'd be interested to see, if you're able to dig anything up, what studies you might be referring to that support the null hypothesis (peak T does not affect strength), as I cannot recall anything on the subject. Conversely, peak T is associated with the increase to hematocrit/hemoglobin, and too frequent intramuscular pinning (e.g., at ~ every t1/2) can lead to the need for phlebotomy that would not otherwise be required, for example. Whereas daily subcutaneous pinning would lead to dramatically reduced peak T (reducing the hematopoietic effects of T).
I really never mentioned strength, just muscle growth. As once receptors are saturated a person can have a higher peak above the saturation point but i doubt that does anything positive. Fouad posted up an interview recently where a Dr. gets into this sort of thing, but have not watched the whole thing yet. When looking at a chart if the same amount of time under the line is equal then i would guess growth is the same everything else being equal( peak vs more stable). Although bro talk these days points to daily being better. But can't say i have seen any good studies done. As there rarely is any good studies on using test for growth. And any real cycle would probably not be done sub-q either due to the volume. As for me hemacratic/hemoglobin on a TRT dose my levels are the same whether it is once a day or week.
 
Got it now, thanks for clarifying. Yes, I agree. Peak T, while commonly understood to be associated with strength/performance (ergogenic), this is not strongly supported by anything particularly persuasive. An analogy would be reports or anecdotes that 17AAs like oxymetholone or oxandrolone pre- training leads to increased strength. It's quite possible, as this use has just never been the subject of rigorous study (insofar as I am aware), however. I'd be interested to see, if you're able to dig anything up, what studies you might be referring to that support the null hypothesis (peak T does not affect strength), as I cannot recall anything on the subject. Conversely, peak T is associated with the increase to hematocrit/hemoglobin, and too frequent intramuscular pinning (e.g., at ~ every t1/2) can lead to the need for phlebotomy that would not otherwise be required, for example. Whereas daily subcutaneous pinning would lead to dramatically reduced peak T (reducing the hematopoietic effects of T).
Based on what you know, do you think tne or suspension has any benefits? Assume someone is already on trt at 200mg. And considering adding 350mg per week via long acting, or, tne (50 Ed pre).

I assume there will be high peaks on the tne and times it isn't active. I assume this would be inferior to adding the same dose via long acting.

The only way I think the tne could benefit is if taken pre, the peak actually does help you lift more. I'd assume orals are better for any benefit someone would gain by using tne or suspension?
 
I really never mentioned strength, just muscle growth. As once receptors are saturated a person can have a higher peak above the saturation point but i doubt that does anything positive. Fouad posted up an interview recently where a Dr. gets into this sort of thing, but have not watched the whole thing yet. When looking at a chart if the same amount of time under the line is equal then i would guess growth is the same everything else being equal( peak vs more stable). Although bro talk these days points to daily being better. But can't say i have seen any good studies done. As there rarely is any good studies on using test for growth. And any real cycle would probably not be done sub-q either due to the volume. As for me hemacratic/hemoglobin on a TRT dose my levels are the same whether it is once a day or week.
Interesting, I've never before seen anyone claim that peak T directly influences hypertrophy, only indirectly by increased strength (in my opinion, this, if it occurs, would ostensibly occur by increased neural drive & nongenomic mechanisms).

A Fouad interview is entertainment, not data really. Whatever the doctor claims therein, transient changes to blood concentrations such as peak blood T would not logically alter AR number, within a muscle cell (which we know to be increased at supra-physiologic concentrations since Forbes' 1985 era dose/response data that failed to find a nonlinear portion to the curve plotting dose vs. muscle LBM & weight increases) and 1990s writings by Bill Roberts on the topic of AR up-regulation. Such a claim sort of reveals a facile, if not absence of, understanding of basic cell biology and androgens - or at least a poor application of one to the other.

There are 4 known mechanisms that regulate AR number: transcription rate (i.e., increased transcriptional AR mRNA synthesis), receptor turnover (i.e., decreased degradation-synthesis balance), translational efficiency (i.e., increased muscle protein synthesis per ribosome) & translational capacity (i.e., increased absolute muscle protein synthesis a la increased ribosomal biogenesis). We have since learned that there is no evidence of increased translational efficiency a la mTOR (i.e., no myogenic markers, nor markers of translational efficiency like rpS6 or p70S6K were altered by T in human skeletal muscle cells). But there is evidence of, at least, increased translational capacity by T (a la increased ribosomal biogenesis). Increased translational capacity is capable to explain, at least in part if not in toto, the increase to AR number by androgen/T.

Suffice it to say, all 4 of these mechanisms regulate intracellular processes, i.e., where androgen has already diffused through the sarcolemma into the cytoplasm where AR are located, and are not related to transient changes to blood/serum concentrations.

Tangentially, more to the point of androgen potentially increasing hypertrophy indirectly by increasing strength, I seem to recall Peter Bond mentioning something a bit obscure that I doubt he had thought too deeply about, that involved some data where muscle fibers exposed to androgen directly in culture showed an increase in specific force or something of that nature (going more to the idea that peak androgen/T might increase strength), but I think he'd walk back that association now and probably chalk it up to more likely rapid nongenomic mechanisms.
 
Interesting, I've never before seen anyone claim that peak T directly influences hypertrophy, only indirectly by increased strength (in my opinion, this, if it occurs, would ostensibly occur by increased neural drive & nongenomic mechanisms).

