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 havegreater gains in muscle mass vis a vis the changes in anabolic hormones. Here's an intriguing study that lookedinto just that notion. Twelve healthy young men (22 yr old) trained their elbowflexors (biceps, brachialis) independently for 15 weeks on separate days andunder different hormonal milieu. Ilike that word, milieu. In onetraining regimen, participants performed isolated arm curl exercise designed tomaintain basal hormone concentrations (low hormone, LH); in the other trainingcondition, participants performed identical arm exercise to the LH conditionfollowed immediately by a high volume of leg resistance exercise to elicit alarge increase in endogenous hormones (high hormone, HH). And they found thatthere was no elevation in serum growth hormone (GH), insulin-like growth factor(IGF-1), or testosterone after the LH protocol but significant increases inthese hormones immediately and 15 and 30 minutes after the HH protocol. Thehormone responses elicited by each respective exercise protocol late in thetraining period were similar to the response elicited early in the trainingperiod, indicating that a divergent postexercise hormone response wasmaintained over the training period.

But does this acute elevation with each training session translate intobetter gains in muscle fiber size? Well that's why they do the studies. They found that muscle cross-sectional area (CSA) increasedby 12% in LH and 10% in HH with no difference between conditions. Similarly, both slow and fast twitchmuscle fiber size increased with training with no effect of hormone elevationin the HH condition. Strength increased in both arms, but the increase was notdifferent between the LH and HH conditions. So what gives?(1) I'vealways maintained that the acute elevations in hormones (as measured in blood)is not as important as local signaling happening at the level of the musclefiber. Also, it is clear that acertain level of anabolic hormone (e.g. GH or testosterone) must be present insupraphysiological or perhaps pharmacological levels to induce real meaningfulhypertrophy. And that my friendsis why exogenous androgens work so well.

Quercitin

Quercetin (QR) is known forits potent antioxidant abilities and it's been shown to reduce oxidative stress in the long-term treatment of streptozotocin (STZ)-induced diabetes in animalmodels. 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 diabetesmellitus. In a recent study, sperm numbers, percentages of sperm viability andmotility, and total serum testosterone increased significantly in QR-treateddiabetic rats compared with control groups. In histopathology, degeneration andinflammation in testes cells associated with diabetes were improved and testesweights in the QR-treated diabetic group decreased significantly also. So even though this stuff was given torats, I'd imagine it's worth trying in us bipeds. I mean who couldn't use a little bit more motility downunder?(2)

Fat and Testosterone arelike 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 ofevery 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 notbe fat besides the fact that it irks the sh#$ outta me when I'm flying acrossthe 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 albuminand other proteins. The free T and the albumin-bound fraction are the biologically active testosterone fractions. Being afat man, especially if you carry it underneath your belt buckle, is associatedwith lower total testosterone [TT], free testosterone [FT] and sexhormone-binding globulin [SHBG], and a greater decline in TT and FT withincreasing age compared with lean men. Also, obese men have reduced spermconcentration and total sperm count compared to lean men.(3) Infact, 40% of obese non-diabetic and 50% of obese diabetic men above the age of45 years have subnormal FT concentrations. Thus, being a fat littlehousehusband is probably the condition most frequently associated with abnormally low FT concentration in males.(4) So if you're all about 'Fat Acceptance,' then bygolly, then you are also all about having low testosterone levels. And that myfriend, is just not a good thing. Wake up and get your fat butt on the treadmill.

Stay away from Statins

The use of statins (drugsused to lower cholesterol) is associated with a reduced testis volume and ahigher prevalence of hypogonadism-related symptoms and signs; also, statinusers have lower levels of total and calculated free T.(5) So ifyou happen to be taking these drugs, don't be surprised that in addition tolowering your cholesterol, it'll lower the ability of your private parts to'stand at attention.' And thatain't good.

No Harmful Effects ButBanned Nonetheless

Anabolic steroids work. Andthey work damn well. Some of themore popular drugs include: methyltestosterone, metandienone, nandrolone,testosterone esters and stanozolol. Recently, nonsteroidal alternatives to anabolic steroids have been developed that selectively activate the androgenreceptor in either muscle tissue or bones. These so-called selective androgenreceptor 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 particularfunctional groups allow for the tissue-selective activation or inhibition ofandrogen receptors and, thus, the stimulation of muscle growth without the riskof severe undesirable effects commonly observed in steroid replacementtherapies.(6) Did youread that? Without the risk of badside effects; then why on earth should they be banned? Should WADA ban cigarette smoking sincethat sh@# kills more people each year than the average population of an urbanChinese city.

Reference

1. WestDW, Burd NA, Tang JE, et al. Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy norstrength of the elbow flexors. J Appl Physiol;108:60-7.

2. KhakiA, Fathiazad F, Nouri M, et al. Beneficial effects of quercetin on spermparameters in streptozotocin-induced diabetic male rats. Phytother Res.

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

4. DhindsaS, Miller MG, McWhirter CL, et al. Testosterone Concentrations in Diabetic andNon-Diabetic Obese Men. Diabetes Care.

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

6. ThevisM, Schanzer W. Synthetic anabolic agents: steroids and nonsteroidal selectiveandrogen receptor modulators. Handb Exp Pharmacol:99-126.