Oral AAS before a workout.

[Juice Authority]

Good response bro...

I can see how you drove Nelson to near madness.

I really don't know how we got off on this tangent. My position or response to Nelson's fact that D-bol raised testosterone levels was that it really doesn't raise test levels that much and that it has a much more pronounced effect on muscle catabolism. Go read what I said.

 

[hhajdo]

The comment that Dbol increases test. levels suggests a clear lack of knowledge about AAS pharmacology.


Pharmacology and Sport; Sport Pharmacology in the Soviet Union

"Numerous examinations of healthy non-athletes by dexamethasone/methandrostenolone test showed that normally administration of these hormones caused a 30-40% reduction of blood cortisol and/or testosterone."


As for the cortisol & glucocorticoid antagonism, the Q is how relevant this is:


http://jcem.endojournals.org/cgi/co...full/82/11/3710

..."Since Kochakian’s early observations that gonadectomy increases nitrogen (protein) loss, and testosterone replacement attenuates that loss or net catabolism (1), studies in both animals and humans have demonstrated that androgens or anabolic steroids increase body weight and lean body mass and often decrease fat mass (1, 3, 5, 21, 26, 34, 43, 44, 45). The anabolic action on lean body mass was largely ascribable to an increase in muscle and was observed in hypogonadal male and female animals or eugonadal men given high dose testosterone or anabolic steroids (1, 3, 5, 21, 26, 34, 43, 44, 45). Although some studies suggested that androgens increased protein mass via decreases in proteolysis (46), most investigations have reported that androgens augment muscle mass through increases in muscle protein synthesis without affecting degradation (5, 21, 43, 45, 47, 48, 49). As a result, an earlier concept that androgens decrease glucocorticoid-mediated increases in muscle protein degradation (46) has been discounted...."


Cytadren maybe isn't the best example, but Glucocorticoid receptor antagonism can also lead to increased cortisol levels.



Muscle protein synthesis is elevated >24 hours after exercise:



Changes in human muscle protein synthesis after resistance exercise.

Chesley A, MacDougall JD, Tarnopolsky MA, Atkinson SA, Smith K.

Department of Physical Education, McMaster University, Hamilton, Ontario, Canada.

The purpose of this study was to investigate the magnitude and time course for changes in muscle protein synthesis (MPS) after a single bout of resistance exercise. Two groups of six male subjects performed heavy resistance exercise with the elbow flexors of one arm while the opposite arm served as a control. MPS from exercised (ex) and control (con) biceps brachii was assessed 4 (group A) and 24 h (group B) postexercise by the increment in L-[1-13C]leucine incorporation into muscle biopsy samples. In addition, RNA capacity and RNA activity were determined to assess whether transcriptional and/or translational processes affected MPS. MPS was significantly elevated in biceps of the ex compared with the con arms of both groups (group A, ex 0.1007 +/- 0.0330 vs. con 0.067 +/- 0.0204%/h; group B ex 0.0944 +/- 0.0363 vs. con 0.0452 +/- 0.0126%/h). RNA capacity was unchanged in the ex biceps of both groups relative to the con biceps, whereas RNA activity was significantly elevated in the ex biceps of both groups (group A, ex 0.19 +/- 0.10 vs. con 0.12 +/- 0.05 micrograms protein.h-1.microgram-1 total RNA; group B, ex 0.18 +/- 0.06 vs. con 0.08 +/- 0.02 micrograms protein.h-1.microgram-1 total RNA). The results indicate that a single bout of heavy resistance exercise can increase biceps MPS for up to 24 h postexercise. In addition, these increases appear to be due to changes in posttranscriptional events.


Mixed muscle protein synthesis and breakdown after resistance exercise in humans.

Phillips SM, Tipton KD, Aarsland A, Wolf SE, Wolfe RR.

Metabolism Unit, Shriners Burns Institute, Galveston, Texas, USA.

