Written by justis berg
04 November 2010

Anabolic Edge by Jose Antonio, Ph.D.

 

Acute Testosterone With Training

You’ve heard the idea that certain types of workout regimens will induce marked increases in the anabolic hormones, such as testosterone, GH and IGF-1. And that by doing these exercises (i.e. following the particular rep-set-rest interval schemes), you’ll have greater gains in muscle mass vis a vis the changes in anabolic hormones.  Here’s an intriguing study that looked into just that notion. Twelve healthy young men (22 yr old) trained their elbow flexors (biceps, brachialis) independently for 15 weeks on separate days and under different hormonal milieu.  I like that word, milieu.  In one training regimen, 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). And they found that there was no elevation in serum growth hormone (GH), insulin-like growth factor (IGF-1), or testosterone after the LH protocol but significant increases in these hormones immediately and 15 and 30 minutes 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.  But does this acute elevation with each training session translate into better gains in muscle fiber size?  Well that’s why they do the studies.  They found that muscle cross-sectional area (CSA) increased by 12% in LH and 10% in HH with no difference between conditions.  Similarly, both slow and fast twitch muscle fiber size 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. So what gives?(1)  I’ve always maintained that the acute elevations in hormones (as measured in blood) is not as important as local signaling happening at the level of the muscle fiber.  Also, it is clear that a certain level of anabolic hormone (e.g. GH or testosterone) must be present in supraphysiological or perhaps pharmacological levels to induce real meaningful hypertrophy.  And that my friends is why exogenous androgens work so well.

 

Quercitin

Quercetin (QR) is known for its potent antioxidant abilities and it’s been shown to reduce oxidative stress in the long-term treatment of streptozotocin (STZ)-induced diabetes in animal models. Scientists have known that antioxidants have significant effects on spermatogenesis, sperm biology and oxidative stress, and changes in antioxidant capacity are considered to be involved in the pathogenesis of chronic diabetes mellitus. In a recent study, sperm numbers, percentages of sperm viability and motility, and total serum testosterone increased significantly in QR-treated diabetic rats compared with control groups. In histopathology, degeneration and inflammation in testes cells associated with diabetes were improved and testes weights in the QR-treated diabetic group decreased significantly also.  So even though this stuff was given to rats, I’d imagine it’s worth trying in us bipeds.  I mean who couldn’t use a little bit more motility down under?(2)

 

Fat and Testosterone are like mixing Oil and Water

According to the NAAFA website: “Founded in 1969, the National Association to Advance Fat Acceptance (NAAFA) is a non-profit civil rights organization dedicated to ending size discrimination in all of its forms. NAAFA's goal is to help build a society in which people of every size are accepted with dignity and equality in all aspects of life. NAAFA will pursue this goal through advocacy, public education, and support.”  Did you get that?  A civil rights organization?  You gotta be f’in kidding me.  Anyhow, I’ll not go into a lecture on why NAAFA masquerading around as a civil rights organization is like Fidel Castrol saying he’s a free-market capitalist. There are so many reasons to not be fat besides the fact that it irks the sh#$ outta me when I’m flying across the country, seated next to someone with the girth of overfed Russian maid.  For instance, we know that testosterone is present in plasma (blood( as free or unbound testosterone, albumin-bound and sex hormone-binding globulin [SHBG]-bound. In lean men, about 2% of testosterone is unbound, 44% is bound to SHBG and 50% is bound to albumin and other proteins.  The free T and the albumin-bound fraction are the biologically active testosterone fractions.  Being a fat man, especially if you carry it underneath your belt buckle, is associated with lower total testosterone [TT], free testosterone [FT] and sex hormone-binding globulin [SHBG], and a greater decline in TT and FT with increasing age compared with lean men. Also, obese men have reduced sperm concentration and total sperm count compared to lean men.(3)  In fact, 40% of obese non-diabetic and 50% of obese diabetic men above the age of 45 years have subnormal FT concentrations. Thus, being a fat little househusband is probably the condition most frequently associated with abnormally low FT concentration in males.(4) So if you’re all about ‘Fat Acceptance,’ then by golly, then you are also all about having low testosterone levels. And that my friend, is just not a good thing.  Wake up and get your fat butt on the treadmill.

 

Stay away from Statins

The use of statins (drugs used to lower cholesterol) is associated with a reduced testis volume and a higher prevalence of hypogonadism-related symptoms and signs; also, statin users have lower levels of total and calculated free T.(5)  So if you happen to be taking these drugs, don’t be surprised that in addition to lowering your cholesterol, it’ll lower the ability of your private parts to ‘stand at attention.’  And that ain’t good.

 

No Harmful Effects But Banned Nonetheless

Anabolic steroids work. And they work damn well.  Some of the more popular drugs include: methyltestosterone, metandienone, nandrolone, testosterone esters and stanozolol. Recently, nonsteroidal alternatives to anabolic steroids have been developed that selectively activate the androgen receptor in either muscle tissue or bones. These so-called selective androgen receptor modulators (SARMs) are currently undergoing late clinical trials (IIb) and will be prohibited by the World Anti-Doping Agency from January 2008. Their entirely synthetic structures are barely related to steroids, but particular functional groups allow for the tissue-selective activation or inhibition of androgen receptors and, thus, the stimulation of muscle growth without the risk of severe undesirable effects commonly observed in steroid replacement therapies.(6)  Did you read that?  Without the risk of bad side effects; then why on earth should they be banned?  Should WADA ban cigarette smoking since that sh@# kills more people each year than the average population of an urban Chinese city.

Reference

1.                  West DW, Burd NA, Tang JE, et al. Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. J Appl Physiol;108:60-7.

2.                  Khaki A, Fathiazad F, Nouri M, et al. Beneficial effects of quercetin on sperm parameters in streptozotocin-induced diabetic male rats. Phytother Res.

3.                  Mah PM, Wittert GA. Obesity and testicular function. Mol Cell Endocrinol;316:180-6.

4.                  Dhindsa S, Miller MG, McWhirter CL, et al. Testosterone Concentrations in Diabetic and Non-Diabetic Obese Men. Diabetes Care.

5.                  Corona G, Boddi V, Balercia G, et al. The Effect of Statin Therapy on Testosterone Levels in Subjects Consulting for Erectile Dysfunction. J Sex Med.

6.                  Thevis M, Schanzer W. Synthetic anabolic agents: steroids and nonsteroidal selective androgen receptor modulators. Handb Exp Pharmacol:99-126.