Roids

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Roids

Notapor DanySam » Sab, 19 Oct 2013, 21:28

Meto ese topic aquí porque sinceramente no me cabe en ninguno (en este tampoco)

Siempre he pensado que los esteroides hacía crecer a quien los tomaba debido a la estimulación o segregación de la hormona del crecimiento, no obstante, ésta no aumenta cuando se estimula o sintetiza de forma exógena (corregidme si me equivoco).
Por lo tanto, que hacen los roids en nuestro organismo?

Gracias.
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Re: Roids

Notapor Fisio » Dom, 20 Oct 2013, 01:29

Son análogos a la Testosterona, modificaciones sintéticas. La hormona del crecimiento no es tan anabólica ni de lejos.
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Re: Roids

Notapor DanySam » Dom, 20 Oct 2013, 11:26

Y la testosterona, aunque se meta de forma externa, anaboliza?
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Re: Roids

Notapor Cobayahumana » Dom, 20 Oct 2013, 11:41

Claro que anaboliza aunque la testosterona es más androgénica que anabólica. Lo que hace es balancear positivo el nitrógeno y eso crea crecimiento si ingieres suficiente proteina y hace que se regeneren antes las fibras musculares, permitiendo entrenar más.
El mejor traje que puedes llevar es la desnudez.

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Re: Roids

Notapor charlyz » Dom, 20 Oct 2013, 13:53

http://books.google.es/books?id=Kwdu8Jl ... ER&f=false


Si vamos a la pag. 69 , el autor explica que la hormona del crecimiento y las somatomedinas ( igf 1 ) son las mayores causantes de hipertrofia , y que la testosterona está más relacionada con la fuerza explosiva ....

Lo que pasa es que ante dosis suprafisiológicas , como sucede con los esteriodes , no sé lo que ocurrirá
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Re: Roids

Notapor Fisio » Dom, 20 Oct 2013, 17:00

charlyz escribió:
Si vamos a la pag. 69 , el autor explica que la hormona del crecimiento y las somatomedinas ( igf 1 ) son las mayores causantes de hipertrofia , y que la testosterona está más relacionada con la fuerza explosiva ....

Lo que pasa es que ante dosis suprafisiológicas , como sucede con los esteriodes , no sé lo que ocurrirá



Pufff... ni de coña. Además muy mal encaminado. Por un lado la hormona del crecimiento tiene un lugar secundario respecto a IGF1 y Testo. Por otro lado, respecto a los análogos de testo, muchos tienen un perfil más anabólico que androgénico. Depende del compuesto y por eso han desarrollado modificaciones sintéticas.

Respecto a la importancia de las hormonas para el crecimiento a niveles fisiológicos, no parece que tengan gran importancia los picos observados con distintos entrenamientos, por lo que no existe una base para recomendar entrenamientos según el efecto en distintas hormonas.

J Physiol. 2009 Nov 1;587(Pt 21):5239-47. doi: 10.1113/jphysiol.2009.177220. Epub 2009 Sep 7.
Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men.
West DW, Kujbida GW, Moore DR, Atherton P, Burd NA, Padzik JP, De Lisio M, Tang JE, Parise G, Rennie MJ, Baker SK, Phillips SM.
Source

Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, 1280 Main Street West, Hamilton, ON L8S 4K1, Canada.
Abstract

We aimed to determine whether exercise-induced elevations in systemic concentration of testosterone, growth hormone (GH) and insulin-like growth factor-1 (IGF-1) enhanced post-exercise myofibrillar protein synthesis (MPS) and phosphorylation of signalling proteins important in regulating mRNA translation. Eight young men (20 +/- 1.1 years, BMI = 26 +/- 3.5 kg m(-2)) completed two exercise protocols designed to maintain basal hormone concentrations (low hormone, LH) or elicit increases in endogenous hormones (high hormone, HH). In the LH protocol, participants performed a bout of unilateral resistance exercise with the elbow flexors. The HH protocol consisted of the same elbow flexor exercise with the contralateral arm followed immediately by high-volume leg resistance exercise. Participants consumed 25 g of protein after arm exercise to maximize MPS. Muscle biopsies and blood samples were taken as appropriate. There were no changes in serum testosterone, GH or IGF-1 after the LH protocol, whereas there were marked elevations after HH (testosterone, P < 0.001; GH, P < 0.001; IGF-1, P < 0.05). Exercise stimulated a rise in MPS in the biceps brachii (rest = 0.040 +/- 0.007, LH = 0.071 +/- 0.008, HH = 0.064 +/- 0.014% h(-1); P < 0.05) with no effect of elevated hormones (P = 0.72). Phosphorylation of the 70 kDa S6 protein kinase (p70S6K) also increased post-exercise (P < 0.05) with no differences between conditions. We conclude that the transient increases in endogenous purportedly anabolic hormones do not enhance fed-state anabolic signalling or MPS following resistance exercise. Local mechanisms are likely to be of predominant importance for the post-exercise increase in MPS.



Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors.
West DW, Burd NA, Tang JE, Moore DR, Staples AW, Holwerda AM, Baker SK, Phillips SM.
Source

Exercise Metabolism Research Group, Dept. of Kinesiology, McMaster Univ., Hamilton, ON L8S4K1 Canada.
Abstract

The aim of our study was to determine whether resistance exercise-induced elevations in endogenous hormones enhance muscle strength and hypertrophy with training. Twelve healthy young men (21.8 +/- 1.2 yr, body mass index = 23.1 +/- 0.6 kg/m(2)) trained their elbow flexors independently for 15 wk on separate days and under different hormonal milieu. In one training condition, participants performed isolated arm curl exercise designed to maintain basal hormone concentrations (low hormone, LH); in the other training condition, participants performed identical arm exercise to the LH condition followed immediately by a high volume of leg resistance exercise to elicit a large increase in endogenous hormones (high hormone, HH). There was no elevation in serum growth hormone (GH), insulin-like growth factor (IGF-1), or testosterone after the LH protocol but significant (P < 0.001) elevations in these hormones immediately and 15 and 30 min after the HH protocol. The hormone responses elicited by each respective exercise protocol late in the training period were similar to the response elicited early in the training period, indicating that a divergent postexercise hormone response was maintained over the training period. Muscle cross-sectional area (CSA) increased by 12% in LH and 10% in HH (P < 0.001) with no difference between conditions (condition x training interaction, P = 0.25). Similarly, type I (P < 0.01) and type II (P < 0.001) muscle fiber CSA increased with training with no effect of hormone elevation in the HH condition. Strength increased in both arms, but the increase was not different between the LH and HH conditions. We conclude that exposure of loaded muscle to acute exercise-induced elevations in endogenous anabolic hormones enhances neither muscle hypertrophy nor strength with resistance training in young men.


Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training

Daniel W. D. West,
Stuart M. Phillips

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Abstract

The purpose of this study was to investigate associations between acute exercise-induced hormone responses and adaptations to high intensity resistance training in a large cohort (n = 56) of young men. Acute post-exercise serum growth hormone (GH), free testosterone (fT), insulin-like growth factor (IGF-1) and cortisol responses were determined following an acute intense leg resistance exercise routine at the midpoint of a 12-week resistance exercise training study. Acute hormonal responses were correlated with gains in lean body mass (LBM), muscle fibre cross-sectional area (CSA) and leg press strength. There were no significant correlations between the exercise-induced elevations (area under the curve—AUC) of GH, fT and IGF-1 and gains in LBM or leg press strength. Significant correlations were found for cortisol, usually assumed to be a hormone indicative of catabolic drive, AUC with change in LBM (r = 0.29, P < 0.05) and type II fibre CSA (r = 0.35, P < 0.01) as well as GH AUC and gain in fibre area (type I: r = 0.36, P = 0.006; type II: r = 0.28, P = 0.04, but not lean mass). No correlations with strength were observed. We report that the acute exercise-induced systemic hormonal responses of cortisol and GH are weakly correlated with resistance training-induced changes in fibre CSA and LBM (cortisol only), but not with changes in strength.




Y es más, el cortisol es el que más se asocia a las ganancias musculares.


Research debunks bodybuilding myth: Growth-promoting hormones don't stimulate strength

New research from scientists at McMaster University reveals exercise-related testosterone and growth hormone do not play an influential role in building muscle after weightlifting, despite conventional wisdom suggesting otherwise.

The findings indicate that bodybuilders who look to manipulate those hormones through exercise routines are wasting their time.

In two separate studies, published in the Journal of Applied Physiology and the European Journal of Applied Physiology, researchers found anabolic hormones—long thought to be essential for building a muscular frame—do not influence muscle protein synthesis, the process that leads to bigger muscles.

"A popular mindset for weightlifters is that increased levels of hormones after exercise play a key role in building muscle," explains Daniel West, lead author of both studies and a graduate student in the Department of Kinesiology at McMaster. "That is simply not the case."

In the first study, researchers examined the responses of both male and female participants to intense leg exercise. Despite a 45-fold difference in testosterone increase, men and women were able to make new muscle protein at exactly the same rate.

"Since new muscle proteins eventually add up to muscle growth, this is an important finding," says West.

"While testosterone is definitely anabolic and promotes muscle growth in men and women at high doses, such as those used during steroid abuse, our findings show that naturally occurring levels of testosterone do not influence the rate of muscle protein synthesis."

In the second study, researchers analyzed the post-exercise hormonal responses of 56 young men, aged 18 to 30, who trained five days a week for 12 weeks in total.

The men experienced gains in muscle mass that ranged from virtually nothing to more than 12 pounds, yet their levels of testosterone and growth hormone after exercise showed no relationship to muscle growth or strength gain.

Surprisingly, the researchers noted that cortisol—considered to have the opposite effect of anabolic hormones because it reduces protein synthesis and breaks down tissue—was related to the gain in muscle mass.

"The idea that you can or should base entire exercise training programs on trying to manipulate testosterone or growth hormone levels is false," says Stuart Phillips, a professor in the Department of Kinesiology. "There is simply no evidence to support this concept."



Cortisol = HORMESIS. Lo mismo que con el estrés oxidativo. Posiblemente forme parte de la señalización catabólica que inicie las respuestas anabólicas mediante un mecanismo hormético. Por eso decía lo de entrenar en ayunas, no es óptimo tener el cuerpo siempre siguiendo un patrón y señalizando vías anabólicas, porque el organismo se adapta.

Y respecto a los derivados de testo, son similares estructuralmente, tan solo varía un enlace en muchos casos, pero esto es suficiente para que varíe el efecto androgénico/anabólico ya que en dosis suprafisiológicas es otro cantar

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