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5th Cycle: Test/Tren/Dbol or Add Mast?

Hi, long time lurker, first time posting.

On gear: 220lbs, 10-12%BF
Off gear: 200lbs, 14%BF

My goal is to hit 230lbs at 8-10%BF.

All my past cycles have been pretty moderate. The last two I ran exactly the same with:
500mg/wk Test E/weeks 1-12
500mg/wk Tren E/weeks 1-12
50mg/day Dbol/weeks 4-12

At week 10, I get bloods. Both times, my ALT, AST, bilirubin, and GGT were all within the normal range (obv. high-normal). This is why I run Dbol for 8 weeks, supplementing with TUDCA, NAC, and curcumin. I run letro for AI throughout the cycle, and my PCT is standard 4-5week Nolva. I also run HCG 750IU/week throughout the cycle to avoid shutdown and make recovery easier.

Anyway, I want to add 500mg/week of injectable for another 12 week cycle, and I’m trying to decide b/w simply upping my dose of Test and Tren from 500mg to 750mg or adding Mast 500mg/week. Honestly, right now I’m leaning Mast b/c of its good side effect profile. Maybe in the future, I’ll run Test and Tren at 750mg each alongside Mast 500-750mg. Definitely not for this next cycle tho…that’s a little much all at once.

What you boys think?

Are you a competitive bodybuilder? This is way overkill for all but the most veteran of rec gym goers.
I mean… Eight weeks of dbol… Not exactly low dose either.

You do know liver damage can occur transiently right? Without any observable elevation in blood markers. Just as you can’t diagnose AAS induced DCM with blood work (perhaps with BNP testing… Maaaybe).

You’re cycling isn’t “moderate” either… 500mg tren is a hefty dose. 50mg dbol is a lot to be running for 8 wks… 500mg test is the only conservative element within this cycle… That would be if it were 500mg test only.

Does trashed lipids count as a side effect… Same with tren, get cholesterol checked on high dose tren/mast, get renal function checked on tren… Unless you’re some sort of God tier responder like Iron Yuppie or Flipcollar you won’t like what you see… At all

200 @6 ft 14 % is pretty good… But you can certainly achieve 230 without 750mg tren/wk (as you’ve proposed)

Edit… Wait, 230 @8% and 6ft is leaps and bounds bigger than Schwarzenegger was if I’m not mistaken… Leads me to question why the average Joe feels he has to be THAT big… It’ll probably cut a good decade or two of you’re lifespan (sustaining that sheer level of mass)

I would agree that these are definitely not moderate and closer to heavy cycles albeit still not what the pros go for. 220 at 10-12% would be more than adequate for me, but we all have our own goals. I don’t quite drop as much as you but I also lose about 10lbs and composition softens a bit as well. I’ve never tried Tren though and likely never will. I seem to get all the sides of everything I touch.

Agreed, however a pro bodybuilder typically dedicates his entire life to the sport of bodybuilding, perhaps he/she even makes money from his/her physique. I don’t understand why the avg Joe needs 750mg tren/wk unless they’ve been cycling for like… a good 10 years and this is what they require to grow (even then I’d say “isn’t there a point wherein you can be happy with what you’ve achieved?”)

I believe Arnold claimed 6’2" and about 250. However Patrick Moore was on stage at 6’0" and 230 lbs, but closer to 5% bodyfat and dry.


Arnold was probably around 8-12%BF come contest time at 225-235, 6’2-6’3

This guy is two inches shorter, wants 230 8-10% bf

I believe in freedom of choice, so long as you’re aware of the potential ramifications you’re decisions entail. Unfortunately the majority aren’t and/or just don’t want to hear it.

750mg is a lot of tren…

Thanks for the reply. Honestly, I find your perspective refreshing because I’m more usually around users who casually run 1.5-2.5g/wk of injectables and are lazy with their cardio, bloodwork, etc.

I’d like to ask you some questions while I’ve got your time.

  1. I don’t doubt that transient liver damage could occur. In what way, though, could this happen without some kind of corresponding increase in these serum liver markers?

