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Psychoactive Drugs and Athletic Performance

Thomas L. Schwenk, MD


In Brief: Some psychoactive drugs have actual performance-enhancing side effects. However, many actually decrease performance, primarily because of adverse cardiovascular effects and impaired judgment. Athletes and nonathletes alike may be knowingly or unknowingly exposed to psychoactive substances if they use over-the-counter, recreational, or prescription drugs. Many national and international sports federations ban or limit psychoactive drug use. The physiologic actions of psychoactive drugs and their use by high school and college athletes are discussed here.

Psychoactive drug use by high school and college athletes is extraordinarily common. A survey of Chicago area high school athletes (table 1) (1) revealed use of various over-the-counter and prescription medications as well as legal and illegal psychoactive drugs. Anabolic steroids, which have received considerable attention in the sports medicine literature, were used relatively infrequently. A more recent study of varsity-level college athletes in the Midwest showed similar results (2), in particular high utilization of smokeless tobacco; alcohol, including binge drinking; and marijuana. At least one study (3) showed that the use of alcohol by athletes was greater than that by sedentary college students.

Table 1. Prevalence of Psychoactive Drug Use Among 1,117 Male High School Athletes in the Chicago Area

Drug Percent

Beer 67.6
OTC drugs 56.7
Wine/whiskey 54.5
Oral smokeless tobacco 32
Cigarettes 27.9
Caffeine 27.1
Marijuana 18.5
Narcotics 9.9
Hallucinogens 9.2
Inhalants 4.9
Amphetamines 3.8
Cocaine 2.4
Anabolic steroids 2.2

Adapted from Forman et al (1).

Primary care physicians must consider the potential for psychoactive drug use by their young patients, athletes or not. The properties and physiologic effects, particularly as related to athletic performance, of a wide range of psychoactive drugs are discussed here. In addition, the current policies of the National Collegiate Athletic Association (NCAA) and the International Olympic Committee (IOC) regarding these drugs are summarized.

Over-the-Counter Drugs

Alpha-adrenergic agents. These drugs are constituents of many over-the-counter medications, some of which are used for weight loss (phenylpropanolamine hydrochloride) and to treat asthma and upper respiratory infections (ephedrine, phenylephrine, and epinephrine). Their primary effect is autonomic cardiac stimulation as well as an amphetamine-like central nervous system (CNS) stimulation that results from their displacement of norepinephrine and other brain monoamines. Possible side effects at commonly used dosages include tachycardia, headache, dizziness, hypertension, anorexia (hence their use by athletes in appearance sports), irritability, anxiety, mania, and, at high doses, psychosis.

Some research (4,5) has demonstrated no effect of alpha-adrenergic agents on strength, endurance, reaction time, anaerobic capacity, or recovery time after prolonged exercise. All systemic use has been banned by the IOC, but topical use is permitted (eg, oxymetazoline hydrochloride and phenylephrine nasal spray).

Ma huang is an herbal form of ephedrine called ephedra that is contained in many herbal products available in health food stores, often in conjunction with chromium. Recent changes in US Food and Drug Administration (FDA) regulations excuse the makers of nutrition supplements from fully identifying the contents of their products. Ma huang has been blamed for the deaths of several high school students who used it as a stimulant or aphrodisiac; the deaths presumably resulted from CNS bleeding or cardiac arrhythmia. Its use is banned by the IOC (6).

Caffeine. This substance has been used as stimulant since the Stone Age. Its concentration ranges from 4 mg per cup in decaffeinated coffee to 220 mg in coffee prepared by the drip method. Concentrations range from 60 to 150 mg in most colas and coffee. The average consumption in the United States is 206 mg per day; 10% of the adult population consumes more than 1,000 mg per day (7). Caffeine is chemically related to the methylxanthines and inhibits the action of cyclic nucleotide phosphodiesterase, leading to increased cyclic adenosine monophosphate (cAMP) levels. A dose of 80 to 200 mg leads to increased alertness, shortened reaction time, and improved concentration, but the response varies greatly among individuals. At doses over 250 mg (2 to 3 cups of coffee), the nonhabitual user usually experiences a headache and nervousness, which is the definition of caffeinism proposed by the American Psychiatric Association (8). For habitual users, abstinence for as little as 24 hours leads to a withdrawal syndrome of headache, irritability, insomnia, and dysphoria.

