It amazes me how often creatine is blamed for various athletic problems. These problems range from dehydration to severe muscle cramps. This is true despite the fact that numerous, well-controlled studies have shown that creatine is safe and is not the cause of these problems. The creatine hysteria peaked back in 1997, when three collegiate wrestlers who were otherwise healthy, abruptly died within a two month time frame. The actual cause of death of the wrestlers turned out to be severe dehydration and kidney failure. In an effort to make weight, the wrestlers had severely restricted their fluid intake, while also exercising vigorously in a hot environment and wearing heavy rubber exercise apparel. Several self-styled experts quickly accused creatine usage as the primary culprit behind the young wrestlers premature demise. But it turned out that there was no evidence that any of the dead wrestlers had used creatine. If anything, they likely avoided creatine shortly before their tragic deaths, because creatine is known to promote a certain level of water retention. And the wrestlers were doing everything they could to lose water.

In the latest incident, 19 high school football players from McMinnville High School in Oregon were afflicted with compartment syndrome, to the extent that most of them had to be hospitalized. Compartment syndrome is a swelling of the connective tissue or fascia that surrounds muscles. If the swelling becomes severe, it can choke off blood vessels, nerves, and destroy muscle tissue. One characteristic of this syndrome, besides pain, is an elevation of creatine kinase (CK), an enzyme found in muscle that functions to add a phosphate group to creatine, allowing the creatine to be stored in muscle. Whenever muscle is damaged, including heart muscle, CK is released into the blood. Normal levels of CK range form 200 to 2,000. The level found in the Oregon football players averaged 40,000. Since compartment syndrome is a relatively rare event in sports, the fact that 19 players on the same time all came down with it at the same time suggested that something was amiss. A finger had to be pointed somewhere, and creatine appeared to be a prominent suspect.

In fact, the players had engaged in a so-called “immersion camp,” that involved intensive pre-conditioning activity in the heat. None of the players had conditioned themselves to do high intensity exercise, much less in a hot environment. They started to complain about excessive swelling in their triceps after doing a series of push-ups and chair dips in a 30-second alternating series of reps over 20 minutes in a hot, humid wrestling room where temperatures averaged 115 to 120 degrees. If the athletes didn’t complete their rep goal, they had to start over again. In addition, they were not permitted to drink any water during the workout. All this is a classic scenario for the onset of rhabdomyolysis, or rapid destruction of muscle tissue. Rhabdo,as it’s often called, is linked to dehydration and unaccustomed exercise in a hot environment. One the primary signs of rhabdo is an extremely high release of CK into the blood. If not rapidly treated, release of a muscle iron pigment called myoglobin can jam up the kidneys, resulting in total kidney failure. There are several case studies on record of bodybuilders who suffered from rhabdo, often from trying a new intense style of training while dehydrated and in hot conditions.

In truth, none of the football players said they had used creatine prior to the disease incident. So why was creatine wrongly accused? My guess is that because creatine can promote water retention, it was thought that this caused the rapid onset of compartment syndrome in the athletes. Also, the fact that the CK levels were extremely high in the players, also pointed to creatine, since CK works with creatine in muscle. But the flaw in these suggestions is that most of the water retained by creatine is intracellular, not extracellular. Extracellular water retention can cause the familiar bloating effect, but that doesn’t happen with creatine. If anything, the extra “internal” water retention promoted by creatine would serve to prevent heat related illness, including rhabdo and the compartment syndrome. Besides, none the football players used creatine anyway. But a convenient scapegoat was needed. The truth of the matter is that the players became ill because of stupid training practices, such as doing unaccustomed intense exercise that they weren’t used to, along with not consuming any fluids. So don’t blame creatine, blame the moron coaches who pushed the players into becoming seriously ill.

Find out the truth about creatine and other popular sports supplements in my e-book, Natural Anabolics, available at jerrybrainum.com.

