Sports medicine

A recent study has provided evidence that testosterone increases muscle strength, but does this translate to enhanced performance? Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia". strength increased considerably in subjects who received placebo, but who were told they were receiving anabolic steroids For almost half a century, athletes have believed that use of anabolic-androgenic steroids can improve sporting performance. The United States physician John Zeigler was so convinced of their positive effects that on his return from the World Powerlifting Championships in Vienna in 1954 he worked on the development of methandrostenolone as a means of enhancing sporting performance. 1 This belief has persisted, leading to the widespread and much-publicised use of these drugs at all levels of sport (professional and amateur). It has been promoted by the banning of these drugs by sporting bodies to ensure fair competition. 2 Media reports and "underground" guides to anabolic steroids have also propagated the use of anabolic-androgenic steroids, which has spread from elite athletes to recreational bodybuilders, amateur athletes and adolescents. 3 Are the athletes and their coaches mistaken in their belief? Theoretically, anabolic-androgenic steroids should improve athletic performance by increasing muscle mass (via increased protein synthesis, nitrogen retention and antiglucocorticoid actions), as well as by increasing aggression and motivation. Moreover, recent isotope uptake studies in humans indicate that androgens may increase muscle protein synthesis, possibly through stimulation of intramuscular insulin-like growth factor-I (IGF-I) gene expression. 4 However, clinical studies have, in general, been inconclusive, partly because of the many unique methodological problems in studying the effects of anabolic-androgenic steroids (see below). In 1991, 16 randomised, placebo-controlled studies that used objective measures of performance were analysed by Elashoff et al. 5 They concluded that, while the possibility of anabolic-androgenic steroids improving sporting performance could not be excluded, "the data are insufficient to allow any firm conclusion about the efficacy of anabolic steroids in enhancing overall athletic performance". Since then, apart from a non-placebo-controlled study that showed an increase in lean body mass in healthy male volunteers receiving weekly injections of testosterone enanthate, 6 there were few real developments in the area until Bhasin et al. 7 published their study in July 1996. This study will probably become, in time, one of the most-cited articles on drugs and sport. Funded by the National Institutes of Health (US), the study examined the effect of high doses of testosterone enanthate in sesame oil (600 mg/week intramuscularly for 10 weeks); the authors made every attempt to remove confounding variables (such as diet, training, and weightlifting experience), and used standardised measures. Forty-three experienced weightlifters were randomly assigned to one of four groups (placebo with or without exercise, or testosterone with or without exercise). Strength was measured by two single weightlifts -- upper-body strength by benchpress, and lower-body strength by squatting. Fat-free body mass was measured by underwater weighing, and muscle size by magnetic resonance imaging. Forty subjects completed the study. Body weight increased only in the two testosterone-treated groups, and fat-free body mass only in the exercise groups, with the greatest change in fat-free mass in the testosterone plus exercise group (increase, 6.1 kg). Percentage body fat did not change in any group. Muscle size increased more in the testosterone groups than in either placebo group. Strength increased in both testosterone groups, as well as in the exercise group receiving placebo, but was greater in the exercise group with testosterone than in the exercise group with placebo. No significant adverse drug reactions were reported. Hence, for the first time, in a well designed study, supraphysiological testosterone did appear to increase muscle strength. One other placebo-controlled study has used higher doses of anabolic steroids (methandrostenolone, 100 mg/day for six weeks). 8 Reported 20 years ago, it used a crossover design, with attempts to control for most variables. The active drug was found to be no better than placebo in increasing strength. However, some caveats should be considered in assessing Bhasin et al.'s data. A placebo response has not been completely eliminated. It was not stated that the placebo was identical to the active drug in terms of pH, viscosity and other factors that may have allowed the code to be broken by either the administrator or recipient of the drug. Indeed, in a controlled study of oral anabolic steroids, all subjects correctly identified the active drug when directly asked. 9 The importance of the placebo response was shown by Ariel and Saville, who found that strength increased considerably in subjects who received placebo, but who were told they were receiving anabolic steroids. 10 Bhasin et al.'s subjects were experienced weightlifters. Although they reported that they had not taken anabolic steroids, these medications are illicit, and thus self-reporting may not be reliable. As 38%-58% of bodybuilders and weightlifters have been reported to use anabolic steroids, 11,12 some of Bhasin et al.'s subjects may well have been able to identify the active drug. Before generalising these results to athletes who use anabolic-androgenic steroids in the community, it should be remembered that they receive and use their supplies in very different ways to the controlled circumstances of Bhasin et al.'s study. Street supplies are often veterinary or illegally manufactured preparations, often combined with other medications such as diuretics and stimulants. Doses and duration are often well in excess of those used in this study. Although no major side effects were reported, the well documented long-term adverse effects of anabolic-androgenic steroids on cardiovascular risk, gynaecomastia, carcinogenesis, prostate and sexual function would not have been evident in a study of this duration. 