The physiologic effects of caffeine include diuresis, gastric acid release, smooth muscle relaxation, increased contractility of skeletal muscle, increased lipolysis, and increased heart rate, blood pressure, oxygen consumption, and metabolic rate. Moderate exercise leads to increased peak plasma concentrations, which explains the experience of many recreational runners who find an additional stimulant effect from the usual consumption of coffee following a morning run. Urinary clearance of caffeine is slowed by oral contraceptives and alcohol.

The effect of caffeine on short-duration, high-intensity performance is negligible at levels under the IOC limit, with animal studies showing an effect only at concentrations 10 times or more that allowed in humans. Caffeine has been shown to increase exercise time during graded incremental performance, but the practical significance of this finding is unclear because of the high dosages used (9). However, during prolonged endurance exercise, the benefits of caffeine are more clear. Studies (7,9) have shown a 7% increase in work output and a 19% increase in exercise time with caffeine use; the proposed explanation is that caffeine enhances lipolysis and free fatty acid release, which would spare muscle glycogen use. Another suggested explanation for caffeine's enhancement of endurance exercise is CNS stimulation, perhaps through catecholamine release.

The only consistent benefit of caffeine is in submaximal, prolonged endurance exercise, but there is controversy as to whether this benefit is realized at the concentrations allowed by the IOC (maximum urinary concentration of 12 micrograms/mL, equal to 8 cups of coffee in 2 to 3 hours) and the NCAA (maximum urinary concentration of 15 micrograms/mL) (6). Some athletes have approached or exceeded the IOC threshold despite seemingly minimal caffeine intake, and athletes should be advised of this possibility. Caffeine is the only substance for which the IOC has set a urinary threshold.

Nicotine. Exposure to nicotine occurs with both cigarette smoking and smokeless tobacco use. The toxicity of tobacco smoke, with its approximately 4,000 chemical constituents, is well known. Because of its immediate cardiorespiratory toxicity, fewer athletes than nonathletes smoke tobacco (1,2), although the prevalence is not as low as one might expect. A fact that can be useful in educating athletes about the hazards of tobacco smoke is that carbon monoxide is a prominent ingredient and that its high affinity for hemoglobin, 200 to 300 times that of oxygen, produces carboxyhemoglobin levels of 5% to 10%, depending on the number of cigarettes smoked per day. These levels are in the lower range of those that might cause mild lethargy as a result of carbon monoxide poisoning from defective natural gas furnaces (10).

Smokeless tobacco is used by 20% to 60% of male college athletes (use varies among sports and is highest in baseball) and 5% to 10% of female college athletes (highest in softball) (1,2). The CNS stimulation and skeletal muscle relaxation produced by nicotine cause athletes to underestimate muscle tension related to athletic performance but do not decrease the rating of perceived exertion (7). Reaction time is not affected. Vasoconstriction leads to an increased heart rate and blood pressure and a decreased stroke volume (by as much as 30% to 40%) (7,8). Nicotine yields no proved benefit in any athletic endeavor, and hence it is not banned by the IOC or NCAA. However, the NCAA has mounted an intense antitobacco campaign and has set regulations regarding use during competition.

Melatonin. This substance is marketed as a "natural" sleep agent and is available in dosages of 1 to 3 mg. At this level, its purported benefits are shortened sleep onset and decreased time to stage 2 sleep without a "hangover" the next morning. Anecdotal reports suggest widespread use by athletes, especially when traveling, but controlled studies of its effects are sparse (11). Interestingly, the usual nocturnal increase in melatonin is greater in amenorrheic than in eumenorrheic athletes, suggesting that melatonin may play a role in exercise-associated menstrual disturbances (12).

