AnoTherBodY
membre approuvé
c'est quoi le hcg exactement?
Cure 100% deca
- Initiateur de la discussion MaRKuS
- Date de début
Nemesis
membre approuvé
Etaye un peu plus tes réponses avec des arguments valables...
Dernière modification par un modérateur:
Nemesis
membre approuvé
clomid= antioestrogenes
Bien sur, je suis d'accord, mais la on parle de pratique et dans la pratique il n'est jamais utilisé en tant que tel.
Nemesis
membre approuvé
prendre le clomid en cure ok , je suis d'accord, mais la on parle de pratique et dans la pratique il n'est jamais utilisé en tant que tel.
Nemesis
membre approuvé
prendre le clomid en cure ok , je suis d'accord, mais la on parle de pratique et dans la pratique il n'est jamais utilisé en tant que tel.
Détrompe toi, j'ai vus des cures sur certains forums ricain ou plusieurs utilisateur utilisé clomid en milieu de cure, aprés sur l'efficacité je peux pas te dire j'ai pas testé, je préfere l'hcg dans ce genre de situation.
Pour ceux qui ne veulent pas passer aux injections le clomid est une bonne alternative dans ce cas.
BlackBaccara
Banni
Non je ne pense pas (ou plutôt je ne sais pas
), il faut bien comprendre que de nombreux facteurs influent sur la pharmacocinétique :"We conclude that the side-chain ester and the injection site and volume influence the pharmacokinetics and pharmacodynamics of nandrolone esters in an oil vehicle in men." (1)Mais je ne peux pas t'en dire davantage, il faudrait une étude comparative, de la même manière dans l'étude que j'ai cité dans mon message précédent le volume d'injection était constant (1ml).
Il semble difficile de construire un modèle mathématique fiable, par exemple si la demi-vie passe de 7 à 12 jours quand on injecte 100mg au lieu de 50, elle est toujours de 12 jours pour une dose de 150mg, cela met en évidence la saturation de certaines voies de métabolisation.
(1) Pharmacokinetics and Pharmacodynamics of Nandrolone Esters in Oil Vehicle: Effects of Ester, Injection Site and Injection Volume
Bien sur, je suis d'accord, mais la on parle de pratique et dans la pratique il n'est jamais utilisé en tant que tel.
En tant qu'oestrogène peut-être par exemple.
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Nemesis
membre approuvé
En tant qu'oestrogène peut-être par exemple.[/QUOTE]
Oui chez la femme et dans un contexte medical, rien a voir avec le dopage des culturistes.
Oui chez la femme et dans un contexte medical, rien a voir avec le dopage des culturistes.
BlackBaccara
Banni
Heu ? le Clomid est un SERM, si tu ne l'utilises pas pour son effet anti-E, ni son effet E, tu l'utilises pour quoi alors ?
TheIrIsh
membre approuvé
pour stimuler l'ovulation :th_goodone:
la LH .
Nemesis
membre approuvé
En bodybuilding, tu l'utilise pour ta relance, en pct ou a la rigeur comme anti-E, mais dans ce cas la on a a notre disposition des produits mieux adapté, novadex... j'ai jamais vu personne l'utiliser comme anti-E dans un programme de dopage.
Pour ce qui est de son effet E, quel interet en dopage?
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BlackBaccara
Banni
Nan mais d'accord ça j'ai bien compris ! Mais le clomid c'est pas the magic pill ! Donc ton effet sur la "relance" c'est un effet E ou anti-E ...
clomid + nolvadex pour la PCT c'est bon ?
musclor
membre approuvé
Bah écoute j'éspere David car c'est ce que je fait aprés Hgc et pour l'instant pas perdu un kilo de muscle
BlackBaccara
Banni
(copié/collé de l'une de mes interventions sur CEM)
Clomid is a SERM and it exerts both antiestrogenic and estrogenlike effects. Bodybuilders always focus on the first but sometimes estrogenic effects could be useful too. On this board there are lot of discussions to determine the best choice between Nolvadex and Clomid for PCT purpose.
When we think about these compounds, we think mostly about their antiestrogenic natures and because tamoxifen is a more potent anti-estrogen, it can be thought to be the best choice. I have often read this sort of reasoning : SERM can induce gonadotropins by counteracting the negative feedback. It is true and easy to understand when we speak about normal men with normal HPT axis. But in the case of PCT this reasoning is irrelevant because androgens are the sole way of enstrogens synthesis. So if androgens are low, estrogens are low too and they cannot exert the feedback and the use of SERM in PCT appears questionable.
From a reported case of a male bodybuilder with prolonged HPTA suppression and impotence disorder : despite a treatment with HCG. LH, FSH and T were low 9 months after that drugs had been discontinuated. A month treatment with clomiphene 100mg ED restored HPT axis to normal men levels.
http://www.pubmedcentral.gov/picren...57&blobtype=pdf
How Clomid can be helpful in PCT despite very low androgens and estrogens levels ?
Maybe because an estrogenic effect, estradiol is known to be both a positive and negative signal for the pituary. So, if LH doesn't raise after the discontinuation of AAS administration, as it is generally the case, the reason can be a pituary desensitization to GnRH signal. In this case the lack of estrogen can explain why the HPT axis can't be restored and the use of an estrogenic compound like Clomid can be helpful and a better choice than an anti-E :
Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro
The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enClomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its EnClomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.
Clomid is a SERM and it exerts both antiestrogenic and estrogenlike effects. Bodybuilders always focus on the first but sometimes estrogenic effects could be useful too. On this board there are lot of discussions to determine the best choice between Nolvadex and Clomid for PCT purpose.
When we think about these compounds, we think mostly about their antiestrogenic natures and because tamoxifen is a more potent anti-estrogen, it can be thought to be the best choice. I have often read this sort of reasoning : SERM can induce gonadotropins by counteracting the negative feedback. It is true and easy to understand when we speak about normal men with normal HPT axis. But in the case of PCT this reasoning is irrelevant because androgens are the sole way of enstrogens synthesis. So if androgens are low, estrogens are low too and they cannot exert the feedback and the use of SERM in PCT appears questionable.
From a reported case of a male bodybuilder with prolonged HPTA suppression and impotence disorder : despite a treatment with HCG. LH, FSH and T were low 9 months after that drugs had been discontinuated. A month treatment with clomiphene 100mg ED restored HPT axis to normal men levels.
http://www.pubmedcentral.gov/picren...57&blobtype=pdf
How Clomid can be helpful in PCT despite very low androgens and estrogens levels ?
Maybe because an estrogenic effect, estradiol is known to be both a positive and negative signal for the pituary. So, if LH doesn't raise after the discontinuation of AAS administration, as it is generally the case, the reason can be a pituary desensitization to GnRH signal. In this case the lack of estrogen can explain why the HPT axis can't be restored and the use of an estrogenic compound like Clomid can be helpful and a better choice than an anti-E :
Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro
The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enClomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its EnClomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.
Dernière modification par un modérateur: