Motivation to go to the gym

They will have effect on your body composition, metabolic rate, nutrient uptake/partitioning, and all the side effects too; however, they will not make you grow any appreciable amount of muscle mass without resistance training and appropriate nutrient intake. You won't gain anything worthwhile or notable without training harder and more frequently to a degree alongside eating more of the right foods.
 
I don't like being contrarian as much as I am but someone has to do it. They absolutely will make you gain more muscle WITHOUT working out AT ALL than a natural who works out EVERY DAY. Training doesn't even have to be a part of the equation with steroids and you'll still be bigger than the naturals. I'm not encouraging the op to go ahead and take steroids now, because the truth of the matter is working out would be one of the last things on my mind if I was living out of my car. So I commend him for the positive attitude.
 
Snarky91 said:
I don't like being contrarian as much as I am but someone has to do it. They absolutely will make you gain more muscle WITHOUT working out AT ALL than a natural who works out EVERY DAY. Training doesn't even have to be a part of the equation with steroids and you'll still be bigger than the naturals. I'm not encouraging the op to go ahead and take steroids now, because the truth of the matter is working out would be one of the last things on my mind if I was living out of my car. So I commend him for the positive attitude.
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The gain in muscle from AAS without training would only seem to be roughly equal to that of a natural who does train in the short term. However those gains plateau rapidly if you don't train. Ultimately a long term natural would far outstrip anyone who took AAS and didn't train.

Probably all the AAS is doing in an untrained subject is altering the equilibrium state induced by myostatin and follistatin/GASP-1 to a slightly higher level. The muscle produced is also pretty worthless, and doesn't improve strength or physical functioning at all.

http://cat.inist.fr/?aModele=afficheN&cpsidt=16649835
 
NeighborMike said:
Im pretty sure you dont gain more muscle from taking aas and doing nothing, just more density?
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CFC and trozzle covered this thing completely.

Altered gene expression of myostatin/follistatin would allow a greater threshold of growth regardless of exercise or lack their of simply because it is disabling the mitigation effects related to the genetic markers that once dictated the aforementioned growth...if that even made sense.

Also having a higher nutrient uptake and metabolic efficiency would increase glycogen storages (muscle swelling effect from glycogen storages temporary increasing due to androgen mechanics) a higher nutritional usage (a lesser degree of nutritional substances being wasted due to spikes in protein synthesis/peptide synthesis, greater activity at the mitochondrial level/ATP)

Now I'm unsure about this, but would an influx in androgens also correlate to hyperplasia occurring in skeletal muscle tissue or is that indicative of exercise rather than supraphysiological androgen levels?
 
GrymReefer said:
Now I'm unsure about this, but would an influx in androgens also correlate to hyperplasia occurring in skeletal muscle tissue or is that indicative of exercise rather than supraphysiological androgen levels?
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I seem to remember supraphysiological AAS is linked modestly to hyperplasia through indirect mechanisms (eg MGF/IGF-1 upregulation). Interestingly myostatin has been potentially implicated in hyperplasia, indicating again the ambiguous/necessary nature of such regulators.
 
Snarky91 said:
When I first started working out I was not only too young but I was also scared to go in the gym and be judged for not being up to par. So I would do push ups and bicep curls with 10 and 15 lb dumbbells at home until I reached a point where I bought some additional equipment and eventually I knew there wasn't enough room and I actually had to go to the gym. You might benefit from just increasing the number of push ups you can do and how many pull ups and sit ups and bicep curls; all relatively easy to do at home or at a playground. It's a catch 22 how do you look fit in the gym and "fit in" without being fit in the first place...

Now, even after a layoff, I will do some pushups at home for a week or two before going back to the gym. And when I do go back to the gym I actually get strongly motivated because of my competitive nature. The girls who dress very provocatively and the guys who don't know what they're doing are an annoyance, but trust me nobody is going to fixate on what you look like or what you're doing. Take it from experience they're probably busy worrying about their own physique and their own challenges - the serious people who know what they're doing, even especially more so.
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There's actually more truth to this than most care to admit... Usually some of the biggest, fittest, most ripped people are the most insecure. Why do you think they kill themselves to look that way anyway? Granted, there are those that aren't, but a good number of people with the "best" bodies in the gym are usually the most self critical and most self conscious. If anything, if they're even looking at you it's probably because the were either 1.) in your place before (or someplace similar) or 2.) they're impressed that you're even there making an effort when you could be at home sitting on the couch eating a bag of potato chips doing nothing. When I see very out of shape people at the gym I usually think nothing of it but if anything I'm impressed that they're even at the gym doing something about it. Doing something is nothing to be embarrassed about, doing nothing is something to be embarrassed about.
 
