Continued discussion from Dizzle's thread

[SwollOnIron]

I don't want to hijack Dizzle's thread, but I want to continue a discussion started by Dinoiii and JSwoll.

...understand that 10 pounds gained in 2 weeks AND MAINTAINED - regardless of who claims it is IS NOT MUSCLE - I hate to break that news to a lot of on-lookers (hate me if you will, but I continue to chose not to blow flowers up your a**).

Sorry, D, I laughed my ass off reading this, actually assembling (not just the storage and compilation of) genetic material into muscle is a very involved process that takes a finite amount (meaning at some point it can no longer be reduced by any agent) and some times I find the weight total funny. But it's true none-the-less, the weight may be there; it just may be rapidly stored fat, water retention, and that last heavy meal you just ate.

OK, in the spirit of debate/education lets explore this a little more:
In my experience most people tend to claim a total amount of weight gained. Then which you can take before and after BF measurements to determine how much is actually lean muscle.

Now an artificial increase in sarcoplasmic fluid (via PH/AAS) may skew the results slightly, it still seems very logical to me that there is SOME true hypertrophy induced in a two week period. You can attribute much of the water weight to this factor. But since muscle is 80% water (if I recall properly)....it seems like you are splitting hairs.

Additionally, hypertrophy is defined as: excessive development of an organ or part; specifically : increase in bulk (as by thickening of muscle fibers) without multiplication of parts.
http://www2.merriam-webster.com/cgi-bin/mwmednlm?book=Medical&va=hypertrophy

or:
The enlargement or overgrowth of an organ or part due to an increase in size of its constituent cells.
http://cancerweb.ncl.ac.uk/cgi-bin/omd?query=hypertrophy&action=Search+OMD

To me, it seems that an increase in water retention = an increase in intracellular (sarcoplasmic) fluid IS hypertrophy.

Now, if we are talking about new protein synthesis...well that happens 24/7. It is a continuous process through out the entire body (intestines, heart, skeletal muscle etc)...it is not an isolate event that only takes place in response to training or nutrient timing.

Additionally, receptor activation and subsequent transcription/translation is fairly straight forward (in theory): with oral PH that are steroids (or convert to steroids), you ingest them; they are absorbed; reach the blood stream; circulate; diffuse across the cell membrane into the cytoplasm then into the nuclear membrane. Inside the nucleus, it binds a nuclear receptor, a conformational change ensues and the receptor is activated. Then transcription/translation proceed.

I am at odds with the thoughts that say initial cellular actions (penetration, binding, transcription/translation) are the ultimate rate limiting step (by taking days or weeks to initiate an effect). Don't get me wrong - the quantity of cellular actions do correlate with the amount of new protein synthesis, but the process does not take days or weeks to become activated. It take minutes. It takes time for a sufficient quantity of receptors to become activated to produce a visible, macroscopic result. But this is in part to the fact that response is dose dependant, receptor saturation takes a finite amount of time, up/down regulation, and quantity of specific receptor availability.

Synthetic hormones can and do produce a much faster response than native hormones simply because of the dose involved in a certain period of time. native steroid hormones are very slowly and gradually released in response to changes in the internal environment. They are not meant to be released in massive, profound, effect inducing amounts. With synthetic steroid hormones / PH, this is exactly what is happening. A large amount of steroid hormone is rapidly introduced to the system. Once again, after absorption, the process from circulation to receptor activation should take minutes. Not days.

Lets look at a steroid hormone that is in certain circumstances released in a very large amount: Cortisol. What is the result of a massive cortisol dump? Mainly gluconeogenesis (and occasionally resulting fat accumulation). If steroid hormones could not induce effects during the same hour, much less the same day they are released, how then does cortisol induce catabolism after exercise, training, fasting etc?

Test injection causes a decline in native test production. This occurs in minutes after injection. The end result (total shut down) is not observed for days or weeks - but this is due to dose administered, normal levels, receptor saturation, up/down regulation, and quantity of specific receptor availability.

