AAS Roundtable Discussion
AAS Roundtable Discussion
Hi guys....I don't post much in this forum (actually I don't post at all).
Anyway, I just got this quarters Strength and Conditioning Journal from the NSCA. They have an AAS roundtable discussion in there (some heavy hitters in the world of sports nutrition).
I have not read it yet, so I don't know what it is going to be talking about particularly. Thought I would post it here for anyone interested.
If you want a PDF version, just drop me a PM with your email addy and I can get that out to you.
Strength and Conditioning Journal: Vol. 28, No. 6, pp. 42–55.
Roundtable Discussion: Anabolic Androgenic Steroids: Part I
G. Gregory Haff, PhD, CSCS
West Virginia University School of Medicine, Morgantown, West Virginia
With the discovery of tetrahydrogestrinone and desoxymethyltestosterone, a widespread conspiracy to supply athletes with anabolic agents, which were not currently on doping control lists, was uncovered. This realization, plus the Congressional Hearings on Steroid Use in Sport, has brought discussions about anabolic-androgenic steroids to the forefront of popular culture. Within this movement, a plethora of nonscientifically sound data has been presented in the popular media. The present roundtable is the first part of a 2-part series designed to present current information on the topic.
Disclaimer: The views expressed by the authors of this manuscript may not reflect the official position stance presented by the National Strength and Conditioning Association (NSCA) or the editorial staff of Strength and Conditioning Journal. The complete NSCA Position Stance on Anabolic Steroids can be found on the NSCA Web site (http://www.nsca-lift.org/Publication...shtml#steroid).
The concept of attempting to improve athletic performance through the use of different types of ergogenic aids has been around for well over 3,000 years (1, 8). With the isolation of the basic chemical compound known as testosterone in 1935 and the subsequent understanding of the anabolic characteristics of the compound (6), some individuals have suggested that testosterone could offer a potentially powerful ergogenic benefit for athletes (2).
Even though synthetic testosterone was not developed as an ergogenic aid for sports, the 1950s saw the first documented incidences of anabolic-androgenic steroid (AAS) use by athletes (5, 9, 11). From the late 1950s through the 1990s, it appears that AAS use grew in silence, although by 1976 AAS had been placed upon the International Olympic Committee's banned substances list (5) and was subsequently classified as a Schedule III Controlled Substance by the United States government in 1990 (4). For the most part, the public believes that the usage of AAS by athletes is minimal (1), even though rough estimates suggest that the black market sale of AAS in the United States exceeds $100 million annually (10).
More recent events, which include the discovery of tetrahydrogestrinone and desoxymethyltestosterone and a widespread conspiracy to supply athletes with illegal and banned ergogenic aids (3, 7), coupled with congressional hearings on steroid use in sport, have created an environment in which AAS have become a popular topic in the popular media. The present roundtable is designed to foster a contemporary discussion about topics that are related to AAS use in sports.
Question 1: How Do Steroids Work (i.e., Possible Mechanisms-of-Action)? Return to TOC
Jose Antonio: AAS exert their actions via the androgen receptor. There is evidence to suggest that the administration of AAS can up-regulate levels of the androgen receptor, can stimulate satellite cell proliferation, and can promote gains in skeletal muscle protein (1, 2, 4, 6, 8). The effects of AAS on skeletal muscle mass are dose dependent. Thus, synthetic testosterone administration improves net muscle protein balance by stimulating muscle protein synthesis, decreasing muscle protein degradation, and improving the reutilization of amino acids (3). According to Bhasin et al., “the muscle protein synthesis hypothesis does not adequately explain testosterone-induced changes in fat mass, myonuclear number, and satellite cell number.” The complete mechanism of action is not entirely understood at this time (3).
Robert Chetlin: This is a question that has captivated the field of exercise science for decades. Though the AAS have been studied extensively in animal models, clinical populations, and otherwise healthy humans, the truth is no single mechanism-of-action (MOA) has been identified. Current theory, however, holds that the MOA of AAS is most likely multifactorial. The basis for this assertion likely is due to the ubiquitous presence of androgen receptors in virtually all tissues in the human body (8, 40). AAS bind androgen receptors in target tissues and these receptors express properties of both anabolism and androgenicity. To date, no drug has been discovered or manufactured that can produce selective anabolic or androgenic effects. Thus, it is most probable that the overall MOA of this class of drugs is not tissue-specific, but tissue-common, producing an array of effects including:
Increased protein synthesis producing hypertrophy, and perhaps hyperplasia, of skeletal muscle by up-regulation of gene transcription and synthesis of messenger RNA (1,29,37,38); proliferation of satellite cells including an increased myonuclei-to-fiber ratio in muscle (19–22, 34); induction of the effects of growth hormone and insulin-like growth factor 1 (1, 19, 37); and possibly heightened stimulation of mesenchymal pluripotent cells (5).
Displacement of cortisol at its receptor, thus inducing an anticatabolic effect. Competitive binding of AAS to glucocorticoid receptors enables these drugs to countermand cortisol's role in the degradation of skeletal muscle protein, indirectly contributing to heightened skeletal muscle anabolism (17).
Elevated synthesis of neuropeptides producing altered perceptions to pain and fatigue (35). Because the central nervous system, including the brain and spinal cord, is rich in steroid receptors, most notably androgen-mediated complexes, AAS administration results in an increased concentration of neurotrans-mitter (e.g., dopamine, serotonin) metabolites (9, 30). Such an effect would beneficially influence exercise adaptation by permitting longer, more frequent, and higher intensity training bouts (9, 11).
To what extent the preponderance of the individual components of this integrated MOA facilitate their effects in a heterogeneous population is unknown.
Jay Hoffman: Testosterone itself is a very poor ergogenic aid. It is degraded quite rapidly when provided exogenously. For exogenous administration of synthetic testosterone to be effective, it is necessary to chemically modify the steroid in order to retard the degradation process. As a result, AAS are maintained at higher concentrations for longer periods of time, permitting the desired anabolic and androgenic changes. The principal mechanism responsible for performance improvements (primarily seen as increases in lean body mass and muscular strength) relate to an increase in protein synthesis and an inhibition of the catabolic effects from high-intensity training. This latter mechanism may function more as an indirect method by providing for a greater anabolic environment. This allows the athlete to maintain a high intensity and a high volume of training, with enhanced recovery processes occurring between exercise sessions. Thus, the athlete can train harder and for a longer duration, providing for a greater training stimulus. It is likely that the improved training stimulus is the direct mechanism of action resulting in performance improvements.
William Kraemer, Jakob Vingren: Exogenous AAS are synthetic forms of testosterone, and as such, they mimic the biological action of testosterone. The AAS-induced cellular regulation is modulated by the binding of AAS to the cytosolic androgen receptor (AR). This testosterone-AR complex (TARC) has an overall stimulating effect on protein synthesis via numerous pathways and mechanisms. The detailed mechanisms for this stimulation, especially in skeletal muscle, have not been fully determined. However, several mechanisms have been proposed. Many endocrine responses are tissue specific; nevertheless, the androgenic mechanisms in nonskeletal muscle tissue can suggest possible androgenic mechanisms in skeletal muscle. The TARC, in combination with its coactivators, can stimulate protein synthesis directly by translocating to the nucleus and then altering target gene transcription by binding to its corresponding DNA response element (6, 8, 11). One such alteration of gene transcription has been reported by Lee (10), who found that the TARC enhances the expression of myogenin, a secondary myogenic regulatory factor.
Recently, this area has become more complex, because a new class of synthetic drugs called nonsteroidal selective androgen receptor modulators (SARMs) has been developed (3). SARMs display similar actions to AAS, but their actions are limited somewhat to a specific target tissue. In this manner, SARMs developed to display an effect in muscle tissue may not have many of the negative side effects in other tissue normally associated with AAS.
Mathew Lively: AAS bind to androgen receptors in skeletal muscle and activate the transcription of genes necessary for muscle growth. This activation causes an increase in protein synthesis that leads to gains in muscle strength and mass, with or without exercise, through both hypertrophy and the formation of new muscle fibers (3, 7, 12, 15, 16). The number of androgen receptors in skeletal muscle is increased by exposure to AAS (2) and also by resistance training (11), which likely explains why exercise and steroid use is additive.
Question 2: Currently, the Popular Media Seems to Suggest That Steroid Use Is on the Rise. Based Upon Your Understanding of the Literature, Is This True and, If So, How Prevalent Is Steroid Use at Various Levels of Athletic Competition (i.e., High School, College, Professional Sports, and International Competitions Such as the Olympics)? Return to TOC
Antonio: The popular media does suggest this; however, my general impression is that journalists in the mainstream press are ignorant of this subject. There are mainstream newspaper reports that dehydroepiandrosterone is an “anabolic” steroid. It certainly is a steroid, but it is certainly not anabolic (5).
Chetlin: The answer to this question has been, and remains, somewhat speculative. Definitive estimates are difficult to obtain because of the inherent weaknesses of historical research, including the use of surveys. Threats to internal validity with such self-report methodology include recall bias and truthfulness-of-response. Nonetheless, survey research is considered valid and is the only process by which to assess demographic patterns of usage. Having stated this, the literature clearly indicates that the evaluation of multitiered (i.e., high school, college, professional) AAS-user trends is highly variable. One national study of high school students reported that 4.9% of respondents admitted to steroid use, whereas another indicated that 6.6% had experimented with anabolic drugs (7, 42). At the collegiate level, one investigation determined that 17% of all athletes have used AAS, with the highest user rate identified in male collegiate football players—about 30% (13). This greatly contrasts with very conservative data from the National Collegiate Athletic Association (NCAA): 4% of collegiate athletes use AAS and only 1.1% of football players rely on AAS for performance enhancement (24). A study among one group of elite amateur athletes (i.e., powerlifters) competing at a national venue indicated that 55% of this population admitted to steroid use (41). Determination of AAS usage in professional athletics is extremely difficult, given the reticence of the governing authorities of these sports to divulge factual information regarding illicit ergogenic enhancement. Nonetheless, testimonials from former professional athletes are somewhat alarming, including some who estimate usage in the National Football League (NFL) and Major League Baseball (MLB) as high as 75–85% (2).
Despite the described limitations with determining AAS consumption patterns, is it still possible to ascertain if certain segments of the population have increased AAS use? The answer, in my opinion, is a conditional yes. Black market availability of AAS is pervasive; steroids smuggled into this country from Mexico and Europe (particularly Eastern Europe) can be obtained easily from insidious sources, and the Internet has become a virtual clearinghouse for anabolic drugs. It is not difficult, therefore, to reasonably speculate that if availability is widespread, then usage is on the rise as well. Some data indicate as much, especially in adolescents, with usage for both boys and girls increasing (13, 18). Determination of usage change in elite and professional athletics is a bit more illusory. Historically, it is widely accepted that the modern advent of AAS usage occurred in the late 1950s and early 1960s, first with the state-sponsored drug programs of the former Soviet Bloc and then the wholesale availability of manufactured drugs in the West, including Dianabol (methandrostenolone). Increases in AAS use are related to circumstantial innovativeness. As coaches, trainers, and athletes became aware of the drugs' effectiveness, typically by word of mouth, their use rose exponentially. The prevalence of AAS usage has spread from one professional venue to the next with seemingly monumental upsurges noted for football in the late 1960s and throughout the 1970s and for baseball in the 1990s. Today, however, there is most likely a saturation effect in the elite amateur and professional ranks. The effectiveness of the drugs is widely known and their use is no longer novel. Most likely, given the finite populace of elite and professional athletic circles, usage has not increased. The perception of rising use, however, in the public domain is sweeping, especially given the heightened state of media and government attention of the AAS issue.
Hoffman: Interestingly, this may not actually be true. Although the scientific literature is limited in regard to surveys on anabolic steroid use, the NCAA has published a survey on anabolic steroid use in the NCAA from 1989 to 2001 (22). According to the results, AAS use actually has decreased, from 4.9% of the surveyed athletes acknowledging being users in 1989 to 1.4% of the surveyed athletes admitting to anabolic steroid use in 2001. The prevalence of AAS use in NCAA football players also has decreased almost 50% from 1985 to 1993, according to several published reports (3–5). The most frightening part of these surveys is the age at which these athletes began to experiment with AAS. The NCAA surveys have shown that initial AAS use among collegiate athletes occurs during high school (>40% of athletes surveyed in 2001). In the past 10 years, the use of AAS at the high school level has been reported to range from 3% (8) to 5.4% (9).
What we actually may be seeing is an increase in media exposure, rather than an increase in use. Over the past few years, high-profile athletes have been associated with steroid usage corresponding with a media accessibility that is unprecedented in sports history. During the 1970s and 1980s, when steroid use was allegedly at its highest in the NFL, the 24-hour sports shows on Entertainment and Sports Programming Network and sports radio did not exist. Thus, we need to be careful how we place this in its historical perspective.
One of the issues that often goes unmentioned is the fact that many of the sport supplements popularly used today, such as creatine, did not exist during the '70s and '80s. In the opinion of this author, the decrease often reported in AAS usage today compared with that era is likely a result of the availability of alternatives that provide the athlete with the desired gains, minimize health risk, and are legal.
Kraemer, Vingren: In the opinion of these authors, the increase in positive tests also might indicate this to be the case, but in reality we do not have any data concerning this point. It is all conjecture and speculation on a limited database with only testable AAS being examined and survey data potentially indicative of the tip of the iceberg—and we do not know how expansive it is.
Lively: There has been a reported increase in AAS among high school students. Survey data from the National Institute on Drug Abuse show the annual use of AAS among high school seniors in the United States has risen steadily from 1.1% in 1992 to 2.5% in 2004 (10). Among college athletes surveyed every 4 years by the NCAA, 1.4% admitted using AAS in 2001, which was slightly higher than the 1.1% reported in 1997, but well below a high of 4.9% in 1989 (14). There is less prevalence data available among professional sports, but when MLB performed league-wide testing in 2003, at least 5–7% of players tested positive for AAS. The lower prevalence among college athletes often is attributed to year-round testing by the NCAA, which is obviously not available at the high school level. It would be interesting to see if the prevalence in MLB decreases now that regular testing is to be instituted.
Question 3: In Your Opinion, Why Do Athletes Take Steroids? Return to TOC
Antonio: In the opinion of this author, recreational athletes take AAS to increase lean body mass and decrease fat mass, whereas competitive athletes take AAS to expedite recovery time and to improve athletic performance.
Chetlin: The reason seemingly cited most often for AAS use in athletes is to seek a competitive advantage in a particular sport, or to achieve equilibrium in an athletic arena where steroid use is known, or even perceived, to be common. In this latter case, the rationale for usage is based upon an assumption of necessity and self-fulfilling enablement (i.e., to keep up with the competition). Given the ferocity of competition at all sporting levels and the enormous pressure from peers, coaches, and an omnipresent media to succeed, it perhaps becomes a bit easier to understand the ultimate decision to use AAS. Depending upon individual sport demands, some athletes also claim a protective or enhanced recovery effect of the drugs. For example, the repeated and potentially injurious collisions inherent in collegiate and professional football, the grueling day-in, day-out schedule demands of professional baseball, and a combination of these expressed factors in professional ice hockey, may facilitate the self-described justification to use AAS.
Additional motive to use may be specific to some related aspect of the sporting endeavor itself and is, therefore, dependent upon the population stratum one is addressing. High school athletes may take these drugs to place themselves in consideration for extensive playing time or a starting role in a team sport, to qualify for regional or state competition in individual athletic pursuits, or to earn a college scholarship. In addition to playing or participation goals, collegiate athletes may take AAS in an attempt to meet the biometric and performance standards to even be qualified for the ranks of professionalism. One can think of no more cogent illustration than the physical requirements professional football scouts assign to specific positions. Offensive lineman, for example, may be unilaterally dismissed as too small, and thus downgraded from draft consideration, if they weigh less than 300 pounds. A running back who does not weigh 220 pounds or run a 4.4-second 40-yd dash, also may suffer such a judgmental fate. Elite Olympic athletes may take AAS to win a gold medal in their respective sports and thus attract very lucrative sponsorship or endorsement contracts, which easily may reach into the millions of dollars. Consider that in some sports contested in the Olympics, where the margin between winning a gold medal and winning no medal at all is decided by tenths or even hundredths of a second, it simply may be too tempting for many athletes to ignore the siren song of future notoriety and the huge sums of money heaped upon Olympic gold medal winners. Professional athletes may utilize AAS to enhance their chances of obtaining performance bonuses, whether stemming from simply number of games played to rarified All-Star or Pro-Bowl status, and thus augment their earning potential. Such achievement also may prove advantageous as the professional athletes approach new or extended contract negotiations with their respective clubs.
Regardless of the population in question, the appeal of anabolic drugs in athletic circles may be cemented in the potential for metamorphosis from mediocrity to excellence, or, in the case of a few, from excellence to greatness. The allure that such transcendence may result in exponential wealth and fame, combined with society's win-at-all-costs attitude, simply has the capacity to overwhelm even the most intelligent and informed athlete.
Hoffman: There are two primary reasons why an athlete may take AAS. The first reason likely involves the athlete trying to achieve personal goals or dreams that may include getting a college scholarship, being a starter on the team, becoming a professional athlete, or winning a competition. Most often, the athlete has been training consistently and with tremendous passion, but has not met the expected or desired performance gains. It is at this point during the training cycle that the athlete becomes frustrated and may look to explore other methods of maximizing performance gains.
A second reason that athletes may use AAS has more to do with the economics of professional sport. This is likely a contributing factor in the alleged rampant use being experienced in professional baseball. Salaries are quite nice for the professional athlete. However, if team owners are willing to give a contract worth 5 times more to someone who hits 40 home runs a year compared with someone who hits 10 home runs a year, the athlete may believe that it is economically feasible to risk taking AAS to achieve the big contract.
Kraemer, Vingren: In the opinion of these authors, athletes take AAS to gain a competitive advantage, either directly as a performance enhancement via the neuromuscular system or other related physiological/psychological system or more indirectly as a means to faster recovery from training, injury, or competition.
Lively: Athletes take AAS in an effort to improve their performance and to give them an edge over their competition. Some athletes begin taking AAS simply to survive in their sport: they perceive that others are taking AAS, and in order to level the playing field, they also must take them. There is also a subset of non-competitive athletes and recreational users who use AAS in order to improve their physiques and body images.
Question 4: Based Upon Your Understanding of the Scientific Literature, Are Steroids as Effective at Therapeutic Dosages Versus Higher Dosages? Return to TOC
Antonio: There is a dose-response relationship (i.e., the more you take, the greater your gains in muscle mass). This may or may not clearly translate into better performance (2). Interestingly, older men are as responsive as young men to synthetic testosterone's anabolic effects; a dose of synthetic testosterone as low as 125 mg taken once per week for 20 weeks was associated with high normal testosterone levels, low frequency of adverse events, and significant gains in fat-free mass and muscle strength (4).
Chetlin: My response to this would be no. What little peer-reviewed scientific literature is available clearly indicates that suprapharmacologic doses are more effective in terms of measurable change in strength, muscle size, and body composition. These results, however, have been derived only from men who are neither athletes nor regularly weight-trained. Suprapharmacologic doses of approximately 600 mg per week of testosterone esters, administered to these subjects over a period of at least 10 weeks, have resulted in significant increases in muscle strength, hypertrophy, and lean muscle mass (3–6, 34). Dosing regimens in the stated amount may raise mean serum testosterone concentration to 1,000 ng/dL or more (11). Given that the normal mean testosterone concentration is approximately 370 ng/dL (accumulated data from 816 independent labs using 14 different assays to measure total testosterone) (10), this would represent a 2.7-fold increase to actualize morphometric and performance enhancement. Current clinical hormone replacement intervention indicates a therapeutic dosage of 200 mg every 2 weeks by parenteral (i.e., intramuscular) injection with an ester of testosterone (i.e., testosterone enanthate) (14). Thus, a threshold supraphysiologic dose appears to be in the range of 6 times an accepted therapeutic one. When combined with weight training, the described effects were permissive and the extent of the noted improvement appears dose dependent (4, 6, 11).
Interestingly, a review of the clandestine literature of state-sponsored drug programs of the former German Democratic Republic reveals that athletes, both male and female, systematically took massive suprapharmacologic doses of AAS over several years, beginning in adolescence or earlier. Demonstrable performance improvements were meticulously noted in Olympic sporting events such as weight-lifting, swimming, track and field, and kayaking, to name but a few (12).
Hoffman: It appears that for AAS to be effective, they need to be taken in pharmacological doses. By providing AAS in physiological dosages (that which is normally produced by endogenous sources), it will simply cause the body to shut down its own supply of testosterone through a negative feedback mechanism. Thus, for any exogenously administered AAS to have any effect, they need to be taken in pharmacological or suprapharmacological dosages. A dose-response curve of the effect of AAS has been demonstrated, with the total dose of AAS having a logarithmic relationship to increases in lean body mass (11).
Kraemer, Vingren: First, AAS work. To argue against this hypothesis is foolhardy. From a scientific perspective, it has been difficult to demonstrate the efficacy per limitations in experimental designs and doses that can be administered. Thus, this leads to conflicting evidence regarding the effectiveness of AAS in promoting hypertrophy and increases in strength and power, leading some scientific panels and position stands in the 1970s to say AAS had no effect. The majority of studies have found that AAS supplementation with resistance training does not increase strength more than resistance training alone in non–testosterone-deficient populations (4, 5, 7, 9; for review, see 13). However, dose was most likely a major problem in these studies.
In a classic set of studies and as stated by Bhasin and colleagues (1) in one of their recent papers, “Supraphysiologic doses of testosterone, especially when combined with strength training, increase fat-free mass and muscle size and strength in normal men.” In that study, they used a dose of 600 mg weekly over 10 weeks. In a subsequent study (2), it was apparent to these investigators that
Although substantial gains in muscle mass and strength can be realized in older men with supraphysiological testosterone doses, these high doses are associated with a high frequency of adverse effects. The best trade-off was achieved with a testosterone dose (125 mg) that was associated with high normal testosterone levels, low frequency of adverse events, and significant gains in fat-free mass and muscle strength.
Therefore, the higher dose is associated with greater adverse effects, but potentially greater gains. Nevertheless, the evidence is very compelling that AAS do in fact work.
Anecdotal and some survey data indicate that the doses of AAS actually taken by athletes are much higher than those used in most controlled human studies, and that these higher doses are effective in increasing muscle mass and strength. In addition, the effect of long-term use (years) of AAS on strength and how long such potential effects may last after AAS use is stopped have not been directly determined experimentally in humans. The lack of positive findings for AAS as ergogenic aids is due most likely to the restriction in the maximal dose allowed in human studies by many institutional review boards and ethics committees. It appears that if such data were to be collected, it would need to be under highly supervised clinical scenarios (as has been done), and even then, side effects would cause dropouts (1, 2). Nevertheless, studies with doses higher than 600 mg per week probably will never be conducted, due to the potential for side effects; the only recourse would be to study these questions indirectly by following athletes who already use AAS. However, the major problems with self-reported studies are the actual content and type of AAS used, due to untested black market and Internet sources.
Question 5: To What Degree Can Performance Really Be Enhanced by the Administration of Anabolic Steroids? Return to TOC
Antonio: Performance is dependent on many factors. Certainly in sports that put a premium on strength and power, it is clear that AAS self-administration can enhance performance. However, AAS use can assist athletes in recovery, which can be of value to endurance athletes.
Chetlin: The answer to this question is also left to some speculation. There is virtually universal agreement that AAS improve athletic performance, but to what degree? Because there are no controlled studies that have specifically examined this question, we are reduced to informed conjecture regarding the magnitude of performance enhancement one might expect to realize in a given sport. Though institutionally protected mechanisms greatly limit even the possibility of facilitating studies to examine AAS-induced performance improvement in otherwise healthy humans (e.g., athletes), the furtive literature left in the wake of past Eastern European regimes reveals specific, predicted advancement in various athletic disciplines. Specific drug protocols lasting several years were associated, for example, with the following forecasted gains: men's shot put 2.5–4 m; women's shot put 4.5–5 m; men's discus throw 10–12 m; women's discus throw 11–20 m; women's hammer throw 6–10 m; women's javelin throw 8–15 m; women's 400-m run 4–5 seconds; women's 800-m run 5–10 seconds; and women's 1,500-m run 7–10 seconds. Across genders and various sports, these illicit state-sponsored programs produced performance gains of approximately 3–20% (12), remarkable gains considering that among groups of homogeneous elite athletes an improvement of 1–2% may mean the difference between winning a gold medal or no medal at all. Exercise scientists employed in these now-defunct governmental programs determined that women derive the greatest AAS-driven improvements in performance, with the most profound enhancements observed in junior athletes after the initial bout of anabolic administration (12).
Given the response variation to AAS, the extent of functional improvement is likely due to a combination of intervening factors, including
Drug dosage—Higher doses may translate into greater performance gains (3, 6, 11).
Drug number—The practice of stacking appears to enhance AAS effects in a permissive fashion (12, 15).
Androgen receptor sensitivity—AR-mediated AAS use may promote up-regulation of these specific receptors (25, 38).
Training status—Younger, less-experienced individuals (especially women) may respond in a more pronounced fashion to AAS effects (12).
Athletic discipline—Sporting endeavors that emphasize speed, strength, power, and aggression (i.e., shorter-duration, higher-intensity efforts) may derive the most benefit from AAS supplementation. This is strictly a comparative assessment; improvement in many sports, with varying degrees of functional and metabolic requirements, may be enhanced with this class of drugs (12).
Genetics—This is an inescapable component; transcriptional and translational expression of specific drug effects probably varies greatly from one individual to the next.
Hoffman: This is an interesting question, due to the fact that a huge mistake was made in study methodology (e.g., use of physiological dosages versus pharmacological dosages typically used by athletes, mode of exercise assessment different from the training stimulus, and the use of novice resistance-trained subjects) during the early research examining the efficacy of AAS use. Early studies were unable to see any significant differences in strength or body mass gains (10, 12, 14, 18, 28). As a result, scientific and medical communities at the time suggested that AAS had little influence on athletic performance. This was contrary to anecdotal evidence emanating from gyms and spreading among competitive athletes, and it created a credibility gap between researchers/medical community and athletes.
