Foro de culturismo, musculación, pesas, fitness y esteroides anabólicos

Eric M. Potratz escribió:Human Chorionic Gonadotropin (hCG) is a peptide hormone that mimics the action of luteinizing hormone (LH). LH is the hormone that stimulates the testes to produce testosterone. (1) More specifically LH is the primary signal sent from the pituitary to the testes, which stimulates the leydig cells within the testes to produce testosterone.

When steroids are administered, LH levels rapidly decline. The absence of an LH signal from the pituitary causes the testes to stop producing testosterone, which causes rapid onset of testicular degeneration. The testicular degeneration begins with a reduction of leydig cell volume, and is then followed by rapid reductions in intra-testicular testosterone (ITT), peroxisomes, and Insulin-like factor 3 (INSL3) – All important bio-markers and factors for proper testicular function and testosterone production. (2-6,19) However, this degeneration can be prevented by a small maintenance dose of hCG ran throughout the cycle. Unfortunately, most steroid users have been engrained to believe that hCG should be used after a cycle, during PCT. Upon reviewing the science and basic endocrinology you will see that a faster and more complete recovery is possible if hCG is ran during a cycle.

Firstly, we must understand the clinical history of hCG to understand its purpose and its most efficient application. Many popular “steroid profiles” advocate using hCG at a dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical (1960’s) hCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency. (21,22) A prolonged LH deficiency causes the testes to desensitize, requiring a higher hCG dose for ample stimulation. In men with normal LH levels and normal testicular sensitivity, the maximum increase of testosterone is seen from a dose of only 250iu, with minimal increases obtained from 500iu or even 5000iu. (2,11) (It appears the testes maximum secretion of testosterone is about 140% above their normal capacity.) (12-18) If you have allowed your testes to desensitize over the length of a typical steroid cycle, (8-16 weeks) then you would require a higher dose to elicit a response in an attempt to restore normal testicular size and function – but there is cost to this, and a high probability that you won’t regain full testicular function.

One term that is critical to understand is testosterone secretion capacity which is synonymous to testicular sensitivity. This is the amount of testosterone your testes can produce from any given LH or hCG stimulation. Therefore, if you have reduced testosterone secretion capacity (reduced testicular sensitivity), it will take more LH or hCG stimulation to produce the same result as if you had normal testosterone secretion capacity. If you reduce your testosterone secretion capacity too much, then no amount of LH or hCG stimulation will trigger normal testosterone production – and this leads to permanently reduced testosterone production.

To get an idea of how quickly you can reduce your testosterone secretion capacity from your average steroid cycle, consider this: LH levels are rapidly decreased by the 2nd day of steroid administration. (2,9,10) By shutting down the LH signal and allowing the testis to be non-functional over a 12-16 week period, leydig cell volume decreases 90%, ITT decreases 94%, INSL3 decreases 95%, while the capacity to secrete testosterone decreases as much as 98%. (2-6)

Note: visually analyzing testes size is a poor method of judging your actual testicular function, since testicular size is not directly related to the ability to secrete testosterone. (4) This is because the leydig cells, which are the primary sites of testosterone secretion, only make up about 10% of the total testicular volume. Therefore, when the testes may only appear 5-10% smaller, the testes ability to secrete testosterone upon LH or hCG stimulation can actually be significantly reduced to 98% of their normal production. (3-5) The point here is to not judge testosterone secretion capacity by testicular size.

The decreased testosterone secretion capacity caused by steroid use was well demonstrated in a study on power athletes who used steroids for 16 weeks, and were then administered 4500iu hCG post cycle. It was found that the steroid users were about 20 times less responsive to hCG, when compared to normal men who did not use steroids. (8) In other words, their testosterone secretion capacity was dramatically reduced because they did not receive an LH signal for 16 weeks. The testes essentially became desensitized and crippled. Case studies with steroid using patients show that aggressive long-term treatment with hCG at dosages as high as 10,000iu E3D for 12 weeks were unable to return full testicular size. (7) Another study with men using low dose steroids for 6 weeks showed unsuccessful return of Insulin-like factor-3 (INSL3) concentration in the testes upon 5000iu/wk of HCG treatment for 12 weeks (6) (INSL3 is an important biomarker for testosterone production potential and sperm production. 20)