A long-standing tenet in bodybuilding is that if you want to promote muscular hypertrophy, or muscle size gains, you need to train heavy, using lower reps. Conversely, training with lighter weights will “tone” muscles, but isn’t effective for promoting gains in muscular size and strength. Much of this is based on a physiological principle called the Muscle fiber recruitment hierarchy. This principle states that the body activates only as many muscle fibers as possible to produce movement, beginning with the slow-twitch, or type-1 muscle fibers. As these fibers fatigue (and fatigue is the key word here, as we shall see), other muscle fibers, namely types 2-a and 2-b, also known as fast-twitch muscle fibers, are brought into play. What activates these fast-twitch fibers are neuromuscular connections. Simply put, when enough resistance is placed on the muscle, a signal is sent to the cerebellum section of the brain requesting more neural input to the muscle fibers in order to recruit the type-2 fibers. For years, it was thought that to recruit the type 2B muscle fibers required a greater neural input, and the best way to do this was to increase the intensity level of the imposed stress on the fibers. The best way to do this was to lift heavy. Indeed, most exercise physiology textbooks say that the fast-twitch type-2 muscle fibers are the fibers most amenable to gains in muscle size and strength. Type-1 slow-twitch fibers are more related to endurance, and would be activated with lower intensity exercise, such as when doing endurance activity, or when using lighter weights for higher reps. Again, it was thought that the body won’t recruit the type-2 fibers unless it was necessary. But note that the type-2 fibers can also be brought into play when the type-1 fibers become fatigued, for whatever reason.

Bodybuilders had larger muscles because of a selective hypertrophy of type 2B fast-twitch muscle fibers, and they achieved this through lifting heavy weights. But in recent years, this notion has come into question. As I reported in an Ironman magazine article a while ago, muscle biopsies of champion bodybuilders showed that they had a preponderance of type 2A fast-twitch muscle fibers, rather than the expected type 2B fibers. Type 2A fibers are considered an intermediate fiber, having characteristics of both type 1 and type 2 fibers. What this pointed to was that the typical bodybuilding workout of doing higher reps, averaging 8-12 per set, would likely produce better muscle gains compared to doing lower reps with heavier weight.While many powerlifters and Olympic weightlifters undeniably are strong, many don’t show the level of muscle hypertrophy that you would expect considering their chronic heavy lifting training routines, which usually involve heavy weights and low reps.

Occlusion training, which involves training with an impediment to blood flow, such as wearing an inflatable cuff while training, has been shown in several studies to produce significant gains in muscle size despite using light weights. Various reasons are offered to explain this effect, but the main mechanism seems to be an increase in localized fatigue products produced in the muscle as a result of the impeded blood flow. This increased fatigue, in turn, is interpreted by the brain as a call to recruit the type-2 muscle fibers, which result in the muscle gains apparent following this type of exercise. I also reported on another study, in which subjects lifted light weights, but under high tension, meaning that they did the exercises slower than normal, and forcefully contracted the trained muscles during every rep. Again, despite using weights only equivalent to 20% of one rep-maximum, which is very light, the subjects made gains in muscle size comparable to that achieved through lifting far heavier weights. The deciding factor here was again the level of local muscle fatigue produced in the trained muscle, which not only fully activated the type-2 fibers, but also promoted a greater release of anabolic hormones, such as growth hormone and IGF-1, which are stimulated by locallly produced muscle fatigue factors, such as increased lactic acid in the muscle.

In the latest study, 15 men, average age, 21, all of whom had at least 6 months of training experience, and had trained at least three times a week 6 months prior to the start of the study, did 4 sets of one-legged extensions using differing training protocols. These protocols were as follows:

1) 90% of one-rep maximum weight to failure (heavy weight)

2) 30% of one-rep maximum matched in reps and load to #1

3) 30% of one-rep maximum done to failure (light)