In studies administering AAS in dosages that are commonly used by experienced resistance-trained athletes, results appear to confirm the anecdotal claims of superior performance and size improvements. The majority of studies examining AAS administration on experienced resistance-trained athletes has reported significant strength and body-mass gains (1, 2, 6, 15, 21, 27, 29, 30). In experienced resistance-trained athletes, strength gains are generally small in comparison with novice lifters. However, when these athletes are given AAS, their strength gains appear to be 2- to 3-fold higher, compared with athletes at a similar level who are not supplementing with AAS (6, 15, 30). Recent research also has demonstrated a 3-fold difference in lean body mass accretion (29). Thus, the evidence is quite convincing that AAS administration in conjunction with a resistance training program and an adequate diet will increase both strength and lean body mass.
Lively: There should no longer be a question as to whether or not AAS are ergogenic. Well-controlled studies (3, 4, 7, 12, 15, 16) have demonstrated that administration of AAS produces both an increase in muscle mass and strength. The literature demonstrates strength improvements in the range of 5–20% over baseline levels, depending on the administered dose and regimen (8). Studies do show that the anabolic effects of AAS are dose dependent (4, 15) and that the combination of strength training and AAS administration leads to larger increases in muscle size and strength than are achieved with either intervention alone (3). In view of the evidence on dose dependence, it is also possible that the literature underestimates the anabolic effects, because it is difficult for a study to mimic the large doses, multiple drugs, and training regimens that are actually used by most AAS users.
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Question 6: What Are the Health Consequences of Steroid Use (i.e., in Women, Men, and Adolescents)? Return to TOC
Antonio: We wrote a review article on this topic several years ago (8). First, let me address the issue of androgen use in men. It has been estimated that 1–3 million male and female athletes in the United States have used androgens. Androgen or AAS use has been associated purportedly with liver dysfunction, altered blood lipids, infertility, musculotendinous injury, and psychological abnormalities. Yet, androgens have been available to athletes for more than 50 years and there is little evidence to show that their use will cause any long-term detriment; furthermore, the use of moderate doses of certain AAS (e.g., testosterone enanthate, nandrolone decanoate) results in side effects that are largely benign and reversible. It is our contention that the incidence of serious health problems associated with the use of androgens by athletes has been exaggerated (8). This is an area where there is perhaps more myth and misinformation (with creatine misinformation coming in a close second) than any other topic. The mainstream press reports of “roid rage,” yet this is more media creation than actual scientific fact (9).
The issue of women and children, of course, is different. Women clearly can become masculinized if they take sufficient doses of AAS. Children, of course, should not be taking AAS due to the potentially detrimental effects on their growth plates. However, there are clinical applications for androgens in children. For instance, one study determined whether oxandrolone administration for 1 year after a burn reverses muscle and bone catabolism in hypermetabolic pediatric burn patients. They discovered that long-term administration of oxandrolone safely improves lean body mass, as well as bone mineral content and density, in severely burned children (7).
Chetlin: This question necessitates a multifactorial answer, based upon length of use, dosage, polydrug practice, and predisposition of the user to diseases exacerbated by AAS. According to my objective review of the literature, otherwise healthy males taking pharmacologic or suprapharmacologic doses of a single AAS, under controlled short-term conditions, apparently may not experience irreversible side effects (3, 4, 11, 31, 32). Please notice that I have made a very qualified comment and have italicized some operative words. Having made this statement, it must be noted that medically established and self-reported adverse effects of individuals abusing AAS are numerous, which may or may not prove reversible. These include hypertension, altered lipoproteins (increased LDLs, decreased HDLs), libido changes (increased or decreased), myocardial arrhythmias, myocardial hypertrophy, thrombosis, hepatotoxicity, hepatic neoplasm, acne, cutaneous striae, alopecia, male-pattern baldness, schizophrenia, and affective disorder (i.e., mania, depression) (11, 16, 23, 27, 28, 33, 36, 39). Gender-specific effects also have been reported in both men (e.g., testicular atrophy, impotence, prostate hypertrophy, gynecomastia) and women (e.g., hirsutism, masculinization, menstrual cessation, clitoral hypertrophy, voice changes) (11,12,15,16). Though some long-term effects in men may prove reversible, side effects associated with androgenization in women may not be reversible or may be only partially reversible with androgen antagonists. Children given AAS may experience premature epiphyseal closure of the long bones, precocious puberty, severe acne, and, in the case of prepubescent girls, various gynecological disorders (e.g., amenorrhea, ovarian cysts) (11, 12). Overall, long-term health risks associated with suprapharmacologic AAS usage are not well established, although there is some evidence to indicate that chronic AAS users, including those who administer more than one drug concurrently (i.e., polydrug practice), may have increased risk for cardiovascular disease and an incidence of mortality 5 times higher than normal (26, 27).
Hoffman: The clinical examination of AAS usage is quite limited. Much of the problem is related to an inability to study this drug in a nonclinical population due to the unwillingness of institutional review boards to approve such studies. As a result, most of the investigations on medical issues associated with AAS use have been performed on athletes self-administering the AAS. Most of the adverse events appear to be seen in athletes who have been using AAS for several years. In addition, anecdotally, there appears to be a disproportionate amount of adverse events seen in bodybuilders compared with strength/power athletes.
Some of the cardiovascular effects associated with AAS use are decreased HDL, increased cholesterol, increased triglycerides, elevated blood pressure, and increased risk of thrombosis. The magnitude of the effect may differ depending upon the AAS used. Of interest is that these effects appear to be reversible when the athlete cycles off the steroid. In regard to left ventricular function, studies suggest that highly strength-trained athletes, with no history of anabolic steroid use, exhibit a high incidence of waveform abnormalities, but athletes self-administering AAS exhibit a higher percentage of waveform abnormalities. In addition, a study on rats has shown that synthetic testosterone administration for 8 weeks will increase left ventricle stiffness and will cause decreases in stroke volume and cardiac performance (17). It was hypothesized by the researchers that increased stiffness may be related to formation of cross-links of adjacent collagen molecules within the heart. AAS administration also may predispose an individual to thrombosis due to AAS-stimulated platelet aggregation. Some evidence exists that shows that anabolic AAS reduce the endothelial nitric oxide dilator system, causing coronary artery occlusion (19). However, this may depend upon the AAS compound used. Generally, issues related to thrombosis have been reported in case studies of bodybuilders with a number of years of steroid use.
Other adverse events generally associated with AAS use include acne, male-pattern baldness, gynecomastia, decreased sperm count, testicular atrophy, impotence, and transient infertility. In addition, increases in the risk of liver tumors and liver damage are often discussed as a consequence of AAS use. This is likely due to the liver being the primary site of steroid clearance. However, the relationship between AAS use and hepatic disease appears to be exaggerated. Dickerman et al. (7) has shown that the blood chemistry of bodybuilders self-administering AAS shows elevations in aspartate aminotransferase (AST), alanine aminotransferases (ALT) and creatine kinase (CK), but no change in gamma-glutamyl-transpeptidase (GGT). This chemistry panel is not suggestive of hepatic dysfunction, but of possible muscle damage. These researchers suggested that AAS-induced hepatotoxicity may be overstated. In another study by that research team (23), surveys were sent to physicians, asking them to provide a differential diagnosis for a 28-year-old AAS-using bodybuilder with an abnormal serum chemistry profile (elevations in AST, ALT, and CK, but with a normal GGT). The majority of physicians (56%) failed to mention muscle damage or muscle disease as a potential diagnosis. The majority of physicians (63%) indicated liver disease as primary diagnosis. If prior reports of hepatic disease and anabolic steroid usage had been based upon increased aminotransferases, the authors concluded that the medical community may have overemphasized AAS-induced hepatotoxicity. In regards to hepatic cancer, it appears that such isolated cases have been reported in nonathletic populations being treated with testosterone for aplastic anemia. Many of these individuals were treated with oral AAS (17a-alkylated) for years of continued use. No cysts or tumors have been reported in athletes using 17b-alkylated AAS. Thus, there does appear to be evidence that the risk of hepatic disease from anabolic steroid use is not as great as the medical community had thought originally.
In the younger athlete using AAS, the risk of premature epiphyseal plate closure does exist. This will result in stunting one's longitudinal bone growth. In addition, AAS also have been associated with an increased risk of tendon tears. Studies in mice have suggested that AAS may lead to degeneration of collagen proportional to duration of steroid administration and potentially lead to a decrease in tensile strength (20). In addition, a decrease in collagen synthesis also has been reported from AAS administration in rats (16). However, there are limited case reports of spontaneous tendon ruptures of weightlifters and athletes. Although experimental data from animal models suggest that AAS may alter biomechanical properties of tendons, ultrastructural evidence supporting this claim is lacking. Evans and colleagues (9) performed an ultrastructural analysis on ruptured tendons from anabolic steroid users. They concluded that AAS did not induce any ultrastructural collagen change causing the tendon ruptures in the anabolic steroid users.