Recreational Drugs

Alcohol. Alcohol blocks the release of acetylcholine, resulting in decreased serotonin turnover and increased noradrenergic activity. The result of these neurotransmitter alterations is euphoria followed by depression (8). Alcohol has long been used as a prerace stimulant (sometimes laced with strychnine), and its prominence in sports promotion and marketing is obvious. College athletes express more negative attitudes about alcohol use than nonathletes do, but this may reflect only socially acceptable responses on questionnaires, since they show the same drinking behaviors, particularly binge drinking, as nonathletes (13).

Controlled studies of alcohol's effect on athletic performance are difficult to blind because of the easily recognizable taste of alcoholic beverages (7). To blind participants to the presence of alcohol, most researchers use vodka, at an insignificant concentration but sufficient for taste, or noseclips and anesthetic throat lozenges. Limited evidence suggests increased isometric muscle strength at low doses of alcohol because of CNS disinhibition of neuromuscular impulses. Other significant effects include impaired gluconeogenesis, lowered resting muscle glycogen levels, poor temperature regulation, diuresis, and direct cardiotoxicity, all of which impair athletic performance. For unclear reasons, alcohol produces an increase in VO2 at submaximal exercise intensity but has no effect on VO2 max, resulting in decreased exercise time to exhaustion and decreased performance in middle-distance running events (7,14).

Athletes engaged in activities that require precise fine motor control, such as archery and shooting, have a perception of reduced tension and increased relaxation as a result of alcohol, but the actual effect is decreased hand-eye coordination and impaired judgment and tracking; this results in a less smooth release in archery, increased reaction time, and confusion. Alcohol is banned by the NCAA for riflery and by the international federations that govern the modern pentathlon, fencing, and shooting.

Marijuana. This drug is tried by at least a third of high school students and may be used more commonly than cigarettes because it is incorrectly perceived to contain fewer toxic irritants and ergolytic chemicals than tobacco smoke (14,15). Tetrahydrocannabinol (THC), the active ingredient, causes sedation and euphoria at low doses and hallucinations and psychosis at high doses. Its effects on athletic performance are increased reaction time, decreased fine-motor coordination, and increased heart rate. These effects, along with the vasodilating effect, cause an athlete to reach maximal heart rate at a lower than normal intensity of exercise, resulting in a decreased maximal work capacity. Chronic marijuana use has been associated with decreased motivation to perform and to give a maximal effort as well as with decreased circulating testosterone levels (8); this second effect may be persuasive when counseling teenage male athletes against marijuana use. Marijuana use is illegal and is banned by the NCAA. National and international sports federations test athletes for marijuana use on a discretionary basis.

Cocaine. This stimulant was isolated in the mid-1800s. Although soldiers in the late 1800s used it to decrease fatigue, its current use is primarily recreational. An estimated 3 million persons in the United States were cocaine users in 1991. Its basic pharmacologic effect is an increased synaptic concentration of dopamine, and its use is reinforced and mediated through dopamine pleasure receptors (8). Cocaine is more addictive than amphetamine, and withdrawal produces fatigue, lack of motivation, and depression. Positron-emission tomography studies of cocaine users have demonstrated decreased glucose metabolism in the cerebral cortex and temporal lobe during cocaine use and rebound increases to above-normal levels upon withdrawal (14,15).

Cocaine is notable for distorting the user's perception of reality; for example, an athlete may perceive increased performance and decreased fatigue in the face of actual decreased performance in both strength and endurance activities. Cocaine produces a catecholamine-induced as well as a direct negative effect on glycogenolysis, which affects athletic performance. Its more important adverse effects include paranoid psychosis, seizures, hypertension-related CNS bleeding in the presence of vascular malformations, coronary artery vasoconstriction and myocardial toxicity leading to arrhythmias and ischemia, and sudden death (14,15). Cocaine use, including its use as a local anesthetic, is banned by both the NCAA and the IOC.

Methylenedioxymethamphetamine (ecstasy, MDMA, XTC). MDMA results from substitutions on the aromatic nucleus of amphetamine, which diminish the agent's stimulant effects and increase its hallucinogenic effects (7,8) It is closely related to 2,3- and 3,4-methylenedioxyamphetamine (MDA), also known as the "love drug," hence the common phrase "to have sex with X[TC]." Whether it offers any benefits as a stimulant in sports is unknown. Recreational use may be revealed by amphetamine drug testing.