The scientists conducting the study calculated various rates of protein synthesis in the trained muscle, measuring both contractile protein synthesis and connective tissue or structural muscle protein synthesis. Increased muscle protein synthesis is directly related to increased gains in muscle size and strength, particularly the contractile proteins. The study results showed that the light weight to failure style (#3) was more effective at increasing muscle protein synthesis compared to #1, or high load, heavy weight. The light training to failure produced a level of muscle protein synthesis that was similar to that of the heavy load 4 hours after exercise, but it was sustained for 24 hours after training only in the light weight to failure training. The study authors suggest that the increased volume of training produced by the lighter weight to failure study resulted in more muscle fatigue, and more positively affected the amplitude of the muscle synthesis process. Only the #3 style of training produced sustained increases in the muscle protein synthesis rate of all proteins found in muscle: contractile, connective tissue, and mitochondrial. This means in simple terms that this style of training may be capable of increasing muscle size, strength, and even endurance simultaneously. The total number of completed reps was 94 in group #3; 19 in #1; and 62 in #2. The greater number of reps in #3 appeared to promote a greater activity of several muscle protein synthesis signaling factors. Group#3 also showed higher indicators of signaling factors for stimulation of muscle satellite cell activity, which is important for promoting muscle size and strength gains.

The authors suggest this information could be useful for prescribing exercise for those who are injured or too old to lift heavy weights.They point out that people over age 70 show an anabolic resistance to weight-training, meaning that they don’t show any significant increases in muscle protein synthesis following weight-training. This resistance,however, can be overcome by increasing the volume of exercise in the aged. This jives with the findings of this new study, which suggests that lifting lighter, but doing reps to muscle failure, is capable of fully turning on the muscle protein synthesis machinery of the body. The key is to induce enough fatigue in the muscle to kick-start the muscle protein synthesis reactions. And according to this study, it can be done by using lighter weights that feature higher reps to failure (reps in the study averaged 34 reps per set  in the light weight to failure sessions). I believe that a key element of these findings is that even in the light weight group, each set was done to muscular failure, no matter how many reps that took.  Just lifting light weights and not training to failure won’t do diddly squat in promoting muscle gains, since it won’t activate the muscle protein synthesis signaling factors that play a central role in producing muscle gains.

Burd, M, et al. Low-load high volume resistance exercise stimulates muscle protein synthesis more than high-load low volume resistance exercise in young men.Plus One 2010;5:e12033.

Learn the truth about various anabolic supplements in my e-book, Natural Anabolics, available at jerrybrainum.com.

Studies continue to be published attesting to the value of beta alanine as an effective ergogenic aid for increasing both training and athletic performance. Beta alanine is an amino acid, and when combined with another amino acid, histidine, it forms the core of carnosine. The significance of carnosine is that it’s a potent antioxidant, and also acts as a primary intramuscular buffer. What this means is that carnosine helps lower elevated acid levels that accrue in muscle following intense exertion, including exercise. Increased acid interferes with the activity of enzymes involved in energy production, so lowering acid levels in muscle would increase athletic performance.

While carnosine is available in supplement form, it’s only marginally effective in boosting intramuscular carnosine levels. A ubiquitous enzyme called carnosinase breaks down most of the ingested carnosine into its constituent beta alanine and histidine forms. But research shows that using supplemental beta alanine at dose of 4 to 6 grams a day does boost intramuscular carnosine as much as 64%. Although hard-training athletes tend to have naturally higher muscle carnosine levels as a result of regular training, these levels still increase when they use supplemental beta alanine.

The typical effects of beta alanine (BA) supplementation is evident by the results of a new study. The study involved 18 high level rowers who used BA for 7 weeks at a dose of 5 grams a day. Other rowers ingested a placebo for the same amount of time. Before and after supplementation, muscle carnosine levels were measured, and performance was evaluated in a 2000 meter ergometer test. The baseline test showed a strong correlation between muscle carnosine levels in the rowers and speed at various distances. After the BA supplementation, carnosine content increased by 45.3% in the soleus muscle (slow-twitch) and 28.2% in the gastrocnemius muscle (fast-twitch). Performance testing also showed that the BA group was 4.3 seconds faster than the placebo group. Prior to BA, they were 0.3 seconds slower. Muscle carnosine levels was positively correlated to 2000 meter rowing performance. As such, carnosine was able to increase speed in these elite athletes. Strength wasn’t measured in the study, although prior studies suggest that BA usage may increase muscle endurance, along with the ability to boost training intensity levels due to less muscle fatigue. What it all points to is that unlike many other sports supplements, BA is the real deal.

