Jump to content
NZ's bodybuilding, strength and fitness community


  • Content count

  • Joined

  • Last visited

  • Days Won


Daz69 last won the day on June 18

Daz69 had the most liked content!


About Daz69

  • Rank
    Senior member
  • Birthday July 5

Profile Information

  • Gender
    Not Telling
  • Location
    Dead for tax purposes...
  • Interests
    Training injured....
  • Steroid use

Recent Profile Visitors

2336 profile views
  1. Look at this paper on hCG: Human chorionic gonadotropin up-regulates insulin-like growth factor-I receptor gene expression of Leydig cells. Nagpal ML1, Wang D, Calkins JH, Chang WW, Lin T. Author information Abstract The effects of hCG, 8-bromo-cAMP, 4 beta-phorbol 12 beta-myristate 13 alpha-acetate, and forskolin on insulin-like growth factor-I (IGF-I) receptor gene expression of Leydig cells were studied. The treatment of purified Leydig cells with hCG caused a dose-dependent increase in [125I]IGF-I binding to Leydig cells without changes in binding affinity, indicating that the increased binding was due to increased receptor numbers and not to increased affinity. The minimal time required for hCG to induce IGF-I binding was 6 h, and it had reached a plateau at 16 h. 8-Bromo-cAMP (1 mM) increased IGF-I binding about 2-fold, and forskolin (10 microM) increased binding about 51%. Using the ribonuclease protection assay, we found that hCG and 8-bromo-cAMP could increase IGF-I receptor mRNA expression as early as 2 h before the increase in IGF-I binding. The induction by hCG was over 3.5-fold at 4 h and decreased to about 2-fold at 6 h. 4 beta-Phorbol 12 beta-myristate 13 alpha-acetate had a very small effect on IGF-I receptor mRNA levels (1.5-fold increase at 2 h and no changes at 4 and 6 h). In conclusion, IGF-I receptors can be up-regulated by hCG, 8-bromo-cAMP, and forskolin. The up-regulation of IGF-I receptor number is associated with transient increases in IGF-I receptor mRNA levels. This could be a mechanism by which hCG and IGF-I interact to enhance Leydig cell steroidogenesis. PMID: 1659515 DOI: 10.1210/endo-129-6-2820
  2. Have a read: Why you should never frontload ('kickstart') a cycle: homeostasis Basically, all bodybuilders are in a battle against homeostasis. We try to overcome the body's tendency to not gain mass by eating more food, training more frequently or harder, taking more supplements, and so on. The idea being that more of [whatever] sends a stronger message for protein synthesis. Let's call all these compounds and techniques 'growth factors'. Well eventually, as we all know, these growth factors stop working. We ramp up the training intensity, take more creatine and so on, but growth plateaus regardless. You may be on a bulk cramming down the burgers, but the body finds a way to overcome this and prevent the growth message getting through - probably by elevating myostatin levels, among other mechanisms. At this point bodyfat may go up quickly, but LBM gain is closing in on zero net growth. So we have to take a break, usually shrink back a bit, and let the body get used to the absence of all these growth factors - creating a new 'normal' or set-point. In the process myostatin and all the other inhibitory mechanisms drop back too - with a slight lag, hence the loss of mass. At this point, hopefully we're holding more mass than when we started the last bulking cycle, and now we're ready to go and repeat it all over again, in the hope of retaining even more at the end of it; rinse repeat; rinse repeat. Steroids fit into this homeostatic cycle in exactly the same way as the other growth factors, albeit to a much higher degree. The growth benefit they confer is not an absolute factor. For instance 300mg of test doesn't build, say, 3 kg of muscle, nor does 600mg build 6kg. Steroids don't work like that. Just like with increasing training intensity or food intake, it's the relative change compared to what you were doing or taking before that accounts for their benefit. To make this obvious, let's use an example: Person A has been on a cycle of 1000mg test for a while