13 On considering the available evidence, it appears that anabolic steroids definitely increase muscle size, and probably strength, but the mechanism is unknown. Further studies, using a crossover design, including inexperienced as well as experienced weightlifters, and the same drug vehicle for both placebo and active drug, with confirmation of subject blinding, should probably be conducted to confirm these findings. In addition, whether androgen-induced muscle hypertrophy translates into improved performance in sports that require skill as well as strength remains to be determined. But such studies should not overshadow the need for significant research into the prevention of anabolic-androgenic steroid abuse. Michael C Kennedy Department of Clinical Pharmacology and Toxicology, St Vincent's Hospital; and Manly Hospital, Sydney, NSW. Anthony J O'Sullivan Departments of Medicine and Endocrinology, St George Hospital, Sydney, NSW. Wade N. Anabolic steroids: Doctors denounce them, but athletes aren't listening. Science 1972; 176: 1399-1403. Skolnick AA. Tougher drug tests for Centennial Olympic Games. JAMA 1996; 275: 348-349. Buckley WE, Yesalis CE, Friedl KE, et al. Estimated prevalence of anabolic steroid use among male high school seniors. JAMA 1988; 260: 3441-3445. Urban RJ, Bodenburg YH, Gilkison C, et al. Testosterone administration to elderly men increases skeletal muscle strength and protein synthesis. Am J Physiol 1995; 269: E820-E826. Elashoff JD, Jacknow AD, Shain SG, Braunstein GD. Effects of anabolic-androgenic steroids on muscular strength. Ann Int Med 1991; 115: 387-393. Forbes GB, Porta CR, Herr BE, Griggs RC. Sequence of changes in body composition induced by testosterone and reversal of changes after drug is stopped. JAMA 1992; 267: 397-399. Bhasin S, Storer TW, Berman N, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med 1996; 335: 1-7. Hervey GR, Hutchinson I, Knibbs AV, et al. "Anabolic" effects of methandienone in men undergoing athletic training. Lancet 1976; 2: 699-702. Freed DLJ, Banks AJ, Longson D, Burley DM. Anabolic steroids in athletics: crossover double-blind trial on weightlifters. BMJ 1975; 2: 471-473. Ariel G, Saville W. Anabolic steroids: the physiological effects of placebos. Med Sci Sports 1972; 4: 124-126. Perry HM, Wright D, Littlepage BNC. Dying to be big: a review of anabolic steroid use. Br J Sports Med 1992; 26: 259-261. Delbeke FT, Desmet N, Debackere M. The abuse of doping agents in competing body builders in Flanders (1988-1993). Int J Sports Med 1995; 16: 66-70. Kennedy MC. Anabolic steroid abuse and toxicology. Aust N Z J Med 1992; 22: 374-381. Reprints: Dr M C Kennedy, Manly Non-Invasive Cardiac Laboratory, Level 4, 22 Darley Road, Manly, NSW 2095.

Michael C Kennedy · Anthony J O'Sullivan

A diving fatality due to oxygen toxicity during a "technical" dive Christopher H Lawrence An experienced diver drowned after a generalised seizure caused by oxygen toxicity during a 19-minute "technical" dive to a depth of 47 m. He had used a 50% oxygen/nitrogen gas mixture inappropriately during the dive. This case attests the risk of oxygen toxicity from oxygen-enriched air during deep dives, the shortcomings of the diver's equipment, and the need to examine, with knowledge of diving physiology and practice, both the body and equipment. (MJA 1996; 165: 262-263) Introduction Scuba diving carries the risks of decompression illness and nitrogen narcosis; these risks increase the deeper the dive. Therefore, recreational scuba divers have been encouraged to avoid depths over 40 m. 1 In the past five years, some recreational divers have used highly specialised equipment and techniques to enable diving to greater depths (known as "technical" diving). These techniques include the use of surface supply and rebreather diving apparatuses and gas mixtures with a lower nitrogen concentration than compressed air to reduce the absorbed nitrogen load, allowing a longer bottom time with less decompression. Another technical diving technique uses oxygen-enriched gas mixtures during decompression to accelerate shedding of absorbed nitrogen from the body ("enriched- air", or "nitrox", diving). Unfortunately, higher concentrations of oxygen may have a toxic effect on the brain, causing generalised convulsions which may lead to drowning. The extent of the toxic effect depends on duration of exposure and is increased by exertion and immersion in water. An oxygen tension limit of 161 kPa (1.6 atm) is often adopted in practical diving for exposures of less than 30 min (National Oceanic and Atmospheric Administration guidelines). 2,3,4 However, oxygen toxicity can occur at tensions as low as 121 kPa (1.2 atm). 2 The "safe" level is currently under review and is clearly dependent on duration of exposure. The dangers of "technical" diving have been shown in a report of eight fatalities during technical dives in the United States in 1992. 