Baguet A, et al. Important role of carnosine in rowing performance. J Appl Physiol 2010;in press.

To learn the scientific truth about various supplements, read my e-book, Natural Anabolics, available at jerrybrainum.com

It’s difficult for men to be treated for low testosterone levels for a number of reasons. This is true even for men with clinically proven low testosterone levels. The reasons for the reluctance of physicians to treat low testosterone levels in men has to do with the notion that testosterone levels are related to both the onset of prostate cancer, as well as adverse cardiovascular effects. I covered in depth the misinformation concerning the relationship of testosterone to prostate cancer in a recent article in Ironman, and interested readers should refer to that article for the truth about testosterone and prostate cancer onset. In relation to cardiovascular disease, a recent article published in the New England Journal of Medicine suggested that providing testosterone therapy to older men (average age, 74) could rapidly result in adverse cardiovascular outcomes, including increased incidence of both heart attacks and strokes. I also discuss this study and the actual effects of testosterone on heart function in an upcoming edition of my Bodybuilding Pharmacology column, also in Ironman.

While the relationship between testosterone replacement therapy (TRT) and cardiovascular disease (CVD)  is specious at best, there is one effect of testosterone that could cause problems in this area. This relates to a thickening of the blood, also known as polycythemia, that can occur when testosterone is provided, particularly in injectable form. For some reason, this side effect is more likely to happen in older men, who are the prime candidates for TRT. It usually occurs when the weekly dose of injectable testosterone exceeds 150 milligrams. The effect is evident by blood tests that reveal an increased hematocrit of the blood. Hematocrit is a measure of the viscosity, or thickness of the blood. Interestingly, one of the primary side effects of blood doping, which involves drug-based increases in the red blood cell content of the blood, is polycythemia. Ironically, when this happens, any athletic edge induced by the increased red blood cell count (which results in increased oxygen delivery to muscle, and therefore, increased endurance) is negated because the blood has now become too thick, which lowers oxygen delivery to tissues, inducing a relative hypoxic (lacking oxygen) state. Testosterone causes a type of natural blood doping because it stimulates the kidneys to produce increased levels of erythropoietin (EPO), which in synthetic form, is used for athletic blood doping. Since EPO works by boosting the synthesis of new red blood cells, it would appear that the higher levels of EPO released by testosterone adminstration could account for the increased blood thickness shown by older men who use injectable forms of testosterone. This is a problem because higher hematocrit levels are linked to increased onset of strokes and heart attacks due to increased clotting activity in the blood.

But a new study found the root cause of higher hematocrit levels in men who use injectable testosterone. The study included both younger (ages 19 to 35) and older (ages 59 to 75) men. These men were provided weekly injections of testosterone enanthate (a long-acting ester of testosterone) in varying doses of 25, 50, 125,300, and 600 milligrams over a course of 20 weeks. The men’s own testosterone production was purposely supressed by providing them with a drug that blocks the secretion of gonadatrophic releasing hormone (GRH), which controls testosterone production in the body. This was done to more precisely determine the effects of the testosterone injections. The men underwent blood tests 5 times over the course of the 20-week study. The study results showed that within one week of getting the testosterone injections at higher doses, a substance called hepcidin was markedly suppressed in the men. The effect was related to the dose of testosterone, and was more likely to occur with the higher doses, above 125 milligrams a week. It also was more pronounced in the older, compared to the younger men in the study, and corresponded to a rise in hemoglobin, or the oxygen-carrying protein in red blood cells. The study concluded that the rise in hematocrit or blood thickness, is related to the supression of hepcidin caused by high dose injectable testosterone. This is probably the most common side effect seen when older men use higher doses of injectable testosterone.

