The Dorian Era: the Science Behind the Stack
Though there is no longer any plausible deniability for the professionals that their natural gifts and hard work are the only factors in creating those incredulous physiques, there remains a sense of magic as to how such works of living art are created. Much like that iconic scene from “The Wizard of Oz,” six-time Mr. Olympia Dorian Yates has “pulled back” the curtain on professional bodybuilding. As he was responding to an open interview, the specifics remain clouded, but the details that can be gleaned are eye-opening.
The following relies upon Mr. Yates’ comments, but is not endorsed or confirmed by him.
In a past issue of Muscular Development, Yates discusses some of the drugs employed during his tenure as Mr. Olympia (1992-1997). In response to numerous questions, Yates has conveyed many of the tools used to achieve a physique with extremely low body fat, all the more impressive as he did so while retaining a superior amount of lean mass in comparison to most of his challengers.
Hard Work, Dedication and Genetics
First, it is critical to note that drugs being mentioned are not safe to be used outside the supervision of a qualified health professional. Though the risk is manageable, these drugs are potent and can lead to adverse effects. It is also illegal to obtain these drugs other than through a licensed pharmacy in the United States. Some are not even available via that route.
Second, though physique-enhancing drugs are the “elephant in the room,” there would be little benefit from this presumptive drug panel without providing the correct conditions. Not uncommonly, “normal” people (including bodybuilding fans) make gestures implying “pill popping” or injections behind the back of professional bodybuilders. It is not undeserved, but most pros would still be different from “normal” people based upon their genetics, discipline and extreme work ethic. So, do not forget that the drugs discussed below work for professional athletes such as Yates because the athletes have:
• The necessary desire to pursue excellence or recognition.
• Willingness to accept the risk of serious adverse effects, harm or even death from their pursuit (not unlike most elite athletes).
• Willpower sufficiently strong to maintain a lifestyle of sacrifice and pain.
• Physical gifts that allow them to train at a level not achieved by most people.
• Genetics that respond to the conditions they create.
• Resources that provide them with training facilities, drug access and dietary advice to advance toward their goals.
• A level of awareness to quickly recognize when things are “not right.”
A Lean and Dry Physique
The pre-contest drug routine Yates outlined strongly supports a lean and dry physique. As opposed to his off-season staples of relatively high-dose testosterone and nandrolone esters, along with daily Dianabol, Yates chose different anabolic-androgenic steroids (AAS) during his pre-contest phase. Note, he continued to use testosterone, but lowered his dose to 300 milligrams per week. This dose agrees with the minimal threshold dose necessary for promoting muscle hypertrophy in young adult men.[SUP]1[/SUP]
Yates did not mention the use of aromatase inhibitors— Nolvadex was more prevalent at the time— but it is likely that he reduced his testosterone dose to a minimal dose effective for his goals, and discontinued the Deca (nandrolone) and Dianabol to minimize the presence of aromatizable steroids (testosterone and Dianabol), as well as the estrogenic and progestinic stimulation evoked by nandrolone.
Water retention is also a factor with all three of his off-season AAS.[SUP]2,3[/SUP] The other two injectable AAS used during his pre-contest phase include Parabolan and Primobolan, two non-aromatizable AAS well known for providing a “dry” physique.[SUP]4[/SUP] Use of highly androgenic AAS agrees with reported observations that AAS with strong affinity for the androgen receptor also act on precursor cells such that they reduce the formation of new fat cells (adipogenesis), and reduce the effect of estrogens in existing fat cells that promote fat storage.[SUP]5[/SUP]
Trenbolone, the steroid component of Parabolan, is capable of promoting fat loss despite not being a substrate for 5-alpha reductase (meaning it is not turned into a super-androgen like testosterone being converted into DHT); trenbolone has three times the affinity for the androgen receptor as compared to testosterone.[SUP]6,7[/SUP] Primobolan is a well-regarded “cutting” AAS, presumably because it does not aromatize.