Prescription Drugs

Anabolic steroids. The metabolic and hormonal effects of anabolic steroids will not be addressed here, but there are significant psychological effects that deserve brief mention. While lacking controlled studies, the literature is full of case reports and case series describing depression, suicidal ideation, psychosis, delirium, mania, aggression, and homicidal behavior as a consequence of anabolic steroid use. The mechanisms of these effects are unclear, but probably involve neurotransmitter receptor systems in such areas as the amygdala (16).

Benzodiazepines. The first benzodiazepine (BZD), chlordiazepoxide hydrochloride, was patented in 1959 and the second, diazepam, in 1963. Today at least 39 BZDs are available for prescription. These drugs block the release of acetylcholine (much as alcohol does) and decrease the turnover of norepinephrine, particularly during periods of stress, producing sedative, hypnotic, anticonvulsant, and muscle relaxant effects (8). The primary anxiolytic effect is mediated through gamma-aminobutyric acid (GABA). BZDs and GABA enhance each other's binding to GABA receptors, resulting in a decreased release of serotonin. The muscle relaxation effects are mediated at the spinal cord level, but other effects are mediated at the cerebral cortex. BZDs are often used to relax muscles following an injury, such as a lumbosacral strain, but there is no evidence that they have an effect on specific muscles, only a CNS-mediated relaxation effect. BZDs alter sleep by increasing total time asleep, reducing sleep latency, and decreasing total time in rapid-eye-movement (REM) sleep; however, the number of REM cycles is increased, resulting in more dreams. Conversely, BZD withdrawal often results in nightmares or bizarre dreams.

The half-life of all BZDs and their metabolites is 6 to 20 hours or more. (This includes flurazepam hydrochloride, which is metabolized to the active metabolite N-desalkylflurazepam and is often suggested, incorrectly, to have short-acting, no-hangover properties.) BZDs are sometimes used by athletes as a sleep aid, particularly during travel to competitions to prevent jet lag, but the predictable morning-after hangover results in a prolonged reaction time and dulled senses (4). These drugs have been promoted by athletes and coaches as a substitute for alcohol in shooting (in the modern pentathlon and biathlon). Their use is banned by some sports federations and by the US Olympic Committee (USOC), although not specifically by the IOC. Their use is absolutely contraindicated for underwater divers.

Gamma-aminobutyric acid (GABA). This substance is widely available in natural food and health catalogs and is rumored to be used for its anxiolytic effect, but little more is known because of inadequate testing methods. GABA receptors are a major mediator of anxiety and depressive disorders and are functionally associated with BZD binding sites, as noted above. BZD binding is enhanced by GABA such that there is a functional, although not an anatomical, relationship between BZD and GABA receptors (8). Plasma and cortical GABA levels are low in intractable depression, but the effects of exogenous GABA are unknown.

Narcotics. Narcotics are used primarily to relieve pain and to enable an athlete to compete despite painful injuries. They have no ergogenic effect on exercise tolerance or VO2 max. Narcotics that are banned, including morphine and meperidine, are banned because they impair judgment and hence the ability to perceive dangerous situations (14,15). Codeine, dihydrocodeine bitartrate, and dextromethorphan hydrobromide are not currently banned by the USOC (codeine was a banned substance until 1994) (6). Narcotic analgesics (other than heroin) are not banned by the NCAA, but since one of the metabolites of codeine is morphine, a positive drug test is possible. The recent highly publicized treatment of pro football quarterback Brett Favre for hydrocodone bitartrate addiction and reports of the ready availability of unlimited quantities of addictive narcotics in team locker rooms and training facilities suggest the extent to which these drugs have become a part of athletic culture.

