Dyskusje o żarciu, treningu i innych czynnikach przełamujących stagnację

ale propa to ladujesz opor, na masie jestes ?

Szybkie pytako w pon poszedl 3strzal deki 200mg e7(oczywiście z susta ;)) czy jak jutro pojde zbadac prolke to juz powinna byc wywalona?bo chce sprawdzic ta deke to narazie nic nie biore na utrzymanie prolki w widlach

Testowo tak, zawsze uwalełem mocno, teraz chcę zobaczyć jak będzie na większej dawce, czy będzie jakaś różnica w pełności sylwetki.

kamilplnk

Szybkie pytako w pon poszedl 3strzal deki 200mg e7(oczywiście z susta ;)) czy jak jutro pojde zbadac prolke to juz powinna byc wywalona?bo chce sprawdzic ta deke to narazie nic nie biore na utrzymanie prolki w widlach

Po pierwsze prolka = testosteronum prolongatum,
po drugie nie kazdemu wywala na dece,
po trzecie na takiej malej dawce to marginalne przypadki zeby komus prolaktyna wzrosla
po czwarte i tak mogloby byc za krotko

Prz1993 ok, zapytam Cie za kilka tyg

Prolka w sensie prolaktyna ;) wiem ze dawka mala podbije na 300e7

Miczelx , ostatnio coraz więcej słyszę paradoksalnie że wysoki estrogen, jest przydatny w spalaniu tkanki tłuszczowe, wiadomo potem obniżamy estradiol IA czy przed zawodami czy amatorsko, jakie masz zdanie na ten konkretny wątek ?

wysoki estrogen???

Seba dokładnie, o to mi chodzi już z trzy lata temu czytałem o tym na forum gh15, zareagowałem podobnie jak Ty.
Jak coś znajdę to wrzucę tobie na fc. teraz jest trochę problem z artami bo na mojej przeglądarce nie chcą tłumaczyć ,od kilku miesięcy a z angielskim u mnie średnio.

kamilplnk

Prolka w sensie prolaktyna ;) wiem ze dawka mala podbije na 300e7

Wiem w jakim sensie, ale cale zycie prolka to byla prolka i bez sensu zmienic teraz nazewnictwo
nie jest to temat na rozpiski w sprawie dawkowania na Twoim cyklu, zaloz swoj osobny w tej sprawie

Wnc,
wielokrotnie do znudzenia pisalem, ze estro nie wplywa na spowolnienie utraty tkanki tluszczowej, ze nie ma znaczenia, takze konsekwetnie w druga strone rowniez nie ma zaleznosci, wg mnie jest bez znaczenia ani na plus ani na minus.

Tu taki art, chcecie to się przetłumaczcie.


Estrogen is the second factor people often consider. Especially steroid and prohormone users are often plagues with a serious misunderstanding of estrogen and its effects on adiposity. Most are convinced that estrogen increases fat gain or retards fat loss, when in effect the opposite is true. Estrogens, and especially estradiol (E2), is probably a more effective fat loss aid than is testosterone. Although like testosterone, it may have certain anti-lipolytic effects by increasing a2 adrenoreceptors in specific female patterning (harder to lose fat in thighs and butt).

First of all, estradiol also reduces LPL (6), just like testosterone does, so uptake of fatty acids in adipocytes is reduced. Apart from that, its effects can be divided in three categories. Its effect on insulin-related events, its effects on Growth Hormone and its effects on reducing appetite.

Estradiol can cause a reduction in weight, with only a minimal effect in insulin itself (8), but that does not mean it does not alter the body's reaction to insulin. Estradiol lowers insulin receptor number (9), and in very high doses even actual insulin sensitivity (10). It does so in various ways, not in the least by reducing GLUT4 recruitment and translocation in adipocytes (11), which results in less glucose uptake in fat cells.

This will result in a negative energy balance and a greater activation of lipolysis, right where we want it, in the fat tissue. The effect of estradiol on insulin is quite acute, and clearly evident in the fact that short-term modulation drastically reduces glucose appearance (release) and disappearance (uptake) (12), suggesting a dysfunctional glucose transport system.

The second way in which estradiol may increase fat loss, is its effect on growth hormone (13,14). Unlike testosterone, which stimulates the GH/IGF-1 axis, the effect of estrogen may actually be in reducing systemic (liver-derived) IGF-1 (13), which lowers inhibition of Growth Hormone.

