Friday, September 28, 2012

Arginine Prior to Training by Jerry Brainum

I always wonder what people are thinking when they eat a full meal immediately before training. Ostensibly, they’re providing energy for the ensuing training session. Of course, food must be digested before it can provide energy or nutrients. Also, exercise profoundly affects the digestive process. Research has shown that high-intensity exercise delays gastric emptying, likely because the exercised muscles get preference for the available blood supply. In other words, food or drink just sits in the stomach for the duration of the training session.
    There are, however, exceptions to the rule. A sports drink containing no more than 7 percent carbohydrate, along with electrolyte minerals such as potassium, magnesium and sodium, is absorbed even faster than plain water. What about amino acids, which are already in their elemental form for uptake into the body?
     That’s a highly relevant question, because many protein or amino acid supplements touted for bodybuilding come with suggestions to take immediately before training. A study presented at the 2006 meeting of the American College of Sports Medicine (ACSM) charted the fate of arginine taken at rest and prior to an intense training session.
     Nine men, average age 27, who fasted for 10 hours before the study measurements, took either a placebo or arginine tablets (50 milligrams per kilogram of bodyweight, or 4,500 milligrams for a 200-pound man) with 400 grams of water. The drinks were taken at rest or just before engaging in a 60-minute weight-training program. The treatment was repeated four times, with a seven-day interval between treatments.
Blood levels of arginine increased after arginine intake both during rest and before exercise. Peak levels occurred after one hour in the rest group but were delayed by the exercise for an additional hour. Clearly, taking amino acids just prior to training leads to delayed absorption of the amino acids, just like anything else.

Mero, A., et al. (2006). Acute effect of strength exercise on plasma arginine after oral ingestion of arginine in men. Med Sci Sports Exerc. 38:S339-S440.


 ©,2012, Jerry Brainum.Any reprinting in any type of media, including electronic and foreign is expressly prohibited.


 Have you been ripped off by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com