4 We report the death of an experienced diver in Australia during a technical dive using an oxygen-enriched gas mixture. This case attests the risk of oxygen toxicity from oxygen-enriched air during deep dives, the shortcomings of the equipment used and the importance of an integrated approach to examination of the body and equipment by those experienced in diving practice and physiology. Clinical record A 47-year-old experienced underwater cave diver, with no significant medical history, was diving with two tanks -- one containing compressed air, the other a 50% mixture of oxygen and nitrogen (nitrox). Towards the end of the 47-m, 19-min dive, he was seen floating head down, unresponsive, with his mouthpiece out of his mouth and "his fins [flippers] moving as if he was shivering" (as reported by another diver to the Coroner). The body was carried up to 15 m depth and then allowed to ascend freely as the other divers decompressed. Cardiopulmonary resuscitation was attempted, but abandoned after 43 minutes as there was no response. Autopsy findings Erect postmortem x-rays and autopsy of the body performed 24 hours after death revealed large amounts of gas in the venous system of the trunk and limbs and in both sides of the heart (Figure 1). The heart weighed 380 g and was normal, apart from foamy blood and gas in all chambers. Analysis of gas from the right ventricle showed O 2 (20.6% by volume), and N 2 (75.9%). There was bruising of the tongue and petechiae on the lungs and heart. The brain (1740 g) showed mild cerebral oedema and a microscopic perivascular haemorrhage in the floor of the fourth ventricle. Figure 1: Postmortem erect chest x-ray, showing gas in both sides of the chest and in the neck veins (a combination of postmortem decompression, perimortem barotrauma and, possibly, decomposition). Examination of diving equipment Examination of the subject's diving equipment (Figure 2) re-vealed that he had been breathing the 50% oxygen/nitrogen mixture for most of the dive. Each tank had a separate first stage connected in an unusual fashion by a two-way switch, which the diver had had made by a local engineering shop. This allowed the diver to switch from one tank to another rapidly. This switch supplied a single second-stage mouthpiece. The two tanks were different colours; the circuit from the black (compressed-air) tank was marked with yellow tape, while the circuit from the yellow (nitrox) tank was unmarked. Figure 2: Equipment used by the diver, showing the 50% oxygen/nitrogen gas tank (yellow, right), compressed-air tank (black, left), yellow tape marking the compressed-air circuit, and two-way valve which controlled the source of the air supply (inset shows close-up of valve). The regulator had a small tear and a bite mark in the mouthpiece. The diver wore a facemask and separate mouthpiece rather than a full facemask, which covers eyes, nose and mouth. Discussion The cause of death, as determined by the Coroner, was drowning after oxygen toxicity. 5 The "shivering" movements and the biting of the tongue and mouthpiece suggested fitting. Using a 50% oxygen/nitrogen mixture at 47 m depth, the diver had been exposed to a partial pressure of oxygen of 291 kPa (2.9 atm), possibly for as long as 19 min. During diving, this gas mixture should be used only at depths less than 14-18 m (depending on the duration of exposure). Cerebral gas embolism and decompression illness were unlikely causes of death, as the subject was unresponsive before ascent. The gas observed at autopsy probably resulted from a combination of postmortem decompression (release of tissue nitrogen), perimortem barotrauma and, possibly, a degree of decomposition. 6 This death resulted from several compounding problems: The diver may have turned the switch to the unmarked nitrox circuit, thinking he was using the circuit to the compressed air in the black tank (the yellow label marked the circuit from the black [compressed-air] tank, not the circuit from the yellow [nitrox] tank). Alternatively, as the two-way valve needed very little pressure to turn, it could have been accidentally switched from a safe to an unsafe gas mix. The diver was using a separate facemask and mouthpiece. During the seizure, the mouthpiece fell out. A full facemask, covering both the mouth and nose, should be worn by divers using oxygen-rich mixtures or carrying out deep diving on compressed air, to reduce the chance of drowning should an oxygen convulsion occur. This technical diving fatality and those reported in the United States in 1992 4 were in experienced divers, who should have understood the dangers. The standard of equipment and of diving practice during technical dives should be that of a commercial operator, with planning of the dive to stay below an appropriate oxygen pressure for the duration of the dive (e.g., below 161 kPa [1.6 atm] for a 19-min dive), 2 use of a full facemask, proper analysis of gas mixtures and access to surface decompression facilities after long deep dives. Use of home-made equipment is not appropriate. During the inquest the New South Wales State Coroner declined to recommend legislation to regulate recreational technical diving, preferring that it remain subject to a voluntary code of conduct. 5 Acknowledgements I thank Sergeant John Marshall, New South Wales Police Divers, for the examination of the equipment. References Moon RE, Vann RD, Bennett PB. The physiology of decompression illness. Sci Am 273: 54-61. Gorman DF. Oxygen and carbon dioxide toxicity. In: Gorman DF, editor. Diving and hyperbaric medicine. 2nd ed. Adelaide: Hyperbaric Medicine Unit, Royal Adelaide Hospital, 1993: 26.2-26.4. Clark JM. Oxygen toxicity. In: Bennett PB, Elliott DH, editors. The physiology and medicine of diving. 4th ed. Philadelphia: WB Saunders, 1993. Menduno M. Safety first, an analysis of recent technical-diving accidents. Technical Diver 1993; 2: 3-10, reproduced in SPUMS J 1993; 23: 177-184. New South Wales State Coroner. Coroner's Court, 1995. File number 94/574. Williamson JA, King GK, Callanan VI, Rich KW. Fatal arterial gas embolism: detection by chest radiography and imaging before autopsy. Med J Aust 1990; 153: 97-100. Author's details NSW Institute of Forensic Medicine, Sydney, NSW. Christopher H Lawrence, BSc(Med), FRCPA, Forensic Pathologist; and Clinical Lecturer in Pathology, University of Sydney, Sydney, NSW. Reprints: Dr C H Lawrence, NSW Institute of Forensic Medicine, PO Box 90, Glebe, NSW 2037. E-mail: IOFM AT OZEMAIL. COM. AU Make a comment - Register to be notified of new articles by email - - To top of article - ©MJA1996 < URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia. We appreciate your comments.