Many people report an increase in strength (even slight) within days of taking PH/AAS (like anavar). IMO, there are two main reasons for this - 1)Myosin heavy-chain synthesis rate is correlated with measures of muscle strength (meaning rapidly induced by the PH/steroid. 2) Additional cellular fluid volume can offer greater buffer capacity, nutrient stores etc. So...the main component of hypertrophy (fluid / cellular size) coupled with an increase in synthesis of the contractile protein myosin = an increase in strength...once again, this IS hypertrophy, and it takes min/hours.

OK, to recap my thoughts:

Hypertrophy (...due to an increase in size of its constituent cells) IS an increase in muscle fluid.

Hyperplasia (...increase in the number of normal cells in normal arrangement in a tissue) is more closely related to the previous time/environmental constraints mentioned by others, and IMO what many people misconstrue hypertrophy to be.

Protein synthesis is a 24/7 continuous process.

Steroid hormone receptor activation and subsequent translation/transcription takes place within minutes of the hormone entering circulation.

Response of all steroid hormones response are dose dependant; receptor saturation takes a finite amount of time; up/down regulation, and quantity of specific receptor availability all effect ultimate transcription/translation.

Synthetic hormones are usually administered in dose much greater than their native counterparts, and as a result of this greater dose, will produce a response QUICKER.

So far, I am forced to conclude that a hypertrophic response can and is induced rapidly after synthetic steroid ingestion/circulation. I cannot see how it will take a synthetic steroid hormone days or weeks to induce change, when native hormones induce change almost instantaneously.


Please feel free to continue the discussion. I hope to learn something ;)

[dinoiii]

I think you have explained your case well...allow me to explain why I don't agree. Namely, you have forgotten an intricate component involved in straited muscle reconstruction - that is the genetic intermediate and how this affects protein synthesis.

Yes, you are undergoing protein synthesis 24/7 (protein synthesis is neither synonomous nor homologous with skeletal muscle hypertrophy) as you suggest but these changes in regards to muscle hypertrophy happening now actually began WEEKS ago. Despite the issue with us having the neuronal response at an almost immediate rate, I cannot disagree - but this is NEITHER influenced by nor the starting point of actual "hypertrophy" without continual stimulation.

As the muscle continues to receive increased demands, the synthetic machinery is upregulated. This upregulation (through our limited means to date - perhaps someone can correct me) appears to begin with the ubiquitous second messenger system (including phospholipases, protein kinase C, tyrosine kinase, and others). These, in turn, activate the family of immediate-early genes, including c-fos, c-jun and myc. These genes appear to dictate the contractile protein gene response. Finally, the message filters down to alter the pattern of protein expression (mind you, as I said earlier - the protein synthesis occuring now had likely been the end result of weeks ago training/myofibril breakdown). It can take as long as two months for actual hypertrophy to begin. The additional contractile proteins appear to be incorporated into existing myofibrils (the chains of sarcomeres within a muscle cell). There appears to be some limit to how large a myofibril can become: at some point, they split. These events appear to occur within each muscle fiber. That is, hypertrophy results primarily from the growth of each muscle cell, rather than an increase in the number of cells (which echos your hypetrophy versus hyperplasia argument, but I think you have gone WAY too simplistic).

This is why what is "thought" to be hypertrophy without allowing these intermediate steps to take place is literal hogwash.




Next, you suggest quite a bit about intracellular fluid, but an intracellular build up WILL NOT OCCUR in vaccuum unless you are suggesting all osmotic regulators to have broken down. That being said, you would likely "celebrate" edematous, ascitic, and other high-fluid conditions well before any "hypertrophy" which is just not the case.




Think too of the simple uniform "enlargement" seen with the prototypical "recreational" PH/PS/AAS user. Do you think ALL users of such product experience growth in a universal manner? The answer is ABSOLUTELY NOT....there is a disproportionate number of receptors in humans throughout the upper arms, chest, and back - the usual response to quoted growth however is universal - which in ANY time frame makes absolutely no sense.





