The Ultimate Anabolic Stack

In recent years, former elite professional bodybuilders have discussed the drugs used in achieving both their off-season gains and pre-competition goals. Bodybuilding’s attraction, lost somewhat in the modern version of the sport/pageant, is a presentation of aesthetics and potency. Size and muscularity are certainly components of this, but of equal or greater importance is achieving a lean physique.

Emphasizing that the following is not condoned— and should not be construed as a recommendation or suggest any warrant of safety— there are several commonalities to “stacks” that provide a lean, even ripped physique for the recreational bodybuilder.

“Ripped” refers to a body fat percentage low enough to allow superficial veins and striations in a flexed muscle to be visible. In terms of numbers, body fat percentage needs to be dropped as low as physiologically possible. For natural bodybuilders, this may be five to six percent without sacrificing lean mass precipitously. Drug-enhanced bodybuilders are capable of maintaining muscle mass under conditions that would normally deplete muscle protein stores, allowing them to reach body fat percentages reportedly as low as the two percent range, though likely in the three to four percent range. At this extreme, it is very difficult to acquire an accurate body fat percentage, regardless of technique, as technical issues and lack of standardization at this end of the scale create a variability that is higher than the measured body fat.

More specific to being “ripped” is depleting subcutaneous fat— under the skin. While it is technically correct to factor visceral, intra-abdominal and organ-associated fat in the calculation, these depots of fat do not affect the presentation of one’s physique. They can adversely affect health, but that is outside the scope of this topic. Further, it does little good to reveal the underlying muscles if they are not well developed.

First, it is important to develop the skeletal muscles, and this is obviously a function of one or more anabolics. Bodybuilders discuss “bulking” versus “cutting” cycles, as they are well aware of the inherent challenges in trying to achieve both simultaneously. Thus, “cutting” cycles generally are the domain of experienced anabolic-androgenic steroids (AAS)-enhanced lifters. This is to acknowledge that the following drugs are generally misused by men who have acquired a self-satisfactory amount of muscle mass.

Pre-contest Cutting Cycle

Other than competitive bodybuilders who are compelled to attain a skin-stretching muscle mass far greater than nature intended, most lifters aim for a look more in line with the classic physique. Frank Zane’s competition form may be a suitable example, or Sylvester Stallone’s in “Rocky III.” Note, as one gets leaner, he appears more muscular and even larger due to the “high-definition” look compared to the soft, rounded appearance when body fat levels are in the double digits.

There is no “one” ultimate cutting cycle, but the following is an example that mimics the pre-contest preparation used by amateur bodybuilders. [Note— this for discussion purposes only, not a recommendation or advice]

testosterone enanthate

300 milligrams per week

trenbolone acetate

~75 milligrams, twice weekly

stanozolol

50 milligrams, twice weekly (intramuscular) or 10-20 milligrams per day (oral)

anastrozole

1 milligram per day

clenbuterol

20 micrograms (mcg) two days on/off; many build up to dosing four times daily or more due to tolerance

T₃ (Cytomel)

25 mcg daily, titrated up to a maximum of 100 mcg in divided doses, pyramiding down

hGH (human growth hormone)

3 international units (IU) per day

Testosterone is the foundation drug, highly effective when used at near-physiologic dosing. Studies have shown benefits with weekly dosing of 300 milligrams of testosterone ester, and greater effect at 600 milligrams weekly; this includes reducing body fat while increasing muscle mass.^1,2 Though these doses are reasonably well tolerated in young adults, older men may experience elevations in hematocrit (red blood cells), and those with a pro-thrombotic condition (tendency to form blood clots) should not use AAS without the supervision of a health care provider.

Some may challenge testosterone’s placement in a cutting cycle due to its propensity to aromatize, which will be discussed further. However, testosterone has a strong ability to maintain size and fullness, and aromatization can be controlled. It is possible that some of testosterone’s actions occur in muscle cells as well, where enzymes produce DHT and estradiol, to affect the muscle directly.³ This is an area that has not been well studied.