An issue that often is raised with AAS use is the associated psychological and behavioral effects. Increases in aggressiveness, arousal, and irritability have been associated with anabolic steroid usage. This potentially has both beneficial and harmful implications. Elevations in arousal and self-esteem may be thought of as a positive side effect. In addition, the increase in aggressiveness is a benefit that athletes participating in a contact sport may wish to achieve. However, increased aggressiveness may not be contained in the athletic arena, posing significant risks for AAS users and those with whom they are in contact. AAS also are associated with mood swings and increases in psychotic episodes. Studies have reported that nearly 60% of AAS users experience increases in irritability and aggressiveness (24, 26). A recent study by Pope (25) reported that significant elevations in aggressiveness and manic scores were seen following 12 weeks of testosterone cypionate injections in a controlled double-blind crossover study. Interestingly, results of the study were not uniform across the subjects. Most subjects showed little psychological effect and few developed prominent effects. A cause-and-effect relationship has yet to be identified in anabolic steroid users, and it does appear that individuals who experience any psychological or behavioral changes do recover when steroid use is discontinued (13).
In women and girls who begin to take AAS, the medical issues are quite different. Deepening of the voice, enlargement of the clitoris, decreased breast size, altered menstruation, and hirsutism are all side effects generally associated with AAS use among female athletes. More so, these effects do not appear to be transient.
The acute health issues associated with AAS use do appear to be transient and may be more prevalent in individuals with genetic predisposition (e.g., hair loss). It is the long-term effects that raise some of the bigger questions. There are only minimal data available, though. One study on mice administered AAS in the relative dosages typically used by bodybuilders. However, the duration of the study was one-fifth of the life span of the mouse, which is relatively greater than that experienced by most athletes on AAS, and it was given without any washout period. Results, though, did demonstrate a shortened life span of the mice, with evidence of liver, kidney, and heart pathology (7). Still, AAS use in strength/power athletes has been reported for more than 50 years. During the 1970s and 1980s, rampant use of AAS in professional football was reported; however, the athletes of that era are now into their middle age and little information is available on any AAS-related diseases or associated deaths in these former strength/power athletes. Further research should be done in this population of former AAS users.
Kraemer, Vingren: The answer to this question may be dramatically overstated in some respects in the attempt to scare athletes from using such drugs. Yet AAS use does impact the body's physiological function, because it causes a drug effect and adverse symptoms have been noted experimentally at higher doses (1, 2). It also interacts differently with each individual and there are concerns as to how it interacts with an individual's own genetics. It is dependent upon the dose, cycles, type of drug, and impact of the drug, so that it is very difficult to give a long laundry list that will affect each person, each regimen, or each AAS. One can easily get into a high degree of speculation and extrapolation of the side effects.
As stated in the classic paper by Bhasin et al. (1):
Supraphysiologic doses of testosterone, with or without exercise, did not increase the occurrence of angry behavior by these carefully selected men in the controlled setting of this experiment. Our results, however, do not preclude the possibility that still higher doses of multiple steroids may provoke angry behavior in men with preexisting psychiatric or behavioral problems.
Our results in no way justify the use of anabolic-androgenic steroids in sports, because, with extended use, such drugs have potentially serious adverse effects on the cardiovascular system, prostate, lipid metabolism, and insulin sensitivity. Moreover, the use of any performance-enhancing agent in sports raises serious ethical issues. Our findings do, however, raise the possibility that the short-term administration of androgens may have beneficial effects in immobilized patients, during space travel, and in patients with cancer-related cachexia, disease caused by the human immunodeficiency virus, or other chronic wasting disorders.
In addition, in another investigation studying younger and older men with different dose levels of testosterone enanthate, Bhasin et al. (2) reported these results:
Older men had 147 adverse and 12 serious adverse events. Twelve serious adverse events occurred in nine older men and included hematocrit greater than 54% (six events), leg edema with shortness of breath (one event), urinary retention (one event), and prostate cancer (two events). There were dose-dependent increases in hemoglobin and hematocrit (dose effect, p < 0.0001…). One older man receiving the 125-mg dose, three receiving the 300-mg dose, and two receiving the 600-mg dose had hematocrits greater than 54%. Leg edema occurred in eight older men: one receiving 50 mg, four receiving 300 mg, and three receiving 600 mg.
There were 55 adverse events, but no serious adverse events, in young men. The frequency of total and serious adverse events and prostate events by testosterone dose was not statistically different between young and older men, although the total number of adverse events was numerically greater in older men than young men. The older men had significantly greater increments in hemoglobin and hematocrit than young men after adjusting for testosterone levels (age effect, p = 0.0001).
Thus, readers are referred to these papers (1, 2) for further study of documented side effects in a clinical study of different doses. Age and AAS used may be a crucial feature interrelated with dose as it influences drug side effects.
In addition, the underground network presents so much information that is only partially right due to rationalization of use that it makes it difficult for the average person to evaluate the veracity of the side effects. The NSCA's 1985 position stand on AAS tried to outline the basics about side effects years ago with an expert panel (12), which I (Kraemer) chaired, to bring some reality checks regarding AAS efficacy and benefits and to note serious concerns about side effects. This was during a time when Sports Illustrated mediated an era of “anabolic steroids mania” with lack of detail and hard data. In fact, in a recent show on HBO's Real Sports, the original author of these articles came back to what the NSCA had presented in its first position stand at the time and said much hyperbole had been put into the articles. Nevertheless, AAS can have dramatically negative side effects from a medical perspective. It all becomes one of ethics in competition with the potential for dramatically negative side effects related to a given individual and his or her genetics and use pattern. Furthermore, the physiological interactions between other drugs and AAS remain unknown in the world of AAS use in athletics.
Lively: Although AAS use certainly carries significant health risks, some of the potential adverse complications have been overstated and most of the harmful effects of AAS are dose dependent and reversible after discontinuation of the drug. Many of the dramatic effects attributed to AAS use are documented anecdotally or by case study, and no causal link between AAS and the disease condition can be established. Controlled studies do, however, objectively show that AAS use can result in undesirable changes in lipid levels (6, 9), blood pressure (13), and liver enzymes (oral formulations) (13). Dermatologic changes of acne, alopecia, and hirsutism may occur along with endocrine effects of testicular atrophy, gynecomastia, and depressed reproductive hormones (1, 5). Psychologically, some AAS users report increased aggression, mania, depression, and withdrawal symptoms (5). Often overlooked as adverse effects, complications of self-administered injections such as abscesses, injection site pain, and nerve injury can be problematic, along with the potential spread of blood-borne pathogens from sharing needles or multidose vials.
References Introduction Return to TOC
1. Berning, J.M., K.J. Adams, and B.A. Stamford. Anabolic steroid usage in athletics: Facts, fiction, and public relations. J. Strength Cond. Res. 18:908–917. 2004. Find this article on other systems
2. Boje, O. Doping. Bull. Health Organ. League Nations. 8:439–469. 1939. Find this article on other systems
3. Catlin, D.H., M.H. Sekera, B.D. Ahrens, B. Starcevic, Y.C. Chang, and C.K. Hatton. Tetrahydrogestrinone: Discovery, synthesis, and detection in urine. Rapid Commun. Mass Spectrom. 18:1245–1049. 2004. Find this article on other systems
4. Evans, N.A. Current concepts in anabolic-androgenic steroids. Am. J. Sports Med. 32:534–542. 2004. Find this article on other systems
5. Hartgens, F., and H. Kuipers. Effects of androgenic-anabolic steroids in athletes. Sports Med. 34:513–554. 2004. Find this article on other systems
6. Kochakian, C.D. Testosterone and testosterone acetate and the protein and energy metabolism of castrated dogs. Endocrinology. 21:750–755. 1937. Find this article on other systems
7. Malvey, T.C., and T.D. Armsey II. Tetrahydrogestrinone: The discovery of a designer steroid. Curr. Sports Med. Rep. 4:227–230. 2005. Find this article on other systems
8. Prokop, L. The struggle against doping and its history. J. Sports Med. Phys. Fitness. 10:45–48. 1970. Find this article on other systems
9. Todd, T. Anabolic steroids : The gremlins of sport. J. Sport Hist. 14:87–107. 1987. Find this article on other systems
10. Williams, M.H., and J.D. Branch. Ergogenic aids for improved performance. In: Exercise and Sport Science. W.E. Garrett and D.T. Kirkendall, eds. Philadelphia: Lippincott, Williams, and Wilkins. 2000. pp. 373–384.