Mixed muscle protein fractional synthesis rate (FSR) and fractional breakdown rate (FBR) were examined after an isolated bout of either concentric or eccentric resistance exercise. Subjects were eight untrained volunteers (4 males, 4 females). Mixed muscle protein FSR and FBR were determined using primed constant infusions of [2H5]phenylalanine and 15N-phenylalanine, respectively. Subjects were studied in the fasted state on four occasions: at rest and 3, 24, and 48 h after a resistance exercise bout. Exercise was eight sets of eight concentric or eccentric repetitions at 80% of each subject's concentric 1 repetition maximum. There was no significant difference between contraction types for either FSR, FBR, or net balance (FSR minus FBR). Exercise resulted in significant increases above rest in muscle FSR at all times: 3 h = 112%, 24 h = 65%, 48 h = 34% (P < 0.01). Muscle FBR was also increased by exercise at 3 h (31%; P < 0.05) and 24 h (18%; P < 0.05) postexercise but returned to resting levels by 48 h. Muscle net balance was significantly increased after exercise at all time points [(in %/h) rest = -0.0573 +/- 0.003 (SE), 3 h = -0.0298 +/- 0.003, 24 h = -0.0413 +/- 0.004, and 48 h = -0.0440 +/- 0.005], and was significantly different from zero at all time points (P < 0.05). There was also a significant correlation between FSR and FBR (r = 0.88, P < 0.001). We conclude that exercise resulted in an increase in muscle net protein balance that persisted for up to 48 h after the exercise bout and was unrelated to the type of muscle contraction performed.


The time course for elevated muscle protein synthesis following heavy resistance exercise.

MacDougall JD, Gibala MJ, Tarnopolsky MA, MacDonald JR, Interisano SA, Yarasheski KE.

Department of Kinesiology, McMaster University, Hamilton, Ontario.

It has been shown that muscle protein synthetic rate (MPS) is elevated in humans by 50% at 4 hrs following a bout of heavy resistance training, and by 109% at 24 hrs following training. This study further examined the time course for elevated muscle protein synthesis by examining its rate at 36 hrs following a training session. Six healthy young men performed 12 sets of 6- to 12-RM elbow flexion exercises with one arm while the opposite arm served as a control. MPS was calculated from the in vivo rate of incorporation of L-[1,2-13C2] leucine into biceps brachii of both arms using the primed constant infusion technique over 11 hrs. At an average time of 36 hrs postexercise, MPS in the exercised arm had returned to within 14% of the control arm value, the difference being nonsignificant. It is concluded that following a bout of heavy resistance training, MPS increases rapidly, is more than double at 24 hrs, and thereafter declines rapidly so that at 36 hrs it has almost returned to baseline.


BTW, most AS increase RBC.

 

[Fonz]

Methandrostenelone will raise blood androgen levels.

HOWEVER, dball's main mode of action is anti-catabolic.

It is capable of reducing endogenous cortisone by 50-70%.
(Please look up the studies done by Ciba in the 50's and 60's)

Hence why it works on everybody.

Fonz

 

[hhajdo]

"It is capable of reducing endogenous cortisone by 50-70%"

Not many studies that have addressed this are available online, some actually suggest that it increases cortisol:

Eksp Klin Farmakol 1992 Jan-Feb;55(1):40-2 Related Articles, Links


[Changes in the endogenous hormonal background due to anabolic steroids]

[Article in Russian]

Chermnykh NS, Andreev IuA, Syrov VN.

Studies into the effects of metandrostenolone and ecdisterone, anabolic steroids of different classes, on the content of hormones in blood plasma made it possible to establish that metandrostenolone produces appreciable changes in the hormonal background: a short-term increase in the content of corticosterone but a decline in the concentration of somatotropic hormone (STH)....


Lancet 1976 Oct 2;2(7988):699-702 Related Articles, Links


"Anabolic" effects of methandienone in men undergoing athletic training.

Hervey GR, Hutchinson I, Knibbs AV, Burkinshaw L, Jones PR, Norgan NG, Levell MJ.

On the drug, plasma-cortisol concentration and urinary cortisol excretion increased, and plasma-testosterone decreased. Although the weight and body-composition changes may demonstrate an anabolic action of methandienone in man, they may alternatively have been caused by an increase in intracellular fluid, and the question of anabolic action therefore remains open.

 

[Juice Authority]

Methandrostenelone will raise blood androgen levels.

HOWEVER, dball's main mode of action is anti-catabolic.

It is capable of reducing endogenous cortisone by 50-70%.
(Please look up the studies done by Ciba in the 50's and 60's)

Hence why it works on everybody.

Fonz

That has been my point on this issue all along regarding the anti-catabolic nature of D-bol.