Christopher H Lawrence

Anabolic steroids and the mind Brian Corrigan MJA 1996; 165: 222-226 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Introduction - Psychological effects - Withdrawal symptoms - Drug dependence - Other psychiatric changes - Acknowledgements - References - Authors' details Register to be notified of new articles by email - - ©MJA1996 Anabolic steroids were first used by weight lifters and others involved in pursuits of strength, but are now taken, often in large doses, by young men interested in enhancing their appearance. The severe psychogenic side effects of these high doses include aggressive and violent behaviour. Problems with drug withdrawal and drug dependence are also common in users of anabolic steroids and these drugs may also provoke psychiatric disorders. I review these complications, as reported in the past decade, and comment on two recent violent murders in Sydney in which anabolic steroid use was implicated. Introduction S ydney has recently witnessed two particularly brutal murders by users of anabolic steroids. One man with recent paranoid tendencies took a claw hammer and battered his wife to death, and then shot himself. In the second murder a man met a woman he knew at a nightclub and they went to the stairwell of a nearby hotel. In the man's words "something snapped" and he murdered the woman. Experienced police described it as the most brutal attack they had encountered. In both these murders the level of aggression and violence fits the descriptive term steroid rage ("roid rage"). The male hormone testosterone, derived mainly from the testes, is an anabolic and androgenic steroid responsible for the production and maintenance of the male physical features, 1 as well as the recognisable male psychological and behavioural attributes. 1-3 Numerous human and animal studies support the psychological and aggressive effects of testosterone use, and some reports correlate testosterone levels with aggressive behaviour and dominance. 2,3 Anabolic steroids are derived by chemical manipulation of the 19-carbon testosterone molecule. Despite well documented problems with their use, they are widely abused in the community for non-medical reasons, mostly by young men to enhance their appearance by "bulking up" (i.e., increasing their lean muscle mass without increasing fat). How common their use is in Australia is not known, but a recent survey in the United States concluded that there were at least three million users at any one time and at least one million former users. 4 Side effects can occur with all anabolic steroids. 5 The higher the dose the higher the risk is the general rule, and side effects can be sudden, severe and unpredictable, and include sudden death. 5 The most common group of side effects involve psychological and/or psychiatric changes. Being psychoactive substances, 3,6 anabolic steroids are expected to produce some degree of psychological change after they have been taken for some time. Indeed, these changes (which include an increase in self-confidence, energy and motivation), if they allow people to train harder, may well be one of the main factors explaining the mechanism of action of anabolic steroids. 7 Psychological effects One of the earliest papers on psychological effects reported the side effects of anabolic steroids in 32 weight-trained men; 8 56% had a subjective perception of increased irritability and aggression. This also applied to a smaller group of 10 weight-trained female athletes. 9 A more recent report compared 13 anabolic steroid users with 14 non-users and 18 former users. 10 Steroid users had more frequent episodes of anger, which were of greater intensity and duration, and a more hostile attitude towards others. In general, psychological changes need to be related to the dose and duration of anabolic steroid use (e.g., taking one or two 5 mg tablets would not produce any changes, but after taking an increasing dose for some days several psychological changes may occur). These changes will develop if anabolic steroids are taken for long enough (just how long could possibly depend upon individual tolerance). The psychological changes that occur can be arbitrarily divided into three groups, representing a continuum of effects from milder through to more severe changes, especially if continued high doses are taken. Early effects are seen as changes in mood and euphoria: there is an increase in confidence, energy and self-esteem, with enhanced motivation and enthusiasm. There is also diminished fatigue, sleeplessness and an ability to train through pain. Libido may be decreased, but is more often increased, sometimes markedly. 11 Irritability, anger, agitation and a "strange edgy feeling" are commonly reported. With larger doses or after taking anabolic steroids for a longer time, there is a loss of inhibition and a lack of judgement, with mood swings or grandiose ideas. Prolonged users become suspicious, quarrelsome, impulsive and more aggressive. 7 Severe effects manifest when these aggressive feelings increase to the extent that violent, hostile, antisocial behaviour develops, meriting the descriptive title, well known in the steroid-taking community, of "roid rages". These rages can result in property damage, self-injury (including reckless driving or crashing cars), assaults, marriage break-ups, domestic violence, 12 child abuse, 12 suicide 13 and attempted murder or murder. 14-20 Partners of anabolic steroid users are at particular risk of serious injury, and there is even a self-help group, Anabolic Steroid Wives Association, 21 to help provide them with support. One group of men who often take anabolic steroids in high doses are those working as security officers or nightclub bouncers; 22 under the influence of the drug they may be provoked into a rage and seriously injure people, and at least one person has been killed as a result. 22 How common these rages are is not known. There is often a great reluctance by anabolic steroid users to report them to doctors, but they may be reported at times by the family. Rages generally result from taking a high dose for a prolonged period; how high a dose and for how long are yet to be defined. In addition, not all people taking high doses develop steroid rages. On the other hand, there are a few reports of rages in those taking quite low doses. 