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Muscle Destruction From Steroids

Several cases of exercise- or drug-related rhabdomyolysis in long-distance runners, football players and military personnel have been reported in the medical literature.


www.ironmanmagazine.comAnabolic steroids are synthetic, structurally modified versions of testosterone. They are termed “anabolics” because they provoke reactions in muscle and other tissues that result in either growth or stabilization of the tissues. Anabolic steroids have legitimate medical uses, such as preventing excessive tissue breakdown. Athletic use of steroids, however, is far more publicized than their medical applications. Bodybuilders and other athletes who use anabolic steroids often self-medicate with dosages far above what medical treatment requires. In line with the adage “Only the dose determines the poison,” those using large doses of steroids or several of the drugs simultaneously can be subject to systemic side effects: liver problems, negative changes in blood lipids and heart structure, fluid retention, gynecomastia in males, virilism in women, inhibition of testosterone production and possible adverse behavioral changes in susceptible individuals.

While all of those side effects are possible in theory, in reality they rarely occur. Athletes monitor themselves for adverse effects, although rarely under the care of a physician. They use other drugs to mitigate some of the side effects of large doses, such as estrogen-blocking drugs to prevent estrogen-related side effects.

Idiosyncratic reactions, however, are always possible. That means some steroid users experience unusual or rare side effects. Why that happens is unknown but probably has something to do with genetics or individual susceptibility. One recent case study illustrates the point.

A 39-year-old previously healthy amateur bodybuilder reported to an emergency room with excruciating pain and inability to move his right shoulder after an injection of steroids in that shoulder, which was followed by a shoulder workout on the same day.1 He trained five days a week and had done so for the previous eight years. For the past seven years he had also used anabolic steroids. Deploying a 23-gauge needle and sterile technique, he injected steroids into his shoulder four times a week. He denied doing any type of abrupt overstretching exercise that could have caused a severe muscle strain.

The physical exam showed that his right deltoid was swollen and tense, with the skin around it red, tender and warm. He had no apparent bruising and no fever. The picture became clearer when blood tests revealed a creatine kinase enzyme level of 18,200—normal is below 195. Creatine kinase is an enzyme that adds a phosphate to creatine in muscle, thereby helping the muscle store creatine. When muscle is damaged, even with intense exercise, CK is released from the muscle into the blood. Having large amounts of it in the blood point to severe muscle damage. Because the bodybuilder’s blood potassium, also released by damaged muscle, was high, the diagnosis was rhabdomyolysis, which means massive muscle destruction.

Rhabdomyolysis can have several causes, among them toxic reactions, lack of blood flow to muscle, infections and inflammation. One type, which is called exertional rhabdomyolysis, occurs when muscle cells are damaged by unaccustomed exercise. For example, untrained persons who exercise in hot, humid weather can develop it, but it can also occur in well-trained athletes. Switching to a new mode of intense training without preparation can bring it on. A few cases have occurred in bodybuilders who abruptly began high-rep—100 reps or more per set—training regimens, particularly in hot weather without drinking adequate fluids.

Destruction of the muscle cell membrane causes the leakage of intramuscular materials, such as CK, minerals and other enzymes. In severe cases myoglobin, the oxygen-carrying protein in muscle, is also released in large amounts and can crystallize in the kidneys. That blocks the kidneys’ filtering units and rapidly induces kidney failure. Without immediate treatment, death follows.

Several cases of exercise- or drug-related rhabdomyolysis in long-distance runners, football players and military personnel have been reported in the medical literature. One published case study involved a 25-year-old male professional dancer who showed up at a hospital complaining about severe thigh and calf pain.2 The pain began after he engaged in a 45-minute aerobic workout on a cross-training machine. He experienced severe muscle cramps and a day later showed up at the hospital. He was given an anti-inflammatory drug but returned two days later, still in severe pain. Tests revealed a high CK level, which led to a diagnosis of rhabdomyolysis. He received intravenous fluids and buffers such as potassium bicarbonate to alkalinize his blood and prevent myoglobin precipitation in the kidneys. He received cortisone to relieve inflammation, Valium to relax his muscles and Tylenol for pain.

The dancer had used two steroid drugs, Winstrol and Primabolan, four ampoules each a week apart. Before his pain set in, he’d used only one ampoule of Primobolan a few days before, injecting it into his thigh. His treatment proved successful, and he was released from the hospital.

Reports involving bodybuilders have been sporadic and may have been written off as severe muscle strains. One 40-year-old bodybuilder who initially denied using any anabolic steroid or other drugs suffered rhabdomyolysis in his biceps. In fact, he’d also injected Winstrol into the affected shoulder, leading the attending physicians to suspect that the injection itself had caused the localized rhabdomyolysis. The doctors suggested that he might have had a toxic reaction to the drug—a not unwarranted assumption, as most forms of injectable Winstrol are veterinary versions not subject to the same quality control as drugs slated for human use. A more likely possibility is that the bodybuilder had a compartment syndrome, the name given to a swelling of the fascia that surrounds muscle. Usually occurring in the calf, it’s rare in the shoulders because of the higher mobility of the shoulder and its attendant fascia. Only three previous cases were reported in the medical literature, and they involved drug overdoses or intoxication after minor trauma.