  2. I’ve heard that a 500mg Tren E dose is roughly equivalent to a 350mg/wk Tren Acetate dose. When I was running 50mg Tren A/day, I experienced more perceived sides than I do w/this 500mg Tren E dose. My lipids and other values are generally pretty bad at the 10-week mark, but never drastically lie outside the upper limit of the reference range. 2-3 months post cycle, they return to normal. Would pushing my luck with 750mg/Tren E for 12 weeks really do me much harm here?

  3. I wasn’t aware that Mast hurts lipid profiles more than other compounds. I was only aware that its perceived sides were much better than tren for example. What compounds do you personally prefer re: safety profiles? Also, I thought that steroids generally hurt the kidneys indirectly through elevated BP. Is there something different about tren that makes it more harmful than others on kidneys?

  4. I realize that you probably have reservations recommending anything 1g/week or more on top of 50mg/day Dianabol (I might bring this down to 6 weeks now), but…hypothetically, if someone were holding a gun to your head and asked you to choose a cycle w/1.5g/week of injectable that included test and tren, what would you choose? Don’t worry btw, only asking for a friend lol

Again, thanks for your response so far. If you don’t mind me asking, what cycles have you personally had success with in trying to achieve your goals safely?

I’m a big fan of mast. Also, have you considered dropping the d-bol and instead running 8 weeks of anavar? I’ve ran just about everything at one time or another and test, tren, mast, and var is my go to cycle now days

These are very, very, very good questions

I’m not an expert, but I will write up a detailed answer when I’m done working (well, I don’t know if farm labour qualifies as work… Taking how tiring it is into consideration I believe farm labour to count as “work”)


Sorry for the super late reply…

No, one can transiently induce liver damage whilst enzymes remain relatively normal. Whilst a relatively rare complication, oral AAS greatly, greatly increase risk for hepatocellular adenomas and/or carcinomas. The liver is largely able to regenerate… but keep knocking it again and again (or damage it enough just once) and the prospect of permanent damage becomes feasible

No, you’ve got to take into account ester weight. The molar mass of base trenbolone is 270.37g/mol, molar mass Tren E is 382.544g/mol, Tren A is 312.409g/mol.

So 270.37/382.544=0.706, 1-0.706=.294. This means 29.4% of tren E (per mg) is ester weight, the rest is pure trenbolone. For every 100mg tren E you’ve got 70.6mg tren E

270.37/312.409=0.865. 1-0.865=0.135 so 13.5% = ester weight. Out of every 100mg you’ve got 86.5mg tren

500mg tren E = 70.6*5 353 (this is rough, I’m rounding to 3 significant figures).
350mg tren A = 86.5 *3.5 = 302.75

86.5*x=353=4.08. 408mg tren A = 500mg tren E.

Lipids are a minor concern compared to the development of cardiomyopathy. A very real prospect when someone uses high dose AAS… Or just tren in general. With higher dosages you’re looking at the very real long term prospect of deleterious cardiac enlargement. I’ll go through potential mechanisms

1: High blood pressure secondary to systemic vascular resistance: Pretty much… high blood pressure causes the heart to enlarge in a deleterious fashion. Systemic vasoconstriction (of which AAS can transiently induce). The heart as a result is required to work harder to pump oxygenated blood throughout the body. In response to being chronically overworked, the heart becomes thicker, stiffens… particularly the left ventricle. I’ll explain later why this is a bad thing. High blood pressure also induces arterial damage, narrowing coronary via increased force put upon arterial walls. This over time will make coronary arteries more prone to plaque build-up, plaque build up damages the fibrous cap surrounding atherosclerosis, making one prone to plaque rupture and thus myocardial infarction. High blood pressure can be induced via a myriad of mechanisms pertaining to AAS use. Firstly, the RAAS system (renal angiotensin aldosterone system) is pivotal for regulation of BP/fluid balance, within the kidney angiotensin II receptors influence sodium reabsorption within the kidney, arterial vasoconstriction etc. How does this relate to AAS use? The answer is yeetfloop! Nah, just kidding… I’m NOT an expert and these mechanisms are controversial however there is a compound within the body called 20 hydroxyeicosatetraenoic acid that regulates vascular resistance. Within rodent models (unsure if this has been demonstrated within humans) 20 HETE within certain circumstances activates Angiotensin converting enzyme, this enzyme converts angiotensin I to the vasoconstrictive Angiotensin II, furthermore the enzymes that generate 20 hydroxyeicosatetraenoic acid appear to be androgen mediated. Thus RAAS dysregulation would be the prime culprit of AAS mediated hypertension if this were to be the case.