17,23-25 Some common features have been noted in men having these rages. They are generally young, come from apparently caring families, have not previously taken drugs or been in trouble with the police, and do not have a history of being aggressive. They usually feel no remorse at all after the rage, however antisocial their behaviour. 21 It has been suggested that there may be an underlying predisposition to this type of behaviour and that excessive drug use "pushes them over the edge"; however, nearly all the cases described in the literature fit the description above. The first two murder cases in which taking anabolic steroids was used as a defence (called the "dumbbell defence" by Newsweek ) were in the United States in 1988; both men were found guilty of murder. Some 20 murders associated with the use of anabolic steroids have been reported in America, 26 but the usual pleas of innocence due to temporary insanity have never been upheld there. Sydney's two cases are summarised in the Box. Withdrawal symptoms All types of steroid drugs, including corticosteroids, produce withdrawal symptoms. 2 Depression is almost invariably one of the symptoms in anabolic steroid users: they miss the feeling of elation induced by the drugs. Other symptoms relate to loss of the positive psychological effects and include listlessness; apathy; loss of appetite, libido and self-esteem; feelings of anxiety; difficulty in concentrating; and mood swings. Withdrawal can also be associated with violent behaviour and rages. Hence, rages may result from taking either a high steroid dose or stopping taking the drug. Severe symptoms of steroid withdrawal may not be a problem in athletes, possibly because they take anabolic steroids in certain well defined phases and because they reduce the dose gradually. Body builders or weight trainers, however, have greater problems with withdrawal. They lose their new improved body image as their recently enhanced musculature shrinks away, and are likely to be driven back to taking steroids again and to have great trouble stopping them in the future. 27 Drug dependence Another related problem is drug dependence; pharmacological, psychological and genetic factors may all have an effect. This problem was first described in 1988 in a 23-year-old body builder; 28 anabolic steroid dependence was later reviewed, 29 and two other case reports followed. 30,31 Brower et al. produced a series of papers on anabolic steroid dependency and its management. 32-37 They initially published a case in a 24-year-old weight trainer with drug dependence, depression and aggression, 32 and later reported eight steroid-using weight lifters (age range, 23-65 years) who showed evidence of dependence at interview according to criteria of the Diagnostic and statistical manual of mental disorders (DSM-III-R). 33 In a review of 49 male weight lifters, average age 24 years, 28 (57%) were considered to be drug dependent. 37 Mechanisms discussed were either that (i) anabolic steroids may affect endogenous opioid 28 or monoaminergic brain systems, or (ii) that dependence may result from social reinforcement and the pleasure of having a muscular body. However, users were more likely to have expressed dissatisfaction with their body size and so dependence was considered to be driven more by negative reinforcement (trying to avoid feeling small). The presence of more than three DSM-III-R criteria is considered consistent with drug dependence, and Brower et al. found anabolic steroid users may have up to six of these ( Box 2). 37 Other psychiatric changes Several psychiatric disorders have been reported in association with anabolic steroid use since the first case was described in 1980. 38,39 The full list includes schizophrenia, 38 hypomania and mania, 40 delirium, 41 depression, 42 suicide, 10,28,43 and paranoia. 44 In the first reported case of anabolic steroid-related psychiatric disorder, in 1980, a 17-year-old male body builder developed acute schizophrenia when taking methandienone; he recovered on stopping the drug, but relapsed when he took it again. 38 In 1992, Freinhar and Alvarez 40 noted that referring doctors "often" commented on mood changes accompanying anabolic steroid therapy, and described a 27-year-old body builder with hypomania who was taking oxandrolone. He recovered on withdrawal of the drug but had a second attack when taking oxymetholone. A toxic confusional state with choreiform movements occurred in another patient taking 200-300 mg a day of oxymetholone; the condition improved on drug withdrawal. 41 Perry et al. studied 20 weight lifters taking anabolic steroids and 20 controls using a self-administered questionnaire and an interview. 45 The questionnaire showed an increase in psychotic features in the users, including paranoid thoughts, depression, increased hostility and aggression. Pope and Katz in 1987 reported two cases of psychosis in anabolic steroid users, 46 and then, in 1988, 41 cases (39 men) with a wide range of psychiatric problems. 47 This study was widely criticised because it was not a controlled, prospective trial and because of its selection of subjects. In 1994, they rectified this with a controlled study of 88 athletes who used anabolic steroids and 68 controls. 48 The Structured Clinical Interview for DSM-III-R was used for diagnosis; 25% showed evidence of drug dependence and 23% hypomania, mania or depression. Aggression or violence "often" accompanied hypomanic or manic episodes. The authors also suggested that steroid users are most vulnerable to major depressive episodes during the first three months after discontinuing anabolic steroid use. Depression has been mentioned previously in relation to drug withdrawal and dependence. Testosterone was formerly used to treat depression, but it is now known to cause it. 49 Suicide may also be a problem with either anabolic steroid drug dependence or after drug withdrawal (especially with sudden withdrawal). It is not often reported in medical journals, but may be reported in the press. Brower et al. reported a body builder who had suicidal thoughts of crashing his car, and warned of the dangers of anabolic steroids and suicide. 