Hepcidin is a 25-amino acid peptide that is produced in the liver. It was discovered in 2000, and is now known to be the master regulator of iron metabolism in the body. It works by directly inhibiting another protein called ferroportin, which works to transport iron out of cells that store the mineral. Ferroportin is present mainly in the cells that line the small intestine, and in immune cells called macrophages. By interfering with the actions of ferroportin, hepcidin reduces iron absorption. When larger doses of injectable testosterone block hepcidin, more iron is released and absorbed into the body. This increased iron, in turn, leads to a greater production of red blood cells, and it is that greater amount of red blood cells that results in the thicker blood or polycythemia that can occur with the testosterone injections. One unanswered question is why this effect of thicker blood with higher dose testosterone injections is more prevalent in older men. One possibility is that older men have lower iron stores than younger men, and this changes when high dose testosterone is used. But that is strictly speculation on my part. The elevated hematocrit effect can be eliminated through either using alternative forms of TRT, such as testosterone creams or gels, or by injecting doses of testosterone that are 125 milligrams or less each week.

Bachman, E, et al. Testosterone suppresses hepcidin in men: A potential mechanism for testosterone-induced erythrocytosis. J Clin Endocrin Metab 2010: in press.

Want to learn the truth about bodybuilding nutrition? Read my book, Natural Anabolics. available at jerrybrainum.com.

Those of us who purchase eggs are offered three main choices: 1) organic eggs;2)free-range eggs, which are also often organic; 3) regular eggs. Organic eggs are often touted for their nutritional superiority over “normal” eggs. To qualify as organic, eggs must be derived from hens that are fed organic feed. Such hens are not allowed to be fed animal byproduct feed, or feed that is derived from genetically modified organisms (GMO) , often called “Frankenfood.” Organic hens are also never provided with antibiotics, except for emergency purposes, such as disease outbreaks. Another advantage of organic eggs is that the chickens that produce such eggs are treated far more humanly compared to eggs produced from chickens on so-called factory farms. In fact, a law was recently passed in California that now prohibits many of the cruel practices that were often used in such factory chicken production, such as crowding of hens in small boxes, and so on.Interestingly, lower stress in chickens actually produces eggs that are of superior quality. One way to reduce stress in chickens is to let them roam freely, rather than being constantly imprisoned in small boxes. The eggs produced by such free roaming birds are appropriately labeled “free range.”  To permit such roaming, small doors are installed on barns, allowing the birds to come and go as they please. On the other hand, one fact not often publisized is that male chicks born on organic or free-range farms are discarded and immediately killed by lethal gas because they don’t produce eggs. This fact tends to temper the otherwise human practices common on such farms.

In a new study conducted by researchers from the Agricultural Research Service, both conventional and organic eggs were accessed for quality, and no differences were found. The main difference between eggs was found between white and brown eggs. Brown eggs weighed more than white eggs, but white eggs  had a higher percentage of total solids and crude fat.  Other than that, there were no significant differences between the eggs. The study examined cage-free, traditional, free-roaming, pasteurized, nutritionally-enhanced, and fertile eggs. Specialty eggs, such as those labeled free-roaming, organic, and cage-free, as well as those that are nutritionally-enhanced, such as with omega-3 fatty acids, are considerably more expensive compared to traditional eggs. But this study says there is little or no differences between eggs. Should you pay extra for the specialty eggs?

I’ve seen other studies indicating that free-range eggs are nutritionally superior to traditional eggs, and those with nutritional enhancement show better balances of fats in the eggs, such as higher omega-3 fat levels. This could be important if you avoid eating fatty fish sources of omega-3, or refuse to take fish oil supplements. In addition, I buy free-range eggs because I’ve had the sad experience to research how chickens are treated on egg factory farms, and trust me when I say that such treatment falls way beyond the inhumane category. For that reason alone, I would continue to purchase free-range eggs. Now if we could just do something to spare those poor little male chicks on organic farms, that would be gratifying and humane, too.