 
 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 

Saturday, September 22, 2012

Arnold’s Heart and Other Tales of Woe by Jerry Brainum

On June 9, 2007, Kris Dim collapsed while training in a gym. The 34-year-old professional bodybuilder underwent immediate emergency surgery. He’d suffered a stroke due to an aortic dissection—that is, the large artery in the heart literally split. Since the aorta delivers blood pumped from the left ventricle of the heart to the pulmonary and all other arteries in the body, a sudden breakdown of the vessel would compromise blood flow—explaining why Dim passed out. Two types of aortic dissection are known: Type A involves the ascending aorta, which requires surgical repair. Type B involves the descending aorta, which can be treated with drugs, such as beta-blockers.
      Dim was lucky. Rapid surgery saved his life. Others with the same condition, such as actor John Ritter, comedienne Lucille Ball and Olympic volleyballer Flo Hyman, weren’t as fortunate. They died from complications of aortic dissection. Last year a 21-year-old University of Toledo basketball player succumbed to aortic dissection. Michael DeBakey, the renowned Texas heart surgeon who devised the surgical procedure for Type A in 1955, fell victim to it himself and was the oldest person to undergo surgery (his own) at age 97 in 2006. Untreated aortic dissection has a 50 percent mortality rate in the first 24 hours. Studies show that two in every 10,000 people have the condition.
      Initial rumors circulated, especially on the Internet, that Dim’s condition was related to his using anabolic drugs. After all, he was a pro bodybuilder—it seemed likely that he used steroids extensively.
Whether Dim used steroids had zero relationship to what happened to him. Although one study compared athletes who use anabolic steroids with drug-free athletes and found increased aortic stiffness in the drug users,1 several reports in the medical literature suggest that merely lifting weights could predispose people with structural deficits in their aorta to a dissection. For example, an aneurysm is a local weakness in the aortic wall. Those who train regularly with heavy weights temporarily raise their blood pressure to extreme levels, which enlarges the aorta. Some doctors don’t agree that an enlarged aorta is a risk factor; however, since connective tissue stiffens with age, people 40 or older who have the condition—or risk factors for it—need to be careful. Doctors have suggested screening would-be weightlifters via echocardiogram, which measures heart rhythm.
     Having high blood pressure may cause aortic dissection in some people, as can intense chest trauma. Most such cases occur in those aged 50 to 70. Using cocaine is a definite risk factor for aortic dissection because cocaine elevates blood pressure. Yet any type of strenuous exercise—even sneezing—may precipitate aortic dissection in a susceptible person. In 2005, researchers from the University of Texas Medical School found that having a genetic mutation in transforming growth factor beta receptor-2 predisposes a person to aortic dissection.
     One susceptibility that could result in aortic dissection is a bicuspid aortic valve. Normal aortic valves are tricuspid, having three cusps, or flaps, but 1 to 2 percent of the population are born with only two cusps. It’s the most common cardiac structural abnormality. One person in this category was none other than Arnold Schwarzenegger.
     In April 1997, Arnold underwent surgery to replace his bicuspid aortic valve. “I never felt sick or had any symptoms at all,” he told the press, “but I knew that I would have to take care of this condition sooner or later.” Since Arnold’s name was almost synonymous with huge muscularity, it didn’t take long for the rumor mill to claim that the condition was the consequence of years of steroid abuse.
    According to standard medical texts, however, problems related to bicuspid aortic valve peak at age 40. Even insurance companies, which aren’t known to give anyone a break, don’t charge extra premiums for this congenital condition, which is four times more prevalent in males than females. As for the steroid connection, there was none. As Arnold noted, in many cases there are no symptoms associated with it. The condition is just considered a structural anomaly of the heart.
     The need for bicuspid aortic valve surgery arises when symptoms do surface. Aortic stenosis, or a narrowing of the aortic valve opening that limits blood flow, is often the result of calcium buildup in the valve over time—for example, the time it takes the body to reach middle age. (Arnold had his surgery at 49.) Aortic regurgitation, the name given to backflow of blood from the aorta into the left ventricle from which it just came because the valve doesn’t close all the way, is another aspect of stenosis. The worst-case scenario is aortic dissection.
     Surgical treatment for bicuspid aortic valve varies. One option is to use valves extracted from pigs; reports that Arnold had a pig valve replacement weren’t true. He opted for a homograft—that is, an organ donation. That type of replacement often lasts 15 to 20 years before it needs to be replaced. Other options are the Ross procedure, which replaces the defective valve with a pulmonary artery. The longest-lasting replacement is mechanical, made of synthetic material rather than body tissue, but that means lifelong use of anticoagulant drugs, which may be the reason Arnold didn’t go for it.
      Arnold’s fame also spawned reports that he was a cardiac invalid. He filed lawsuits against several publications and won them all. The important point was that Arnold’s condition was so benign that he never experienced symptoms during his entire bodybuilding career or most of his acting career. Since he’s publicly admitted using steroids when he competed, it seems clear that the drugs had no effect on his valve. Of course, he probably had no idea he had the condition at the time.
      A recent study confirmed that many athletes have the same condition but that it doesn’t interfere with their training or sport participation.2 Of the 2,273 athletes evaluated in sports ranging from basketball to soccer to tennis to cycling to swimming, 58, or 2.5 percent, had a bicuspid aortic valve. Among the 2.5 percent, nine had normal valve function, 47 had abnormal valve function with mild regurgitation, and two had moderate stenosis. Their ages ranged from eight to 60.
      Asymptomatic bicuspid aortic valve doesn’t show up during normal medical exams unless the doctor hears a faint heart murmur or click. That’s rare, which is why diagnosis depends on an echocardiogram. In any case, the odds of having it are low. Contrary to Internet B.S., anabolic drugs of any kind have no relation to the condition and won’t escalate symptoms.

                                                       Can Hormones Protect Your Brain?

     You hear so many bad things about testosterone and growth hormone that it’s easy to overlook what happens to bodies that don’t have them. Public prejudice is fueled by sensationalist reports in popular media. Anabolic-drug use by professional athletes, such as baseball players, leads the uninformed to believe that such drugs are no use to “normal” people.
     Nothing could be further from the truth, which is readily available in the medical literature. The following studies—none of which rated publication in the popular media—relate to preventing degenerative brain disorders.
     In one study mice that were injected with a protein called beta amyloid, a type of which is considered the root of Alzheimer’s disease,3 developed memory loss and confusion—exactly what occurs in Alzheimer’s patients. Some of the mice, however, got human growth hormone. The mice with induced Alzheimer’s experienced an increase in free radicals, toxic by-products of oxygen metabolism that destroy the neurons that produce acetylcholine, a neurotransmitter associated with memory and learning. In the mice that got GH, those effects were blocked. Human studies have demonstrated that those who are clinically deficient in GH suffer from accelerated brain degeneration.
     The prefrontal cortex is vital for guiding behavior, thinking and working memory. Damage to it—common with aging—can result in a failure to plan and organize behavior. It partly explains the frequent memory deficits (“Where are those keys?”) that start about age 40. The prefrontal cortex is sensitive to levels of norepinephrine, a catecholamine hormone also involved in fat oxidation. In the brain, moderate levels of norepinephrine bind to alpha-2 adrenergic receptors and improve prefrontal cortex function, which means alertness and memory retention.
     Since the brain also contains beta-adrenergic receptors, a new study tested the effects of the drug clenbuterol on brain function.4 Clenbuterol is normally prescribed as an asthma drug in Europe but was never approved for use in the United States. Since it is structurally similar to catecholamines, it binds to beta-2 adrenergic receptors in the body.
     Clenbuterol was directly injected into the brains of young and old rats that showed mental deficits linked to poor prefrontal cortex function. The drug was also supplied to monkeys. Previous studies have shown that clenbuterol selectively affects the amygdala and hippocampus, which have to do with emotions and memory.
The study found that clenbuterol increased brain function. While that points to possible therapeutic uses of clenbuterol in treating brain disorders, there are some problems. Bodybuilders use clenbuterol for muscle growth and fat loss, but it can also cause bone loss, which can lead to fractures in older people. Excess clenbuterol produces such side effects as heart arrhythmia, tremors and possibly heart attacks. Less well-known potential side effects are testicular damage and immune suppression. Even low-dose clen can damage heart muscle.
     The doses the monkeys got in the study were similar to what’s prescribed for asthma. That dose doesn’t cause cardiovascular problems, though it does induce transient tremors. The initial research looks promising, but further human studies are needed to clarify whether and how clenbuterol might be used to treat human brain disorders.
     A study that examined the impact of estrogen and insulinlike growth factor 1 in the brain indicates that they partner to protect the brain against the damaging effects of cortisol, a stress hormone that attacks the sections of the brain that govern learning and memory.5 That’s why long-term stress is considered a major cause of brain aging.
     IGF-1 rises in response to exercise and a high-protein diet, as well as in the presence of growth hormone. Estrogen is produced in much greater amounts in women than in men, and some researchers think that it helps preserve women’s brains. Estrogen has beneficial cardiovascular effects, such as maintenance of high-density-lipoprotein cholesterol, and possibly long-term brain protection, although that’s not as evident in men is as it is in women.

References
1 Kasikcioglu, E., et al. (2007). Aortic elastic properties in athletes using anabolic-androgenic steroids. Int J Cardiol. 114:132-134.
2 Stefani, S.L., et al. Bicuspid aortic valve in competitive athletes. Brit J Sports Med.2008;42:31-35
3 Ling, F.A., et al. (2007). Protective effect of recombinant human somatotropin on amyloid B-peptide induced learning and memory deficits in mice. Growth Hor IGF-1 Res. In press.
4 Ramos B.P., et al.). Beta-2 adrenergic agonist, clenbuterol, enhances working memory performance in aging animals. Neurobiol Aging.2008;7:1060-9.
5 Garcia-Segura, L.M., et al. (2007). Estradiol, insulin-like growth factor-1 and brain aging. Psychneuroendocrin. In press.