Here’s a decent article on it

2: Sympathetic nervous system dominance/up-regulation: effect on beta adrenergic receptors (testosterone in replacement dosages modulate function B adrenergic receptors in numerous tissues), in supra physiologic dosages it’s been hypothesised (can’t find the studies, but I’ve read them prior, will link them when I find them… could be in a day, could be in a week. Not losing sleep over it, but I am losing sleep over… not sleeping due to anxiety), GABA-ergic dysregulation, dopaminergic dysregulation etc… these numerous modifications predispose one to arrhythmia. Some especially sensitive to the pro-arrythmiac effects of AAS will notice dramatically increased RHR’s on even low dose cycles/TRT. Beta adrenergic receptor up-regulation may furthermore be a liable culprit for sympathetic nervous system dominance, however there is little data regarding this. Rodent studies indicate 19-nortestosterone can increase cardiac beta 2 adrenergic receptor expression. Beta 2 adrenergic receptors act as binding sites for catecholamines such as epinephrine. Epinephrine is pro-arrythmiac, increases cardiac output, contractility, pulse rate etc. Studies indicate those on gear have cardiac autonomic dysfunction, impaired post-exercise HR recovery times

3: direct myocardial injury (AR mediated): Direct AR binding can induce myocardial apoptosis potentially via activation of capsase, AIF etc. Furthermore, when cardiac myocytes grow to a certain extent (depending on the cause of growth) cells will under go programmed cell death as a protective mechanism of sorts. As a result fibrotic tissue will replace dead cells… this tissue stiffens the heart, impairs contractility… predisposes one to arrhythmia. Furthermore cardiac hypertrophy via direct AR binding can induce apoptosis once the cell reaches a certain size. LVH with myocardial scarring is a fairly well documented side effect amongst those extensively abusing AAS.

4: indirect myocardial injury: AAS dose dependently induce oxidative stress, excess oxidative stress will/can trigger cellular apoptosis

5: Kidneys: AAS decrease excretion of calcium, can induce hypercalcemia (severe hypercalcemia can induce arrhythmia). Hypercalcemia can induce vasoconstriction as it initiates smooth muscle contraction, this can decrease renal blood flow, put strain on the kidney. Severe hypercalcemia can even induce acute renal failure, of which has been documented in those using tren, orals etc. One study looking at bodybuilders found a large majority had FSGS (focal segmental glomerulosclerosis), whilst diuretics could also cause this, rodent models (and one human study) indicates AAS tend to stress the kidneys (human study found boldenone markedly impacted markers of renal function). Chronic nandrolone administration to rabbits induces profound nephrotoxicity associated with oxidative stress, other AAS probably aren’t any better, nandrolone merely has more studies associated with it because it’s used widely within medicine compared to say, trenbolone, dbol or EQ… it’s also one of the more commonly abused compounds.

6: Haematological: also looking at clotting factor alteration + haematological alterations (increased RBC/HCT etc) leading to an excessively hyper coagulable state, thus potentially increasing the risk for a thrombosis to form.

7: Extensive vasoconstriction inducing coronary vasospasm: Systemic vasoconstriction can induce coronary vasospasm, AR mediated effect on arteries inhibit alter smooth muscle tone (altered activity regarding iron channels of which typically induce vasodilatation)… hence why using cocaine and cyclic doses of anabolic steroids is SUCH a bad idea. For whatever reason, stanozolol is particularly implicated regarding the induction of coronary vasospasm.

I’ll add more eventually, but honestly I don’t really feel like it… nothing against you, it’s more alongside the lines of I find writing these detailed responses to be time rather consuming. I’m not an expert by any means btw… but 500mg test 500mg tren (the tren in particular) is in no way, shape or form safe.

