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To keep your gains, do you have to keep on cycling?
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lefler
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interesting read i found on-line:
Muscle growth is a specialized form of protein synthesis. As we saw above, a steroid hormone (testosterone) enters the muscle cell by diffusing directly across the cell membrane, combines with a receptor in the cell and then stimulates gene transcription and protein formation via the DNA -> mRNA -> tRNA -> protein pathway. Specific receptors and genes are involved.
Muscle cells, as mentioned before, are long cells called myofibrils. They differ from most other cells in that when muscles grow, the individual cells simply become thicker and longer instead of dividing into entirely new cells. Muscle cells also differ from most other body cells in that muscle cells are multinucleated. A myofibril may increase in size up to 28 times its initial size.
The interesting questions come in as we start looking at exactly how and when this process occurs. Human growth hormone (hGH) and insulin-like growth factors (IGFs) seem to play an important, though somewhat unclear, role.
hGH is released from the anterior pituitary and travels through the blood. It acts on the liver to release IGFs. Both IGFs and hGH are peptide hormones; IGFs are structurally very similar to a large section of the insulin molecule - hence their name.
What precisely happens at the muscle cell is not known, but we can make some fairly well-informed speculation. Since IGFs are similar to insulin, it makes sense to think that they would also have a similar function. So IGFs probably work to increase uptake of amino acids and glucose into muscle cells. It is not clear whether muscle cells have receptors for hGH, but if they do, then it could be that hGH increases nuclear division in muscle without triggering cellular division (mitosis).
We have seen how DNA and RNA are critical to protein synthesis, so it is clear that having more nucleii within muscle would be very beneficial for more rapid protein synthesis (muscle growth). It turns out that each nucleus has a sort of effective "range". When the muscle grows, it can only grow as far as the nucleii will "reach". So the number of nucleii control the ultimate size of the muscle fiber. One of the major functions of hGH is to stimulate cell division. Now, if there are hGH receptors in muscle, but muscle cells lack the ability to divide, and hGH has an anabolic effect on muscle, it stands to reason that hGH is increasing the nuclear division process (and thus the total number of available nucleii in the muscle), but the cytoplasmic separation process never kicks in. Perhaps the mechanism for it that is found in most cells has been lost over time in muscle as an evolutionary adaption. (There is no doubt that muscles are very important to survival!)
It seems then that hGH and IGFs might have complementary functions in stimulating muscle growth. hGH could be instructing the muscle cells to "build more factories" for muscle while IGFs could be stimulating the cells to take in more "building blocks" for protein synthesis. Both hGH and IGFs may affect other important components in the process as well - such as increasing the production of hormone receptors or tRNA or activating enzymes that accelerate transcription.
Multinucleation might explain the longstanding anecdotal phenomenon most bodybuilders call "muscle memory". Muscle memory is recognized when someone who has had a substantial muscular mass and then lost it due to injury or layoffs from training, returns to training and regains the majority of the mass in a much shorter time than was initially required to develop it. What could be happening is this: the specific muscle proteins in the muscle were cannibalized by the body for energy production during non-use. However, the muscle retains the higher than average number of nucleii that the previous exercise stress caused the body to create. When presented with exercise and proper nutrients, new protein synthesis can occur at an accelerated rate.
Muscle growth is a specialized form of protein synthesis. As we saw above, a steroid hormone (testosterone) enters the muscle cell by diffusing directly across the cell membrane, combines with a receptor in the cell and then stimulates gene transcription and protein formation via the DNA -> mRNA -> tRNA -> protein pathway. Specific receptors and genes are involved.
Muscle cells, as mentioned before, are long cells called myofibrils. They differ from most other cells in that when muscles grow, the individual cells simply become thicker and longer instead of dividing into entirely new cells. Muscle cells also differ from most other body cells in that muscle cells are multinucleated. A myofibril may increase in size up to 28 times its initial size.
The interesting questions come in as we start looking at exactly how and when this process occurs. Human growth hormone (hGH) and insulin-like growth factors (IGFs) seem to play an important, though somewhat unclear, role.
hGH is released from the anterior pituitary and travels through the blood. It acts on the liver to release IGFs. Both IGFs and hGH are peptide hormones; IGFs are structurally very similar to a large section of the insulin molecule - hence their name.
