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Bodybuilding Pharmacology: The Case of the Fainting Bodybuilder

In late fall, 1998, a 36-year-old bodybuilder walked into a local hospital emergency room after fainting twice at home. During one episode he fell on his face, causing a deep cut that required stitches. While in the emergency room he fainted again but rec

In late fall, 1998, a 36-year-old bodybuilder walked into a local hospital emergency room after fainting twice at home. During one episode he fell on his face, causing a deep cut that required stitches. While in the emergency room he fainted again but recovered in a few seconds. As it turned out, he wasn’t having a seizure but was instead experiencing a type of heart rhythm disturbance called atrial fibrillation. The atria are the two uppermost chambers of the heart, and during fibrillation the atrial portion of the heart beats chaotically.

The bodybuilder told attending doctors that he’d had a few fainting spells in his teens, especially under stressful conditions. At the time he walked into the hospital, he was taking the anabolic steroid Dianabol, five milligrams four times daily. He’d also recently started using another drug at night called bromocriptine (trade name Parlodel) at a dose of 2.5 milligrams. He’d missed his evening meal that night but had taken the Parlodel anyway. He had no apparent cardiac risk factors and no family history of heart disease.

According to the attending doctors, the man had passed out repeatedly due to a combination of a very strict diet and his having taken Parlodel while in a fasting state. Some believe that Parlodel is an effective drug for fat-burning purposes, despite a dearth of evidence to prove it. Parlodel works by inhibiting the release of a posterior pituitary gland hormone called prolactin, which initiates the lactation process in women and is often prescribed to prevent lactation. It’s also used to treat Parkinson’s disease and acromegaly, which is characterized by an excessive secretion of growth hormone, usually caused by a small tumor in the pituitary gland. Parlodel would decrease GH release, making it a dubious drug at best for fat loss.

The fainting bodybuilder was treated and released with no further episodes of either fainting or atrial fibrillation.1 Despite warnings from doctors, however, he not only continued taking anabolic steroids but also added growth hormone and insulin to his drug regimen.

While the atrial fibrillation in his case appeared to result from a combination of Parlodel and a strict diet, another report links it entirely to anabolic steroid use.2 The bodybuilder in this case was 22 years old, with no history of any health problems. He didn’t use any medications, didn’t drink alcohol, didn’t smoke and said he didn’t use drugs. Despite his denial, the sharp-eyed examining physicians noted that he had pronounced gynecomastia and was muscular at 6’2′, 265 pounds. He’d walked into the emergency room complaining of a ‘funny feeling’ in his chest, along with excessive sweating, weakness, anxiety and shortness of breath.

After the doctors gave him antianxiety drugs to reduce his sweating and anxiety, the bodybuilder relaxed enough to admit to using a weekly steroid stack consisting of the following:

‘200 milligrams of testosterone cypionate
‘200 milligrams of Extrabolin Decanoate (a Greek brand of nandrolone decanoate, or Deca-Durabolin)
‘120 milligrams of Winstrol

He’d used that regimen each Tuesday and Friday for the five weeks before the symptoms began. He was discharged from the hospital two days later with no signs of any symptoms. To prevent any problems related to his diagnosed atrial fibrillation, the doctors gave him the drug Inderal, a beta-blocker that eases cardiac workload, and a tablet of aspirin a day. The aspirin was likely included to prevent any chance of strokes, since atrial fibrillation is a known risk factor for them. Ten weeks after he was discharged from the hospital, he was again training five days a week, had lost 18 pounds and was drug-free’or so he said.

Why would anabolic steroids precipitate an episode of atrial fibrillation in an otherwise healthy young bodybuilder? One possibility involves the adverse changes in thyroid hormone status induced by steroids. Steroids can reduce the level of a protein that binds with thyroid hormone in the blood. While that doesn’t produce overt thyroid disease, it does increase the level of active, or free, thyroid hormone. The increased thyroid hormone can then overstimulate the heart, resulting in atrial fibrillation.

In a worst-case scenario atrial fibrillation can lead to a wandering blood clot that lodges in the lungs, known as a pulmonary embolism. Some cases of steroid-associated deaths have been linked to that. Older people who acquire atrial fibrillation, often as a by-product of chronic high blood pressure, are usually prescribed anticlotting drugs such as Coumadin. Aspirin also helps in that regard.

A more recent report, however, casts doubt on anabolic steroids as a direct cause of atrial fibrillation in athletes.3 It involved a 35-year-old powerlifting champion who was dubbed ‘the World’s Strongest Man.’ At 5’9′ he weighed 245 pounds. His lifts included a 1,030-pound record squat. Prior examination had shown that the man had the greatest degree of left ventricle wall thickness yet measured’the inner wall of his left ventricle, the pumping chamber of the heart, had hypertrophied far beyond normal dimensions.