Beta-adrenergic agents. Clenbuterol is the most notorious of the beta-adrenergic agents, which have been found to have anabolic properties. Several studies of laboratory animals and livestock have demonstrated marked increases (13% to 65%) in muscle mass with clenbuterol as well as with several other long-acting beta-agonists (7). These anabolic effects are not mediated through testosterone, growth hormone, or insulin. Beta-adrenergic agents are illicitly used to maintain anabolic effects after steroid use is discontinued; their potency is approximately 25% of that of anabolic steroids. They also enhance lipid metabolism, increase lipolysis, decrease fat deposition, and increase lean body mass and the lean-to-fat ratio.

Clenbuterol has the longest half-life of all the commonly available beta-agonists (35 hours, compared with 5 hours for albuterol sulfate) and is considered to be the most potent by athletes (7). A long half-life may be necessary to produce an anabolic effect, but human studies have shown a 14% to 18% increase in hamstring and quadriceps muscle strength at oral albuterol dosages of 8 mg twice a day (a dose at which most humans have significant side effects). Side effects of clenbuterol are the expected ones for a beta-agonist: tachycardia, palpitations, muscle tension, headache, and dizziness.

Beta-adrenergic agents are most commonly used therapeutically in inhaled form to treat asthma. Approximately 10% to 15% of athletes at most levels of competition have exercise-induced bronchospasm, and an additional few have more severe inflammatory forms of asthma. The use of all beta-adrenergic agents in inhaled form was permitted by the IOC until 1992, when the anabolic properties of these drugs were quantified. At that time, all long-acting inhaled and oral forms, including clenbuterol (available only in Europe and for veterinary use) and salmeterol xinafoate, were banned by the IOC and were classified as "stimulants" and "other anabolic agents." Inhaled albuterol and terbutaline sulfate are permitted by the IOC after approval subject to verified medical indication. Use of salmeterol in inhaled form also is now permitted by the IOC, since studies have demonstrated a negligible anabolic effect (6,17). Clenbuterol was banned by the NCAA in 1993 as an "anabolic steroid," but all other long-acting beta-adrenergic agents are permitted by the NCAA in inhaled form; oral forms are banned as "stimulants." The NCAA allows the use of theophylline and cromolyn.

Beta-adrenergic antagonists (beta-blockers). Beta-blockers are commonly used to treat hypertension, angina, arrhythmias, migraine headache, and anxiety and are frequently given after myocardial infarction. Their central anxiolytic effect occurs in direct proportion to their lipophilic binding, but their propensity to cross the blood-brain barrier also contributes to CNS-mediated side effects such as nightmares, depression, insomnia, and fatigue (8).

Beta-blockers have no effect on strength or power, but they reduce available energy by decreasing insulin release, glycogenolysis, and lipolysis. Their inotropic and chronotropic effects, ie, decreased heart rate, stroke volume, cardiac output, and VO2 max, are undesirable for endurance athletes. Beta-blockers can markedly reduce catecholamine-mediated palpitations, tremor, flushing, and diarrhea (13,15). Metoprolol tartrate use has been associated with a 13% improvement in shooting, the greatest effect being observed for the best shooters (3). Beta-blockers were originally banned by the IOC in 120215, but this restriction was subsequently eased and now affects only those sports for which enhanced performance is likely, including archery, shooting (the only sport listed by the NCAA), fencing, equestrian events, biathlon and modern pentathlon (because of the shooting event), bobsled, luge, diving, synchronized swimming, and ski-jumping.

Beta-blockers are commonly used to reduce performance anxiety in musicians, teachers, and business executives, although reports are mostly anecdotal, with a recommendation for a short-acting, low-dose preparation, such as propranolol hydrochloride 10 to 20 mg. In a double-blind, controlled crossover comparison of 40 mg nadolol and 2 mg diazepam, the measured psychological anxiety was the same with both medications, but technical performance was better with nadolol due to an attenuation of the expected increase in heart rate and tremor. Diazepam resulted in a deterioration of performance (18).

Methylphenidate hydrochloride and related amphetamines. Methylphenidate hydrochloride is one of several structurally related amphetamines; its increased use in the treatment of patients who have attention deficit hyperactivity disorder (ADHD) has made it the amphetamine that most physicians encounter most often.