32 A different view of anabolic steroid complications was taken by Dimeft and Malone: 50 in 31 current users, 45 previous users and 88 non-users, they found psychiatric diagnoses to be more common in previous users, suggesting that psychiatric disorder may either predispose a person to, or result from, anabolic steroid use. There is one study which gives a contrary view. Bahrke et al., 51 using two valid psychometric inventories, studied 50 men (12 current steroid users, 14 previous users, and 24 non-users) and concluded that users taking an average daily dose of 45 mg showed minimal psychiatric effects. In conclusion, this brief review highlights some of the psychological problems encountered with anabolic steroid use. It does not appear that these problems are very common, but future research will show how much disability they cause. Acknowledgements I sincerely thank the librarians at Concord Hospital (Ms Kaye Lee) and Manly Hospital (Ms Diane James) for all their help, as well as Ms Kathleen Roach and Ms Nicki Vance at the Australian Sports Drug Agency. References Mooradian AD, Morley JE, Korenman SG. Biological actions of androgens. Endocr Rev 1987; 8: 1-28. Bahrke MS, Yesalis CE, Wright JE. Psychological and behavioural effects of endogenous testosterone levels and anabolic steroids among males. A review. Sports Med 1990; 10: 303-337. Hoberman JM, Yesalis CE. The history of synthetic testosterone. Sci Am 1995; Feb: 60-65. Yesalis CE, Kennedy NJ, Kopstein AN, Bahrke MS. Anabolic androgenic steroid use in the United States. JAMA 1993; 270: 1217-1221. Corrigan B. Drugs in sport. Sports Coach 1988; 12: 11-17. Parrott AC, Choi PY, Davies M. Anabolic steroid use by amateur athletes: effects upon psychological mood states. J Sports Med Phys Fitness 1994; 34: 292-298. Lombardo JA, Sickles RT. Medical and performance-enhancing effects of anabolic steroids. Psychiatr Ann 1992; 22: 19-23. Strauss RH, Wright JE, Finerman GAM. Side effects of anabolic steroids in weight-trained men. Physician Sportsmed 1983; 11: 86-96. Strauss RH, Ligget MT, Laaese RR. Anabolic steroid use perceived effects on weight-trained women athletes. JAMA 1985; 253: 2871-2873. Lefavi RG, Reeve TG, Newland MC. Relationship between anabolic steroid use and selected psychological parameters in male bodybuilders. J Sport Behav 1990; 13: 157-166. Moss HB, Panzak GL, Tarter RE. Sexual functioning of male anabolic steroid abusers. Arch Sex Behav 1993; 22: 1-12. Schulte HM, Hail M, Boyer M. Domestic violence associated with anabolic steroid abuse. Am J Psychiatry 1993; 150: 348. Brower KJ, Blow FC, Eliopulos GA, Beresford P. Anabolic androgenic steroids and suicide. Am J Psychiatry 1989; 146: 1075. Lubell A. Does steroid abuse cause or excuse violence? Physician Sportsmed 1989; 17: 177-185. Choi PY, Parrot AC, Cowan D. High dose anabolic steroid in strength athletes: effects upon hostility and aggression. Hum Psychopharmacol 1990; 5: 349-356. Pope HG, Katz DL. Homicide and near homicide by anabolic steroid users. J Clin Psychiatry 1990; 51: 28-31. Dalby JT. Brief anabolic steroid use and sustained behavioral reaction. Am J Psychiatry 1992; 149: 271-272. Moss HB, Panzac GL. Steroid use and aggression. Am J Psychiatry 1992; 150: 1616. Yates WR, Perry P, Murray S. Aggression and hostility in anabolic steroids users. Biol Psychiatry 1992; 31: 1232-1234. Choi PY, Pope HG. Violence towards women and illicit anabolic androgenic steroid use. Ann Clin Psychiatry 1994; 6: 21-25. Cooper CJ, Noakes TD. Psychiatric disturbances in users of anabolic steroids. S Afr Med J 1994; 84: 509-510. Drugs in Sport. Second Report of the Senate Standing Committee (Chairman John Black). Canberra: AGPS, 1990; 357-368. Barker S. Oxymetholone and aggression. Br J Psychiatry 1987; 151: 564. Conacher GN, Workman DG. Violent crime possibly associated with anabolic steroid use. Am J Psychiatry 1989; 146: 679. Su TP, Pagliariio RN, Schmidt PJ, et al. Neuropsychiatric effects of anabolic steroids in male normal volunteers. JAMA 1993; 269: 2760-2764. Moss DC. And now the steroid defence. Am Bar Assoc J 1988; 74: 22-23. Yesalis CE, Vicary JR, Buckley WE, et al. Indications of psychological dependence among anabolic steroid abusers. In: Lin GC, Erinoff L, editors. Anabolic steroid abuse. National Institute on Drug Abuse. Washington, DC: US Department of Health and Human Services (National Institute on Drug Abuse), 1990: 196-214. (NIDA Research Monograph 102.) Tennant PH, Black D, Voy RO. Anabolic steroid dependence with opioid-type features. N Engl J Med 1988; 319: 578. Kashkin KB, Kleber HD. Hooked on hormones? An anabolic steroid addiction hypothesis. JAMA 1989; 262: 3166-3169 . Hays LR, Littleton S, Stillner V. Anabolic steroid dependence. Am J Psychiatry 1990; 147: 122. Allnutt S, Chaimowitz G. Anabolic steroid withdrawal depression: a case report. Can J Psychiatry 1994; 39: 317-318. Brower KJ, Blow F, Beresford TP, Fuelling C. Anabolic androgenic steroid dependence. J Clin Psychiatry 1989; 50: 31-33. Brower KJ, Eliopulos GA, Blow FC, et al. Evidence for physical and psychological dependence on anabolic androgenic steroids in eight weight lifters. Am J Psychiatry 1990; 147: 510-512. Brower KJ. Rehabilitation for anabolic androgenic steroid dependence. Clin Sports Med 1989; 1: 171-181. Brower KJ. Anabolic steroids: addiction, psychiatric and medical consequences. Am J Addict 1992; 1: 100-114. Brower KJ. Anabolic steroids. Psych Clin North Am 1993; 16: 97-103. Brower KJ, Blow FC, Young JP, Hill EM. Symptoms and correlates of anabolic steroid dependence. Br J Addict 1991; 86: 759-768. Annitto WJ, Layman WA. Anabolic steroids and acute schizophrenic episode. J Clin Psychiatry 1980; 41: 143-144. Uzych JD. Anabolic steroids and psychiatric-related effects: a review. Can J Psychiatry 1992; 37: 23-28. Freinhar JP, Alvarez W. Androgen-induced hypomania. J Clin Psychiatry 1985; 46: 354-355. Tilzey A, Heptonstall J, Hamblin T. Toxic confusional state and choreiform movements after treatment with anabolic steroids. BMJ 1981; 283: 349-350. Bourget D, Bradford JMW. Affective disorder and homicide: a case of familial filicide. Theoretical and clinical considerations. Can J Psychiatry 1987; 32: 222-225. Elofson G, Elofson S. Steroid claimed my son's life. Physician Sportsmed 1990; 18: 15-16. Wilson IC, Prange AJ, Lara PP. Methyltestosterone and imipramine in men: conversion of depression to a paranoid reaction. Am J Psychiatry 1985; 131: 21-24. Perry PJ, Anderson KH, Yates WR. Illicit anabolic steroid use in athletes. A case series analysis. Am J Sports Med 1990; 18: 422-428. Pope HG, Katz DL. Bodybuilder's psychosis. Lancet 1987; 1: 863. Pope HG, Katz DL. Affective and psychotic symptoms associated with anabolic steroids use. Am J Psychiatry 1988; 145: 487-490. Pope HG, Katz DL. Psychiatric and medical effects of anabolic steroid use. A controlled study of 160 athletes. Arch Gen Psychiatry 1994; 51: 375-382. Alschule MD, Tillotson KJ. The use of testosterone in the treatment of depression. N Engl J Med 1948; 239: 1036-1038. Dimeft R, Malone D. Psychiatric disorders in weight lifters using anabolic steroids. Med Sci Sports Exerc 1991; 23: 18. Bahrke MS, Wright JE, Strauss RH, Catlin DH. Psychological moods and subjectively perceived behavioural and somatic changes accompanying anabolic steroid use. Am J Sports Med 1992; 20: 717-724. Author's details Institute of Sports Medicine, Concord Hospital, Sydney. Brian Corrigan , AM, FRACP, FACRM, Consultant Physician. Reprints: Dr B Corrigan, 1 Lookout Avenue, Dee Why, NSW 2099. - - To top of article - ©MJA1996 < URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Brian Corrigan