  
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
 

Have you been ripped off by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com

 
 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 

Friday, September 14, 2012

Fire in the Whole by Jerry Brainum


             Control Inflammation to Get Bigger, Stronger and Healther

The body responds to injuries, infections and irritations with inflammation. In an acute stage, inflammatory processes aid healing. Uncontrolled, or chronic inflammation, however, is the cornerstone of every major disease.
    Research shows that uncontrolled inflammation is the underlying cause of cardiovascular disease, cancer and asthma. Some diseases, such as arthritis, are obviously driven by inflammation. In others the effects of inflammation are more subtle but just as damaging. In Alzheimer’s disease inflammation leads to the gradual destruction of the brain.
     While cholesterol and saturated fat are often implicated as the main players in cardiovascular disease, the true villain is underlying inflammation. Some studies show that C-reactive protein, a general indicator of inflammation in the body, is a more reliable indicator of incipient cardiovascular disease than is blood cholesterol.
     Inflammatory responses involve several body systems, among them hormones and immune cells. The positive side of inflammation is that it sets the stage for the healing process, along with the eradication of invading pathologens like bacteria and viruses. Special proteins called cytokines signal immune cells like neutrophils and macrophages to migrate to sites of injury or damage, where they enable the body to keep the invasion localized and marshal a more focused defense.
Inflammation and Training

Inflammation has both good and bad effects on exercise. The muscle-growth process is initiated by exercise-induced injury. The body compensates for the injury by stepping up processes such as muscle protein synthesis, which leads to increases in muscle size and strength. As with any injury, the body’s initial response to exercise-induced muscle damage is localized inflammation. It’s a positive effect, as the arrival of neutrophils and other immune cells results in the clearance of debris and preparation of the damaged muscle for repair.
    Neutrophils are produced in bone marrow and circulate in the blood, where they represent 50 to 60 percent of circulating leukocytes—a.k.a. white blood cells. They constitute the first line of defense against infection. Neutrophils produce free radicals, which are used to kill invading bacteria. Unfortunately, it’s a shotgun approach in that free-radical release also damages the cell membranes of healthy tissue.
Neutrophils begin to appear at the site of muscle damage within an hour after the damage occurs. They can remain there for up to five days. They can gobble up excess debris in the damaged area—a process known as phagocytosis—and they produce proteases, or protein-digesting enzymes, that further degrade cellular debris produced by muscle damage.1 Meanwhile, the other immune cells that react to muscle inflammation, such as macrophages, release cytokines and help mop up the excess debris damage that would otherwise impair efficient muscle repair and regeneration.
     The effects of the initial immune responses are tempered and controlled by nitric oxide. Without nitric oxide, the free radicals that immune cells produce could damage healthy tissue, delaying the healing process.
The muscle damage exercise inflicts also breaks down the fatlike outer layer of muscle cells, which leads to the release of arachidonic acid, an omega-6 fatty acid found in meat and eggs. Arachidonic acid is the precursor of a number of inflammatory chemicals, such as prostaglandins. Cyclooxygenases, or COX enzymes, are required to convert the arachidonic acid into active prostaglandins—the substances responsible for most of the pain caused by inflammation.
     One prostaglandin, PGF2A, is involved in several aspects of postexercise muscle repair, including nitric oxide release and protein synthesis. The more damaging the exercise, the greater the release of PGF2A. So eccentric muscle contractions, which usually involve lowering weights, release more PGF2A because they damage the muscle more. Using over-the-counter painkillers, including aspirin and ibuprofen, appears to inhibit postexercise muscle repair because they inhibit the COX enzymes your body needs to convert arachidonic acid into PGF2A. Research supporting that conclusion, however, used doses of 2,400 milligrams of ibuprofen or higher, far more than what’s used routinely to treat pain. Most studies show that a 400-milligram dose—the amount typically used to treat acute pain—doesn’t interfere with PGF2A synthesis.