Perhaps you can enlighten me to something different here, but this argument is not simply one of hypertrophy versus hyperplasia, nor does it center on intracellular versus extracellular......I will offer one more piece of anectdotal evidence before I go and it is a very important point. This "anabolism" suggested with all of these various products falters at one thing which is why post-cyclers actually are quoted at "losing all their gains" should they not do PCT well - which is so not true of an actual hypertrophic state on a cellular level (hence, the evolution of topics such as "muscle memory", et al. but I will save that one for a later date).

[Jswoll]

Not ignoring, just working and long threads are hard to read here, will look at this and respond as time allows.

[SwollOnIron]

Hey thanks for the response Dinoiii ! I was very interested in a more detailed view of your thoughts.
Above you mentioned that current hypertrophy is the result of previous and continued stimulation (which I agree with).

But if it can take up to two months for true hypertrophy to begin, how then will shorter oral PH cycles ever generate hypertrophy (cycles lasting less than 2 months)?

OK, to help me understand this better - what time frame are you suggesting that oral PH use can actually contribute to true hypertrophy?

Most oral cycles are not 2 months long, and appear to average 3-6 weeks. Are any of these cycles effective of stimulating true hypertrophy since the agent is only on board for a short time?

Also, back to the intracellular / intrasarcoplasmic fluid topic - creatine (along with many other agents) is touted as being a "cell volumizer" to which many people can attest to an increase in fullness, pump etc while on creatine. I have never encountered anyone who suffered from edema as a result of creatine ingestion. Many people have experience bloating on mono, but that seems to have been resolved for most people with the use of CEE or CMC. So, I am just throwing this out there...how then can creatine cause an increase in skeletal muscle cell volume without say, increasing whole body cellular volume (epithelial, smooth muscle, etc)....
To me it seems you answered this question for me by pointing out the differences of receptor location/density - but at the same time this would seem to reinforce IMO, that a rapid site specific increase in cellular volume can take place with the use of oral PH.

[dinoiii]

All things considered - hyprtrophy can be expedited at best...you have not delved into the alternative mechanisms of action for anabolics like their anti-catabolic nature....I talk about this more in PCT:ACV II. Prevention of current catabolic effects could easily accelerate hypertrophic processes begun into action months prior as it is easy to imagine that AAS/PH/PS users aren't picking up a weight for the first time.

one thing you are forgetting too is with 17 alpha alkylated ones that the extended half-life of the essential metabolite lingers well beyond your cycles dates, which offers potential rationale as to why you would get prolonged effects or hold on to gains for those that report it.


Some time ago, I offered up the notion that I felt that short cycles were NOT worth it and got chastized for it and pulled out b/c it was claimed I was irresponsible and the like when people weren't getting what I said and reading into things interestingly....that being said, I feel that a longer cycle is a necessity to see true cycle effects maximized and "worthwhile" in attempt to steer away from what I would call transient gains. People will likely spit at me and call my mother names based on that response, but it is true. I feel no different from the current PH era that I did the one prior, and this one is a tad more suspect.







Some studies have shown that creatine supplementation increases both total and fat-free body mass, though it is difficult to say how much of this is due to the training effect. Since body mass gains of about 1 kg (about 2.2 pounds) can occur in a week's time, several studies suggest that the gain is simply due to greater water retention inside the muscle cells. However, studies into the long-term effect of creatine supplementation suggest that body mass gains cannot be explained by increases in intracellular water alone. In the longer term, the increase in total body water is reported to be proportional to the weight gains, which means that the percentage of total body water is not significantly changed. The magnitude of the weight gains during training over a period of several weeks argue against the water-retention theory.

It is possible that the initial increase in intracellular water increases osmotic pressure, which in turn stimulates protein synthesis. A few studies have reported changes in the nitrogen balance during creatine supplementation, suggesting that creatine increases protein synthesis and/or decreases protein breakdown. Again, while hypothesized, this remains unproven.