Jones DR, et al. Physical quality and composition of retail eggs.Poultry Science 2010;89:in press.

Learn the truth about anabolic supplements in my e-book, Natural Anabolics, available at jerrybrainum.com.

Ah, the vicissitudes of life. You can be up one day, down the next, or as Forest Gump memorably noted,”Life is like a bunch of chocolates, you never know what you’re going to get next.” Take for example Lou Tellegen. What’s that? You never heard of Lou Tellegen? Perhaps you may recall some of his more notable films, such as The Things We love, or The Woman and the Puppet. Who can forget his performance in The Sporting Chance. You can be forgiven if you don’t recall these films, since they were made in 1918, 1920, and 1925 respectively. Tellegen is all but forgotten today, but he was the George Clooney of the silents, causing female hearts to swoon when Rudy Guguelmi, better known by his stage name of Rudolph Valentino, was working as a busboy and dancing for dollars in New York.

Tellegen was born as Isadore Louis Edmon Van Dommelen in Holland in 1881, the illegitimate progeny of a Dutch army lieutenant and his girlfriend. He made his stage debut in 1903, and developed enough of a following to the point where he was invited to perform on the Paris stage. But when he arrived in Paris, he got into a scrape with a woman, and wound up in prison. While trying to make it as an actor, he worked various odd jobs, including working the high trapeze in a circus. He was once jailed in Russia for selling pamphlets about birth control to women. One wonders if this was done in his own self-interest rather than any concern about overpopulation. After his short performance in the French penal system, a friend hooked him up with the biggest female star of her day, Sarah Bernhardt, with whom Tellegen soon developed a romantic relationship. He made his silent film debut along co-starring with Bernhardt in a 1910 French silent film. That same year, he traveled with Sarah to the United States, where the New York Times announced the impending marriage of Bernhardt and Tellegen, despite Bernhardt being  37 years his senior. He never married Bernhardt, but did marry a well-known opera star named Geraldine Farrar in 1916. The marriage lasted seven years, but Tellegen had previously been married to a countess for two years. He later married two more times, with both marriages also being short-lived.

Tellegen was a major star in the early silent films, most of the time playing a dashing leading man in intensely romantic films. But life took a turn for the worse for Tellegen when his face got severely burned in a fire. With the advent of “talkies,” Tellegen was out of a job, since his high, squeaky voice didn’t lend itself to the new talking pictures. He soon went into deep debt and bankruptcy. Tellegen, once a major

Lou Tellegen and Geraldine Farrar in happier times

star, was reduced to selling hot dogs at a stand located just outside of the studio where he made many of his popular films. Overnight, he was all but forgotten. Then he found out that he had cancer. That proved too much for Tellegen. On October 29, 1934, the 50-year-old former star locked himself into a bathroom at a house located near the fabled Hollywood and Vine streets. He then proceeded to shave and powder his face. The bathroom was lined with newspaper articles about his past theatrical triumphs. In front of a full-length mirror, Lou Tellegen performed his final dramatic scene as he plunged a pair of scissors into his chest seven times. When asked to comment on his death, wife #2, Geraldine Farrar replied,”Why should that interest me?” Three years earlier, Tellegen had published his autobiography, entitled,”Women Have Been Kind.” Dorothy Parker, a leading wit at the time, said that the book should have been called “Women have been kind–and dumb.”

Tellegen was cremated and his ashes were scattered at sea. But he’s made a comeback of sorts. Today he has a blog appearing on My Space. One can only wonder if he’s still ready for his close-up.

Few would argue that testosterone helps to build muscle. Proof of this exists throughout the existing medical literature. One study, for example, showed that when a drug that blocks the effects of testosterone were provided to young men involved in a weight-training program, the men immediately stopped making any gains in muscular size and strength. A more obvious effect of testosterone is evident in athletic performance, and in the appearance of competitive bodybuilders who use large doses of various anabolic steroid drugs, all of which are based on testosterone. One question that arises: can you build a significant amount of muscle without using anabolic steroids and other drugs? The answer to that question is admittedly ambiguous. While you can significantly increase the size and strength of muscles without resorting to drugs, the likelihood of achieving the look shown by most professional bodybuilders is beyond of the capability of the large majority of people who eschew anabolic drug usage.