In doing so it obviously reduces the anabolic capacity of the body (which is why we don't use estrogen to build muscle) but increases the fat burning capacity since whole-body IGF-1 is reduced, leading to a reduction in adipogenic markers (since IGF-1 and insulin activate the same cascades) and a concurrent increase in Growth Hormone, leading to further decreases in LPL and upregulation of beta-adrenoreceptors (cfr. Part 4). Estradiol may even reduce IGF-1, while increasing IGFBP-3 (15).

This may in effect be the reason why estradiol does not promote growth, since unbound IGFBP-3, which is under normal circumstances the main carrier or IGF-1 in circulation, has been attributed charachteristics that inhibit growth (16). It acts as a pro-apoptotic agent to activate cysteine proteases, much in the same manner that cortisol or TNFalpha would (cfr. Part 4).

This implies that as long as we are seeing an increase in estradiol accompanied by an equal or larger increase in testosterone, we are reaping positive effects, on both fat loss and muscle retention since testerone increases IGF-1, while estradiol prolongs the half-life and effect of the hormone by increasing IGFBP-3 and IGF1-receptor density (20). Without the testosterone increase, it may however increase muscle loss (and potentially increase fat loss further by enhancing apoptosis of fat cells ?).

A third way in which estradiol helps as a fat loss agent is by reducing appetite. It reduces sensations of hunger via modulation of melanin-concentrating hormone. We have discussed the role of orexigenic (hunger inducing) peptides once or twice previously, specifically NPY.

Obviously NPY isn't the only peptide involved. For instance Agouti-related peptide is also involved, as is melanin-concentrating hormone (MCH). When energy intake is restricted, MCH levels sky-rocket, leading to an increased sense of hunger. Estradiol was able to completely abolish this increase in MCH (17), making it a very potent appetite suppressor during low-calorie diets.

Lastly, estradiol increases both the release of arachiconic acid (18) and the actions of cyclo-oxygenase (19) in certain cell types. This results in a quick and effective increase in several prostaglandins, including PGF2 and PGI2, that are related to lower body-fat levels. Because these effects can be highly varying in different cell types it should not automatically assumed that these events do occur, or that they necessarily contribute to fat loss however.

Estradiol can also prevent muscle loss, once again only in the presence of testosterone, by blocking the low affinity glucocorticoid receptors (22), protecting against the effects of cortisol. Testosterone, or another blocker of the high affinity receptors must be present however, otherwise the blocking of the low affinity receptor would not yield very good results.

On a closing note, as with testosterone, the effects of estradiol are not uniformly positive. It has been shown to enhance PPARgamma (20), so modulation of testosterone/estradiol levels should occur in the presence of a PPARgamma blocker for maximal effects on fat loss. And lastly, estrogen increasing products are often omitted during diets for the simple reason that estradiol increases aldosterone (21), a hormone that increases sodium retention, and as a result water retention.

Excess levels of estrogen often lead to water retention and a puffed up look. While this does not affect fat loss one iota, and can be addressed quickly, in only 1 or 2 days, it does make it difficult for the dieter to judge his progress accurately.



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7. Woodhouse LJ, Gupta N, Bhasin M, Singh AB, Ross R, Phillips J, Bhasin S. Dose-dependent effects of testosterone on regional adipose tissue distribution in healthy young men. J Clin Endocrinol Metab. 2004 Feb;89(2):718-26.

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11. Sugaya A, Sugiyama T, Yanase S, Terada Y, Toyoda N. Glucose transporter 4 (GLUT4) mRNA abundance in the adipose tissue and skeletal-muscle tissue of ovariectomized rats treated with 17 beta-estradiol or progesterone. J Obstet Gynaecol Res. 1999 Feb;25(1):9-14.

12. Carter S, McKenzie S, Mourtzakis M, Mahoney DJ, Tarnopolsky MA. Short-term 17beta-estradiol decreases glucose R(a) but not whole body metabolism during endurance exercise. J Appl Physiol. 2001 Jan;90(1):139-46.

13. Shah N, Evans WS, Bowers CY, Veldhuis JD. Oral estradiol administration modulates continuous intravenous growth hormone (GH)-releasing peptide-2-driven GH secretion in postmenopausal women. J Clin Endocrinol Metab. 2000 Aug;85(8):2649-59.

14. Genazzani AD, Gamba O, Nappi L, Volpe A, Petraglia F. Modulatory effects of a synthetic steroid (tibolone) and estradiol on spontaneous and GH-RH-induced GH secretion in postmenopausal women. Maturitas. 1997 Sep;28(1):27-33.



Zmieniony przez - wnc1964 w dniu 2016-01-27 12:46:30