Clinical Practice Clinical exercise stress testing -- Safety and performance guidelines* The Cardiac Society of Australia and New Zealand Clinical exercise testing has wide application in medicine, including the assessment of functional capacity, ventilatory function, gas exchange, muscle function, and endocrine and metabolic function, and as a test for claudication in peripheral vascular disease. The major use of exercise testing, however, is as a stress test in patients with known or suspected coronary artery disease. This article outlines the minimum safety and performance guidelines for exercise stress testing with electrocardiography, although many of the safety guidelines are common to other types of exercise tests, particularly exercise stress scintigraphy and echocardiography. MJA 1996; 164: 282-284 Introduction - Exercise equipment - Electrocardiograph (ECG) - Blood pressure measurement - Documentation - Postexercise period - Resuscitation equipment - Personnel - References - Authors' details - - Articles on similar material Introduction Clinical exercise stress testing with exercise electrocardiography is usually performed in patients with known or suspected coronary artery disease (see Box 1). It is thus not without risk: one in 10 000 people will die, and two to three in 10 000 will have a major morbid event such as myocardial infarction, a major arrhythmia requiring resuscitation, severe hypotension, severe heart failure or unstable angina pectoris. (The complication rates may be higher in some laboratories because of the mix of referred patients.) Those who perform exercise stress testing must thus be able to recognise and exclude patients at high risk, and have the clinical skills and equipment to recognise and deal effectively with complications. They should also obtain informed consent from the patient before performing the test. Exercise equipment Energy expenditure is best quantified by measurement of oxygen consumption (Vo2), expressed in METS, during exercise. A MET unit is the energy expenditure at rest, equivalent to an oxygen uptake of approximately 3.5 mL O2 per kilogram bodyweight per minute. This is the most precise measurement of metabolic load, and therefore cardiovascular load, and can vary considerably between individuals with differing exercise efficiency working at the same treadmill or cycle ergometer setting. Vo2 is not usually measured directly; energy expenditure in METS can be estimated from nomograms1 which assume that energy expenditure can be quantified as watts (cycle ergometer) or as speed and grade (treadmill). Treadmills must be motorised and calibrated, and should be capable of providing measured increases in speed and gradient. The treadmill speed can be easily checked by measuring the visible length of belt, multiplying by two, and multiplying this by manually counted belt revolutions/ minute to give km/hour. Treadmill inclination can be checked by a protractor. Cycle ergometers must be able to vary the external workload and quantify it in watts. Preference is for electrical or mechanical braking, although wind-braking is probably adequate. Thumb-screw braking is not adequate as the load cannot be quantified and is not reproducible. Simple step devices (including "Masters two-step"), or any other form of non-quantified and unmonitored exercise, are not adequate for clinical exercise stress testing. Equipment should be serviced on a regular basis to ensure performance within specifications. Electrocardiograph (ECG) Use 12-lead ECG equipment, recording on a 3-channel device with adequate low frequency and phase response. Devices which record only one or three ECG leads, even if these are bipolar chest leads, are not adequate. If the device provides computer-averaged complexes, raw ECG traces should also be inspected at each stage of exercise, or at least every three minutes, to avoid incorrect interpretation resulting from noise or artefact. Electrodes must be firmly fixed to the patient's skin with adhesive or continuous suction, and have good contact with the ECG lead, to prevent movement artefact in the ECG trace. Use an alcohol solution to remove oil from the patient's skin and abrade the horny layer of the epidermis with fine sandpaper or a disposable abrasive device. Record a standard supine ECG (with limb leads on the limbs) for each patient, and an additional supine ECG with the limb electrodes on the torso if this is where they will be placed during exercise. Monitor the ECG continuously during the exercise period and for five minutes after the cessation of exercise on a video display of two or three leads, preferably selected to be semiorthogonal (i.e., an inferior lead, V5, and V1 or V2). Monitoring a single lead is suboptimal for detecting arrhythmias and ischaemic patterns during exercise. Monitoring devices should have a memory loop capable of providing hard copy or storing rhythm traces on request by the operator. Record further ECGs with the patient upright; during each stage of exercise (or at least every three minutes); at peak exercise; immediately upon cessation of exercise; and at least twice during the post- exercise period. Blood pressure measurement Measure blood pressure before, during (ideally every minute but at least every three minutes, coinciding with each stage of exercise) and after exercise (at least two measurements). If possible, a measurement should be made at peak exercise. Additional measurements may be required depending on clinical circumstances. Documentation Document the resting and peak heart rate and blood pressure, and any abnormalities of these or the ECG. The peak rate-pressure product (heart rate x systolic