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Resistence Exercise and Androgen Levels
by: Karl Hoffman

Ratamess and coworkers recently published the results of a study that looked at the hormonal profile and androgen receptor content in the vastus lateralis muscle (a portion of the muscles comprising the quadriceps) of men following two exercise protocols [1]. The results were a bit surprising in light of some previous studies, and suggest a possible supplement regimen to offset some of the negative effects that were observed. The salient results of their research were (a) an increase in both cortisol and testosterone levels after multiple sets of squats; and (b) a significant downregulation of the androgen receptor in biopsied muscle tissue.

Several previous studies have examined hormonal changes in cortisol, testosterone, and growth hormone (GH) during and following resistance exercise [2–4]. In [2] Kraemer observed an increase in both testosterone and GH after heavy resistance exercise. Hakkinen and Pakarinen observed increases in free and total testosterone, cortisol, and GH after an acute bout of heavy squatting [3]. Kraemer examined plasma hormone changes after an intense bout of cycling and noted a significant increase in cortisol [4]. The current study and the earlier ones cited show a trend of increased cortisol and testosterone immediately after strenuous exercise.

The current study by Ratamass is the first to look at androgen receptor content in worked muscle immediately post-exercise. While the elevated testosterone that occurs after exercise sounds beneficial, if receptor levels are low, then the increased testosterone would be of less anabolic value than if receptor levels were unchanged or increased. In fact, a depressed level of AR is exactly what Ratamass and coworkers found. The downregulation of AR coupled with high cortisol levels post-exercise would be expected to make for a metabolic state characterized by net catabolism.

To quote from the current study under investigation, “…acute hormonal elevations are without context unless subsequent interaction with a specific membrane bound or nuclear receptor occurs and the appropriate signal is transduced”.

In other words, what good is the extra testosterone produced during lifting if the receptors aren’t there to accept it?

In the current study, 9 young resistance trained men performed two exercise protocols. One consisted of a single set (SS) of 10 reps of heavy squats. The second exercise involved 6 sets of 10 reps of squats (MS). Weights were determined for each individual by measuring their 1 Rep Max (RM) and then having them squat at 80 – 85% of the (RM). The average RM was 330.4 lbs.

Plasma testosterone and cortisol were measured every 15 minutes for 1 hour after both sessions. The vastus lateralis was biopsied to determine AR content 1 hour after training. The results, taken from [1] are shown below.

As can be seen, there was no significant change in cortisol in is SS group, while cortisol rose about 40% in the MS group after 30 minutes

Similarly, testosterone did not change in the SS group but showed a transient increase of 20% in the MS group.

The bar graph below from [1] shows relative vastus lateralis AR content at baseline and 1 hour after completion of exercise. The drop in AR content in the worked muscle is clear

The authors of the present study attribute the decline in androgen receptors to an overall loss of protein due to the demands of strenuous exercise. Cortisol is highly catabolic to proteins and does not discriminate between contractile proteins and noncontractile proteins, such as the androgen receptor, which itself is a protein. A number of studies have shown that the AR is upregulated after a longer post exercise time period. For example, Bamman & Shipp reported that in humans AR messenger RNA in the vastus lateralis increased 63% and 102% respectively 48 hours following 8 sets of 8 reps of either eccentric (110% of 1 RM) or concentric ( 85% of 1RM) squats [5]. Thus resistance exercise may ultimately upregulate the AR, but the initial response appears to be a catabolic one, based on the current study.

One might be tempted to speculate that the increased testosterone and decreased AR may cancel each other out. This may not be the case. Another interesting finding of this study was the individual baseline 1 RM was independent of plasma testosterone levels, but correlated highly with androgen receptor content. So an individual’s AR levels may be more indicative of their strength than their testosterone levels.

Certain anabolic steroids such as Anavar (oxandrolone) that are considered to have a very high anabolic to androgenic ratio are noted for their ability to upregulate the AR [6].

Since it is generally believed that protein synthesis peaks in the few hours after a training session, it makes sense to attempt to limit the downregulation of the AR that seems to occur after exercise. One strategy might be to supplement with amino acids, especially Branched Chain Amino Acids rich in leucine. Besides being anabolic in and of itself, leucine taken as a supplement will be preferentially oxidized for fuel, sparing body proteins, which would likely include the AR.

Another strategy would be to combine a cortisol blocker such as 7-oxo DHEA and/or phosphatidyl serine to the BCAA mix to help limit protein catabolism. While I don’t advocate the use of anabolic steroids, clearly agents such as Anavar which upregulate the AR would likely prove helpful as well.