He also showed atrial fibrillation, which was attributed to his greatly enlarged left ventricle wall. The left ventricle had grown that large due to years of blood pressure spikes caused by heavy lifting. Even though he’d used anabolic steroids for more than a decade, the powerlifter’s enlarged heart was a more likely cause of his heart problem. The steroids in his case were merely contributing factors. His heart had actually exceeded the upper limit of size, causing the abnormal heart rhythms.

The Case of the Disappearing Pituitary Gland

Most hormones in the body work by a negative-feedback mechanism. The body attempts to maintain a state of homeostasis and detects use of any exogenous, or out-of-the-body, hormones or chemicals. It responds by slowing down its own production of hormones, and if the exogenous hormones exceed a certain level, hormone synthesis and release are cut off completely.

When that happens, the affected gland may shrink or atrophy, since it’s not getting the stimulating hormone from the brain’s pituitary gland that directs glandular synthesis of hormones. An example is what happens when large doses of testosterone are injected over an extended time. The brain’s hypothalamus detects the larger-than-usual amount of testosterone in the blood and responds by not secreting gonadotrophic-releasing hormone (GRH). GRH normally travels in the brain’s special blood system to the pituitary gland, which responds by synthesizing and secreting luteinizing hormone (LH). LH then travels in the blood to the testes, where it regulates the synthesis of testosterone in a series of enzymatic steps. While the alphabet soup of hormones may be a bit complex, the net effect is clear: Glands that aren’t stimulated regularly by them shrink or atrophy. If they aren’t resuscitated in time, a permanent deficiency of hormones could result, requiring the person to use hormone drugs just to maintain normal health.

The master gland of the body is the pituitary gland, located in the brain just behind the top of the nose. While the pituitary gland is under the control of the brain’s hypothalamus, another gland structure that monitors constant changes in the internal environment of the body, it’s the pituitary that produces the tropins that govern the direct release of hormones from glandular structures in the body. Included in this system are hormones from the testes (testosterone) and thyroid gland. The pituitary gland releases growth hormone, which itself is regulated by a feedback system.

That raises a question: If the pituitary gland is the master gland and hormones work through a negative feedback system, how would taking large amounts of drugs such as anabolic steroids, growth hormone and thyroid drugs over long periods affect the pituitary gland?

One clue comes from the case of a 39-year-old competitive bodybuilder who was 5’11’ and weighed 285 pounds.4 Although he was healthy and had no overt medical symptoms, he and his wife had attempted to conceive a child 18 times with no success. That led him to a medical clinic for a fertility checkup, which found a high level of prolactin, a pituitary hormone usually associated with lactation in women and impotence in men. The doctors ruled out a tumor that could cause excessive prolactin secretion.

When questioned, the bodybuilder revealed that he had trained an average of 90 minutes a day, five days a week for the past 20 years. He’d used anabolic steroids intermittently for 17 years, using them consistently for the past four years. He’d also added growth hormone and thyroid hormone during the past two years. The precise medications he took were as follows:

‘ Ibuprofen (a nonsteroidal anti-inflammatory) to treat joint pain, 200 milligrams, twice daily
‘ Testosterone enanthate, 600 milligrams weekly
‘ Oxymetholone (Anadrol-50), 25 milligrams once daily
‘ Nandrolone decanoate (Deca-Durabolin), 400 milligrams weekly
‘ Methandrostenolone (Dianabol), 30 milligrams daily
‘ Humatrope (growth hormone), eight units daily
‘ Cytomel (T3 thyroid drug), 25 micrograms daily

The most remarkable finding occurred during a magnetic resonance imaging test of his brain, when it was noted that he had an atrophied pituitary gland, a condition medically known as ‘partial empty sella syndrome,’ since that’s the area of the brain where the pituitary gland is located. Testosterone can lead to pituitary atrophy through the negative-feedback effect described above. The condition is also a normal anatomic variant in 9 percent of the population. Besides hormonal mechanisms, the condition can occur with age, with increased intracranial pressure and through means that remain unknown.

The doctors who examined the bodybuilder suggest that his shrunken pituitary gland may have been caused by either his long-term hormone use or an increased intracranial pressure that occurs intermittently during heavy training. It may increase pressure within the head enough to literally flatten the pituitary gland. That last hypothesis is speculative’and it had better be. Otherwise it doesn’t bode well for anyone who engages in long-term heavy lifting.

The more likely cause was the bodybuilder’s long-term drug use, especially considering that he stayed on hefty doses of various anabolic drugs for four years straight. Anyone on a regimen like that would expect to pay some kind of price’wouldn’t he?

1 Manoharan, G., et al. (2002). Syncopal episodes in a young amateur bodybuilder. Br J Sports Med. 36:67-68.
2 Sullivan, M.L., et al. (1999). Atrial fibrillation and anabolic steroids. J Emergency Med. 17:851-857.
3 Qualls, E.J., et al. (2001). Surpassing the upper limits of physiologic concentric left ventricular hypertrophy: atrial fibrillation in an elite power athlete. Int J Cardiology. 81:275-276.
4 Dickerman, R.D., et al. (2001). Secondary partial empty sella syndrome in an elite bodybuilder. Neurol Res. 23:336-338.

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