                           Who’s Inflamed?

     While a controlled amount of postexercise muscle inflammation fosters muscle repair and regeneration, too much slows muscle repair. Many older people are in a chronic state of inflammation, which leads to the release of substances, such as cytokines and cortisol, that are linked to muscle breakdown. If the process continues unabated, sarcopenia, or severe muscle loss, can result in frailty and weakness.
      A recent study, however, demonstrated that older people who took ibuprofen and similar drugs had a dramatic increase in muscle mass, almost as if they used anabolic steroids. How can that happen if the same painkillers interfere with muscle growth? Out-of-control inflammation has a catabolic effect on older people’s muscle because of excess cytokines and other inflammatory chemicals. Block the inflammation with drugs, and the muscles perk up rapidly.
     The obese are also affected by excess inflammation. While in the past fat tissue was thought to be inert—or merely a storage depot for excess energy—recent research shows that fat cells release more than 100 mostly inflammatory substances, collectively known as adipokines. In other words, people who are carrying excess bodyfat are in a chronic state of inflammation and are in a position to develop cancer, cardiovascular disease and diabetes.
      The worst is the deep-lying abdominal bodyfat. Known as visceral fat, it’s far more dangerous than fat found on the thighs or hips because it’s constantly being broken down and released. That means adipokines are constantly being released into the blood.
     Research shows that it’s harder for those who have excess bodyfat to build muscle. One reason is that they are releasing more free fatty acids into their blood. Excess blood fat stimulates a protein called nuclear factor beta, which in turn activates proinflammatory genes—a kind of double whammy of inflammation. Among the substances it activates, tissue necrosis factor alpha, or TNF-a, is particularly catabolic in muscle, which may partially explain why it’s so much harder for those who have too much bodyfat to build muscle.
      Exercise blunts the release of many inflammatory compounds, making exercise itself anti-inflammatory. On the other hand, moderate-to-low-intensity exercise (50 percent of maximum oxygen intake or less), such as mild walking, is inflammation-neutral.2 Exercise must therefore be of sufficient intensity to impart any anti-inflammatory benefits.
Inflammatory Compounds and Muscle

   Recent studies show that contracting muscle produces cytokines that act on muscle in ways different from what happens with other parts of the body. For example, a cytokine called interleukin-6 exerts inflammatory effects in most tissues of the body. In fact, it also works in concert with cortisol to break down muscle, an effect most often seen in older people. One study indicates that having an abundance of inflammatory markers, including interleukin-6, limits the body’s capacity for processing oxygen.3
Active people have less interleukin-6 and other inflammatory mediators. Older people, who have more interleukin-6 in their bodies, are more likely to have chronic inflammation as well.4
     One hypothesis is that overtraining sets in due to an excess release of interleukin-6.5 That appears to be more likely with extended endurance exercise rather than shorter bouts of high-intensity work, like bodybuilding training. In any case, interleukin-6 can penetrate the protective blood-brain barrier, and once in the brain, it triggers ACTH release, which in turn triggers the release of cortisol. Interleukin-6 in the brain also aids the synthesis of serotonin, leading to feelings of fatigue. Other triggers for excess interleukin-6 release are hypoglycemia, or low blood sugar, and dehydration.
    By and large, interleukin-6 is beneficial. It’s released directly within muscle as a result of muscular contraction. As with PGF2A, the extent of interleukin-6 release in muscle depends on the duration, intensity and mass involved in exercise.