These studies show that postponing hCG usage until the end of a steroid cycle increases your need for a higher dose of hCG, and decreases your odds of a full recovery. As a consequence to using a higher dose of hCG at the end of a cycle, estrogen will be increased disproportionately to testosterone, which then causes further HPTA suppression (from high estrogen) while increasing the risk of gyno. (11) For example, high doses of hCG have been found to raise estradiol up to 165%, while only raising testosterone 140%. (11) Higher doses of hCG are also known to reduce LH receptor concentration and degrade the enzymes responsible for testosterone synthesis within the testes (12,13,19 ) -- the last thing someone wants during recovery. While these negative effects of hCG can be partly mitigated by the use of a SERM such as tamoxifen, it will create further problems associated with using a toxic SERM (covered in another article).

In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. We must protect our testicular sensitivity. Besides, with hCG being so readily available, and such a painless shot, it makes you wonder why anyone wouldn’t use it on cycle.

Based on studies with normal men using steroids, 100iu HCG administered everyday was enough to preserve full testicular function and ITT levels, without causing desensitization typically associated with higher doses of hCG. (2) It is important that low-dose hCG is started before testicular sensitivity is reduced, which appears to rapidly manifest within the first 2-3 weeks of steroid use. Also, it’s important to discontinue the hCG before you start PCT so your leydig cells are given a chance to re-sensitize to your body’s own LH production. (To help further enhance testicular sensitivity, the dietary supplement Toco-8 may be used)

A more convenient alternative to the above recommendation would be a twice a week shot of 200iu hCG, or possibly a once a week shot of 500iu. However, it is most desirable to adhere to a lower more frequent dose of hCG to mimic the body’s natural LH release and minimize estrogen conversion. If you are starting hCG late in the cycle, one could calculate a rough estimate for their required hCG ‘kick starting’ dosage by multiplying 40iu x days of LH absence, since the testes will be desensitized, thus requiring a higher dose. (ie. 40iu x 60 days = 2400iu HCG dose)

Note: If following the on cycle hCG protocol, hCG should NOT be used for PCT.

Recap –

For preservation of testicular sensitivity, use 100iu hCG ED starting 7 days after your first AAS dose. At the end of the cycle, drop the hCG two weeks before the AAS clear the system. For example, you would drop hCG about the same time as your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the hCG about 10 days before your last oral dose. This will allow for a sudden and even clearance in hormone levels, while initiating LH and FSH production from the pituitary, to begin stimulating your testes to produce testosterone. Remember, recovery doesn’t begin until you are off hCG since your body will not release its own LH until the hCG has cleared the system.

In conclusion, we have learned that utilizing hCG during a steroid cycle will significantly prevent testicular degeneration. This helps create a seamless transition from “on cycle” to “off cycle” thus avoiding the post cycle crash.



References -

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robin1 escribió:Esto esta muy interesante, se podrian sacar varias conclusiones para el uso del hcg, mañana me pondre manos a la obra xq la verdad q ahora no tengo muxas ganas jajajajaja, pero prometo volver mañana para dar mas.
Saludos

Inge AX escribió:

robin1 escribió:Esto esta muy interesante, se podrian sacar varias conclusiones para el uso del hcg, mañana me pondre manos a la obra xq la verdad q ahora no tengo muxas ganas jajajajaja, pero prometo volver mañana para dar mas.
Saludos

Como que no traes ganas joven maravilla? Recuerda...no dejes para manana lo que puedes hacer hoy, ok

Saludos

ismaele00 escribió:El aumento testicular normal (la vuelta a los niveles normales de testosterona) se consigue con dosis únicamente de 250 UI, con un aumento consiguiente de 500 UI.