and his growth has plateaued. So he increases the dose by 500mg for the next 10 weeks (it could just as easily be a different compound he's adding instead, btw). And suddenly, he experiences some new growth. Just what we want and what we would expect. Person B has also been training for years and his growth is at a plateau. So he's just starting a cycle, which is 500mg test total for 10 weeks. In other words, they are both doing exactly the same thing in adding 500mg testosterone to their bodies after hitting a plateau. But all other things being equal, who is going to gain more from that 500mg over the next 10 weeks? No prizes for guessing Person B. Person B is experiencing a dramatic change in his testosterone levels of several multiples of what he produces naturally. Meanwhile Person A was only increasing his testosterone level by 50%. For Person A to even have a chance at a similar result, he'd probably need to take something like 3-4000mg, which would be a relatively similar increase. So what does this mean for our normal gains-hungry bodybuilder? Well if you take this fundamental physiological fact, and now programme it into a regular cycle, you can see that ultimately the most effective strategy for overcoming homeostasis on AAS must be to continuously create as much relative change as you can. To be constantly tapering-up the dose from the lowesteffective level. Now I ask anyone, if you intend to frontload your cycle with 1000mg of testosterone for a few weeks (or an oral steroid or whatever), how the f*ck do you plan on creating much relative change after? You're starting out so high, the only way up is through the stratosphere. And since it's only a frontload, your serum levels may actually start to decline after peaking in the first month! So fine, you'll bloat up quickly at first and it will look like an amazing idea because the changes come on fast and you'll leave Mr Tortoise behind. But good luck if you thought those bloated 10lbs were solid real muscle. And good luck maintaining that pace for a solid 12 weeks of continuous real growth while your testosterone levels flatten out or even decline. This is one reason most cycles stop being productive after about 8 weeks or so - the body's homeostatic mechanisms kick in so quickly that you're fighting a losing battle from that point onwards. Meanwhile Mr Tortoise, who started out low and slow but keeps upping the dose, soon overtakes you despite still being on less AAS, all the while staying harder and drier and never once resembling the bloated watery Pufferfish you became thanks to your frontload. Which is why I say frontloading is logically one of the most retarded practices there is. By boosting AAS levels up to a peak within the first weeks, you are literally killing off your future growth potential. You're wasting your most effective tool for growth (relative change) by throwing it all in at the start. And you're deluding yourself that the rapid changes you saw were real keepable gains post-cycle. The clever approach to cycling - and indeed bodybuilding in general, given our battle with homeostasis - is to always be 'confusing' the body (and overcoming inhibitors like myostatin) by upping whatever variable you're playing with (be it food intake, training intensity, supplements or AAS) from the lowest effective starting point. Thus I advise guys to do the complete opposite of frontloading. Start your cycle on a dose that's barely over natural levels, so you can then spend the next 12-15+ weeks gradually raising the dose, achieving the solid relative change we all want, while still staying at a sensible level and without experiencing all the negative side-effects that high doses entail. This should be common sense, even on the most anecdotal level and to the most novice trainee - after all, we all know our bodies plateau sometime after we make a change. So to be constantly changing (periodising) and tapering up various compounds and strategies from their lowest effective level is self-evidently the most efficient - and healthy - way to build muscle.
  3. No pct after cycle