11. Yesalis, C.E., S.P. Courson, and J.E. Wright. History of anabolic steroid use in sport and exercise. In: Anabolic Steroids in Sports and Exercise. C.E. Yesalis, ed. Champaign, IL: Human Kinetics. 1993. pp. 35–48.
Antonio Return to TOC
1. Antonio, J., J.D. Wilson, and F.W. George. Effects of castration and androgen treatment on androgen-receptor levels in rat skeletal muscles. J. Appl. Physiol. 87:2016–2019. 1999.
2. Bhasin, S. The dose-dependent effects of testosterone on sexual function and on muscle mass and function. Mayo Clin. Proc. 75: (Suppl.). S70–S75. discussion S75–S76. 2000.
3. Bhasin, S., W.E. Taylor, R. Singh, J. Artaza, I. Sinha-Hikim, R. Jasuja, H. Choi, and N.F. Gonzalez-Cadavid. The mechanisms of androgen effects on body composition: Mesenchymal pluripotent cell as the target of androgen action. J. Gerontol. A Biol. Sci. Med. Sci. 58:M1103–M1110. 2003.
4. Bhasin, S., L. Woodhouse, R. Casaburi, A.B. Singh, R.P. Mac, M. Lee, K.E. Yarasheski, I. Sinha-Hikim, C. Dzekov, J. Dzekov, L. Magliano, and T.W. Storer. Older men are as responsive as young men to the anabolic effects of graded doses of testosterone on the skeletal muscle. J. Clin. Endocrinol. Metab. 90:678–688. 2005.
5. Dayal, M., M.D. Sammel, J. Zhao, A.C. Hummel, K. Vandenbourne, and K.T. Barnhart. Supplementation with DHEA: Effect on muscle size, strength, quality of life, and lipids. J. Womens Health (Larchmt.). 145) 391–400. 2005.
6. Jasuja, R., D.H. Catlin, A. Miller, Y.C. Chang, K.L. Herbst, B. Starcevic, J.N. Artaza, R. Singh, G. Datta, A. Sarkissian, C. Chandsawangbhuwana, M. Baker, and S. Bhasin. Tetrahydrogestrinone is an androgenic steroid that stimulates androgen receptor-mediated, myogenic differentiation in C3H10T1/2 multipotent mesenchymal cells and promotes muscle accretion in orchidectomized, male rats. Endocrinology. 146:4472–4478. 2005.
7. Murphy, K.D., S. Thomas, R.P. Mlcak, D.L. Chinkes, G.L. Klein, and D.N. Herndon. Effects of long-term oxandrolone administration in severely burned children. Surgery. 136:219–224. 2004.
8. Street, C., J. Antonio, and D. Cudlipp. Androgen use by athletes: A reevaluation of the health risks. Can. J. Appl. Physiol. 21:421–440. 1996.
9. Tricker, R., R. Casaburi, T.W. Storer, B. Clevenger, N. Berman, A. Shirazi, and S. Bhasin. The effects of supraphysiological doses of testosterone on angry behavior in healthy eugonadal men—A clinical research center study. J. Clin. Endocrinol. Metab. 81:3754–3758. 1996.
Chetlin Return to TOC
1. Bamman, M., J. Shipp, J. Jiang, B. Gower, G. Hunter, A. Goodman, C. McClafferty, and R. Urban. Mechanical load increases muscle IGF-1 and androgen receptor mRNA concentrations in humans. Am. J. Physiol. Endocrinol. Metab. 280:E383–E390. 2001.
2. Berning, J., K. Adams, and B. Stamford. Anabolic steroid usage in athletics: Facts, fiction, and public relations. J. Strength Cond. Res. 184) 908–917. 2004.
3. Bhasin, S., T. Storer, N. Berman, K. Yarasheski, B. Clevenger, J. Phillips, W. Lee, T. Bunnel, and R. Casaburi. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N. Engl. J. Med. 335:1–7. 1996.
4. Bhasin, S., T. Storer, N. Berman, K. Yarasheski, B. Clevenger, J. Phillips, W. Lee, T. Bunnel, and R. Casaburi. A replacement dose of testosterone increases fat-free mass and muscle size in hypogonadal men. J. Clin. Endocrinol. Metab. 82:407–413. 1997.
5. Bhasin, B., W. Taylor, R. Singh, J. Artaza, I. Sinha-Hikim, R. Jasuja, H. Choi, and N. Gonzalez-Cadavid. The mechanism of androgen effects on body composition: Mesenchymal pluripotent cells as the target of androgen action. J. Gerontol. A Biol. Sci. Med. Sci. 5812) M1103–M1110. 2003.
6. Bhasin, S., L. Woodhouse, R. Casaburi, A. Singh, D. Bhasin, N. Berman, X. Chen, K. Yarasheski, L. Magliano, C. Dzekov, J. Dzekov, R. Bross, J. Phillips, I. Sinha-Hikim, R. Shen, and T. Storer. Testosterone dose-response relationships in healthy young men. Am. J. Physiol. Endocrinol. Metab. 281:E1172–E1181. 2001.
7. Buckley, W., C. Yesalis, K. Friedl, W. Anderson, A. Streit, and J. Wright. Estimated prevalence of anabolic steroid use among male high school seniors. JAMA. 260:3441–3445. 1988.
8. Creutzberg, E., and A. Schols. Anabolic steroids. Curr. Opin. Clin. Nutr. Metab. Care. 2:243–253. 1999.
9. Daly, R., T. Su, P. Schmidt, D. Pickar, D. Murphy, and D. Rubinow. Cerebrospinal fluid and behavioral changes after methyl testosterone administration: Preliminary findings. Arch. Gen. Psychiatry. 58:172–177. 2001.
10. Elin, R., and S. Winters. Current controversies in testosterone testing: Aging and obesity. Clin. Lab. Med. 24:119–139. 2004.
11. Evans, N. Current concepts in anabolic-androgenic steroids. Am. J. Sports Med. 322) 534–542. 2004.
12. Franke, W., and B. Berendonk. Hormonal doping and androgenization of athletes: A secret program of the German Democratic Republic government. Clin. Chem. 437) 1262–1279. 1997.
13. Ghaphery, N. Performance-enhancing drugs. Orthop. Clin. North Am. 26:433–442. 1995.
14. Gooren, L., and M. Bunck. Androgen replacement therapy: Present and future. Drugs. 6417) 1861–1891. 2004.
15. Hartgens, F., and H. Kuipers. Effects of anabolic-androgenic steroids in athletes. Sports Med. 348) 513–554. 2004.
16. Haupt, H. Anabolic steroids and growth hormone. Am. J. Sports Med. 21:468–474. 1993.
17. Hickson, R., S. Czerwinski, M. Falduto, and A. Young. Glucocorticoid antagonism by exercise and anabolic-androgenic steroids. Med. Sci. Sports Exerc. 22:331–340. 1990.
18. Johnston, L., P. O'Malley, and J. Bachman. Monitoring the future national survey results on drug use. 1975–2001. Volume I : Secondary School Students. Bethesda, MD: National Institute on Drug Abuse. 2002. NIH Publication No. 02-5106.
19. Kadi, F. Adapatations of human skeletal muscle to training and anabolic steroids. Acta Physiol. Scand. 646: (Suppl.). 1–52. 2000.
20. Kadi, F., P. Bonnerud, A. Eriksson, and L. Thornell. The expression of androgen receptors in human neck and limb muscles: Effects of training and self-administration of androgenic-anabolic steroids. Histochem. Cell Biol. 113:25–29. 2000.
21. Kadi, F., A. Eriksson, S. Holmner, G. Butler-Browne, and L. Thornell. Cellular adaptations of the trapezius muscle in strength-trained athletes. Histochem. Cell Biol. 111:189–195. 1999.
22. Kadi, F., A. Eriksson, S. Holmner, and L. Thornell. Effects of anabolic steroids on the muscle cells of strength-trained athletes. Med. Sci. Sports Exerc. 31:1528–1534. 1999.
23. Millman, M., and B. Ross. Steroid and nutritional supplement use in professional athletes. Am. J. Addictions. 12:S48–S54. 2003.
24. National Collegiate Athletic Association (NCAA). Steroid and nutritional supplement use in professional athletes. Newsletter. 1997.
25. Negro-Villar, A. Selective androgen receptor modulators (SARMs): A novel approach to androgen therapy for the new millennium. J. Clin. Endocrinol. Metab. 84:3459–3462. 1999.
26. Parssinen, M., U. Kujala, E. Vartiainen, S. Sarna, and T. Seppala. Increased premature mortality of competitive power lifters suspected to have used anabolic agents. Int. J. Sports Med. 21:225–227. 2000.
27. Parssinen, M., and T. Seppala. Steroid use and long term health risks in former athletes. Int. J. Sports Med. 23:83–94. 2002.
