First Cycle--Low Dose

It seems the majority of experienced posters here recommend a person’s first cycle to be a relatively high dose one, with the reasoning that the body is most receptive at this point (?), and it would be the smart way to maximize gains.

Personally I’m hoping to start out with pretty low doses (for example, test e 3-400 mg/wk, eq 2-300 mg/wk, run for 10-12 weeks), especially since I’m not really looking for a big amount of hypertrophy, but rather performance, joint repair and strength gains. But at the same time I don’t want to waste my first cycle if it really does make that much of a difference with regard to later cycles being less productive.

I’ve done a couple searches, but mostly I’m getting people recommending what I just said, which is fine, but I haven’t really seen much to back it up scientifically, or anyone posting much anecdotally on it.

So, would anyone mind sharing their own experiences with their first cycle being a low dose one? Thanks for reading.

Doing a weak first cycle doesn’t impair later cycles.

Thank you.

no equipose for the firstimers, as no long esters

nandrolone fenil
test prop
winstrol

suit great for the first cycles when on a good diet

Would you mind sharing why not?

I wouldn’t consider winny because it would have the opposite effect on my joints that I’m looking for.

Test prop, nandrolone phenyprop, and winstrol is a poor first cycle.

Test E at 500mg/wk for 8-10 weeks with an AI and SERM PCT is plenty. If you really want to add in another compound, throw in Dbol at the end of the cycle for 4-6 weeks.

Thank you for replying.

The reason I’m being stubborn about Eq (or possibly Deca) is that I’m really looking for something that’ll work synergistically to help repair my crumbling joints (I do kickboxing in addition to lifting). From my research it doesn’t look like Dbol will do that.

[quote]nickels wrote:
Thank you for replying.

The reason I’m being stubborn about Eq (or possibly Deca) is that I’m really looking for something that’ll work synergistically to help repair my crumbling joints (I do kickboxing in addition to lifting). From my research it doesn’t look like Dbol will do that.[/quote]

No steroid will repair your joints. Deca will lubricat them so the pain goes away. But once you come off your joints will go back to the way they felt before hand. And if you gain strength and are moving bigger weights off cycle than you previously had been, your joints may take an even bigger beating.

GH is a much better option for long term joint health. At the proper dosage.

Thanks.

I thought I’d read that some aas can enhance collagen synthesis, which to my understanding would actually do some good in joint repair, but I could be misguided on that point.

At any rate, I’d love to run HGH, but I’m having trouble getting some at the moment. Probably next time…

My usual issue is that my joints get sore when i’m in a cycle and the pain usually isn’t very bad afterwards even though my weights in the gym aren’t changing very much. And it is strictly my elbows.

[quote]nickels wrote:
Thanks.

I thought I’d read that some aas can enhance collagen synthesis, which to my understanding would actually do some good in joint repair, but I could be misguided on that point.

At any rate, I’d love to run HGH, but I’m having trouble getting some at the moment. Probably next time…[/quote]

You almost certainly DID read that. I think we all have. But the problem is that no one knows where the information came from. There are numbers floating around that EQ increases collagen sythesis by 300something % and Deca by 270something but there are never any sources cited with those numbers.

Okay thanks.

Yeah, it would be nice if someone could confirm or disprove that info. Seems like it could be anything from extremely applicable to strength sports, to nothing but sly marketing.

At least one mechanism is from glucocorticoid receptor effects.

Evidence towards this:

Fed Proc. 1984 Oct;43(13):2793-8.
Effect of topically applied steroidal and nonsteroidal anti-inflammatory agents on skin repair and regeneration.
Alvarez OM, Levendorf KD, Smerbeck RV, Mertz PM, Eaglstein WH.

We studied the effects of topically applied steroidal and nonsteroidal anti-inflammatory agents on dermal and epidermal wound healing. Superficial wounds (0.3 mm deep) on the skin of domestic pigs were treated daily with either 0.1% triamcinolone acetonide (TA), 1% hydrocortisone (HC), 1% nandrolone decanoate (ND), 1% ND + 0.1% TA, 10 mg ibuprofen, 10 mg meclofenamate sodium, 3 mg indomethacin, vehicle (USP petrolatum or 70% ethanol), or control (untreated). Wounds were excised on days 2-7 after wounding and the epidermis was separated from the dermis. The dermis was assayed for collagen biosynthesis and the epidermis was evaluated for reepithelialization. A significant decrease (P less than 0.01) in relative collagen synthesis was observed in the wounded dermis in both HC- and TA-treated groups on day 3 after wounding,

(corticosteroids decreased collagen synthesis)

but there were no significant differences on days 4-7. Depressed collagen and noncollagenous protein production was also noted in vehicle-treated wounds on day 3. Topical application of ND did not affect collagen synthesis,

(note the above)

but when combined with TA it eliminated the inhibitory effect observed as a result of TA alone.