6 The primary stimuli to interleukin-6 release in muscle are the following:

• Low muscle glycogen
• Intake of niacin, a B-complex vitamin
• Heat
In contrast, here are the factors that blunt interleukin-6 release:
 • Carbohydrate intake
• Antioxidant use
• Anti-inflammatory drugs, such as ibuprofen
• Moderate endurance exercise
     The same interleukin-6 that produces inflammatory effects in nonmuscle tissue has anti-inflammatory effects in muscle. For example, it blocks the release of inflammatory mediators such as TNF-a. TNF-a is also suspected of being an agent of insulin resistance, a precursor of diabetes. Exercise may protect against insulin resistance when a muscle contraction signals the release of interleukin-6. That may also help explain the 60 percent reduction in diabetes produced by weight training.
     Although the genes that produce interleukin-6 in muscle are silent at rest, activated only through intense muscle contraction, interleukin-6 also acts as an energy sensor. If you’re low on muscle glycogen, interleukin-6 released from muscle aids in the breakdown of bodyfat for energy.7 It works by activating a protein that helps your body use fat for energy and another protein that boosts glucose uptake into muscle. That helps account for why contracting muscle protects against insulin resistance—and diabetes—by releasing interleukin-6.
     A recent mouse study illustrates perhaps the most interesting effect related to bodybuilding and interleukin-6.8 It found that mice lacking the substance cannot develop larger muscles, even when they overload their muscles during exercise as weight-training humans do. Mice that produced interleukin-6 in their muscles, however, did increase muscle mass. The effect was traced to a stimulation of satellite cells, the major muscle repair cells, by interleukin-6.
     Still another muscle-produced cytokine or myokine is interleukin-15. Researchers observed a gradual rise in that substance after subjects lifted weights, with it peaking in 24 hours. In muscle, it produces potent anabolic effects and blocks muscle breakdown. It also appears to encourage bodyfat loss. No doubt interleukin-15 will emerge in the future as an “ergogenic aid” to building muscle and losing fat.
Controlling Bad Inflammation

   While controlled inflammation in muscle is helpful if you’re looking for mass gain and bodyfat loss, chronic overall inflammation is a harbinger of disability and mortality. There are several ways to temper the flames, the most important by far being to reduce excess bodyfat.9
    Eating a lot of trans fats is associated with higher concentrations of inflammatory chemicals in the body.10 Taking dietary antioxidants can neutralize much inflammation damage.11 One of the most efficient dietary supplements for reducing inflammation is fish oil. It increases a natural anti-inflammatory agent in the body called resolvin E1 and interferes with arachidonic acid’s production of inflammatory prostaglandins. Taking in too much omega-6 fatty acids, which are abundant in most vegetable oils, leads to excessive amounts of inflammatory prostaglandins and pain. Since omega-6 sources are already abundant in most people’s diets, stick with fish oil supplements and avoid the ones that contain omega-6s. For purposes of reducing out-of-control inflammation in the body, take 10 to 15 grams a day of fish oil in divided doses. Use liquid versions; trying to get that amount from capsules would mean swallowing 10 to 15 pills a day.
                                                 
                                                         References
1 Tidball, J.G. (2005). Inflammatory processes in muscle injury and repair. Am J Physiol Regul Integr Comp Physiol. 288:R345-R353.
2 Markovitch, D., et al. (2008). Acute moderate intensity exercise in middle-aged men has neither an anti nor pro-inflammatory effect. J Appl Physiol. In press.
3 Kallo, I.J., et al. (2007). Markers of inflammation are inversely associated with VO2 max in asymptomatic men. J App Physiol. 102:1374-1379.
4 Maggio, M., et al. (2006). Interleukin-6 in aging and chronic disase: A magnificent pathway.


  
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

Have you been ripped off by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com