Anavar (oxandrolone) was the sole oral AAS used during his pre-contest phase. Oxandrolone is regarded as a “mild” AAS, but has the same propensity for causing liver strain as other 17 alpha-alkylated oral steroids. It is remarkable that oxandrolone has been reported to decrease abdominal fat in numerous studies at a dose of 20 milligrams per day or lower; Yates reported taking 50 milligrams per day.[SUP]8.9[/SUP] One proposed mechanism involves increased fatty acid oxidation (fat burning) in the liver, and a resultant increase in ketone production.[SUP]10[/SUP]
Human Growth Hormone
In addition to AAS, Yates admitted using human growth hormone (hGH), apparently utilizing hGH as an anabolic; he saw little anabolic benefit at a dose of four IU/day (within clinical replacement protocols). Two issues may account for this— anabolic effects occur at a higher threshold than the lipolytic effect; and Yates’ body mass was much so greater than the “normal” person that he likely was underdosed based on bodyweight.[SUP]11 [/SUP]When he increased his daily hGH dose to eight IU, he noted better results, stating, “It helped kick-start me to the next level.”
hGH is thought of as a “growth” hormone, but a more pronounced and useful effect is an increase in lipolysis (breakdown of stored fat). This lipolytic effect occurs at a lower dose, which allows one to avoid the increased water retention noted at the higher doses necessary for muscle growth.[SUP]12,13[/SUP] Further, Yates noted that he added insulin to his regimen in 1997, presumably after six years of hGH misuse. It is not surprising that a substantial gain in size with the combination was experienced, as hGH may antagonize the anti-proteolytic (preventing muscle breakdown) effects of insulin in the muscle.[SUP]14[/SUP] The observation by Yates that he only experienced abdominal distension when he added insulin to his drug regimen is interesting, as hGH is usually blamed for the distended bellies seen onstage during the late 1990s. Of course, insulin has nothing to do with fat loss in a bodybuilding drug regimen, as its effect on the fat cell is the opposite— promoting fat storage.
DNP and Thyroid Hormones for Fat Loss
Three final comments were offered by Yates relevant to his fat-loss drug protocol. Two stand in contrast to the actions of some of his contemporaries; another followed the standard for that period. First, there was a wave of DNP use to facilitate a rapid and extreme fat loss among elite and recreational bodybuilders. This was due in large part to the strong following enjoyed by steroid guru Dan Duchaine. DNP is a chemical uncoupler. This means that it “disconnects” the energy-producing function from the calorie-burning function in the mitochondria of the cell.[SUP]15[/SUP] The cell is not getting as much energy, so it burns more calories to finally get its ATP needs fulfilled. A consequence of this is that the additional calories burned are let off as heat, raising the body temperature considerably. More than one death has been attributed to DNP use. Yates clearly stated he never used DNP, and his approach to his entire drug-support actions was one of caution and effectiveness.
Thyroid hormones, especially T3 (aka Cytomel), are effective fat burners frequently used by bodybuilders and perhaps more so by fitness competitors. Though effective at increasing the metabolic rate (boosting the number of calories burned at rest or during exercise), thyroid hormone misuse can result in long-standing suppression of natural thyroid hormone production. Additionally, the more active T3 has a narrow window, and to reach the concentration where fat loss is increased causes non-specific catabolism. This means you lose muscle faster as well.
Many bodybuilders depend upon T3 to guarantee their metabolism is not slowed by overtraining or hypocaloric diets, even with a low body fat.[SUP]16[/SUP] hGH given at doses similar to those reported by Yates have been shown to suppress the release of TSH (pituitary hormone) without lowering free T4 or free T3 during a 21-day trial. It is unknown if hGH protects or suppresses thyroid function over the course of months or years at the doses taken by this group of men.[SUP]17[/SUP] If the dose becomes elevated to an unsafe level, heart arrhythmias can occur. Though no bodybuilder has reportedly died from T3-associated arrhythmia, the risk is present. This is magnified in the presence of stimulant drugs. Yates again reported that he did not resort to the use of thyroid medications, which may explain how he was able to retain so much lean mass when he was in “show shape.”
