Steroids: Not Really All That Bad

/ Posted 02.04.2012
Whenever you hear or read anything about anabolic steroids, it’s almost always bad news.

Whenever you hear or read anything about anabolic steroids, it’s almost always bad news. The media have demonized them, leading the average person to believe that anabolic steroids have little medicinal or health value and are mainly a means for athletes to cheat their way to glory. You can’t turn to the typical medical doctor for answers, either. Most doctors have little or no actual experience with anabolic steroids. They are rare in most routine medical practices, and the fact that they’re Schedule III drugs means that any doctor who prescribes them can expect some government heat. About the only positive thing you hear about steroids relates to testosterone-replacement therapy for men who are clinically deficient in the hormone. Even there, however, most doctors are quick to suggest that it causes prostate cancer—despite the overwhelming evidence that being low in testosterone is what predisposes a man to the disease.

Anabolic steroids share characteristics with other drugs in that side effects are based on time and dosage. The longer you stay on the drugs and the higher the dose, the greater the chance of serious side effects. Most athletes who engage in high-dose steroid regimens do experience side effects, but they’re usually mild and transient and can include elevated liver enzymes, indicative of minor liver inflammation, and adverse changes in blood lipids, including a dramatic lowering of beneficial high-density-lipoprotein cholesterol in those who use oral steroids. Some bodybuilders have also experienced higher blood pressure while on the drugs. In rare instances the temporary side effects linked to steroids have led to severe outcomes, ranging from heart attacks to strokes. In most cases, though, any side effects recede when an athlete gets off the drugs.

Among the benefits cited by athletes who have used anabolic steroids are better exercise recovery and less fatigue during training. Indeed, some of the high-volume training routines favored by pro bodybuilders would be impossible without steroid help. Some studies have suggested that the mechanisms of increased exercise efficiency include a modification of metabolic enzymes; an increase in the size of mitochondria, cellular structures that are the site of both energy production and fat oxidation; and beneficial changes in muscle composition.

During training, more free radicals, also known as reactive oxygen species, are produced as a by-product of exercise intensity and greater oxygen intake. Interestingly, heightened free-radical production has both good and bad effects. Having fewer free radicals means increased muscle force production. Having more leads to muscle fatigue characterized by muscle contractile dysfunction.

Normally, the body compensates for increased free-radical production by boosting the activity of its innate neutralizing antioxidant systems, such as the enzymes superoxide dismutase and catalase. Free radicals themselves are just unpaired electrons but seeking to combine with other electrons. When that happens, they can seriously interfere with cellular function, particularly cell membranes.

While multiple sites in the cell can produce free radicals, the mitochondria, because they processes oxygen, are the primary source. Interestingly, testosterone and other anabolic steroids boost antioxidant cell defenses. In a new study, scientists sought to determine whether and how anabolic steroids could protect cells, especially mitochondria, against oxidative damage. It involved isolating mitochondria from the gastrocnemius muscle of both sedentary and acutely exercised rats. Some of the rats had been given the anabolic steroid stanozolol, trade name Winstrol, a drug popular with bodybuilders and other athletes. An injectable form of stanozolol led to the disqualification of Canadian track star Ben Johnson during the ’88 Summer Olympic Games in Seoul.

The study found that stanozolol did protect rat muscle mitochondria from the effects of increased oxidative damage during exercise. The reason was not an increase in antioxidant protection but rather a drop in mitochondrial free-radical production. That has interesting implications because loss of mitochondria is considered one of the primary causes of muscle aging and loss. If you could maintain mitochondria integrity with age, your muscles would age much more slowly, and as a result you’d maintain more muscle and strength.

How did Winstrol help protect mitochondria during exercise? The authors couldn’t isolate a precise mechanism, but they did offer a plausible theory. In the rats that exercised but weren’t given Winstrol, mitochondrial cell membranes had a marked increase in the DHA content. DHA stands for docosahexaenoic acid, one of two primary omega-3 fatty acids found in natural food sources, such as fatty fish and fish oil. The increased DHA in the mitochondrial membranes is thought to be stimulated by the greater release of catecholamines, such as epinephrine and norepinephrine, produced during exercise. Exercise can cause a 64 percent increase in the DHA in cell membranes.

Normally, DHA in cell membranes is a good thing. It keeps them fluid rather than stiff, as occurs when excess cholesterol is deposited in them. Having more membrane fluidity also increases interactions of cell receptors with their respective hormones. For example, it enables insulin to react more effectively with its cell receptors, which increases insulin sensitivity. The downside of having more DHA in the membranes is that as a highly polyunsaturated fat, it is prone to oxidation, which produces free radicals that, paradoxically, damage the cell membrane.

It turns out that giving rats a steroid such as Winstrol prevents the accumulation of DHA that would otherwise occur during exercise. That in turn means less chance of oxidation. The whole thing adds up to increased mitochondrial protection. How Winstrol does that is also not known, but it may involve modifying the actions of catecholamines, which as noted are the primary stimulus for increased DHA deposition in cell membranes.

So Winstrol—and probably all other anabolic steroids—may considerably support mitochondrial stability. That has broad implications for preventing muscle loss and maintaining a more youthful muscle function with the passing years. Based on those findings, should Winstrol and other steroids be considered antiaging drugs?

Another study involved an animal isolated-cell design, so its result may or may not be duplicated in human tissues. In any case, stanozolol has some properties that may overrule its use as an antiaging drug. For one thing, the oral version can cause liver problems if used for too long or at too high a dose. As a DHT-derivative, stanozolol can lead to male-pattern baldness, acne and prostate problems. Then there’s that lowering of protective HDL, which can predispose users to cardiovascular disease.

Stanozolol is also effective at blocking cortisol, a catabolic hormone. While that produces greater anabolic activity, when you get off stanozolol, either oral or injectable, you get a rebound cortisol effect that can lead to muscle loss. When on stanozolol, you’ll feel more joint pain because of its interference with cortisol’s anti-inflammatory properties.

Still, the new rat study’s findings about stanozolol’s mitochondrial protection are intriguing. I doubt you’ll read about it in the popular media, since anything positive about anabolic steroids doesn’t seem to sell.

Editor’s note: Jerry Brainum has been an exercise and nutrition researcher and journalist for more than 25 years. He’s worked with pro bodybuilders as well as many Olympic and professional athletes. To get his new e-book, Natural Anabolics—Nutrients, Compounds and Supplements That Can Accelerate Muscle Growth Without Drugs, visit www.JerryBrainum.comIM

References

Saborido, A., et al. (2011). Stanozolol treatment decreases the mitochondrial ROS generation and oxidative stress induced by acute exercise in rat skeletal muscle. J Appl Physiol. 110(3):661-9.


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