Training to induce muscle growth produces two types of pain. The first is the pain felt during actual exercise, caused by an increase in lactic acid resulting from anaerobic metabolic reactions in muscle. The other type of pain is delayed-onset muscle soreness. It usually becomes apparent about a day after training and is most associated with eccentric, or negative, repetitions, which involve a lengthening of muscle and are known to cause the most extensive muscle fiber damage.
Other types of training-related pain, often chronic, are linked to injuries, such as joint or tendon pain. They’re commonly treated immediately by application of the RICE technique, an acronym for rest, ice, compression and elevation. Acute pain requires the use of some kind of pain-killing drug, the most popular of which are aspirin; nonsteroidal anti-inflammatory drugs (NSAIDs), meaning that they don’t contain any anti-inflammatory steroids, such as cortisol; and acetaminophen, commonly sold under trade names such as Tylenol.
Both aspirin and NSAIDs work by inhibiting the activity of enzymes that convert fatty acids into prostaglandins. The prostaglandins, which are part of a larger group of fat-derived substances called eicosanoids, have both inflammatory and anti-inflammatory functions. Analgesic drugs target the inflammatory prostaglandins, which markedly reduces pain.
The problem with that approach is that it’s a shotgun technique’not only are the prostaglandins associated with pain reduced but so too are some benefical prostaglandins, such as those that protect the lining of the gastrointestinal tract from irritation. Other prostaglandins offer protection for the kidneys, which explains why long-term use of even aspirin can lead to kidney damage or failure if regularly taken in large doses.
Another little-known function of prostaglandins is the role they play in muscle growth. That information leaked out about two years ago via some Internet articles written by a self-styled drug guru. The mysterious expert reported that the latest secret drug being used by pro bodybuilders was prostaglandin injections. While the drugs were normally used only to promote lactation and pregnancy in cows, some research did show they also appeared to be involved in muscle hypertrophy.
Based on such studies, would-be bodybuilders seeking localized muscle growth were advised to somehow obtain the drugs, then inject them in stubborn muscle groups. As a side benefit the drugs would also obliterate any fat cells hanging around in the area. When I queried a few well-known and successful pro bodybuilders, none knew anything about it, although all expressed an interest in trying it. Those who did, however, quickly abandoned it, since the injections were extremely painful and produced a host of nasty side effects, including nausea. It was clearly an idea that worked on paper but didn’t fare well in the real world.
The one unquestionable aspect is that certain prostaglandins are involved in the muscular-growth process. The question is, If prostaglandins are needed for promoting muscle growth, what happens if you use pain-killing drugs that may inhibit or block anabolic prostaglandin activity?
We can get a good idea from a forthcoming study.1 It focused on the effects of two popular over-the-counter analgesics, ibuprofen (Advil, Motrin and so on) and acetaminophen (Tylenol) on muscle protein synthesis following high-intensity eccentric weight training, which is the most damaging type of exercise. The study involved 24 men who were assigned to one of three groups, which received 1) ibuprofen, 1,200 milligrams daily divided into three doses’the maximum OTC dose; 2) acetaminophen, the maximal dose of 4,000 milligrams, also divided into three doses; or 3) a placebo. Acetaminophen is thought to kill pain through a different mechanism from either aspirin or NSAIDs, by somehow interacting with pain messages conveyed in the central nervous system. As such, it’s not supposed to affect prostaglandin metabolism.
But the study found that while those in the placebo group showed a 76 percent increase in muscle protein synthesis 24 hours after the eccentric workout, the ibuprofen and acetaminophen groups had completely blocked muscle-protein-synthesis rates, although levels of muscle protein breakdown weren’t affected in any of the groups. Prostaglandin synthesis was blocked through enzyme inhibition induced by the drugs.
What does that mean? The researchers say, ‘We speculate that the continued attenuation of the normal increase in muscle protein synthesis after each resistance-training bout would result in a blunting of the hypertrophic response.’ In other words, using common analgesic drugs blocks muscle growth. They note that the long-term effect on muscle growth is unknown. Clearly the lesson here is to avoid habitually using the drugs unless you really need them, since they may interfere with your training progress.
Another study found that using acetylsalicylic acid, better known as aspirin, inhibited the release of pituitary hormones during exercise.2 That led to decreases in several hormones normally released as a result of exercise stress, including cortisol. The latter would constitute an anticatabolic effect. Beta-endorphin release was also blunted during exercise, which is paradoxical, since beta-endorphin is a natural analgesic substance made in the body.
Anabolic Steroids and Sex Drive
Anecdotal evidence indicates that anabolic steroids enhance sex drive in both men and women. That makes sense, since testosterone controls libido, or sex drive, in both sexes. But the situation regarding steroids and sexual function isn’t as clear-cut as it seems. Many other factors enter into the picture, particularly psychological ones. Someone once said that the sexiest organ in the human body is the brain because much of what constitutes successful sex depends on how and what you perceive. In short, hormones may set the stage, but the brain is the major actor in sex’along with the sex organs, of course.