Testosterone is typically combined with other AAS to reduce the dependence on this aromatizable AAS. Nandrolone decanoate (aka Deca) is commonly used, as it is widely available and considered to be a reasonably well-tolerated AAS. However, Deca can promote water retention, and may worsen gynecomastia when used with testosterone, making this a less-than-optimal cutting AAS. Unlike testosterone, nandrolone has direct activity at progesterone receptors, and can be inefficiently converted into an estrogen via a non-aromatase pathway.^4,5 For those seeking to stay ripped, Deca can contribute to muscle mass, allowing for a lower dose of testosterone.

Anecdotally, Deca provides the best “bang for the buck” in a cutting stack when dosed around 100 milligrams per week, or lower. Deca is sometimes included in cutting cycles to relieve joint pain, apparently a function of its progestin-like properties. Note, nearly all AAS can induce edema (water retention), especially around the feet and ankles. This usually subsides, but can be an indication to cease treatment in older men.⁶

Trenbolone, Stanozolol and Anastrozole

Other injectable AAS offer more directed aid, but are less common as they are not commercially available in the United States for human use. Trenbolone is an AAS that was highly regarded when it was available, but has since been pulled from the market— other than for veterinary use. There is research indicating it would be a suitable SARM, or selective androgen receptor modulator— the politically correct term for predominantly non-steroidal anabolics being developed by pharmaceutical companies.⁷ However, recent research suggests that it may accelerate the development of Alzheimer’s dementia when present as a pollutant from animal feedlots in community water supplies, or potentially when used as a bodybuilding drug.⁸

Trenbolone not only provides a dry, hard look, but also promotes satellite cells into differentiating and fusing with myofibers when used in cattle, presumably in humans as well.⁹ This process allows for a higher ceiling in future muscle growth. “Test and tren” stacks provide results that satisfy the goals of many AAS misusers/abusers, but can cause serious mood disruption during and after the cycle. Trenbolone was long the “go to” cutting AAS during the 1970s and 1980s under the brand name Parabolan.

Similar to trenbolone, stanozolol has long been used during “cutting” phases, as it also provides a dry and hardened look. Both trenbolone and stanozolol share the common trait of being 5 alpha-reduced, which prevents any aromatization (conversion of an AAS into an estrogenic steroid). This reduces any potential fat accretion or water retention common to the aromatizing AAS (such as testosterone). There is little functional difference between oral and injectable versions of stanozolol, as the drug is modified to protect against being metabolized by enzymes in the liver and intestines. However, this modification can result in liver damage and a lowering of HDL cholesterol (good cholesterol), which is more pronounced with oral use.¹⁰

Anastrozole is a non-competitive, third-generation aromatase inhibitor, developed to block estrogen production in women with breast cancer. Testosterone and other aromatizable androgens can be converted into estrogenic steroids, unless they are protected by certain modifications. Dihydrotestosterone (DHT)-like AAS are stronger androgens and do not convert into estrogens. Anastrozole is frequently prescribed during testosterone replacement therapy (TRT) to prevent a supraphysiologic estradiol response, more common in older men.

Though there are two slightly more potent aromatase inhibitors, it is the lower potency of anastrozole that is its strength in this comparison. Aromasin is a competitive, and thus irreversible inhibitor. It is referred to as a suicide inhibitor, as it binds the aromatase enzyme permanently, preventing any further action until new enzyme is formed. Letrozole is similar to anastrozole, but penetrates tissue better and has a slightly greater inhibition.