ismaele00 escribió:Si usted ha permitido que sus testículos queden desensibilizados debido a la aplicación de un ciclo de esteroides normal (8- 16 semanas), entonces se requerirán unas dosis mayores de HCG para reactivar y recuperar los testículos, en un intento por restaurar el tamaño y las funciones originales. Pero se ha expuesto (se entiende al no usar HCG durante el ciclo) a que sus testículo no recuperen sus funciones y tamaño originales (o recuperación completa).

ismaele00 escribió:Los niveles de LH se reducen considerablemente (o rápidamente) a partir del 2º día de la administración de esteroides. Cerrando la señal de la LH (pituitaria --> testículos) y produciendo que los testículos dejen de funcionar alrededor de la semana 12- 16 (se produce en menor medida en ciclos más cortos como ya sabemos), se reduce la célula de Leydig en un 90%, disminución de la TIT en un 94%, reducción de la INSL3 un 95%, mientras que la capacidad de producir testosterona se reduce en un 98%.

ismaele00 escribió:La disminución de la capacidad de secretar testosterona por parte de los testículos se demostró en un estudio en el que los atletas tomaban esteroides durante 16 semanas y posteriormente se les trataba con HCG (4500 UI). Se encontró (o demostró) que los usuarios de esteroides eran cerca de 20 veces menos sensibles a la HCG que aquellos que no había tomado esteroides. Es decir, su capacidad de producir testosterona se redujo drásticamente al no recibir ningún estímulo de LH durante 16 semanas. Básicamente, los testículos perdieron sensibilidad y perdieron tamaño (o se redujeron).

ismaele00 escribió:Lo que demuestran estos estudios es que la posposición del uso de HCG (se entiende que hasta después del ciclo) aumenta la necesidad de una cantidad mayor de HCG y DISMINUYEN las posibilidades reales de recuperación. Por consiguiente una dosis más alta de HCG al final de un ciclo lo que hará (o producirá) es un aumento de los estrógenos desproporcionado respecto a la testosterona, que entonces causará la supresión de la HPTA (el estrógeno alto) y aumentará, por otra parte, el aumento de riesgo de sufrir ginecomastia.
Por ejemplo, las altas dosis de HCG han producido aumentos del estradiol de hasta un 165%, mientras que el aumento de la testosterona tan sólo aumentó un 140%.

ismaele00 escribió:Y dosis más altas de HCG producen la reducción de concentración de receptores de LH y degradan las enzimas responsables de la síntesis de la testosterona dentro de los testículos. Aunque estos efectos se puede reducir con el uso de algunso SERMs, por ejemplo tamoxifeno, estos generarán a su vez otros inconvenientes (importante recordar que estamos hablando siempre de problemas que sucederán si no se usan de forma correcta durante el ciclo).

ismaele00 escribió:Una mejor alternativa a la anterior, es usar pinchazos de HCG dos veces por semana a razón de 200 UI o una vez por semana 500 UI.
Para preservar la sensibilidad testicular, el uso de 100 UI/ ED (o los similares, anteriormente citados) de HCG debería comenzar 7 días después de la administración de los esteroides. Al final del ciclo, la retirada del HCG se debe producir 2 semanas antes de la eliminación total de los esteroides del cuerpo.
Por ejemplo se debería de dejar de usar el HCG al mismo tiempo que pasa el efecto de su último pincho de Enantato. O 10 días antes de su última toma de esteroides orales. Esto permitiría un aumento considerable en los niveles de hormonas, mientras que se inicia la producción de LH y FSH pituitario, para comenzar a estimular sus testículos y la producción de testosterona.
Recuerde que la recuperación no comenzará hasta que la HCG exógena desaparezca de su cuerpo y entonces se empiece a producir su propia LH.

ismaele00 escribió:Bien ese resumen, excepto una cosa:

"Usar el HCG 7 días después de meter los esteres" --> esto es meter HCG a partir de la 2ª semana no de la 1ª.

1ª semana lunes --> meto roids + 7 días = 2ª semana lunes --> meto HCG.

El resto es como se viene diciendo desde hace algún tiempo en el foro, que es mejor durante todo el ciclo que no sólo al final, la recuperación es más lenta, se necesita más cantidad y se podría no llegar a producir.

Saludos, buen resumen.