Amphetamine was synthesized in 1920 and was initially used as a nasal decongestant. It was commonly used to reduce fatigue and to increase alertness in soldiers during World War II. Amphetamine use has been shown to increase the speed of learning new tasks and to increase physical energy, confidence, and ambition on a short-term basis. At least four mechanisms of action have been proposed: enhanced release and reduced re-uptake of dopamine, norepinephrine, or serotonin, leading to enhanced neurotransmitter agonist activity; and monoamine oxidase inhibition (8). Amphetamines are highly addictive, particularly when absorbed through mucosal surfaces. High school students are known to use sublingual absorption to enhance the stimulant effect of methylphenidate.

Amphetamines are not known to enhance athletic performance, but enhanced confidence and aggression (possibly on a placebo basis) may lead to a 1% to 2% increase in short-term power activities. At elite levels of competition, such an improvement may be significant. Athletes who use amphetamines may be able to tolerate a longer period of anaerobic metabolism, although credible data on this effect are not available.

Of greatest importance are the serious, and sometimes fatal, side effects of amphetamine use, such as heatstroke due to shunting of blood away from the skin. A more common problem is impaired judgment, which may cause the athlete to participate while injured, possibly leading to worse injuries and putting others at risk. Amphetamines are banned by both the IOC and the NCAA, although the NCAA does permit the use of methylphenidate for ADHD if this need is documented. The practical implementation of this exception has yet to be fully assessed because of the imprecision of ADHD diagnosis and the theoretical possibility that methylphenidate prescribed for legitimate purposes may be used inappropriately.

Tricyclic antidepressants (TCAs). Imipramine, the first TCA, was developed for the treatment of psychotic agitation (8). All TCAs inhibit the neuronal uptake of norepinephrine and serotonin to various degrees. These drugs are most effective in the treatment of severe, melancholic, major depressive disorder, particularly with psychomotor agitation (because of its neuroleptic origins) and postpsychotic depression. They are also effective for obsessive-compulsive disorder (eg, clomipramine hydrochloride), panic disorder, generalized anxiety disorder, and posttraumatic stress disorder.

Most TCAs (particularly amitriptyline hydrochloride) produce numerous side effects relating to multiple receptor systems; each drug in the class causes various degrees of antihistaminic, antimuscarinic, alpha-adrenergic-antagonistic, and anticholinergic effects. Tricyclic antidepressants reduce cardiac capacity and increase the risk of arrhythmias as a result of quinidine-like effects, such as QT prolongation. Some studies have demonstrated increased running or swimming time to exhaustion in rats given imipramine hydrochloride or desipramine hydrochloride. The side effects of TCAs, particularly cardiac conduction abnormalities, preclude their use by athletes with clinical depression. These drugs are banned by the IOC only for athletes in shooting events (including the modern pentathlon and biathlon) because of their anxiolytic effects.

Fenfluramine hydrochloride. This is a serotonergic agent recently approved for the long-term treatment of obesity. It is chemically related to amphetamines but has a minimal stimulant effect and a low potential for abuse. This drug appeals to athletes such as gymnasts, wrestlers, and rowers because of its anorexigenic effect. Fenfluramine is not currently banned by any athletic organization or federation.

Selective serotonin reuptake inhibitors (SSRIs). An SSRI is the first-line medication used to treat most patients with depression in the United States. Fluoxetine hydrochloride, with over $2 billion in annual sales, is the most frequently prescribed antidepressant (19). This class of psychiatric drug was the first designed with specific predetermined criteria in mind. SSRIs have a nearly exclusive effect on neuronal uptake of serotonin and minimal to no effect on the receptor systems affected by TCAs.

SSRIs produce numerous but relatively minor side effects, including nausea, headache, diarrhea, dyspepsia, agitation, and tremulousness. Sexual dysfunction is the most troublesome side effect for many patients. The relative lack of serious side effects makes an SSRI a better choice than a TCA for the treatment of clinical depression in athletes. These drugs can produce ergogenic effects, including prolonged running time to exhaustion, decreased central fatigue, and enhanced motivation and self-esteem, which may improve training and performance (20,21) These drugs are banned by the IOC for shooting sports (including modern pentathlon and biathlon) because of their anxiolytic effects.