Actually (not to sound snarky) there is some "half-truth" to this... In rats, yes suppression of myostatin and an increase in follistatin resulted in a huge amounts of muscle muscle mass gain. However, the same concept was applied to humans (naturally much much lower myostatin levels than rats) and there wasn't near as much growth seen. The pharmaceutical industry has been trying to solve this mystery for years to help treat muscular dystrophy and finally it looks like there's a breakthrough on the horizon. I'll copy and past an article from a thread I started on BYM338 aka bimagrumab by Novartis. Simply reducing the amount of myostatin in humans was ineffective. What was effective was creating a monoclonal antibody against a family of Transforming Growth Factor (TGF) receptors, specifically the TGF-Beta family receptor Activin Type IIb, which binds myostatin. By inhibiting the function of the receptor, they were able to alter the level of muscle mass one can attain and retain.
 
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This is one of my posts from December of last year that details BYM338 and why alteration of follistatin and myostatin levels don't actually have a significant effect on muscle mass generation and retention in humans.

Well, I did a site wide search for both BYM338 and Bimagrumab and came up with absolutely nothing so I wanted to open the door to the discussion of this compound (and all related compounds) as it pertains to gains (something most all of us are in the eternal pursuit of). I'm sure there are people more knowledgeable on this topic and specific antibody than I, so it'd be great to start a discussion/information thread.

BYM338 is a fully human monoclonal antibody, currently under development by Novartis Pharmaceuticals Corporation in Switzerland for treatment of sporadic inclusion body myositis (sIBM). sIBM is a rare muscle degenerative disease that usually affects adult men and women. The antibody blocks activin type IIb (and to a very small degree, type IIa) receptors, which bind ligands belonging to the Transforming growth factor beta superfamily.1 So... why's this important?

Well, I'm sure many of us are familiar with myostatin, also known as growth differentiation factor 8 (GDF-8). For those who aren't, myostatin is a protein in humans encoded via the MSTN gene and it is a member of the TGF beta protein family which is responsible for negatively regulating muscle hypertrophy and differentiation. To oversimplify, the higher the circulating plasma myostatin levels, the less muscle mass growth and development one can expect to experience. If you were to research myostatin deficiency, one of the first things you would come across would be either "Wendy the Whippet" or "Belgian Blue bulls". Both of these animals have genetic mutations in both copies of their MSTN (for reference, I'm using the human gene) gene, and as such they are significantly more muscular than their mutant-free counterparts.

Seeing as how blocking myostatin could be extraordinarily profitable, the research into myostatin inhibition has been booming since it's discovery in 1997. However, despite what any supplement or pharmaceutical company would like to claim, all human trials seeking to show a significant increase in muscle mass due to myostatin attenuation have failed. In multiple rodent models, the reduction or inhibition of myostation altogether has produced nothing short of extraordinary results. But, when the same model was applied to humans, no significant elevation in muscle mass could be observed - simply suppressing the circulating levels of myostatin in humans (through using of myostatin inhibitors, increasing follistatin levels, etc.) wouldn't do the trick.2,3

Now, however, with Novartis' fully human monoclonal antibody which blocks activin type IIb receptors (primarily responsible for binding myostatin), rather than actually lowering myostatin levels, they seem to have found some success.4 Initial trials in vitro and in vivo have demonstrated a significant increase in muscle mass in human cell cultures, rodents, and humans after treatment with the antibody.5 This antibody from Novartis seems to be just one of many approaches to blocking the activin type IIb receptors, which in itself could open up a whole new arena in regard to supplements, gene-doping, and ultimately, (at least what most of us are interested in) super-physiological muscle growth and development. The antibody is currently in phase 2, where the safety and efficacy of treatment over 52 weeks is being assessed in sIBM patients. The outlook is promising, and the trial is estimated to be completed by December of 2015.6

Cheers!

References:
1 Neurology. 2014 Nov 7. pii: 10.1212/WNL.0000000000001070.
2 Am J Pathol. 2011 Mar;178(3):1287-97. doi: 10.1016/j.ajpath.2010.11.071.
3 Cell Mol Life Sci. 2014 Nov;71(22):4361-71. doi: 10.1007/s00018-014-1689-x. Epub 2014 Jul 31.
4 Mol Cell Biol. 2014 Feb;34(4):606-18. doi: 10.1128/MCB.01307-13. Epub 2013 Dec 2.
5 Expert Opin Investig Drugs. 2014 Dec;23(12):1655-69. doi: 10.1517/13543784.2014.942729. Epub 2014 Jul 24.
6 www.clinicaltrials.gov/ct2/show/NCT01925209
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pharmbiak said:
This is one of my posts from December of last year that details BYM338 and why alteration of follistatin and myostatin levels don't actually have a significant effect on muscle mass generation and retention in humans.
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Yes I do agree, however it's the 'significance' of effect that's relevant to the speculation being made here - ie not very.

You may enjoy this recently published paper which helps further elucidate the regulatory paradox between myostatin and GASP-1/FLRG(FSTN) in muscle mass homeostasis:

(It's open access so free for all to read!)



Skeletal Muscle 2015, 5:21

Myostatin as a mediator of sarcopenia versus homeostatic regulator of muscle mass: insights using a new mass spectrometry-based assay

H. Robert Bergen12†, Joshua N. Farr34†, Patrick M. Vanderboom2, Elizabeth J. Atkinson5, Thomas A. White4, Ravinder J. Singh6, Sundeep Khosla34 and Nathan K. LeBrasseur47*


http://www.skeletalmusclejournal.com/content/5/1/21
 
The Effects of Supraphysiologic Doses of Testosterone on Muscle Size and Strength...

http://www.nejm.org/doi/full/10.1056/NEJM199607043350101#t=articleResults

Well, this is the study I have in mind. Trust me, I hate reading studies as much as the next person. They often have flaws that become apparent once you take a very close look at the methodology. I can name a dozen flaws that encompass SO MANY studies.

1. Conducted on animals and elaborated to humans.
2. Small sample size.
3. Indicating an "association" as tantamount to causation.
4. Sampling method biases/recruitment method biases.
5. Weak correlation.
6. Non-replicable results.
7. Neglecting to control for confounding variables.
8. Projecting findings taken in vitro and ex vivo to in vivo.
9. Samples that are representative of a specific population being extrapolated to populations for which they are not representative.
10. Measurement errors.
11. Improper administration including giving cues and suggestions.
12. Tampering with results.
13. Inability to ensure participants' compliance with study design.

I'm sure there are more issues I can imagine on a case by case basis, but these are some I can think right off the top of my head.

That said, the study I linked above is probably not immune to all of these problems. However, it does address some of the biggest problems; namely, this study was conducted on humans and there were human controls. That means a lot to me. Also, take a look at who commissioned the study. Is it a supplement research company... no. I always ask myself, what would the study authors/sponsors stand to gain, given the results they have presented. Call it cynical, but money corrupts most people.

In this case (my own wording), the results show that taking "600 mg of testosterone enanthate in sesame oil" and no exercise, each week for 10 weeks, induces greater gains ["fat free mass"](muscle) than taking intramuscular placebo and exercise each week for 10 weeks.

In plain english: there were four groups (hereafter the group #s are labeled in no particular order and with no significance or relation to specific naming convention(s) in the study)

Group 1. Placebo and no exercise.
Group 2. Placebo and exercise.
Group 3. Testosterone and no exercise.
Group 4. Testosterone and exercise.

[Group 1.] "Fat-free mass did not change significantly in the group assigned to placebo but no exercise"
[Group 2.] "...those in the placebo-plus-exercise group had an increase of 1.9 kg."
[Group 3.] "The men treated with testosterone but no exercise had an increase of 3.2 kg in fat-free mass..."

[Group 4.] "The increase in the testosterone-plus-exercise group was substantially greater (averaging 6.1 kg). The percentage of body fat did not change significantly in any group (data not shown)."


TO MAKE A LONG STORY SHORT.