What precisely happens at the muscle cell is not known, but we can make some fairly well-informed speculation. Since IGFs are similar to insulin, it makes sense to think that they would also have a similar function. So IGFs probably work to increase uptake of amino acids and glucose into muscle cells. It is not clear whether muscle cells have receptors for hGH, but if they do, then it could be that hGH increases nuclear division in muscle without triggering cellular division (mitosis).
We have seen how DNA and RNA are critical to protein synthesis, so it is clear that having more nucleii within muscle would be very beneficial for more rapid protein synthesis (muscle growth). It turns out that each nucleus has a sort of effective "range". When the muscle grows, it can only grow as far as the nucleii will "reach". So the number of nucleii control the ultimate size of the muscle fiber. One of the major functions of hGH is to stimulate cell division. Now, if there are hGH receptors in muscle, but muscle cells lack the ability to divide, and hGH has an anabolic effect on muscle, it stands to reason that hGH is increasing the nuclear division process (and thus the total number of available nucleii in the muscle), but the cytoplasmic separation process never kicks in. Perhaps the mechanism for it that is found in most cells has been lost over time in muscle as an evolutionary adaption. (There is no doubt that muscles are very important to survival!)
It seems then that hGH and IGFs might have complementary functions in stimulating muscle growth. hGH could be instructing the muscle cells to "build more factories" for muscle while IGFs could be stimulating the cells to take in more "building blocks" for protein synthesis. Both hGH and IGFs may affect other important components in the process as well - such as increasing the production of hormone receptors or tRNA or activating enzymes that accelerate transcription.
Multinucleation might explain the longstanding anecdotal phenomenon most bodybuilders call "muscle memory". Muscle memory is recognized when someone who has had a substantial muscular mass and then lost it due to injury or layoffs from training, returns to training and regains the majority of the mass in a much shorter time than was initially required to develop it. What could be happening is this: the specific muscle proteins in the muscle were cannibalized by the body for energy production during non-use. However, the muscle retains the higher than average number of nucleii that the previous exercise stress caused the body to create. When presented with exercise and proper nutrients, new protein synthesis can occur at an accelerated rate.
Hahnb
New member
krishna said:
I think you need to do some more research, deca or eq does not strengthen tendons-this is a common misconception. Take a look at this...
Number one would be the direct impact AAS have on type III collagen synthesis, collagen fibrils dysplasia, and the consequent reduction on tendon tensile strength, rupture strength and the normal biomechanics of the extremities (1,2,3,4,5,6,7,8). In a nutshell, the use of AAS in order to heal tendon injuries or to simulate collagen synthesis and therefore building stronger tendons seems to a load of crap. That famous post on AAS and collagen synthesis which throws a bunch of percentage on collagen synthesis with no references whatsoever is at best extremely doubtfull.
This alterations in the type of collagen III to type I ratio could in itself lead to the development of what is known as tendinosis (see link posted above).
Number two would be the reduction in growth factors shown to stimulate the synthesis of type I collagen on connective tissue, such as GH (9), IGF-1 (10,11,12,13,14) and TGF-beta1 (15,16), all of which could potencialy help reversing this altered ratio of collagen types due to heavy androgen use.
This reduction could happen by various motives.
One would be the androgen induced hipogonadism in the PCT period. Testosterone levels have been shown to directly correlate with GH and other growth factors release (17,18,19,20,21,22) so the low testosterone could have a negative impact on some of the growth factors that could potencially reverse the damage done by androgens.
Another motive would be the use of tamoxifen during and after a steroid cycle.
Tamoxifen has been linked to reduction in IGF-1 levels that range from 19% to 47%(23,26,27,28,29,30,31,32,33,34), and in GH response to GHRH (24,25,27). Since GH seems to be not only regulating both IGF-1 but also TGF levels, tamoxifen may also be contributing to the aggravation of the tendon issues initiated by AAS.
In my case, all the episodes of tendinosis happened either when using tamoxifen during PCT teraphy (so while hipogonadal), after usage of androgens that stimulate collagen type III production, or during tamoxifen use with AAS in order to combat gynecomasty.