 
 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 




Saturday, September 8, 2012

Get Off the Pot? by Jerry Brainum



Richard Lake (not his real name, for reasons that will soon be apparent) was a top professional bodybuilder in the mid to late ’60s. Although he did use anabolic steroids, he disavowed using most drugs later in his career—with one notable exception. Lake had a preworkout ritual that he claimed enabled him to train more intensely and concentrate more effectively throughout his training session.
     The secret source of his preworkout ritual became evident one day in the locker room of Gold’s Gym. The gym had a defunct sauna room, located in the back of the men’s locker room. It was the perfect place to engage in clandestine behavior, which was exactly what Lake wanted. What he couldn’t conceal, however, was the grassy fumes that diffused into the nearby gym floor.
      Lake smoked marijuana in that room—and not just a puff on one “joint,” either. No, Lake reveled in a marijuana orgy, losing his thoughts in the smoke that rose slowly toward the ceiling in his secret alcove. He would emerge in an hour or so and head directly to the gym floor, working out with no apparent sign of his activity.
      Although marijuana is illegal, many athletes, not just bodybuilders, regularly smoke weed as a means of relaxation and mind expansion. Erstwhile bodybuilding champion and current politician Arnold Schwarzenegger openly smoked a joint in the 1977 film “Pumping Iron.” In a 1989 interview with a Los Angeles Times reporter, Arnold noted, “We smoked pot once or twice a week before we went to the gym. Sometimes at parties someone would pass around a joint. It never interfered because it was so casual.” A long-held tenet of the drug culture is that marijuana emphasizes the mood you’re already in. Thus, if you feel good, you’ll feel even better after THC, the intoxicating component of pot, does its job on your brain.
Marijuana has always been considered relatively innocuous compared to other mind drugs, such as cocaine and heroin. Entire volumes have been written documenting its physiological effects, but few people are aware of its true effects on the body. Since this is a bodybuilding magazine, let’s examine the impact of marijuana relevant to bodybuilding and health.
Active Ingredients
       Known to botanists as Cannabis sativa, marijuana grows wild throughout the world in temperate climates. Analysis of the 100-species plant yields 460 compounds, of which 60 are cannabinoids. The only one to have psychoactive effects, however, is delta-9-THC, the ingredient that makes you feel high. Interestingly, not long ago scientists discovered nerve receptors in the brain that are specifically affected by THC, suggesting that the body produces its own natural form of the substance.
      In 1992 a cannibislike chemical was isolated from pig brain. It was made in the body from arachidonic acid, the precursor of other chemicals called prostaglandins, most of which cause inflammatory reactions. The substance was named anandamide, derived from the Sanskrit word for bliss.
      Different parts of the marijuana plant vary in THC content. The bracts, flowers and leaves have the most, while the stems, seeds and roots contain lesser amounts. The most concentrated form is hash oil, the distilled liquid resin of the female marijuana plant. It contains up to 65 percent THC, compared to the 1 to 3 percent found in the average joint. Street pot has gradually increased in potency through the years, and current versions are thought to be five to 10 times more potent than the stuff used to “turn on and tune in” in the ’60s. In the ’70s the average joint contained 10 milligrams of THC; today the average is 60 to 150 milligrams or more.
      When inhaled, THC is rapidly absorbed. Studies show its systemic bioavailability is about 18 percent, with heavier users absorbing more than casual smokers. Compare that to the mere 6 percent of oral uptake (as from a pill). The peak effects occur within 20 to 30 minutes and last for two to four hours.
THC circulates throughout the body and, being highly fat soluble, easily enters the brain. About 80 to 90 percent of an intravenous dose of THC is excreted from the body in five days, although metabolites remain detectable in urine for 10 days after a single dose and more than 20 days after chronic use. Due to its proclivity for storage in fatty tissues of the body, in some cases THC may take up to a month to be eliminated.
      How marijuana affects a person varies with individuals. A recent study funded by the United States National Institute on Drug Abuse involving identical twins found a genetic basis in whether you’ll find pot enjoyable. The effects can even vary in the same person.Users of the drug frequently describe a dreamy, relaxed state, in which they feel more in tune with their senses. You get a false sense of time—it appears to pass more slowly. Others, however, get what the drug culture of the ’60s used to call a “paranoid reaction,” characterized by panic and dread. Much depends on such factors as the user’s mood, expectations and personality.