A Mixture of Androgens, Anabolics and Agonists
The last element in his fat-loss regimen was clenbuterol, a potent and selective beta2-agonist. This means it is a very strong drug that acts on the “adrenalin” receptor involved in muscle function and the breakdown of stored fat in fat cells. Clenbuterol remains in strong demand, though the practical use of it is complex due to receptor downregulation. The anabolic effects of clenbuterol reported in animals has only been repeated in humans using doses that would be deadly if not used with a beta1-blocker to prevent a racing heart beat. Clenbuterol is in a class by itself as a stimulant weight-loss drug, and is not marketed in the United States other than the black market. Yates did not detail his clenbuterol schedule, which would have been enlightening.
Top bodybuilding physiques appear to be magical, but for those who find drug use appalling or unethical, they would be no more than illusions. Dependent upon the base of hard work, dedication and genetics, the genie in the bottle is a mixture of androgens, anabolics and agonists. One must recognize the effort and sacrifice made by these men and women, but realize the magic is not alchemy, but chemistry. Mr. Yates was frank and honest in his revelations. It should be noted that his drug use, as well as Kevin Levrone’s and Shawn Ray’s, was much simpler and more rational than the “more is better” and “anything goes” attitude espoused by those who accomplish much less. Kudos to those men for allowing us a glimpse behind the curtain.
References:
1. 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.
2. Yule AG, Macfie J, et al. The effect of an anabolic steroid on body composition in patients receiving intravenous nutrition. Aust N Z J Surg 1981;51:280-4.
3. Freed DL, Banks AJ, et al. Anabolic steroids in athelics: crossover double-blind trial on weightlifters. Br Med J 1975;2:471-3.
4. Vernon BG, Buttery PJ. The effect of trenbolone acetate with time on the various responses of protein synthesis of the rat. Br J Nutr 1978;40:563-72.
5. 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.
6. Yarrow JF, Conover CF, et al. 17beta-Hydroxyestra-4,9,11-trien-3-one (trenbolone) exhibits tissue selective anabolic activity: effects on muscle, bone, adiposity, hemoglobin, and prostate. Am J Physiol Endocrinol Metab 2011;300:E650-60.
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. Schroeder ET, Zheng L, et al. Effects of androgen therapy on adipose tissue and metabolism in older men. J Clin Endocrinol Metab 2004;89:4863-72.
9. Lovejoy JC, Bray GA, et al. Oral anabolic steroid treatment, but not parenteral androgen treatment, decreases abdominal fat in obese, older men. Int J Obes Relat Metab Disord 1995;19:614-24.
10. Vega GL, Clarenbach JJ, et al. Oxandrolone enhances hepatic ketogenesis in adult men. J Investig Med 2008;56:920-4.
11. Hoffman AR, Strasburger CJ, et al. Efficacy and tolerability of an individualized dosing regimen for adult growth hormone replacement therapy in comparison with fixed body weight-based dosing. J Clin Endocrinol Metab 2004;89:3224-33.
12. Copeland KC, Nair KS. Acute growth hormone effects on amino acid and lipid metabolism. J Clin Endocrinol Metab 1994;78:1040-7.
13. Fryburg DA, Barrett EJ. Growth hormone acutely stimulates skeletal muscle but not whole-body protein synthesis in humans. Metabolism 1993;42:1223-7.
14. Fryburg DA, Louard RJ, et al. Growth hormone stimulates skeletal muscle protein synthesis and antagonizes insulin's antiproteolytic action in humans. Diabetes 1992;41:424-9.
15. Grundlingh J, Dargan PI, et al. 2,4-dinitrophenol (DNP): a weight loss agent with significant acute toxicity and risk of death. J Med Toxicol 2011;7:205-12.
16. Pakarinen A, Häkkinen K, et al. Serum thyroid hormones, thyrotropin and thyroxine binding globulin in elite athletes during very intense strength training of one week. J Sports Med Phys Fitness 1991;31:142-6.
17. Sgrò P, Guidetti L, et al. Effect of supra-physiological dose administration of rhGH on pituitary-thyroid axis in healthy male athletes. Regul Pept 2010;165:163-7.