NO EXERCISE AND NO GEAR OVER TEN WEEKS = ~0 lbs muscle increase/decrease
EXERCISE AND NO GEAR OVER TEN WEEKS = ~4 lbs muscle increase
NO EXERCISE AND GEAR OVER TEN WEEKS = ~7 lbs muscle increase
EXERCISE AND GEAR OVER TEN WEEKS = ~13.5 lbs muscle increase
 
The results of your study are pretty similar to those of the one I posted. But as said, the subject taking AAS and not training will not continue to grow, he will plateau, whereas the natural athlete will continue to gain - albeit slowly - over a much longer period of time. This is not to say AAS do nothing taken alone, but that they are still not the short-cut to an amazing body that so many believe them to be.
 
As I understand it, 6-12 weeks is considered the proper length of a cycle because gains rapidly decelerate toward the end. The study cycle length was 10 weeks; it examined a moderate-high dose of testosterone. Simply increasing the length of the cycle, increasing doses (diminishing returns be damned), and adding a second steroid such as trenbolone (or even a third) will, in my personal opinion, blow away the natural's best intentions. Moreover, steroids increase metabolism and thus increase caloric intake; Just gaining 10 lbs through eating - some will go to muscle, as a natural. With the steroid modulated increase in caloric intake, coupled with the tendency for steroids to partition comparatively greater slice of nutrients toward processes of building muscle, there's no doubt in my mind that someone hopped up on testosterone, trenbolone, and deca, will gain more muscle without training than a natural with training.

Also, the aas have fat burning properties and the quality of muscle sits on much lower body fat. Take a natural at 10% he looks like a coat hanger connected to brooms. Yet the aas user sports all the size and quality with moderate body fat.
 
I respectfully disagree. I see too many people who already train hard, eat well and also use AAS who don't make gains beyond 10-15 weeks to accept that someone not even training will do better, regardless of dose or compound used.
 
I think some of this is confused with the fact that after 25 most people stop producing GH and Test naturally..or it declines at least. So you restore that back to normal and youre probably just hitting a mini fountain of youth...if it was logical to run this test on a teenager i dont think the results would be the same
 
Well, teenagers in normal health would have medium-high levels of natural testosterone; I think the normal range is 300-850 ng/dl (give or take 50-150 ng/dl on either end).
The study participants had normal baseline testosterone. The groups were 20s and early 30s. They all had similar baseline testosterone. 10wk (week 10) testosterone levels were 5-8x higher than baseline levels. At best, one might add another control group of men who would receive small injections of testosterone to put them at the high end of the range. Those are small doses, but they would approximate the profile of a high testosterone adolescent. Let the high testosterone adolescent (low testosterone group) train to his fill. Yes, he will have more muscle because he has more testosterone. However, he only has physiological levels and the other groups have supra-physiological levels 3x higher than top end of normal range.

Your idea would make sense if the testosterone taking groups had lower levels of testosterone than the "control and exercise" and "control and no exercise group." Then you might argue the testosterone taking participants had low level of testosterone to begin with and the exogenous hormones merely caught them up in testosterone and muscle mass that they were lacking compared to those who didn't take testosterone. In that case, you're arguing the calibration standard is off because the scale was -10 lbs. Correcting the scale would add 10 lbs and give the illusion that one had gained in comparison to those who had a proper functioning scale to begin with. Tenuous theory; more, it is demonstrably untenable because the control data don't support it.

One might also argue the groups with testosterone had background in weightlifting and the testosterone mediated an increase due in part to muscle memory. But the men were assigned randomly to each group, so training experience was balanced. The study is solid. It's why I see big guys in the gym working with moderate weights. They don't need much stimulus to grow significantly. Naturals always have a decent strength level because they will not grow if they do not take proper advantage of the damage/demand-adaptation relationship.

Having said all that, natural muscle will not disappear if you take a few months off. It is quick to reconstitute in the capacity what it's already adapted before. It is denser and tougher and stronger... it can do more work per cross section of muscle than a steroid user. It is more efficient. It grows through processes with tight time limited constraints. The coefficient is what matters at the end of the day. You can be big at high body fat, but your greater absolute muscle does not translate to muscle quality. Superior muscle is well adapted to handling high relative strength loads. Natural muscle mass is tightly related to body fat levels. A mechanic's forearms show sinews and striations from years of labor. The steroid user's forearms blow up to eye-catching dimensions, but they are not strong because they have weak connections at the elbow and can't work dynamically. Naturals seldom worry about strength that overburdens their connective tissues.

Natural muscle is superior. But people don't take steroids to see the fruits of hard work; they take them to be bigger and badder than the local gym rat.
 
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