(in other words, it countered the adverse effect of the added corticosteroid, but apparently made no significant difference with the physiological levels of the pigs.)

Topical ND accelerated wound reepithelialization by 12.5% compared with vehicle and by 26% compared with untreated controls. TA delayed epidermal resurfacing by 22%, but when combined with ND (ND + TA) the rate of reepithelialization was similar to vehicle-treated wounds. HC enhanced resurfacing when compared with untreated wounds but did not differ markedly from its vehicle. The nonsteroidal anti-inflammatory drugs when topically applied markedly reduced inflammation (erythema, heat, and edema) but did not influence the healing process.

As an example of the sort of thing cited to claim nandrolone enhances collagen synthesis:

Sichuan Da Xue Xue Bao Yi Xue Ban. 2004 Jul;35(4):508-11.
[Effects of nandrolone phenylpropionate on fibroblasts after injury in rats]
[Article in Chinese]

Cen Y, Liu N, Liu XX, Li K.

Department of Burn and Plastic Surgery, West China Hospital, Sichuan University, Chengdu 610041, China.
OBJECTIVE: To explore the effects of nandrolone phenylpropionate (NP) on fibroblasts after injury in rats. METHODS: Thirty-two Wistar rats with a deep second-degree scald injury and 20% total body surface area were randomly divided into two groups to receive either 5 mg/kg NP (NP group) or normal saline as placebo (control group) every other day. Integrated optical density (IOD) of androgen receptor (AR) and mRNA expression level of alpha1 (I) procollagen were measured by immunohistochemistry and quantitive fluorescent RT-PCR individually on the post-burn days 4, 7, 14 and 21. Fibroblasts were isolated from granulation tissue of a Wistar rat and were cultured in RPMI1640 with the addition of NP at different concentrations. Cell viability of fibroblasts was measured by MTT test, and the proliferative index, by flow cytometry (FCM). RESULTS: (1) Compared with the A value of the concurrent control group, higher A values were seen in NP groups containing different concentrations of NP, and significant difference of proliferative index was observed in NP group, P<0.05. (2) The expression of alpha1 (I) procollagen mRNA in NP groups was much higher than that in control groups. A significant difference between the two groups was noted on the post-burn days 7, 14 and 21, P<0.05, but no difference was seen on day 4. (3) The density of AR on fibroblasts in NP group was higher than that in control group at each time point. And a positive correlation between the expression of alpha1 (I) procollagen mRNA and the quantity of AR on fibroblasats was confirmed (r = 0.836). CONCLUSION: Nandrolone phenylpropionate could promote fibroblast replication, increase the mRNA level of alpha1 (I) procollagen and enhance the density of AR on fibroblasts.

But as for claims of stanozolol slowing collagen synthesis:

J Invest Dermatol. 1998 Dec;111(6):1193-7.
Stimulation of collagen synthesis by the anabolic steroid stanozolol.
Falanga V, Greenberg AS, Zhou L, Ochoa SM, Roberts AB, Falabella A, Yamaguchi Y.

University of Miami School of Medicine, Department of Dermatology, Miami Veterans Affairs Medical Center, Florida, USA.
There is evidence that anabolic steroids, which are derived from testosterone and have markedly less androgenic activity, promote tissue growth and enhance tissue repair; however, the mechanisms involved in their anabolic activities remain unclear. In this report, we measured the effect of the anabolic steroid stanozolol on cell replication and collagen synthesis in cultures of adult human dermal fibroblasts. Stanozolol (0.625-5 microg per ml) had no effect on fibroblast replication and cell viability (p = 0.764) but enhanced collagen synthesis (p < 0.01) in a dose-dependent manner (r = 0.907). Stanozolol also increased (by 2-fold) the mRNA levels of alpha1 (I) and alpha1 (III) procollagen and, to a similar extent, upregulated transforming growth factor-beta1 (TGF-beta1) mRNA and peptide levels (p < 0.001). There was no stimulation of collagen synthesis by testosterone. The stimulatory effects of stanozolol on collagen synthesis were blocked by a TGF-beta1 anti-sense oligonucleotide, by antibodies to TGF-beta, and in dermal fibroblast cultures derived from TGF-beta1 knockout mice. We conclude that collagen synthesis is increased by the anabolic steroid stanozolol and that, for the most part, this effect is due to TGF-beta1. These findings point to a novel mechanism of action of anabolic steroids.

As for claims of different percent values, there is no way that anabolically-equivalent doses were being compared, except perhaps by the purest freak chance. So no seriousness should be given to the figures or differences between them.

Thank you for your input. I’ll keep doing research.