Though there is no longer any plausible deniability for the professionals that their natural gifts and hard work are the only factors in creating those incredulous physiques, there remains a sense of magic as to how such works of living art are created. Much like that iconic scene from “The Wizard of Oz,” six-time Mr. Olympia Dorian Yates has “pulled back” the curtain on professional bodybuilding. As he was responding to an open interview, the specifics remain clouded, but the details that can be gleaned are eye-opening.
The following relies upon Mr. Yates’ comments, but is not endorsed or confirmed by him.
In a past issue of Muscular Development, Yates discusses some of the drugs employed during his tenure as Mr. Olympia (1992-1997). In response to numerous questions, Yates has conveyed many of the tools used to achieve a physique with extremely low body fat, all the more impressive as he did so while retaining a superior amount of lean mass in comparison to most of his challengers.
Hard Work, Dedication and Genetics
First, it is critical to note that drugs being mentioned are not safe to be used outside the supervision of a qualified health professional. Though the risk is manageable, these drugs are potent and can lead to adverse effects. It is also illegal to obtain these drugs other than through a licensed pharmacy in the United States. Some are not even available via that route.
Second, though physique-enhancing drugs are the “elephant in the room,” there would be little benefit from this presumptive drug panel without providing the correct conditions. Not uncommonly, “normal” people (including bodybuilding fans) make gestures implying “pill popping” or injections behind the back of professional bodybuilders. It is not undeserved, but most pros would still be different from “normal” people based upon their genetics, discipline and extreme work ethic. So, do not forget that the drugs discussed below work for professional athletes such as Yates because the athletes have:
• The necessary desire to pursue excellence or recognition.
• Willingness to accept the risk of serious adverse effects, harm or even death from their pursuit (not unlike most elite athletes).
• Willpower sufficiently strong to maintain a lifestyle of sacrifice and pain.
• Physical gifts that allow them to train at a level not achieved by most people.
• Genetics that respond to the conditions they create.
• Resources that provide them with training facilities, drug access and dietary advice to advance toward their goals.
• A level of awareness to quickly recognize when things are “not right.”
The pre-contest drug routine Yates outlined strongly supports a lean and dry physique. As opposed to his off-season staples of relatively high-dose testosterone and nandrolone esters, along with daily Dianabol, Yates chose different anabolic-androgenic steroids (AAS) during his pre-contest phase. Note, he continued to use testosterone, but lowered his dose to 300 milligrams per week. This dose agrees with the minimal threshold dose necessary for promoting muscle hypertrophy in young adult men.[SUP]1[/SUP]
Yates did not mention the use of aromatase inhibitors— Nolvadex was more prevalent at the time— but it is likely that he reduced his testosterone dose to a minimal dose effective for his goals, and discontinued the Deca (nandrolone) and Dianabol to minimize the presence of aromatizable steroids (testosterone and Dianabol), as well as the estrogenic and progestinic stimulation evoked by nandrolone.
Water retention is also a factor with all three of his off-season AAS.[SUP]2,3[/SUP] The other two injectable AAS used during his pre-contest phase include Parabolan and Primobolan, two non-aromatizable AAS well known for providing a “dry” physique.[SUP]4[/SUP] Use of highly androgenic AAS agrees with reported observations that AAS with strong affinity for the androgen receptor also act on precursor cells such that they reduce the formation of new fat cells (adipogenesis), and reduce the effect of estrogens in existing fat cells that promote fat storage.[SUP]5[/SUP]
Trenbolone, the steroid component of Parabolan, is capable of promoting fat loss despite not being a substrate for 5-alpha reductase (meaning it is not turned into a super-androgen like testosterone being converted into DHT); trenbolone has three times the affinity for the androgen receptor as compared to testosterone.[SUP]6,7[/SUP] Primobolan is a well-regarded “cutting” AAS, presumably because it does not aromatize.