So we're all clear at relational theory here that will put things in better light:
Serum Sodium = Total Body Sodium / Total Body Water.....the stuff we measure is not remotely telling the story and it is imperative to keep this basic equation in mind to aid figuring out what happens between Water/Sodium balance which essentially piggyback one another and contribute to your "true water weight" gain while on mono OR any other brand of creatine....you have a certain saturation of creatine stores people seem to always forget.....you take a 20 oz container and fill it with 25 oz., there is a good chance that 5 oz. falls to the table. Same story with total body water concentration....it fills certain areas. When you add something like creatine to water, you are in the process of creating a hypertonic solution....I ask you to look back at our equation above....if you throw more water into the collective process, your osmotic processes will DECREASE serum sodium in response....this causes an OSMOTIC SHIFT OUT OF CELLS not in as the pretty ads and pictures lead you to believe. The body will NOT allow these substances to cross the cell membrane (muscle tissue or otherwise provided saturation) because of the osmotic gradients that are created.

How did many supplement "gurus" with companies (which I guess makes you a guru) attempt to solve getting more creatine in the cell....oh wonder boys decide to add glucose (sugar)...terrific - hyperglycemia increases osmotic pressure ad water shifts from cells into the extracellular compartment (it actually leads to a dilutional hyponatremia which is why you tend to feel thirsty when you have a lot of creatine product or why you become dehydrated when you decide to not allow your body water in response - again, see our equation above). For every 100mg/dL increase in blood glucose above normal levels, the serum sodium level decreases about 3 mEq/L. Note that the actual sodium content in the ECF is unchanged. If this happens abruptly enough....remember water piggybacks sodium....and they both ride hand in hand with glucose in attempt to dilute the solution.



For those that did not follow the above....the extracellular fluid or ECF is made up of plasma and interstitium (area between cells) - this is where MOST fluid equilibrium occurs and likely the place that harbors extra water in ALL of these situations - whether it be creatine, a PH/PS, or otherwise.

[Jswoll]

started typing, will have thoughts posted in the morning, too much to do on such a busy work day.

[SwollOnIron]

How did many supplement "gurus" with companies (which I guess makes you a guru) ...


Hope you are not referring to me here- I have no company, make no claims to fame, and am simply trying to lean/understand things better.

Thanks for your response...the "anticatabloic" effect of PH/AAS is an interesting notion that I have not previously considered.

Based on previous comments, I am still curious as to what you would say the 'minimum' length of an oral PH cycle should be. I am guessing greater than 4 weeks, and possibly 2 months. At this point though (2 months), I would think that we are also getting close to a safety threshold. If you are not comofrotable posting that, just PM me :)

[MVP]

I'm all ears-following intently.

[dinoiii]

Hope you are not referring to me here- I have no company, make no claims to fame, and am simply trying to lean/understand things better.

...

Based on previous comments, I am still curious as to what you would say the 'minimum' length of an oral PH cycle should be. I am guessing greater than 4 weeks, and possibly 2 months. At this point though (2 months), I would think that we are also getting close to a safety threshold. If you are not comofrotable posting that, just PM me :)

I was not insinuating anything of the sort with the company thing to you at all - it was an indirect industry statement. hope that's clarified.

Now, based on what I have said - a "minimum" length is dependent upon goals. I believe anabolic microcycling actually could have benefits if simply trying to use them as anti-catabolics, but in the anabolic sense - I think it is clear what I think needs to be done (i.e. - > 4 weeks - YES, however, not necessarily 2 months provided other factors are in check - this is where additionally supplementation and diet/lifestyle play a HUGE role in recovery time. I ALWAYS say get all other items in check FIRST and then consider anabolic routes.). As far as the "safety threshold" - hell, there is a dose-response curve for ALL items whether you use them in a 2 week time frame or a 4 week one. the trade-off is what kind of efficacy you'll see without first reaching peak plasma levels, second inadequate time to respond to the various reconstruction demands (i.e. - back to our hypertrophy argument).