    Try time restricted eating.. (google Dr Rhonda Patrick time restricted eating)... Drop carbs, increase fats, consume veggies, fruit (berries) nut, seeds, full fat protein sources... drop grains and all gluten..
  4. TRT in Oamaru

    Never admit to exogenous hormone use..!!!
  5. TRT in Oamaru

    You have to present with symptoms of low test, lethargy, tiredness, low sex drive, lack of motivation, depression etc... (exaggerate your symptoms to your Dr)... Blood tests will have to show consistent low for up to 6 months to qualify..!!! Endo, expect $400-$600.... If not ACC.... Maybe try claiming for a fall, injuring your testicles to qualify for ACC.... (state symptoms started after initial trauma)....
  6. Tren High BP

    Unfortunately bodybuilding is not a healthy sport, expect hypertension, and other deleterious cardiovascular issues the longer you run AAS, and the more cycles you do the worse it can get.. (as you increase skeletal muscle mass)... And myocardium becomes thicker and less flexible... (that's why old school bodybuilders employed time off, to give the body especially the heart time to return to normal).... Blast and cruise is particularly harmful to the heart... Systolic of 180 is high, but diastolic (the lower figure) is well within range and is a greater concern than elevated systolic, as it is the pressure of the heart at rest.. Yours is fine... Don't worry too much....!!! A trick to drop systolic is, breath very deeply (full lungs) fully exhale several times, holding your breath for a brief period before exhaling, this will crash your systolic...!!!!
  7. TRT in Oamaru

    Won't happen, TRT can only be prescribed by an endocrinologist.. Dr can issue repeat prescriptions after endo has approved medication... Expect a long drawn out process to be issued TRT meds... If you qualify..
  8. My DNP Cycle Log

    Don't you need carbs for DNP to work effectively..??
  9. Of course you would need carbs, it's the response to insulin that opens GLUT4 transporter allowing glucose to enter cells.. What do you mean by anabolic refractory period..???
  10. It's one of insulin's mechanism of actions, to increase muscle protein synthesis.. Along with Growth/gene expression, glycogen synthesis, fat synthesis, and glucose transport.. Effect of insulin on human skeletal muscle protein synthesis is modulated by insulin-induced changes in muscle blood flow and amino acid availability: In conclusion, physiological hyperinsulinemia promotes muscle protein synthesis as long as it concomitantly increases muscle blood flow, amino acid delivery and availability. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2804964/
  11. No pct after cycle

    Remember hormones act slowly... End of cycle he likely had estrogen dominance, this can affect not only testosterone but progesterone, prolactin, cortisol, thyroid etc.. Plus we don't know what esterified testosterone his cycle consisted of, neither does he, or if other longer estered compounds were mixed with what he thought he had...
  12. A lot of the popular forums don't seem as busy anymore, like you say it's a shame there used to be quite a community here, some knowledgeable people.. Plus products were more available back then, so that caused discussion, as products have got less and much harder to source the discussion has dried up.. Also people tend to get fed up with answering the same old questions, get bored and move on, pharmacokinetics/pharmacodynamics of hormones doesn't change..
  13. No pct after cycle

    Any use of SERM's should be dependant upon whether you are presenting with primary (testicular) or secondary (hypothalamic) hypogonadism..!! If secondary, Clomiphene 25mg/day reduced to 12.5mg over several weeks, or a single dose of triptorelin might kickstart things.. If primary (on-cycle damage to testes via R.O.S) maybe try hCG, as this paper should explain: Human Chorionic Gonadotropin Up-Regulates Insulin- Like Growth Factor-I Receptor Gene Expression of Leydig Cells* MADAN L. NAGPAL, DELI WANG, JO H. CALKINS, WEIWEI CHANG, AND TU LIN Medical and Research Services, W. J. B. Dorn Veterans Hospital, and Department of Medicine, University of South Carolina School of Medicine, Columbia, South Carolina 29208 https://www.ncbi.nlm.nih.gov/pubmed/1659515
  14. DHEA in pct ?

    Shame about cessation of Losartan it has proven cardioprotective benefits.. Basically there are androgen receptors in myocardium, AAS cause thickening of myocardium and loss of flexibility/fibrosis (which is more of a concern) Losartan has been shown to break up fibrotic accretions in heart tissue leaving a much healthier more flexible muscle, which puts less stress upon the pumping ability of the heart... Are you sure Losartan was causing headaches..? Did you try 24 hr BP monitoring..? It's quite relevant, as there should be natural drop at night, which has been shown in research to be very important for the timing of your medication, as this nocturnal drop is an important marker for future heart issues (if it doesn't take place)... I doubt you will be prescribed Clomiphene, as I tried with my Dr,and was told its a female cancer drug so no chance for males...Unless via a sympathetic endocrinologist....
  15. DHEA in pct ?

    Tren and nandrolone are pretty suppressive of the hypothalamus, Clomiphene might be appropriate.. bisoprolol ..? Beta blocker seems a little strange.? Losartan might have been more prudent and cardio protective due to AAS use.. PCV 0.568...... you need venesection.... (donation)... 56 is too high, blood is too thick, which in turn puts extra stress upon the heart...