Anavar (oxandrolone) was the sole oral AAS used during his pre-contest phase. Oxandrolone is regarded as a “mild” AAS, but has the same propensity for causing liver strain as other 17 alpha-alkylated oral steroids. It is remarkable that oxandrolone has been reported to decrease abdominal fat in numerous studies at a dose of 20 milligrams per day or lower; Yates reported taking 50 milligrams per day.[SUP]8.9[/SUP] One proposed mechanism involves increased fatty acid oxidation (fat burning) in the liver, and a resultant increase in ketone production.[SUP]10[/SUP]
Human Growth Hormone
In addition to AAS, Yates admitted using human growth hormone (hGH), apparently utilizing hGH as an anabolic; he saw little anabolic benefit at a dose of four IU/day (within clinical replacement protocols). Two issues may account for this— anabolic effects occur at a higher threshold than the lipolytic effect; and Yates’ body mass was much so greater than the “normal” person that he likely was underdosed based on bodyweight.[SUP]11 [/SUP]When he increased his daily hGH dose to eight IU, he noted better results, stating, “It helped kick-start me to the next level.”
hGH is thought of as a “growth” hormone, but a more pronounced and useful effect is an increase in lipolysis (breakdown of stored fat). This lipolytic effect occurs at a lower dose, which allows one to avoid the increased water retention noted at the higher doses necessary for muscle growth.[SUP]12,13[/SUP] Further, Yates noted that he added insulin to his regimen in 1997, presumably after six years of hGH misuse. It is not surprising that a substantial gain in size with the combination was experienced, as hGH may antagonize the anti-proteolytic (preventing muscle breakdown) effects of insulin in the muscle.[SUP]14[/SUP] The observation by Yates that he only experienced abdominal distension when he added insulin to his drug regimen is interesting, as hGH is usually blamed for the distended bellies seen onstage during the late 1990s. Of course, insulin has nothing to do with fat loss in a bodybuilding drug regimen, as its effect on the fat cell is the opposite— promoting fat storage.
Three final comments were offered by Yates relevant to his fat-loss drug protocol. Two stand in contrast to the actions of some of his contemporaries; another followed the standard for that period. First, there was a wave of DNP use to facilitate a rapid and extreme fat loss among elite and recreational bodybuilders. This was due in large part to the strong following enjoyed by steroid guru Dan Duchaine. DNP is a chemical uncoupler. This means that it “disconnects” the energy-producing function from the calorie-burning function in the mitochondria of the cell.[SUP]15[/SUP] The cell is not getting as much energy, so it burns more calories to finally get its ATP needs fulfilled. A consequence of this is that the additional calories burned are let off as heat, raising the body temperature considerably. More than one death has been attributed to DNP use. Yates clearly stated he never used DNP, and his approach to his entire drug-support actions was one of caution and effectiveness.
Thyroid hormones, especially T3 (aka Cytomel), are effective fat burners frequently used by bodybuilders and perhaps more so by fitness competitors. Though effective at increasing the metabolic rate (boosting the number of calories burned at rest or during exercise), thyroid hormone misuse can result in long-standing suppression of natural thyroid hormone production. Additionally, the more active T3 has a narrow window, and to reach the concentration where fat loss is increased causes non-specific catabolism. This means you lose muscle faster as well.
Many bodybuilders depend upon T3 to guarantee their metabolism is not slowed by overtraining or hypocaloric diets, even with a low body fat.[SUP]16[/SUP] hGH given at doses similar to those reported by Yates have been shown to suppress the release of TSH (pituitary hormone) without lowering free T4 or free T3 during a 21-day trial. It is unknown if hGH protects or suppresses thyroid function over the course of months or years at the doses taken by this group of men.[SUP]17[/SUP] If the dose becomes elevated to an unsafe level, heart arrhythmias can occur. Though no bodybuilder has reportedly died from T3-associated arrhythmia, the risk is present. This is magnified in the presence of stimulant drugs. Yates again reported that he did not resort to the use of thyroid medications, which may explain how he was able to retain so much lean mass when he was in “show shape.”