Both anastrozole and letrozole suppress estrogen concentration by >98 percent in women, but in men the suppression is less— due to the vastly higher testosterone availability, magnified when AAS are used. Aromatase inhibition in adult men suppresses the estradiol:testosterone ratio by approximately 80 percent.¹¹ Near-complete suppression of aromatase can result in less muscle hypertrophy, loss of bone density, mood changes and other effects involving neural pathways in the brain, etc. By allowing estradiol to be maintained in a physiologic range, this negates some of the negative effects seen in traditional cutting cycles that utilized only non-aromatizing AAS. Further, its lesser suppression of aromatase activity in tissue means beneficial cellular functions, and viability is less affected. This includes skin cells, muscle tissue, libido, tendon healing, etc.

The use of testosterone, trenbolone and likely, stanozolol, promotes the differentiation of precursor cells that can divert into either fat cells or muscle cells to enter the muscle (satellite) cell pool; as well, lipolysis (release of stored fat) is increased.¹² Anastrozole may reduce the influence of estrogens to promote fat storage.

Clenbuterol, Thyroid Hormone and hGH

The drugs discussed up to this point serve mainly to promote muscle mass development and maintenance, while they also reduce fat cell development and accretion of fat mass. Androgen-based inhibition of glucocorticoid receptor activity also reduces fat gain, especially in the presence of an aromatase inhibitor. Now we’ll look at drugs that primarily serve to promote energy expenditure (calorie burning) and release of stored fat.

Clenbuterol is an adrenalin-like drug that has a relative specificity for the beta2-adrenoreceptor. Fat cells have approximately 30 percent beta1-adrenoreceptors and 70 percent beta2-adrenoreceptors that can both activate lipolytic processes.¹³ However, as the heart rate can be dangerously elevated when stimulated at the beta1-adrenoreceptor, clenbuterol offers a significant advantage over non-specific stimulants. Unfortunately, clenbuterol is not exclusively a beta2-agonist, and can cause tachycardia and arrhythmias, which can require immediate hospitalization.

Bodybuilders embraced clenbuterol, as it was shown in animal studies to also be anabolic, but the dose required is fatal without adequate beta1-blockade. As a fat-loss agent and thermogenic, clenbuterol is without equal among the available adrenergics, and has been a staple for decades. It is even widely used by actors and models. However, the receptors necessary for the thermogenic effect are rapidly downregulated, so various patterns of clenbuterol dosing have evolved to prolong its effect. The popular scheme is to alternate two days on and two days off, or to alternate weekly; some add an antihistamine (ketotifen), as it has been shown to improve adrenoreceptor response in asthmatics with daily or more frequent use of clenbuterol.¹⁴

Thyroid hormone is present in two main forms, T₄ and T₃, with T₃ having much greater activity. Many bodybuilders and fitness competitors misuse thyroid hormone as it increases the metabolic rate, thus the number of calories burned throughout the day. Further, it helps increase fatty acid oxidation and uncoupling, which “wastes” those calories.¹⁵ However, Synthroid (T₄) is an inappropriate choice, as the body will not “activate” it to T₃ inappropriately, thus the drug of choice for bodybuilders is T₃. Excess T₃ can cause serious heart rhythm problems and lead to muscle wasting. Further, several amateur and professional competitors have become lifetime dependent on thyroid medication, after they were unable to restore natural function due to the suppression that occurs from taking it for weight-loss purposes. It is a step that can have serious consequences, even if tolerated well during the cycle.

Human growth hormone is often thought of as an anabolic, but in moderate dosing, aids in releasing stored fat. Fat cells have receptors for hGH, and respond by breaking down stored fat.¹⁶ Improved body composition is one of the most apparent benefits of hGH replacement therapy, and the doses used are similar to that supporting fat loss.

This stack is not dissimilar from that mentioned by six-time Mr. Olympia Dorian Yates in his revelations of preparing for his Mr. Olympia contests. The cycles used by modern-day competitors are much more complex, and dangerous. However, Mr. Yates was known for his extremely lean condition, especially for a man with his size. The drugs involve a number of health and legal risks, and should not be considered without appreciating potential harm. However, it is important to acknowledge the common practices, and understand that the extreme dosing written about in many forums is unnecessary, and compounds the risk manyfold.