A Fouad interview is entertainment, not data really. Whatever the doctor claims therein, transient changes to blood concentrations such as peak blood T would not logically alter AR number, within a muscle cell (which we know to be increased at supra-physiologic concentrations since Forbes' 1985 era dose/response data that failed to find a nonlinear portion to the curve plotting dose vs. muscle LBM & weight increases) and 1990s writings by Bill Roberts on the topic of AR up-regulation. Such a claim sort of reveals a facile, if not absence of, understanding of basic cell biology and androgens - or at least a poor application of one to the other.

There are 4 known mechanisms that regulate AR number: transcription rate (i.e., increased transcriptional AR mRNA synthesis), receptor turnover (i.e., decreased degradation-synthesis balance), translational efficiency (i.e., increased muscle protein synthesis per ribosome) & translational capacity (i.e., increased absolute muscle protein synthesis a la increased ribosomal biogenesis). We have since learned that there is no evidence of increased translational efficiency a la mTOR (i.e., no myogenic markers, nor markers of translational efficiency like rpS6 or p70S6K were altered by T in human skeletal muscle cells). But there is evidence of, at least, increased translational capacity by T (a la increased ribosomal biogenesis). Increased translational capacity is capable to explain, at least in part if not in toto, the increase to AR number by androgen/T.

Suffice it to say, all 4 of these mechanisms regulate intracellular processes, i.e., where androgen has already diffused through the sarcolemma into the cytoplasm where AR are located, and are not related to transient changes to blood/serum concentrations.

Tangentially, more to the point of androgen potentially increasing hypertrophy indirectly by increasing strength, I seem to recall Peter Bond mentioning something a bit obscure that I doubt he had thought too deeply about, that involved some data where muscle fibers exposed to androgen directly in culture showed an increase in specific force or something of that nature (going more to the idea that peak androgen/T might increase strength), but I think he'd walk back that association now and probably chalk it up to more likely rapid nongenomic mechanisms.
I see post from people often asking about getting the most out of their shot to get a higher peak , get faster absorption, which time of day is best etc. From a wide range of drugs. Personally i don't think it matters much in general, as once it is in it will get used at some point. As the body thinks how it is best used at that time. I quit trying to micromanage my body a long time ago as i found out it worked about as well as my boss(when i had one) trying to micromanage me. I would guess a good double blind placebo controlled study would show a lot of what people thinks works has much to do with the power of belief. And the real world application would be fairly negligible. But i am a glass half empty sort of guy by nature so take that into consideration with my view point on things as well!
 
I see post from people often asking about getting the most out of their shot to get a higher peak , get faster absorption, which time of day is best etc. From a wide range of drugs. Personally i don't think it matters much in general, as once it is in it will get used at some point. As the body thinks how it is best used at that time. I quit trying to micromanage my body a long time ago as i found out it worked about as well as my boss(when i had one) trying to micromanage me. I would guess a good double blind placebo controlled study would show a lot of what people thinks works has much to do with the power of belief. And the real world application would be fairly negligible. But i am a glass half empty sort of guy by nature so take that into consideration with my view point on things as well!
I basically agree, especially I think that people interested in drug effects focus too much on pharmacokinetics (half life, t1/2; time to peak; peak, etc.) - blood concentrations basically, rather than pharmacodynamic (changes in relevant parameters of biological activity of the drug). To wit, people talk about rhGH's short terminal half life, rather than its pharmacodynamic effects with respect to metabolic effects, growth effects, etc.
 
I see post from people often asking about getting the most out of their shot to get a higher peak , get faster absorption, which time of day is best etc. From a wide range of drugs. Personally i don't think it matters much in general, as once it is in it will get used at some point. As the body thinks how it is best used at that time. I quit trying to micromanage my body a long time ago as i found out it worked about as well as my boss(when i had one) trying to micromanage me. I would guess a good double blind placebo controlled study would show a lot of what people thinks works has much to do with the power of belief. And the real world application would be fairly negligible. But i am a glass half empty sort of guy by nature so take that into consideration with my view point on things as well!
Couldn't agree more. The peak C(max) means little. AUC over time maybe factor. But gene activation and the resultant protein synthesis does not follow the C(max) parameter of pharmacokinetics. In other words, you can't set your watch by/on biological functions. Maybe some by circadian rhythms but I highly doubt that applies to anabolism brought about by the introduction of exogenous chemicals that promote anabolism.

Although as @Type-IIx said, it may apply to psychological and aggression factors. I may be wrong though, but this is what I gather from my own personal experience and literature re the clinical pharmacology and various studies involving these compounds and other general opinions (e.g. Bill Roberts, et al).
 
Seriously man, even up to 400mg of test I never saw a rise in PSA with Subq even at 6 months..was also running prescribed deca..my “blast” before that was the same and my PSA went to 1.5
Would you mind sharing what gauge and length you are using for the sub q oil?
 
Can you do quad shot with an insulin needle ?
sure depends on a few variables I can think of

the leaner you are with more muscle, the easier it will be to achieve so yes its possible I did it for a long time. Sometimes It would get irritated.

other variables can affect it , needle size, the gear you are using, sterility upon injecting and aftercare etc. sauna afterwards always helped me recover from ANY SHOT
 
sure depends on a few variables I can think of

the leaner you are with more muscle, the easier it will be to achieve so yes its possible I did it for a long time. Sometimes It would get irritated.

other variables can affect it , needle size, the gear you are using, sterility upon injecting and aftercare etc. sauna afterwards always helped me recover from ANY SHOT
I do wud shots all the time with insulin needles..I’ve found that it really only depends on the amount of fluid in the syringe..I’m not using more than .33 ml a day so it’s not an issue
 

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