Fonz, I believe it was you who originally suggested that D-bol doesn't raise test levels that much if at all.

 

[Fonz]

That has been my point on this issue all along.

Fonz, I believe it was you who originally suggested that D-bol doesn't raise test levels that much if at all.

Yes, that was me.

Dball isn't really that anabolic.

Reason why people stack Dball w/ test.

Test is primarily an anabolic. Its has next to no anti-catabolic properties(It raises protein synthesis almost as much as protein degradation).

Dball gives you a pronounced anti-catabolic effect while test gives you a pronounced anabolic effect.

Fonz

 

[Juice Authority]

Yes, that was me.

Dball isn't really that anabolic.

Reason why people stack Dball w/ test.

Test is primarily an anabolic. Its has next to no anti-catabolic properties(It raises protein synthesis almost as much as protein degradation).

Dball gives you a pronounced anti-catabolic effect while test gives you a pronounced anabolic effect.

Fonz

Ok. That's perfectly in line with what I've been saying all along which sparked this whole controversay in the first place.

 

[Juice Authority]

This thread should be moved to "Best of Elite". There's a shitload of good information on this thread. It's been very informative.

 

[celica]

great post ......

 

[hhajdo]

DBol doesn't have high affinity for AR, but its anabolic activity is caused by formation of its metabolites.

Its anabolic activity is vastly reduced when androgen receptor antagonist is added...


from Q&A by Patric Arnold (AnabolicExtreme)


Q: I hear that there are two classes of steroids. Class I bind to the androgen receptor to impart their activity and they include nandrolone and testosterone. Class II do not bind to the androgen receptor but impart their actions by as yet undetermined means. Class II steroids include d-bol and 4-AD and these are supposed to stack awesomely with Class I. Do I have this right?

A: There are not two classes of anabolic steroids. This theory has no acceptance, let alone mention, in the scientific literature, but is instead the belief of the exceptionally outspoken dudes over at Testosterone.net.

This theory can be blown out of the water by one simple fact. D-bol, 4-AD, anadrol and the other so called“Class II” steroids have very high androgenic activity. Androgenic activity is manifested through the classic androgen receptor and there is no argument about that. Therefore these “Class II” compounds, like the “Class I”, are exerting at least some part of their effects through the androgen receptor.

You want proof? Consider the following article:


--------------------------------------------------------------------------------

Effect of steroids with antiandrogenic properties on androgenic and myotrophic activity of testosterone and some of its derivatives.
Neurosci Behav Physiol.,1980


May-Jun;10(3):227-31.

In this article they use an anti-androgen (receptor antagonist) to test
effects on various tissues when taken along with a variety of
anabolic steroids. The effect with dianabol is described as follows:
"The results obtained upon joint administration of dianabol and the
antagonist were somewhat unexpected. The latter in doses of 2.5 and
7.5mg/rat/day caused a decrease in the response to dianabol only on the
part of the muscle and inhibited the stimulatory effect of dianabol on
the mass of the accessory (androgen sensitive) organs only in the
maximum dose."


--------------------------------------------------------------------------------

Dianabol is described by the T-Mag theorists as being a classic "Class
2" (acts anabolically not by the androgen receptor). This study
completely contradicts their theory because when administered with an
androgen receptor antagonist, dianabol's anabolic activity was vastly
reduced. Reduced even more so than it was with testosterone (a
purported "Class 1" steroid). I mean, these results are the total opposite of what
would be expected from the “Class Theory” of steroids!!

There is a very simple explanation why some steroids do not bind much to the androgen receptor in-vitro, yet exert strong anabolic / androgenic effects in-vivo. Hey, I did not make up this explanation, it is the one accepted by the scientists themselves. You see, many drugs do not exert their effects in their original form but are instead metabolized into the active compounds. Such drugs are termed “prodrugs”. So even though these Class II compounds have negligible binding to the androgen receptor in their parent form, they have metabolites that do bind very well. For instance, oxymetholone (anadrol) metabolizes into 17alpha methyl-DHT (mestanolone) which binds very strongly to the AR.

No, there are not two classes of anabolic steroids. The evidence does not suggest this at all. So why did such a theory get proclaimed with such confidence? Why did it get accepted by the lame ass public just because “they said so”? I dunno!