It is important to close with the understanding that even potent drugs such as discussed here will not combat a poor diet or slovenly work ethic. The results so many people envy in others are typically the result of dedication and discipline, with some acceptance of risk. It is not an endorsement of these practices, and does not mean that they are safe, even in a relative sense.

References:

1. Bhasin S, Woodhouse L, et al. Testosterone dose-response relationships in healthy young men. Am J Physiol Endocrinol Metab 2001;281:E1172-81.

2. Sinha-Hikim I, Artaza J, et al. Testosterone-induced increase in muscle size in healthy young men is associated with muscle fiber hypertrophy. Am J Physiol Endocrinol Metab 2002;283:E154-64.

3. Sato K, Iemitsu M. Exercise and sex steroid hormones in skeletal muscle. J Steroid Biochem Mol Biol 2015;145:200-5.

4. Attardi BJ, Page ST, et al. Mechanism of action of bolandiol (19-nortestosterone-3beta,17beta-diol), a unique anabolic steroid with androgenic, estrogenic, and progestational activities. J Steroid Biochem Mol Biol 2010;118:151-61.

5. Yoshiji S, Yamamoto T, et al. Aromatization of androstenedione and 19-nortestosterone in human placenta, liver and adipose tissues. Nihon Naibunpi Gakkai Zasshi 1986;62:18-25. [Article in Japanese]

6. Johannsson G, Gibney J, et al. Independent and combined effects of testosterone and growth hormone on extracellular water in hypopituitary men. J Clin Endocrinol Metab 2005;90:3989-94.

7. Yarrow JF, McCoy SC, et al. Tissue selectivity and potential clinical applications of trenbolone (17beta-hydroxyestra-4,9,11-trien-3-one): A potent anabolic steroid with reduced androgenic and estrogenic activity. Steroids 2010;75:377-89.

8. Ma F, Liu D. 17beta-trenbolone, an anabolic-androgenic steroid as well as an environmental hormone, contributes to neurodegeneration. Toxicol Appl Pharmacol 2015;282:68-76.

9. Johnson BJ, Halstead N, et al. Activation state of muscle satellite cells isolated from steers implanted with a combined trenbolone acetate and estradiol implant. J Anim Sci 1998;76:2779-86.

10. Carson P, Hong CJ, et al. Liver Enzymes and Lipid Levels in Patients With Lipodermatosclerosis and Venous Ulcers Treated With a Prototypic Anabolic Steroid (Stanozolol): A Prospective, Randomized, Double-Blinded, Placebo-Controlled Trial. Int J Low Extrem Wounds 2015;Feb 3. [Epub, ahead of print]

11. de Ronde W, de Jong FH. Aromatase inhibitors in men: effects and therapeutic options. Reprod Biol Endocrinol 2011;9:93.

12. Gupta V, Bhasin S, et al. Effects of dihydrotestosterone on differentiation and proliferation of human mesenchymal stem cells and preadipocytes. Mol Cell Endocrinol 2008;296:32-40.

13. Mauriège P, De Pergola G, et al. Human fat cell beta-adrenergic receptors: beta-agonist-dependent lipolytic responses and characterization of beta-adrenergic binding sites on human fat cell membranes with highly selective beta 1-antagonists. J Lipid Res 1988;29:587-601.

14. Huszar E, Herjavecz I, et al. Effects of ketotifen and clenbuterol on beta-adrenergic receptor functions of lymphocytes and on plasma TXB-2 levels of asthmatic patients. Z Erkr Atmungsorgane 1990;175:141-6.

15. Barbe P, Larrouy D, et al. Triiodothyronine-mediated up-regulation of UCP2 and UCP3 mRNA expression in human skeletal muscle without coordinated induction of mitochondrial respiratory chain genes. FASEB J 2001;15:13-15.

16. Berneis K, Keller U. Metabolic actions of growth hormone: direct and indirect. Baillieres Clin Endocrinol Metab 1996;10:337-52.

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