Published medical research examining the effects of anabolic steroids on sexual drive and function is ambiguous. Complicating the picture is the fact that anabolic steroids, although all based on the basic testosterone structure, vary in their effects on sexuality. To put it in the vernacular, some drugs make you horny, and others have the opposite effect.
A study of rats illustrates this concept.3 The rats were given six anabolic steroid drugs, representing each of three different classes of steroids: 17-alpha oral drugs, such as methyltestosterone, methandrostenolone (Dianabol), stanozolol (Winstrol) and oxymetholone (Anadrol-50); the 19-nor drug nandrolone decanoate (Deca-Durabolin); and testosterone cypionate. The rats received the drugs in either high, medium or low doses for 12 weeks.
The results showed that high-dose regimens of all oral, or 17-alpha, drugs totally eliminated male sexual behavior in the rats. The injectable drugs (Deca and testosterone) had minimal effects on sexual behavior at any dose. When taken in low-to-medium doses, the oral drugs didn’t appear to adversely affect sexual function in the rodents. None of the drugs caused any other harmful effects on health, so it wasn’t a case of the rats getting sick and losing interest in sex.
It appears that anabolic steroids do affect sexual function in rats, but what applies to rats doesn’t necessarily apply to humans. In humans, as noted, sex isn’t dictated just by hormones; the brain and perception come into play. For example, if your hormones are raging and you encounter a potential sexual partner who turns you off in some way, you’ll likely not continue to have sexual thoughts about that person.
The human studies pertaining to the effect of anabolic steroids on sexual function are paradoxical; some reported a heightened libido, while others found sexual dysfunction induced by steroids. As you might expect, the greater the dose of steroids, the greater the risk of interference with sexual function. Some athletes who’ve used steroids report an initial increase in sex drive, followed by a loss of interest in sex later in the steroid cycle. Those side effects usually recede when you stop using steroids, but some cases of sex problems have lasted a year or longer.
One study reported that in athletes who stopped using steroids, 20 percent experienced a notable decrease in sex drive. On the other hand, other studies show increased sex drive and sexual activity in men using steroids. Studies involving the use of testosterone injections as a male contraceptive show that it appears to increase levels of sexual desire and arousal but not frequency of sexual behavior. In short, the men thought about it more than they did it.
Another thing to consider is that athletes who use anabolic steroids usually take several at once. Such regimens may include both oral and injectable drugs. Since steroids vary in their effects on sexual function in men, some steroids may cancel the libido-lowering effects of others.
Age comes into play too. Another study involving rats found that teenage rats had increased sex drive with steroid usage as well as a quick return to normal when they were off the drug.4 In older rats, however, the same doses of steroids led to permanent loss of cells in the portion of the testes where testosterone is synthesized. In cases of testosterone deficiency, which can occur in older men, testosterone injections can remarkably increase a lagging libido.
What about women? Testosterone is the hormonal arbiter of libido in both sexes. Recently, it became evident that many women lack sufficient testosterone, which is expressed as a lack of interest in sex. Providing them with judicious amounts of testosterone’but not enough to cause masculinizing effects’restores sagging sex drives.
One study sought to determine how long it took women to respond to a sublingual testosterone supplement.5 To speed things along, the subjects watched a few porn films. Although plasma testosterone levels peaked in only 15 minutes, dropping to baseline by 90 minutes, the women showed evidence of sexual arousal only 4 1/2 hours later. On the other hand, the study used genital arousal as a means of determining libido. In fact, under the right conditions, the women may have responded far sooner. Let’s face it: If women actually took an average of 4 1/2 hours to become sexually aroused, we all would have lost interest eons ago.
Based on the confusing evidence published thus far, we can conjecture that using anabolic steroids will increase sex drive in both sexes, but using too large a dose for too long will likely result in a loss of sexual interest. In some cases that may be an extended effect’and I’m not talking about particular organs here.ALL References
1 Trappe, T.A., et al. (2002). Effect of ibuprofen and acetaminophen on postexercise muscle protein synthesis. J Applied Physiol. In press.
2 Di Luigi, L., et al. (2001). Acetylsalicyclic acid inhibits the pituitary response to exercise-related stress in humans. Med Sci Sports Exer. 33:2029-2035.
3 Clark, A.S., et al. (1997). Anabolic-androgenic steroid effects on the sexual behavior of intact male rats. Hormones and Behavior. 31:35-46.
4 Feinberg, M.J., et al. (1997). The effect of anabolic-androgenic steroids on sexual behavior and reproductive tissues in male rats. Physio Behav. 62:23-30.
5 Tuiten, A., et al. (2000). Time course of effects of testosterone administration on sexual arousal in women. Arch Gen Psychiatry. 57:149-153.
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