28. Pope, H., E. Kouri, and J. Hudson. Effects of supraphysiologic doses of testosterone on mood and aggression in normal men. Arch. Gen. Psychiatry. 57:133–140. 2000.
29. Rogozkin, V. Anabolic steroid metabolism in skeletal muscle. J. Steroid Biochem. 11:923–926. 1979.
30. Rubinow, D., and P. Schmidt. Androgens, brain, and behavior. Am. J. Psychiatry. 153:974–984. 1996.
31. Sattler, F., E. Schroeder, M. Dube, S. Jaque, C. Martinez, P. Blanche, S. Azen, and R. Krauss. Metabolic effects of nandrolone decanoate and resistance training in men with HIV. Am. J. Physiol. Endocrinol. Metab. 283:E1214–E1222. 2002.
32. Schroeder, E., A. Singh, S. Bhasin, T. Storer, C. Azen, T. Davidson, C. Martinez, I. Sinha-Hikim, S. Jaque, M. Terk, and F. Sattler. Effects of an oral androgen on muscle and metabolism in older, community-dwelling men. Am. J. Physiol. Endocrinol. Metab. 284:E120–E128. 2002.
33. Shahidi, N. A review of the chemistry, biological action, and clinical applications of anabolic-androgenic steroids. Clin. Ther. 23:1355–1390. 2001.
34. Sinha-Hikim, I., J. Artaza, L. Woodhouse, N. Gonzalez-Cadavid, A. Singh, M. Lee, T. Storer, R. Casaburi, R. Shen, and S. Bhasin. Testosterone-induced increase in muscle size in healthy young men is associated with muscle fiber hypertrophy. Am. J. Physiol. Endocrinol. Metab. 283:E154–E164. 2002.
35. Su, T., M. Pagliaro, and P. Schmidt. Neuropsychiatric effects of anabolic steroids in male normal volunteers. JAMA. 269:2760–2764. 1993.
36. Trenton, A., and G. Currier. Behavioural manifestations of anabolic steroid use. CNS Drugs. 197) 571–595. 2005.
37. Urban, R., Y. Bodenburg, C. Gilkison, J. Foxworth, A. Coggan, R. Wolfe, and A. Ferrando. Testosterone administration to elderly men increases skeletal muscle strength and protein synthesis. Am. J. Physiol. 269:E820–E826. 1995.
38. Wolf, D., T. Herzinger, H. Hermeking, D. Blaschke, and W. Horz. Transcriptional and posttran-scriptional regulation of human androgen receptor expression by androgen. Mol. Endocrinol. 77) 924–936. 1993.
39. Yates, W. Testosterone in psychiatry: Risks and benefits. Arch. Gen. Psychiatry. 57:155–156. 2000.
40. Yeap, B., J. Wilce, and P. Leedman. The androgen receptor mRNA. Bioessays. 266) 672–682. 2004.
41. Yesalis, C. Self-reported use of anabolic-androgenic steroids by elite powerlifters. Phys. Sports Med. 16:91–100. 1988.
42. Yesalis, C. Epidemiology and pattern of anabolic-androgenic steroid use. Psychiatr. Ann. 22:7–18. 1992.
Hoffman Return to TOC
1. Alen, M., K. Häkkinen, and P.V. Komi. Changes in neuromuscular performance and muscle fibre characteristics of elite power athletes self-administering androgenic and anabolic steroids. Acta Physiol. Scand. 122:535–544. 1984.
2. Alen, M., M. Reinila, and R. Vihko. Response of serum hormones to androgen administration in power athletes. Med. Sci. Sports Exerc. 17:354–359. 1985.
3. Anderson, W.A., M.A. Albrecht, and D.B. McKeag. Second replication of a national study of the substance use/abuse habits of college student athletes. Final Report. NCAA News. 1993.
4. Anderson, W.A., M.A. Albrecht, D.B. McKeag, D.O. Hough, and C.A. McGrew. A national survey of alcohol and drug use by college athletes. Phys. Sportsmed. 19:91–104. 1991.
5. Anderson, W.A., and D.B. McKeag. The Substance Use and Abuse Habits Of College Student Athletes. Research Paper No. 2. Mission, KS: National Collegiate Athletic Association. 1985.
6. Blazevich, A.J., and A. Giorgi. Effect of testosterone administration and weight training on muscle architecture. Med. Sci. Sports Exerc. 33:1688–1693. 2001.
7. Dickerman, R.D., R.M. Pertusi, N.Y. Zachariah, D.R. Dufour, and W.J. McConathy. Anabolic steroid-induced hepatotoxicity: Is it overstated?. Clin. J. Sport Med. 9:34–39. 1999.
8. Durant, R.H., L.G. Escobedo, and G.W. Heath. Anabolic-steroid use, strength training, and multiple drug use among adolescents in the United States. Pediatrics. 96:23–28. 1995.
9. Evans, N.A., D.J. Bowrey, and G.R. Newman. Ultrastructural analysis of ruptured tendon from anabolic steroid users. Injury. 29:769–773. 1998.
10. Fahey, T.D., and C.H. Brown. The effects of an anabolic steroid on the strength, body composition, and endurance of college males when accompanied by a weight training program. Med. Sci. Sports Exerc. 5:272–276. 1973.
11. Forbes, G.B. The effect of anabolic steroids on lean body mass: The dose-response curve. Metabolism. 34:571–573. 1985.
12. Fowler, W.M. Jr, G.W. Gardner, and G.H. Egstrom. Effect of an anabolic steroid on physical performance in young men. J. Appl. Physiol. 20:1038–1040. 1965.
13. Fudula, P.J., R.M. Weinrieb, J.S. Calarco, K.M. Kampman, and C. Boardman. An evaluation of anabolic-androgenic steroid abusers over a period of 1 year: Seven case studies. Ann. Clin. Psychiatry. 15:121–130. 2003.
14. Golding, L.A., J.E. Freydinger, and S.S. Fishel. The effect of an androgenic-anabolic steroid and a protein supplement on size, strength, weight, and body composition in athletes. Phys. Sportsmed. 2:39–45. 1974.
15. Hervey, G.R., A.V. Knibbs, L. Burkinshaw, D.B. Morgan, P.R.M. Jones, D.R. Chettle, and D. Vartsky. Effects of methandienone on the performance and body composition of men undergoing athletic training. Clin. Sci. 60:457–461. 1981.
16. Karpakka, J.A., M.K. Pesola, and T.E. Takala. The effects of anabolic steroids on collagen synthesis in rat skeletal muscle and tendon. A preliminary report. Am. J. Sports Med. 20:262–266. 1992.
17. Legros, T., D. McConnell, T. Murry, M. Edavettal, L.A. Racey-Burns, R.E. Shepherd, and A.H. Burns. The effects of 17 α-methyl-testosterone on myocardial function in vitro. Med. Sci. Sports Exerc. 32:897–903. 2000.
18. Loughton, S.J., and R.O. Ruhling. Human strength and endurance responses to anabolic steroids and training. J. Sports Med. Phys. Fitness. 17:285–296. 1977.
19. Melchert, R.B., and A.A. Welder. Cardiovascular effects of androgenic-anabolic steroids. Med. Sci. Sports Exerc. 27:1252–1262. 1995.
20. Michna, H. Organisation of collagen fibrils in tendon: Changes induced by an anabolic steroid. I. Functional and ultrastructural studies. Virchows Arch. B Cell Pathol. Incl. Mol. Pathol. 52:75–86. 1986.
21. National Collegiate Athletic Association. NCAA study of substance use habits of college student-athletes. Available at: http://www.ncaa.org/library/research...use_habits.pdf. Accessed June, 2001.
22. O'Shea, J.P. The effects of anabolic steroids on dynamic strength levels of weightlifters. Nutr. Reports Int. 4:363–370. 1971.
23. Pertusi, R., R.D. Dickerman, and W.J. McConathy. Evaluation of aminotransferases elevations in a bodybuilder using anabolic steroids: Hepatitis or rhabdomyolysis?. J. Am. Osteopath. Assoc. 101:391–394. 2001.
24. Pope, H.G., and D.L. Katz. Psychiatric and medical effects of anabolic-androgenic steroid use. A controlled study of 160 athletes. Arch. Gen. Psychiatry. 51:375–382. 1994.
25. Pope, H.G., E.M. Kouri, and J.I. Hudson. Effects of supraphysiologic doses of testosterone on mood and aggression in normal men. Arch. Gen. Psychiatry. 57:133–140. 2000.
26. Silvester, L.J. Self-perceptions of the acute and long-range effects of anabolic-androgenic steroids. J. Strength Cond. Res. 9:95–98. 1995.
27. Stamford, B.A., and T. Moffatt. Anabolic steroid : Effectiveness as an ergogenic aid to experienced weight trainers. J. Sports Med. Phys. Fitness. 14:191–197. 1974.