While elevated cortisol is a likely contributor to protein catabolism, other proteolytic mechanisms may be at work as well. The body has three independent systems for degrading and disposing of proteins. These are the so-called lysosomal and calcium mediated proteases, and the ATP-ubiquitin dependent proteolytic pathway. However, cortisol has been implicated in activating the ATP-ubiquitin proteolytic pathway [7], which may ultimately be the mechanism by which cortisol exerts its catabolic action; so here again cortisol blockers might help.

We mentioned Anavar above. Besides upregulating the AR, Anavar also antagonizes the catabolic actions of cortisol [8]. Calcium mediated proteolysis is suppressed by cyclic adenosine monophosphate (cAMP), and forskolin is well know to elevate cAMP. Thus forskolin may be a worthwhile supplement to defend against this pathway of protein breakdown. Beta adrenergic agonists, either synthetic such as clenbuterol or albuterol, or naturally occurring epinephrine and norepinephrine also elevate cAMP and suppress calcium mediated protein breakdown [9]. Ephedrine elevates cAMP directly by binding to beta receptors, and indirectly by increasing levels of the body’s naturally occurring hormone/neurotransmitter norepinephrine.

Newly published research also shows that clenbuterol, besides inhibiting calcium dependent proteolysis, also acts to block ATP-ubiquitin mediated protein breakdown [10].

Finally, both the lysosomal breakdown of protein and the ATP-ubiquitin proteolytic system are suppressed by insulin [11,12], so adequate carbohydrate intake prior to, during and after strenuous exercise should help blunt these pathways of protein breakdown.

Thus we have several strategies for reducing the breakdown of androgen receptor proteins after exercise, some as simple as eating to elevate insulin, as well as perhaps even increasing those receptor numbers with the use of certain anabolic steroids such as oxandrolone.


1) MR, French DN, Vescovi JD, Silvestre R, Hatfield DL, Fleck SJ, Deschenes MR. Androgen receptor content following heavy resistance exercise in men. J Steroid Biochem Mol Biol. 2005 Jan;93(1):35-42.

2) Kraemer WJ, Gordon SE, Fleck SJ, Marchitelli LJ, Mello R, Dziados JE, Friedl K, Harman E, Maresh C, Fry AC. Endogenous anabolic hormonal and growth factor responses to heavy resistance exercise in males and females. Int J Sports Med. 1991 Apr;12(2):228-35.

3) Hakkinen K, Pakarinen A. Acute hormonal responses to two different fatiguing heavy-resistance protocols in male athletes. J Appl Physiol. 1993 Feb;74(2):882-7.

4) Kraemer WJ, Patton JF, Knuttgen HG, Marchitelli LJ, Cruthirds C, Damokosh A, Harman E, Frykman P, Dziados JE. Hypothalamic-pituitary-adrenal responses to short-duration high-intensity cycle exercise. J Appl Physiol. 1989 Jan;66(1):161-6.

5) Bamman MM, Shipp JR, Jiang J, Gower BA, Hunter GR, Goodman A, McLafferty CL Jr, Urban RJ. Mechanical load increases muscle IGF-I and androgen receptor mRNA concentrations in humans. Am J Physiol Endocrinol Metab. 2001 Mar;280(3):E383-90.

6) Sheffield-Moore M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN, Wolfe RR, Ferrando AA Short-term oxandrolone administration stimulates net muscle protein synthesis in young men. J Clin Endocrinol Metab. 1999 Aug;84(8):2705-11.

7) Tiao G, Fagan J, Roegner V, Lieberman M, Wang JJ, Fischer JE, Hasselgren PO. Energy-ubiquitin-dependent muscle proteolysis during sepsis in rats is regulated by glucocorticoids. J Clin Invest. 1996 Jan 15;97(2):339-48.

8) Zhao J, Bauman WA, Huang R, Caplan AJ, Cardozo C. Oxandrolone blocks glucocorticoid signaling in an androgen receptor-dependent manner. Steroids. 2004 May;69(5):357-66.

9) Navegantes LC, Resano NM, Migliorini RH, Kettelhut IC. Catecholamines inhibit Ca(2+)-dependent proteolysis in rat skeletal muscle through beta(2)-adrenoceptors and cAMP. Am J Physiol Endocrinol Metab. 2001 Sep;281(3):E449-54.

10) Yimlamai T, Dodd SL, Borst SE, Park S. Clenbuterol induces muscle-specific attenuation of atrophy through effects on the ubiquitin-proteasome pathway. J Appl Physiol. 2005 Mar 17;

11) Wolfe RR. Effects of insulin on muscle tissue. Curr Opin Clin Nutr Metab Care. 2000 Jan;3(1):67-71

12) Bennett RG, Hamel FG, Duckworth WC. Insulin inhibits the ubiquitin-dependent degrading activity of the 26S proteasome. Endocrinology. 2000 Jul;141(7):2508-17.

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