A Few Common Bodybuilding Myths
by
Karl Hoffman
ANABOLIC STEROIDS DOWNREGULATE THE ANDROGEN RECEPTOR
Or is it upregulate? It seems there are two schools of thought on this, with the answer probably lying somewhere in between. Short-term in vitro and in vivo studies generally show that androgens upregulate the androgen receptor (AR) in skeletal muscle. For example, in humans given 15 mg of oxandrolone daily for 5 days, the skeletal muscle AR density nearly doubled (15). When exposed to testosterone in vitro, skeletal muscle AR expression increased significantly (16).
In longer-term studies the picture is somewhat different. One study looked at AR expression in androgen treated sedentary rats vs nontreated exercised rats over 8 weeks. To quote from the abstract:
Results show that contractile muscular activity always increased the quantity of receptors whereas the steroid treatment decreased it. Thus for EDL (extensorum digitorum longus) and SOL (soleus) of control trained rats the quantity of receptors was 0.78 and 0.82 fmol/mg protein, respectively, compared to 0.23 and 0.43 fmol/mg protein for sedentary testosterone-treated rats. (17)
In long term studies in humans we get yet a different picture. In work conducted by Sheffield-Moore et. al., (18) older men were supplemented with testosterone so as to bring their testosterone levels into the mid-to-high physiological range. Androgen receptor expression had more than doubled after one month of treatment, yet by 6 months had returned to baseline. This pattern suggested to the authors that cycling androgen replacement much as bodybuilders cycle AAS might be a viable strategy:
This pattern of AR expression raises the possibility that cycling of testosterone administration could produce effects on skeletal muscle analogous to continuous administration. Such a paradigm would be beneficial by administering significantly less testosterone for similar anabolic outcomes, thus minimizing the possibility of side effects.
So despite the passion with which advocates of either AR upregulation or downregulation defend their positions, the research is equivocal. Would exercise combined with AAS maintain increased AR expression, or would the addition of exercise serve to offset the AAS induced AR downregulation observed in the study by Bricout et al? These are just a couple of questions that require further research, and could lead to answers on why exercise combined with AAS use is so much more productive than simply using steroids alone when it comes to building muscle mass.
(15) Sheffield-Moore M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN, Wolfe RR,
Ferrando AA
J Clin Endocrinol Metab 1999 Aug;84(8):2705-11
(16) Doumit ME, Cook DR, Merkel RA..Endocrinology 1996 Apr;137(4):1385-94
(17) Bricout VA, Germain PS, Serrurier BD, Guezennec CY.Cell Mol Biol (Noisy-le-grand) 1994 May;40(3):291-4
(18) Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7
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