A Mixture of Androgens, Anabolics and Agonists
The last element in his fat-loss regimen was clenbuterol, a potent and selective beta2-agonist. This means it is a very strong drug that acts on the “adrenalin” receptor involved in muscle function and the breakdown of stored fat in fat cells. Clenbuterol remains in strong demand, though the practical use of it is complex due to receptor downregulation. The anabolic effects of clenbuterol reported in animals has only been repeated in humans using doses that would be deadly if not used with a beta1-blocker to prevent a racing heart beat. Clenbuterol is in a class by itself as a stimulant weight-loss drug, and is not marketed in the United States other than the black market. Yates did not detail his clenbuterol schedule, which would have been enlightening.
Top bodybuilding physiques appear to be magical, but for those who find drug use appalling or unethical, they would be no more than illusions. Dependent upon the base of hard work, dedication and genetics, the genie in the bottle is a mixture of androgens, anabolics and agonists. One must recognize the effort and sacrifice made by these men and women, but realize the magic is not alchemy, but chemistry. Mr. Yates was frank and honest in his revelations. It should be noted that his drug use, as well as Kevin Levrone’s and Shawn Ray’s, was much simpler and more rational than the “more is better” and “anything goes” attitude espoused by those who accomplish much less. Kudos to those men for allowing us a glimpse behind the curtain.
References:
1. 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.
2. Yule AG, Macfie J, et al. The effect of an anabolic steroid on body composition in patients receiving intravenous nutrition. Aust N Z J Surg 1981;51:280-4.
3. Freed DL, Banks AJ, et al. Anabolic steroids in athelics: crossover double-blind trial on weightlifters. Br Med J 1975;2:471-3.
4. Vernon BG, Buttery PJ. The effect of trenbolone acetate with time on the various responses of protein synthesis of the rat. Br J Nutr 1978;40:563-72.
5. 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.
6. Yarrow JF, Conover CF, et al. 17beta-Hydroxyestra-4,9,11-trien-3-one (trenbolone) exhibits tissue selective anabolic activity: effects on muscle, bone, adiposity, hemoglobin, and prostate. Am J Physiol Endocrinol Metab 2011;300:E650-60.
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. Schroeder ET, Zheng L, et al. Effects of androgen therapy on adipose tissue and metabolism in older men. J Clin Endocrinol Metab 2004;89:4863-72.
9. Lovejoy JC, Bray GA, et al. Oral anabolic steroid treatment, but not parenteral androgen treatment, decreases abdominal fat in obese, older men. Int J Obes Relat Metab Disord 1995;19:614-24.
10. Vega GL, Clarenbach JJ, et al. Oxandrolone enhances hepatic ketogenesis in adult men. J Investig Med 2008;56:920-4.
11. Hoffman AR, Strasburger CJ, et al. Efficacy and tolerability of an individualized dosing regimen for adult growth hormone replacement therapy in comparison with fixed body weight-based dosing. J Clin Endocrinol Metab 2004;89:3224-33.
12. Copeland KC, Nair KS. Acute growth hormone effects on amino acid and lipid metabolism. J Clin Endocrinol Metab 1994;78:1040-7.
13. Fryburg DA, Barrett EJ. Growth hormone acutely stimulates skeletal muscle but not whole-body protein synthesis in humans. Metabolism 1993;42:1223-7.
14. Fryburg DA, Louard RJ, et al. Growth hormone stimulates skeletal muscle protein synthesis and antagonizes insulin's antiproteolytic action in humans. Diabetes 1992;41:424-9.
15. Grundlingh J, Dargan PI, et al. 2,4-dinitrophenol (DNP): a weight loss agent with significant acute toxicity and risk of death. J Med Toxicol 2011;7:205-12.
16. Pakarinen A, Häkkinen K, et al. Serum thyroid hormones, thyrotropin and thyroxine binding globulin in elite athletes during very intense strength training of one week. J Sports Med Phys Fitness 1991;31:142-6.
17. Sgrò P, Guidetti L, et al. Effect of supra-physiological dose administration of rhGH on pituitary-thyroid axis in healthy male athletes. Regul Pept 2010;165:163-7.