      A 1970 medical review of marijuana described the following effects in a user of the drug:2
“Typically, the user feels a series of jittery ‘rushes’ soon after inhaling. A sense of relaxation and well-being follows. There is awareness of being intoxicated not unlike that produced by alcohol. The user becomes acutely conscious of certain stimuli to the extent that his whole attention is focused, immersed and at times lost with the sensory experience. In this state, jokes are funnier, misfortunes more poignant and human relations more deeply perceived.
“The appreciation of food, sex and, in particular, music is intensified. The user may believe that his thoughts are unusually profound (an impression rarely shared with observers). Paranoid thoughts and feelings of depersonalization have been reported by subjects and observed in the laboratory. Visual imagery is increased, and in larger doses, colors may shimmer and visual distortions occur. There are feelings of changed body proportion. Among the most striking perceptual changes is the subjective slowing of time.”
At least two effects rapidly occur in most people who smoke marijuana: The eyes redden, and the heart beats faster. The increased load on the heart tends to impede athletic performance, as shown in some studies. That’s because while pot speeds the heart, the cardiac stroke volume, or amount of blood pumped by the heart, decreases.3 One study showed that in men cycling against increasing workloads, pot decreased exercise performance.
      A recent case study reported on a 21-year-old man who suffered a heart attack, despite showing no apparent cardiac risk factors, other than drinking too much the night before. THC can cause vasospasms, or contractions, of blood vessels, particularly in the brain, that may predispose to stroke. The substance is also linked to causing heart rhythm disturbances secondary to increased release of catecholamines, such as epinephrine.
      The body’s amandamide promotes increased blood platelet activation. That, in turn, can result in the formation of a blood clot in the coronary arteries that is the most prevalent cause of heart attacks.
Those facts have led some researchers to suspect marijuana use as a factor in heart attacks with normal (not blocked) coronary arteries, which occurs in only 6 percent of heart attacks, but at a frequency of 10 percent in those under age 35.
      Another study showed a general decrement in standing steadiness, simple and complex reaction times, and other athletic skills in 161 men and women who took THC.5 Contrary to the beliefs of the bodybuilder described at the beginning of this article, pot, if anything, decreases training concentration and focus—an effect so potent that it can’t even be overcome with concomitant amphetamine use.6
     From a bodybuilding perspective, a crucial question is how smoking pot affects anabolic hormones, such as testosterone.
Marijuana and Hormones
      A brief report concerning the appearance of gynecomastia, or male breast development, in three male pot smokers published in 1972 sparked a number of subsequent studies that examined the relationship between marijuana use and testosterone levels.7 Gynecomastia, however, is not a common side effect of marijuana use.
      The condition is usually the result of an imbalance between testosterone and estrogen in men, with something increasing the latter. Various studies have shown that the active ingredients in pot don’t have any estrogenic activity; however, a recent study did find potent estrogenlike substances in the smoke emitted from a marijuana joint.
8 Since joints are inhaled deeper than cigarettes (which, by the way, also provide estrogenic compounds), you are getting a considerable estrogenic effect from smoking marijuana.

References
1 Jones, R. (1984). Marijuana: Health and treatment issues. Psychiatric Clinics of North America. 7:703.
2 Pillard, R.C. (1970). Marijuana. New England J Med. 283:294.
3 Tashkin, D.P. (1978). Cannibis: 1977 UCLA Conference. Annals of Internal Medicine. 89:539-549.
4 Caldicott, D.G., et al. (2005). Keep off the grass: Marijuana use and cardiovascular events. Eur J Emerg Med. 12:236-44.
5 Bird, K.D., et al. (1980). Intercannabinoid and cannabinoid-ethanol interactions and their effects on human performance. Psychopharmacology. 71:181-188.
6 Forney, R., et al. (1976). The combined effect of marijuana and dextroamphetamine. Ann NY Acad Sci. 281:162.
7 Harmon, J., et al. (1972). Gynecomastia in marijuana users. New England J Med. 287:936.
8 Lee, S.Y., et al. (2006). Estrogenic effects of marijuana smoke condensate and cannabinoid compounds. Toxicol Appl Pharmacol. 214:270-78.

©,2012, Jerry Brainum.Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

JERRY BRAINUM'S BOOK AT www.jerrybrainum.com