28. Stromme, S.B., H.D. Meen, and A. Aakvaag. Effects of an androgenic-anabolic steroid on strength development and plasma testosterone levels in normal males. Med. Sci. Sports. 6:203–208. 1974.
29. Van Marken Lichtenbelt, W.D., F. Hartgens, N.B.J. Vollaard, S. Ebbing, and H. Kuipers. Body-builders' body composition: Effect of nandrolone decanoate. Med. Sci. Sports Exerc. 36:484–489. 2004.
30. Ward, P. The effect of an anabolic steroid on strength and lean body mass. Med. Sci. Sports. 5:277–282. 1973.
Kraemer, Vingren Return to TOC
1. Bhasin, S., T.W. Storer, N. Berman, C. Callegari, B. Clevenger, J. Phillips, T.J. Bunnell, R. Tricker, A. Shirazi, and R. Casaburi. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N. Engl. J. Med. 335:1–7. 1996.
2. Bhasin, S., L. Woodhouse, R. Casaburi, A.B. Singh, R.P. Mac, M. Lee, K.E. Yarasheski, I. Sinha-Hikim, C. Dzekov, J. Dzekov, L. Magliano, and T.W. Storer. Older men are as responsive as young men to the anabolic effects of graded doses of testosterone on the skeletal muscle. J. Clin. Endocrinol. Metab. 902) 678–88. 2005.
3. Brown, T.R. Nonsteroidal selective androgen receptors modulators (SARMs): Designer androgens with flexible structures provide clinical promise. Endocrinology. 145:5417–5419. 2004.
4. Crist, D.M., P.J. Stackpole, and G.T. Peake. Effects of androgenic-anabolic steroids on neuromuscular power and body composition. J. Appl. Physiol. 542) 366–370. 1983.
5. Fahey, T.D., and C.H. Brown. The effects of an anabolic steroid on the strength, body composition, and endurance of college males when accompanied by a weight training program. Med. Sci. Sports. 54) 272–276. 1973.
6. Griffin, J.E. Male reproductive function. In: Textbook of Endocrine Physiology. J.E. Griffin and S.R. Ojeda, eds. New York: Oxford University Press. 1996. pp. 243–264.
7. Hervey, G.R., I. Hutchinson, A.V. Knibbs, L. Burkinshaw, P.R. Jones, N.G. Norgan, and M.J. Levell. “Anabolic” effects of methandienone in men undergoing athletic training. Lancet. 2:699–702. 1976.
8. Hosohata, K., P. Li, Y. Hosohata, J. Qin, R.G. Roeder, and Z. Wang. Purification and identification of a novel complex which is involved in androgen receptor-dependent transcription. Mol. Cell. Biol. 23:7019–7029. 2003.
9. Johnson, L.C., G. Fisher, L.J. Silvester, and C.C. Hofheins. Anabolic steroid : Effects on strength, body weight, oxygen uptake, and spermatogenesis upon mature males. Med. Sci. Sports. 41) 43–45. 1972.
10. Lee, D.K. Androgen receptor enhances myogenin expression and accelerates differentiation. Biochem. Biophys. Res. Commun. 294:408–413. 2002.
11. McKenna, N.J., R.B. Lanz, and B.W. O'Malley. Nuclear receptor coregulators: Cellular and molecular biology. Endocr. Rev. 20:321–344. 1999.
12. NSCA position statement: Use and abuse of anabolic steroids. Natl. Strength Cond. Assoc. J. 75) 44–59. 1985.
13. Ryan, A.J. Anabolic steroids are fool's gold. Fed. Proc. 4012) 2682–2688. 1981.
Lively Return to TOC
1. Bagatell, C., and W. Bremner. Androgens in men—Uses and abuses. N. Engl. J. Med. 334:707–714. 1996.
2. Bamman, M., J. Shipp, and J. Jiang. Mechanical load increases muscle IGF-1 and androgen receptor mRNA concentrations in humans. Am. J. Physiol. Endocrinol. Metab. 280:E383–E390. 2001.
3. Bhasin, S., T. Storer, and N. Berman. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N. Engl. J. Med. 335:1–7. 1996.
4. Bhasin, S., L. Woodhouse, and R. Casaburi. Testosterone dose-response relationships in healthy young men. Am. J. Physiol. Endocrinol. Metab. 281:E1172–E1181. 2001.
5. Evans, N. Gym and tonic: A profile of 100 male steroid users. Br. J. Sports Med. 31:54–58. 1997.
6. Glazer, G. Atherogenic effects of anabolic steroids on serum lipid levels: A literature review. Arch. Intern. Med. 151:1925–1933. 1991.
7. Griggs, R., W. Kingston, and R. Jozefowicz. Effect of testosterone on muscle mass and muscle protein synthesis. J. Appl. Physiol. 66:498–503. 1989.
8. Hartgens, F., and H. Kuipers. Effects of androgenic-anabolic steroids in athletes. Sports Med. 34:513–554. 2004.
9. Hartgens, F., G. Rietjens, H. Keizer, H. Kuipers, and B.H. Wolffenbuttel. Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein(a). Br. J. Sports Med. 38:253–259. 2004.
10. Johnston, L., P. O'Malley, J. Bachman, and J.E. Schulenberg. Monitoring the Future National Results on Adolescent Drug Use: Overview of Key Findings. Bethesda, MD: National Institute on Drug Abuse, 2004. NIH Publication No. 05–5726.
11. Kadi, F., P. Bonnerud, and A. Eriksson. The expression of androgen receptors in human neck and limb muscles: Effects of training and self-administration of androgenic-anabolic steroids. Histochem. Cell Biol. 113:25–29. 2000.
12. Kadi, F., A. Eriksson, S. Holmner, and L.E. Thornell. Effects of anabolic steroids on the muscle cells of strength-trained athletes. Med. Sci. Sports Exerc. 31:1528–1534. 1999.
13. Lenders, J., P. Demacker, J. Vos, P.L. Jansen, A.J. Hoitsma, A. Van'T Laar, and T. Thien. Deleterious effects of anabolic steroids on serum lipoproteins, blood pressure, liver function in amateur body builders. Int. J. Sports Med. 9:19–23. 1988.
14. NCAA Research Staff. NCAA Study of Substance Use Habits of College Student-Athletes. Indianapolis: National Collegiate Athletic Association. 2001.
15. Sinha-Hikim, I., J. Artaza, and L. Woodhouse. Testosterone-induced increase in muscle size in healthy young men is associated with muscle fiber hypertrophy. Am. J. Physiol. Endocrinol. Metab. 283:E154–E164. 2002.
16. Urban, R., Y. Bodenburg, and C. Gilkison. Testosterone administration to elderly men increases skeletal muscle strength and protein synthesis. Am. J. Physiol. 269:E820–E826. 1995.
Jose Antonio is the chief executive officer of the International Society of Sports Nutrition. He currently serves on the Board of Directors of the National Strength and Conditioning Association (NSCA) Robert Chetlin serves as an assistant professor in the Division of Occupational Therapy, Department of Human Performance at the West Virginia School of Medicine Jay Hoffman is professor and chair in the Department of Health and Exercise Science at the College of New Jersey. He currently serves on the Board of Directors of the NSCA William J. Kraemer is a professor of kinesiology, as well as a professor of physiology and neurobiology, in the Department of Kinesiology and Human Performance Laboratory at the University of Connecticut. He is editor-in-chief of the Journal of Strength and Conditioning Research and a past president of the NSCA Mathew Lively is an associate professor of Internal Medicine and Pediatrics at the West Virginia University (WVU) School of Medicine and is the medical director of the WVU Department of Intercollegiate Athletics Jakob Vingren is a doctoral fellow in the Department of Kinesiology and Human Performance Laboratory at the University of Connecticut
Optimum Sports Performance
"In the beginners mind there are many possibilities, in the experts there are few."
-Buddha's Little Instruction Book
Have you read through this Funk? I find most articles on AAS usage are quite bias one way or another. How do you rate it?(if you have read it)
I'm sure S&C journal is legit, but with the legalities and all of AAS it is hard to find a good article that looks objectively.
haven't read it yet. I have been reading the other articles. I will get around to it tomorrow and let you know.
Originally Posted by fufu
Optimum Sports Performance
"In the beginners mind there are many possibilities, in the experts there are few."
-Buddha's Little Instruction Book
okay, just finished reading it.
Originally Posted by fufu
Part 2 comes out next quarter.
It was actually pretty good. Not biased at all (and actually was kind of pro-steroids....talking about the benefits, the benefits to athletic performance and dispelling myths about side effects that the media creates).
Optimum Sports Performance
"In the beginners mind there are many possibilities, in the experts there are few."
-Buddha's Little Instruction Book
Great read! I'd say some of them had an agenda, but they were very professional and non-biased, in general.
I'll have to give it a peek once my brain lets me.
Originally Posted by P-funk
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