The analysis was that the bodybuilder suffered increased compartment syndrome due to the injected fluid, causing a blood clot, which decreased the elasticity in the shoulder fascia. Compounded by the bodybuilder’s growing shoulder muscle mass, those factors increased the intracompartmental pressure. The shoulder workout that followed amplified the effect of limited blood flow, which resulted in the characteristic muscle breakdown. His treatment proved successful, and he returned to normal training with no evidence of kidney problems.

How Nolvadex Really Works

Tamoxifen citrate, or Nolvadex, is used to treat breast cancer, particularly in older women who have estrogen-sensitive breast cancer; 70 to 80 percent of all breast cancers are estrogen-sensitive. For years it’s also been used by male bodybuilders on anabolic steroids to help prevent gynecomastia, or the formation of male breast tissue.

Gyno is caused by an imbalance between estrogen and testosterone, favoring increased estrogen. The steroid drugs convert into estrogen through the actions of aromatase, an enzyme found throughout the body. The usual practice for preventing estrogen-related side effects, which include excess water and fat retention, is to take drugs that either interfere with aromatase activity, such as Arimidex, or block estrogen cell receptors, such as Nolvadex.

Nolvadex is the older of the two “estrogen solutions,” and most athletes looking to lower estrogen now rely on aromatase-inhibitors because of the notion that they’re more reliable in diminishing estrogen. Nolvadex is also thought to interfere with the activity of growth hormone and its anabolic product, insulinlike growth factor 1. On the other hand, lowering estrogen too much, which is possible with extended use of aromatase inhibitors, may interfere with the anabolic reactions involving androgen receptors and testosterone.

Nolvadex is structurally similar to estrogen and can bind to estrogen cell receptors, thereby blocking estrogen from binding to them. If estrogen cannot interact with its cellular receptors, it cannot exert biological activity and becomes inert. Nolvadex also interferes with the negative feedback signal sent by circulating estrogen in the blood to the pituitary gland. That results in blunting release of gonadatropins, including luteinizing hormone, which controls testosterone synthesis at the Leydig cells in the testes. The reduced estrogen-feedback signal induced by Nolvadex results in greater release of luteinizing hormone and higher blood testosterone. One author has noted that using 20 milligrams of Nolvadex daily—a standard bodybuilding dose—can raise blood testosterone by 150 percent. On the other hand, Nolvadex has both agonist and antagonist properties. That is, when used in high doses for extended times, it may act more like an estrogen agonist. Animal studies show that extended use of Nolvadex interferes with the activity of two testicular enzymes involved in testosterone synthesis, although that hasn’t been confirmed in human studies.

What’s interesting about Nolvadex is that recent research that directly compared it to the newer and supposedly more effective aromatase-inhibiting drugs found that Nolvadex appears to be more effective in preventing gynecomastia and other estrogen-related effects in men. How can that be?

A study presented at a scientific conference related to breast cancer research may provide the answer. Researchers from the famed Mayo Clinic explained that Nolvadex isn’t active but is rather like a pro-hormone. In the liver, enzymes convert Nolvadex into two metabolites that are the effective versions of the drug, endoxifen and 4-hydroxytamoxifen. The study sought to explain why using Nolvadex helps some women with breast cancer but not in others. The researchers found that an enzyme system in the liver called CYP2D6 must convert Nolvadex into its active metabolites in order for the drug to work. In some women that system isn’t as active, which means that they don’t convert the Nolvadex into its most active metabolite, endoxifen. For them Nolvadex doesn’t effectively treat breast cancer.

Most surprising, however, was the finding that endoxifen didn’t just block the estrogen cell receptor, as was previously supposed, but actually degraded it. No receptor means no estrogen cell activity. So drug researchers are now at work producing a direct endoxifen drug, since that’s the actual active form of Nolvadex. The direct form won’t depend on liver enzymes to become active.

While this study involved in vitro, or isolated-cell, protocols, there is no reason to believe that the results don’t apply to men. The findings explain why Nolvadex works better in preventing estrogen-related side effects in some men more than others. In addition, the fact that this active metabolite of Nolvadex actually degrades estrogen receptors explains why the head-to-head studies comparing Nolvadex to aromatase inhibitors showed Nolvadex to be superior in preventing estrogen-related side effects in men. A notable bonus: Nolvadex is far less expensive than most aromatase inhibitors.

References

1 Farkash, U., et al. (2009). Rhabdomyolysis of the deltoid muscle in a bodybuilder using anabolic-androgenic steroids: A case report. J Athlet Training. 44:98-100.

2 Adamson, R., et al. (2005). Anabolic steroid-induced rhabdomyolysis. Hosp Med. 66:362.

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