Finally… Neurotoxicity, Androgen receptors exist within the brain, numerous studies indicate direct AR binding in the brain can induce neuronal apoptosis. Some studies indicate those who use AAS have impaired/stunted cognition compared to controls, others indicate no difference can be observed (perhaps the difference exists regarding being on vs off the drugs)… what is striking is the structure of one’s brain, connectivity within certain regions is strikingly different (deleteriously, not positively) within AAS users and non-users. The drug aspect makes sense, many kids/people who use gear may end up gravitating towards crowds who use recreational drugs as they tend to be less judgemental. Furthermore the effect of AAS on neurology may make one more prone to making impulse/rash decisions (feel invincible, why not try that line of coke etc)

However studies like this one https://www.ncbi.nlm.nih.gov/pubmed/31033318
Don’t account for the fact that AAS exposure was also correlated (strongly) with exposure to recreational drugs… other studies do account for this, whilst the alterations in cognitive performance may not always reach significance within said studies, the structural alterations within the brain of an AAS user still remains significantly altered from that of the avg joe, if I recall correctly one of the changes hinted at enhanced glutamate turnover being present (potentially hinting at a neurodegenerative effect). Rodent models indicate trenbolone, methandienone, testosterone etc at high dosages are neurodegenerative/neurotoxic… but tren is probably the worst by far given how harsh it is neurologically.

Steroids aren’t safe, they aren’t as dangerous as the media makes them out to be either (when used responsibly)… but nowadays people are going full retard all the time without doing a shred of research.

Many of these mechanisms (absent of lipid alterations) will accelerate the rate of atherosclerosis regardless of whether lipids stay within the normal ranges or not

Shit, I forgot… LVH is bad because electrical conduction is deleteriously altered and/or blood can’t pump efficiently if the left ventricle becomes too concentrically enlarged and/or eccentrically enlarged weakens the walls, thus the heart isn’t strong enough to pump blood. Athletes heart is a different scenario wherein the enlargement is associated with improvement within certain parameters of cardiac function (increased stroke volume etc). There are certain differences within athletes heart/cardiomyopathy, within athletes using PED’s/in general sometimes these factors can overlap, causing a dilemma for medical professionals regarding whether they’re fit to play. Undiagnosed hypertrophic cardiomyopathy is one of the leading causes of sudden cardiac death during strenuous exercise for young people.

As time elapses (perhaps hours, perhaps days) I’ll be linking sources/literature. A large portion of this is off the top of my head, so perhaps some facts are slightly incorrect as I haven’t done a whole lot of research on this in a little while (not as relevant to me as it once was)

Stay safe, there are ways one can go about minimising risk factors, but it’s impossible to entirely eliminate risk. I’d hypothesise AAS (used reasonably) is about on par with the risk induced by regularly smoking cigarettes (daily)

AAS/cognition and/or structural brain imaging

I actually think you’re not far from it and the hate you got from some members for explaining pharmacology and giving your opinion was completely unjustified. Nobody expects to get a response from an “expert” in a forum, otherwise they would’ve gone to an expert in person.
Secondly: what defines expert? I studied pharmacy for 5 years in Germany. We study pharmacology together with medicine students. Your post exceeds what we learned in university. Clearly there’s some guys like me who read papers outside of university and have more knowledge than what is taught. Our profs expect this from everyone but the people who actually do it don’t exceed 4% of students. So the knowledge a medicine student has is not that great, and so is the knowledge most docs have.
I can verify a lot of what you’re writing and it is not only explained with a lot of detail but well researched.
Another one: an expert in the medical community is typically one who researches subjects himself, teaches and practices. The practice in these scenarios usually does not take up a lot of his time. So getting an expert to treat you would be extremely difficult and is reserved for very special cases.

My point is: you don’t have to write you’re not an expert two times in every post only because some guys didn’t like some of your posts. You’re doing well and if you become a doctor you’d be a great one with vastly more knowledge than most of them. And I, for my part, enjoy your write ups about pharmacology.

Is this your birthday or is there another reason why there’s cake after your name? :smiley:

Thank you for the kind words

It isn’t my birthday, the slice of cake means this is the date wherein I joined up with T-nation (made an account). When it’s my birthday a full cake appears at the top of my avatar…

This is my last year as a teenager… and a strange one at that indeed. I didn’t exactly intend to spend my gap year confined to my house.

Here’s that one study I was talking about regarding ND and B2 adrenergic receptors in the myocardium

@berserker87 read the post two posts above this one