If anyone wants to discuss this and try to debunk my theory or my interpretation of the research, please go ahead.
There's txt file attached with most abstracts from studies referenced here
References:
1-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.
2-Collagen synthesis in postmenopausal women during therapy with anabolic steroid or female sex hormones.
Hassager C, Jensen LT, Podenphant J, Riis BJ, Christiansen C.
Department of Clinical Chemistry, Glostrup Hospital, University of Copenhagen, Denmark.
3-The effects of anabolic steroids on rat tendon. An ultrastructural, biomechanical, and biochemical analysis.
Inhofe PD, Grana WA, Egle D, Min KW, Tomasek J.
Department of Orthopaedic Surgery, University of Oklahoma College of Medicine,
Oklahoma City, USA.
4-The effect of anabolic steroids on the biomechanical and histological properties of rat tendon.Miles JW, Grana WA, Egle D, Min KW, Chitwood J.
University of Oklahoma Health Sciences Center, Oklahoma City.
5-Anabolic steroid-induced tendon pathology: a review of the literature.Laseter JT, Russell JA.
Joe W. King Orthopedic Institute, Houston, TX 77030.
6-The effect of exercise and anabolic steroids on the mechanical properties and crimp morphology of the rat tendon.
Wood TO, Cooke PH, Goodship AE.
Comparative Orthopaedic Research Group, University of Bristol, England.
7-Tendon injuries induced by exercise and anabolic steroids in experimental mice.
Michna H.
8-Organisation of collagen fibrils in tendon: changes induced by an anabolic
steroid. I. Functional and ultrastructural studies.
Michna H.
9-Growth hormone influences the content and composition of collagen in the aorta from old rats.
Bruel A, Oxlund H.
Department of Connective Tissue Biology, Institute of Anatomy, University of
Aarhus, DK-8000, Aarhus, Denmark. [email protected]
10-Allampallam K, Chakraborty J, Robinson J. Effect of ascorbic acid and growth factors on collagen metabolism of flexor retinaculum cells from individuals with and without carpal tunnel syndrome. J Occup Environ Med 42(3):251-9, 2000.
11-Conti N A, Dahners L E. The effect of exogenous growth factors on the healing of ligaments. Trans Orthop Res Soc 18:60, 1993.
12-Letson A K, Dahners L E. The effect of combinations of growth factors on ligament healing. Clin Orthop 308;207-212, 1994.
13-Kurtz C A, Loebig T G, Anderson D D, DeMeo P J, Campbell P G. Insulin-like growth factor I accelerates functional recovery from Achilles tendon injury in a rat model. Am J Sports Med May-Jun;27(3):363-69, 1999.
14-Abrahamsson S O. Similar effects of recombinant human insulin-like growth factor I and II on cellular activities in flexor tendons of young rabbits: experimental studies in vitro. J Orthop Res Mar;15(2):256-62, 1997
15-Chang J, Thunder R, Most D, Longaker M T, Lineaweaver W C. Studies in flexor tendon wound healing: neutralizing antibody to TGF-beta1 increases postoperative range of motion. Plast Reconstr Surg Jan;105(1):148-55, 2000.
16-Chang J, Most D, Stelnicki E, Siebert J W, Longaker M T, Hui K, Lineweaver W C. Gene expression of transforming growth factor beta-1 in rabbit zone II flexor tendon wound healing: evidence for dual mechanisms of repair. Plast Reconstr Surg Sep;100(4):937-44, 1997.
17-Activation of the somatotropic axis by testosterone in adult men: evidence for a role of hypothalamic growth hormone-releasing hormone.Bondanelli M, Ambrosio MR, Margutti A, Franceschetti P, Zatelli MC, degli Uberti EC.Department of Biomedical Sciences and Advanced Therapies, Section of
Endocrinology, University of Ferrara, Ferrara, Italy.
18-Serum levels of insulin-like growth factor I and insulin-like growth factor-binding protein 1 correlate with serum free testosterone and sex hormone binding globulin levels in healthy young and middle-aged men.
Erfurth EM, Hagmar LE, Saaf M, Hall K.