But there is no getting around the fact that testosterone is still required to develop muscle. The main reason for this is that testosterone promotes muscle protein synthesis, which is the root mechanism in promoting gains in muscular size and strength. Men past 40 often notice that it’s far more difficult to both build and maintain muscle size. A primary reason for this is that testosterone levels begin a gradual nosedive starting around age 40. But there are other factors behind this loss of muscle size and strength with age. If the cause was only testosterone, simply using a bunch of anabolic steroids should be able to make a 60-year-old as muscular and as strong as a 25-year-old, but that just doesn’t happen. Other factors beyond the realm of testosterone come into play, such as the loss of type-2 fast twitch muscle fibers with age. This is significant because these are the muscle fibers most amenable to gains in size and strength. Taking oodles of anabolic steroids will have no effect whatsoever on restoring these fibers, although if taken in time, testosterone therapy will probably delay considerably the age-related loss of these fibers, especially if combined with regular weight-training.

A more controversial anabolic hormone is growth hormone. Similarly to testosterone, GH levels gradually decline, at an average rate of 14% per decade, starting around age 40. Until recently, the drop in GH with age was considered a primary reason for the changes in body composition common with aging, such as a loss of lean mass and a gain in bodyfat. But it turns out that while GH levels are important, they aren’t as critical to maintaining muscle mass as is testosterone. On the other hand, studies with older people who lack both GH and testosterone show that providing both hormones produces far more pronounced effects on muscle strength and bodyfat loss than when providing either hormone separately. The true player in promoting muscle gains is insulinlike growth factor-1 (IGF-1) produced in muscle as a result of exercise. IGF-1 is also produced in the liver as a result of stimulation by GH. But the systemic IGF-1 that results has little or no effect in promoting muscle gains, although it does impart other benefits, such as preservation of heart and brain cells with age. An important consideration here is that promoting testosterone release in the body also promotes the release of intramuscular IGF-1, and it’s this combination that provides the real anabolic effects of exercise. To be complete,however, you also must include insulin, since much of the loss of muscle with age is caused by a loss of muscle insulin insensitivity, which increases the catabolic effects, or breakdown of muscle with age.

All three anabolic hormones can be controlled with exercise. Simply working various muscles will increase insulin sensitivity. Training with minimal rest periods between sets (one minute or less) maximizes the output of GH, and secondarily muscle IGF-1. For boosting testosterone levels, you need to rest longer between sets. For this purpose, resting 90 seconds to two minutes between sets will boost testosterone levels, while not resting enough between sets negates any testosterone boost. The big debate among researchers is whether this exercise-induced hormonal boost actually does anything to help build muscle and strength. This is controversial because all anabolic hormones return to resting levels within 30 minutes after a workout. But even that problem can be overcome by ingesting essential amino acids before and after training. Another aspect to consider is that if you control cortisol levels during and after training, you will likely derive more benefit from the increased flow of anabolic hormones. Cortisol levels during training can be significantly lowered by sipping a drink containing 6% carbs. But this technique is only effective if your workout exceeds one hour.

Should you consider using any of the reputed “testosterone-boosting” supplements on the market?  I’ve never seen any scientific proof that any of these supplements do anything more than enrich the bank accounts of those selling them. If you do consider buying them, ask the company selling them for proof that these supplements significantly boost testosterone levels, and more importantly, increase muscle size and strength. Don’t accept anecdotal evidence, such as “we have many satisfied customers who say they have built tons of muscle using our supplement.” Such “evidence” is worthless, since users are highly susceptible to the placebo effect. In short, they make gains not because of the supplement, but because of their expectation to make such gains. And never, ever, listen to testimonials provided about supplements on various Internet forums  or on Facebook. These are often left by shills from the company selling the products, and are totally worthless.