blood pressure) should be calculated as this provides the best estimate of myocardial load. Question the patient about symptoms such as angina, anginal equivalents, shortness of breath, presyncope and claudication during and after exercise. Identify the major symptom which limits exercise and record its intensity, at least descriptively, but ideally with a quantitative measure such as the Borg scale2 (see Box 2). Also record the duration of exercise and the maximum workload achieved. Postexercise period Patients should be observed for at least 10 minutes after cessation of exercise. Continue ECG monitoring for at least five minutes, or longer if clinically indicated. The duration of ECG monitoring may be abbreviated to three minutes in special circumstances, such as thallium scintigraphy, when imaging must commence as soon as possible after exercise. In such cases, the patient should be closely observed for the first 10 minutes after exercise. Resuscitation equipment Exercise stress test laboratories must be adequately equipped to provide advanced life support in the event of a cardiac arrest (see Box 3). The exercise room must be sufficiently large to allow the patient to be removed from the treadmill or cycle and be placed on the ground for resuscitation if complications occur. All resuscitation equipment must be easily accessible and maintained and tested on a regular basis. Personnel Two people (at least one of whom is a registered medical practitioner, see Box 4) should be present in the exercise room at all times during exercise stress testing and the immediate postexercise period. Both should be trained in cardiopulmonary resuscitation and in the recognition of the major arrhythmias and ischaemic patterns on the ECG. No regular specific courses are currently available in exercise stress testing. The assistant for exercise stress testing should be a professional person with training in an area related to health (e.g., ECG technician, graduate of a course approved by the Australian Association for Exercise and Sports Sciences, coronary care-trained nurse, physiotherapist, occupational therapist). He or she must be able to perform cardiopulmonary resuscitation, obtain a high quality ECG trace, and recognise the major arrhythmic and ischaemic ECG and clinical manifestations likely to occur during exercise stress testing. He or she should also have observed exercise stress tests under the supervision of a cardiologist and performed tests under supervision of an experienced assistant. A retraining program in cardiopulmonary resuscitation should be undertaken every two years. References The Committee on Exercise, American Heart Association. Exercise testing and training of apparently healthy individuals: a handbook for physicians. Dallas, TX: American Heart Association, 1972: 13. Noble BJ, Borg GAV, Jacobs I, et al. A category-ratio perceived exertion scale: relationship to blood and muscle lactates and heart rate. Med Sci Sports Exerc 1983; 15: 523-528. * Adapted from a Cardiac Society guideline document, copies of which are available from Professor Freedman. Authors' details 145 Macquarie Street, Sydney, NSW 2000. The Cardiac Society of Australia and New Zealand. No reprints will be available. Correspondence: Professor Ben Freedman, Honorary Secretary. ©MJA 1998 Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1998 Medical Journal of Australia. 1: Indications for exercise stress testing* As a diagnostic test in patients with suspected coronary artery disease (e.g., men with symptoms that are atypical for myocardial ischaemia, patients with symptoms consistent with recurrent exercise-induced cardiac arrhythmias). To assist in identifying patients with documented coronary artery disease who are at high risk (e.g., due to advanced disease and/or left ventricular dysfunction). To evaluate patients after coronary artery bypass surgery or angioplasty. To quantify a patient's functional capacity, prognosis or response to therapies, and to follow the natural course of disease at appropriate intervals (e.g., after uncomplicated myocardial infarction, in selected patients with congenital heart disease). General contraindications Unstable angina prior to a period of stabilisation Untreated life-threatening arrhythmias Uncompensated severe congestive heart failure Advanced atrioventricular heart block Acute myocarditis Critical aortic stenosis * Adapted from: Guidelines for exercise testing. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Cardiovascular Procedures (Subcommittee on Exercise Testing). J Am Coll Cardiol 1986; 8: 725-738. Back to text 2: Borg scale2 for ratings of perceived exertion 0Nothing at all0.5 Very, very weak1 Very weak2 Weak3 Moderate4 Somewhat strong5 Strong67 Very strong8910 Very, very strong(maximal)Back to text 3: Essential resuscitation equipment Defibrillator with electrogel or electrode pads Suction (motor driven or gas cylinder [Venturi] device with appropriate plastic or metal suckers) Airway plus self-inflating ventilation bag Oxygen and appropriate masks Drugs, intravenous cannulas and giving sets, including atropine, lignocaine, adrenaline, and sotalol or amiodarone for intravenous use, a β2-agonist inhaler (e.g., salbutamol), and short-acting nitrates (e.g., sublingual glyceryl trinitrate or isosorbide dinitrate, or glyceryl trinitrate spray) Alarm to summon nearby personnel and a telephone to call an intensive care ambulance in the event of an emergency Back to text 4: Medical practitioners supervising exercise stress tests should be able to: Evaluate indications for exercise stress testing and recognise contraindications. Interpret all the major abnormalities that can be detected on 12-lead electrocardiography, particularly those associated with ischaemic heart disease; those likely to preclude interpretation of the exercise ECG; those which might indicate deferral of the exercise test; and the tachy- and bradyarrhythmias that may occur during exercise. Differentiate ischaemic from non-ischaemic symptoms during exercise. Perform basic and advanced life support with skill in an emergency situation, and show evidence of continuing competence by, for example, attending retraining courses at two-yearly intervals. Demonstate previous experience in exercise stress testing supervised by a cardiologist, including determination of the most appropriate protocol for individual patients. Back to text

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