07-25-2005, 01:21 AM
As far as I understand HST does not believe in overtraining of muscles, other than the CNS burnout. Does this mean that you are not in danger of muscle atrophy as a result of overuse? If this is the case, would the only drawback to training too frequently be conditioning the muscles so that they do not grow any further? If there is no such thing as overtraining of the muscles what is it about anabolic steroids that allows a person to recover in order to train at a higher intensity and frequency without overtraining? Do "steroids" help prevent CNS burnout?
07-25-2005, 01:53 PM
HST does acknowledge overtraining of the muscle tissue itself, but the effects are inflammatory in nature and result in injuries that do not heal up properly but instead leave scar tissue in the muscle.
Any loss in the size of a muscle with high volume/high frequency training is the result of altered glycogen and water distribution.
Endurance training, as apposed to overtraining, can result in atrophy of muscle tissue if the training is of sufficient duration and consistency. Some muscle fibers will shrink in order to facilitate metabolic activities.
As for steroids, yes, androgens act as direct CNS stimulants through nongenomic pathways. The long term traditional effects of using testosterone are as follows:
Enhanced protein synthesis
Enhanced growth factor activity (e.g. GH, IGF-1, etc.)
Enhanced activation of myogenic stem cells (i.e. satellite cells)
Enhanced myonuclear number (to maintain nuclear to cytoplasmic ratio)
New myofiber formation
Many people are unfamiliar with the nongenomic effects however. Most people know that there is only one classical androgen receptor (AR). The AR exerts its differing effects through differences in the binding affinity and duration of testosterone and its 5-alpha-reduced metabolite DHT. Both the binding affinity and the duration of binding will lead to different physiological effects.
Recently (ok, not that recently) however, more attention has been drawn to what are called nongenomic effects of steroids. They are called nongenomic because the don’t directly involve the steroid bound to the AR acting directly on the cells DNA.
It is known that steroids bound to its receptor can act on the cell membrane to bring about various second messenger effects. These second messenger pathways involve kinase pathways driven by classical receptors (MAPk, ERK, MEK, etc), as well as cyclic AMP, lipase and other kinase pathways (PI3K, PKA, PKC, etc), including ion fluxes (Ca++), which are driven by nonclassical receptors. All in all, steroids affect cells through several different pathways and at least one additional receptor, none of which involve what most people consider the true mechanism of steroid action.
Concerning the topic of this thread, most all of these nongenomic affects of steroids are acute, or immediate. Meaning, they occur within seconds or minutes of the steroid interacting with the cell. This helps to explain why so many different organs have androgen receptors or are sensitive to androgen levels. For example, in tissues taken from rats, (in order of sensitivity):
Bulbocavernosus muscle (penis)
The hypothalamus, part of the CNS, has a higher concentration of ARs than even the quads. That is an interesting fact. Of course this is from rats but human would no doubt show “similar” distributions though not exactly alike.
It is perfectly reasonable that androgens act at a direct CNS stimulant (not to mention Ca++ agonist) through nongenomic pathways such as cAMP. Keep in mind that this is the same second messenger pathway utilized by catecholamines and like drugs (adrenaline, noradrenaline, ephedrine, caffeine, etc)
Here are some references: (There are many many more like these)
1. Losel R, Wehling M. Nongenomic actions of steroid hormones. Nat Rev Mol Cell Biol. 2003 Jan;4(1):46-55.
2: Schmidt BM, Christ M, Falkenstein E, Wehling M. Nongenomic steroid actions: completing the puzzle. Aldosterone as an example. Exp Clin Endocrinol Diabetes. 1998;106(6):441-5.
3: Cato AC, Nestl A, Mink S. Rapid actions of steroid receptors in cellular signaling pathways. Sci STKE. 2002 Jun 25;2002(138):RE9.
4: Christ M, Haseroth K, Falkenstein E, Wehling M. Nongenomic steroid actions: fact or fantasy? Vitam Horm. 1999;57:325-73.
5: Falkenstein E, Tillmann HC, Christ M, Feuring M, Wehling M. Multiple actions of steroid hormones--a focus on rapid, nongenomic effects. Pharmacol Rev. 2000 Dec;52(4):513-56.
6: Wehling M. Specific, nongenomic actions of steroid hormones. Annu Rev Physiol. 1997;59:365-93.
7: Schmidt BM, Gerdes D, Feuring M, Falkenstein E, Christ M, Wehling M. Rapid, nongenomic steroid actions: A new age? Front Neuroendocrinol. 2000 Jan;21(1):57-94.
8: Gerdes D, Christ M, Haseroth K, Notzon A, Falkenstein E, Wehling M. Nongenomic actions of steroids--from the laboratory to clinical implications. J Pediatr Endocrinol Metab. 2000 Jul-Aug;13(7):853-78.
9: Joels M. Modulatory actions of steroid hormones and neuropeptides on electrical activity in brain. Eur J Pharmacol. 2000 Sep 29;405(1-3):207-16.
10: Spindler KD. Interactions between steroid hormones and the nervous system.
Most people feel an almost immediate increase in exercise tolerance when they begin using testosterone. This allows them to train harder, longer and more frequently. As you can see from the traditional effects of testosterone it also helps to prevent scarring in muscle tissue by upregulating growth factors and satellite cell activity.
07-25-2005, 02:25 PM
Thanks for taking the time to answer my question thoroughly.
Much appreciated, but I have more questions. LOL
Is stimulating synonymous with recovery or does the stimulation facilitate recovery?
If so then would taking effedrine and caffeine help my CNS recover faster?
While studying Intro to Psychology in college, I was taught that stimulating the CNS with cocaine, caffeine, and "steroids" *and other drugs etc. actually destroys the nerves and makes it more dull and resistant to stimulation, is this true?
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