Clinical Implications

Psychoactive drug use among young athletes often results from these drugs' perceived, and sometimes actual, enhancement of performance. The use of many psychoactive drugs is regulated or banned by national and international sports federations, which does provide a deterrent effect. Primary care physicians must be mindful of both deliberate and unintentional psychoactive drug use among their young athletic patients and the potential for serious or life-threatening complications related to this use.


  1. Forman ES, Dekker AH, Javors JR, et al: High-risk behaviors in teenage male athletes. Clin J Sport Med 1995;5(1):36-42
  2. Kokotailo PK, Henry BC, Koscik RE, et al: Substance use and other health risk behaviors in collegiate athletes. Clin J Sport Med 1996;6(3):183-189
  3. Nattiv A, Puffer JC: Lifestyles and health risks of collegiate athletes. J Fam Pract 1991;33(6):585-590
  4. Constantinou D: Ergolytic and harmful drugs in sport. S Afr J Sports Med 1995;Jun:10-14
  5. Powles AC: The effect of drugs on the cardiovascular response to exercise. Med Sci Sports Exerc 120211; 13(4):252-258
  6. Fuentes RJ, Rosenberg JM, Davis A (eds): Athletic Drug Reference 1996. Durham, NC, Allen & Hanburys, Division of Glaxo Wellcome Inc, Clean Data, 1996
  7. Mottram DR (ed): Drugs in Sport. London, E&FN Spon, Chapman and Hall, 1996
  8. Schatzberg AF, Nemeroff CB (eds): The American Psychiatric Press Textbook of Psychopharmacology, ed 1. Washington DC, American Psychiatric Press, 1995
  9. Graham TE, Spriet LL: Caffeine and exercise performance. Sports Science Exchange (Gatorade Sports Science Institute) 1996;9:1-6
  10. Zwillich CW: Diseases of ventilatory control, in Kelly WK (ed): Textbook of Internal Medicine. Philadelphia, Lippincott, 120219
  11. Zhdanova IV, Wurtman RJ, Lynch HJ, et al: Sleep-inducing effects of low doses of melatonin ingested in the evening. Clin Pharmacol Ther 1995;57(5):552-558
  12. Laughlin GA, Loucks AB, Yen SS: Marked augmentation of nocturnal melatonin secretion in amenorrheic athletes, but not in cycling athletes: unaltered by opioidergic or dopaminergic blockade. J Clin Endocrinol Metab 1991;73(6):1321-1326
  13. Overman SJ, Terry T: Alcohol use and attitudes: a comparison of college athletes and nonathletes. J Drug Educ 1991;21(2):107-117.
  14. Jonas PA, Sickles T, Lombardo JA: Substance abuse. Clin Sports Med 1992;11(2):379-401
  15. Eichner ER: Ergolytic drugs in medicine and sports. Am J Med 1993; 94(2):205-211
  16. Brower KJ: Anabolic steroids: addictive, psychiatric and medical consequences. Am J Addiction 1992;1: 100-114
  17. Brukner P: Drugs in Sport. Canberra, Australia, Sports Medicine Australia, 1995
  18. James I, Savage I: Beneficial effect of nadolol on anxiety-induced disturbances of performance in musicians: a comparison with diazepam and placebo. Am Heart J 120214;108(4 pt 2):1150-1155
  19. Olfson M, Klerman GL: Trends in prescription of antidepressants by office-based psychiatrists. Am J Psychiatry 1993;150(4):571-577
  20. Bailey SP, Davis JM, Ahlborn EN: Effect of increased brain serotonergic activity on endurance performance in the rat. Acta Physiol Scand 1992;145(1):75-76
  21. Kramer PD: Listening to Prozac. New York City, Viking, 1993

Dr Schwenk is professor and chair in the Department of Family Practice at the University of Michigan Medical School in Ann Arbor. He is a fellow of the American College of Sports Medicine. Address correspondence to Thomas L. Schwenk, MD, Department of Family Practice, University of Michigan Medical Center, 1018 Fuller St, Ann Arbor, MI 48109.