Department of Internal Medicine, University of Lund, Sweden.
19-Low circulating levels of insulin-like growth factors and testosterone in chronically institutionalized elderly men.
Abbasi AA, Drinka PJ, Mattson DE, Rudman D.
Department of Medicine, Medical College of Wisconsin, Milwaukee.
20-Testosterone increases serum 1,25-dihydroxyvitamin D and insulin-like growth factor-I in hypogonadal men.
Hagenfeldt Y, Linde K, Sjoberg HE, Zumkeller W, Arver S.
Department of Clinical Chemistry I, Huddinge University Hospital, Sweden.
21-Chronic sex steroid exposure increases mean plasma growth hormone concentration and pulse amplitude in men with isolated hypogonadotropic hypogonadism.Liu L, Merriam GR, Sherins RJ.
22-Serum insulin-like growth factor-I and serum testosterone status of elderly men in an inpatient rehabilitation unit.
Kosasih JB, Abbasi AA, Rudman D.
Department of Physical Medicine & Rehabilitation, Medical College of Wisconsin, Milwaukee, USA.
23-Effect of low dose tamoxifen on the insulin-like growth factor system in healthy women.Bonanni B, Johansson H, Gandini S, Guerrieri-Gonzaga A, Torrisi R, Sandri MT, Cazzaniga M, Mora S, Robertson C, Lien EA, Decensi A.
24-Effect of tamoxifen on GH and IGF-1 serum level in stage I-II breast cancer patients.Mandala M, Moro C, Ferretti G, Calabro MG, Nole F, Rocca A, Munzone E, Castro A, Curigliano G.Division of Medical Oncology, European Institute of Oncology, Via Ripamonti 435, 20141-Milan, Italy. [email protected]
25-Inhibitory action on GHRH-induced GH secretion of chronic tamoxifen treatment in breast cancer.De Marinis L, Mancini A, Izzi D, Bianchi A, Giampietro A, Fusco A, Liberale I, Rossi S, Valle D.
Institute of Endocrinology, Catholic University School of Medicine, Rome, Italy.
[email protected]
26-Effect of tamoxifen on lipoprotein(a) and insulin-like growth factor-I (IGF-I) in healthy women.
Decensi A, Robertson C, Ballardini B, Paggi D, Guerrieri-Gonzaga A, Bonanni B, Manetti L, Johansson H, Barreca A, Bettega D, Costa A.
FIRC Chemoprevention Unit, European Institute of Oncology, Milan, Italy.
[email protected]
27-Effect of acute and chronic administration of tamoxifen on GH response to GHRH and on IGF-I serum levels in women with breast cancer.Corsello SM, Rota CA, Putignano P, Della Casa S, Barnabei A, Migneco MG, Vangeli V, Barini A, Mandala M, Barone C, Barbarino A.Institute of Endocrinology, Catholic University School of Medicine, Rome, Italy.
28-Enhancement of tamoxifen-induced suppression of insulin-like growth factor I gene expression and serum level by a somatostatin analogue.Huynh H, Pollak M.Department of Medicine, Lady Davis Research Institute, Jewish General Hospital,
Montreal,
29-In vivo inhibition of insulin-like growth factor I gene expression by tamoxifen.Huynh HT, Tetenes E, Wallace L, Pollak M.Department of Medicine, McGill University, Montreal, Quebec, Canada
30-Suppression of serum insulin-like growth factor-1 levels in breast cancer patients during adjuvant tamoxifen therapy.Friedl A, Jordan VC, Pollak M.Department of Pathology and Laboratory Medicine, University of Wisconsin, Madison
53792.
All in all eq and deca can actually weaken tendons by stimulating type 3 collagen synthesis-leading to tendinosis.
silverbackn
New member
I like steroids.
R
roidpuple
Guest
Steroids help us build more muscle.. so we are able to add more to our frame than we could of natrually... some peopls body can hold more muscle but the problem is getting it there... so i think with the help of steroids adding the muscle.. we then after use can hold more muscle on our bodies then we would have been able to because we would have never been able to get it there in the 1st place at that amount... I think you can hold about 20lbs -40 extra pounds of mucles .. after a cycle.. and going back natty...
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