You’re probably wondering who the old woman in the photo is. She’s an Indonesian woman who claims to be 157 years old. She’s never used GH or testosterone. And that stuff she’s eating isn’t whey protein.

Want to learn which supplements will help you make muscular gains without using anabolic drugs? Read my e-book, Natural Anabolics, available at jerrybrainum.com.

In 1990, I had the occasion to meet Dorian Yates. Yates was making his American debut at the Night of the Champions professional bodybuilding contest, which I was covering for a bodybuilding magazine. Yates was a sensation in his native Great Britain, but he was unknown in the United States. While in the lobby of the hotel I was staying at one night, an associate asked me if I wanted to take a look at Dorian Yates, who was staying at the same Manhattan hotel. We then proceeded up to Yate’s room. The first thing I noticed about Yates was his massive and well-defined calf development. Since the calves are considered the most difficult of all muscles in the body to develop, the natural question for Yates was,”Are those natural calves?”  “Natural” in this sense had nothing to do with anabolic drug usage, but rather referred to whether his calf development was more genetically-based in origin. Yates responded that they were not only not natural, but that his calves were quite small when he began training. “They were only 17-inches,”he told me. Dorian seemed to be unaware that a 17-inch calf is impressive for anyone, much less a guy who had never previously touched a weight, nor done any direct calf exercises.

In bodybuilding, the adage is that when it comes to calves, you either have them or you don’t. Indeed, the most impressive sets of calves have belonged to bodybuilders who were blessed with a head start in this area. Names that come to mind for having the genetic gift of huge calves include Dorian, Steve Reeves, Mike Matarrazo, and Eric Fankhouser, whose calves are so huge that they should be called cows. From what I understand, he rarely trains them. Since the majority of bodybuilders don’t have great calves, when a competitor does show up with great calves, he or she tends to stand out from the rest. Many black bodybuilders are hampered with poor calf development. This is often attributed to having fewer muscle fibers in the calves, which is seen as having “high calves.” Shorter muscle bellies usually indicate fewer muscle fibers, and therefore less potential to achieve massive muscle size. But the statement that black bodybuilders tend to have under par calf development is a general statement not always applicable. Evidence for exceptions to the rule comes in the persons of men such as 1982 Mr.Olympia, Chris Dickerson, and pro competitor, Vince Taylor, as well as three-time Mr.Olympia, Sergio Oliva, all of whom had tremendous calf development.

This is not to say that you can’t improve on initially poor calf development. Several bodybuilders over the years have started out with poor calf development, yet managed to build an impressive set of calves. One name that comes to mind here is Arnold Schwarzenegger. Arnold lost the 1966 NABBA Mr.Universe to American bodybuilder Chet Yorton, because Yorton had superior calf development compared to Arnold. Arnold then focused on improving his calves, getting advice from his bodybuilding mentor, Reg Park. Arnold went on to develop a pair of calves that were so huge that rumors circulated that he had calf implants inserted. I don’t know about the implants, but I can verify that Arnold trained his calves hard year-round. Even when he slacked off on the rest of his training, Arnold always ensured that he trained his calves a couple of times a week during the contest off-season. I also witnessed my good friend, the late Dennis Tinerino, build a nice set of calves from intensive workouts. When he began training, his calves looked like toothpicks.

Still, for most bodybuilders, the calves remain the most recalcitrant of muscles. The question is why. Several studies have examined the reason behind the stubbornness of calf development. Most of them have concluded that the calves show a relatively poor blood circulation when compared to muscles that are closer to the heart. In many cases, the amount of blood circulation in the calves remains poor, even under exercising conditions. This explains the common advice that you should do higher reps  when training calves in the belief that this will increase blood circulation and promote greater growth. Indeed, a routine published in Ironman magazine in the mid 1960s involved doing one very long set of standing calf raises. This special calf routine was said to add up to an inch to even stubborn calves. I tried it at a crowded gym in Manhattan when I was about 15. Since the routine involved using the calf machine for about 12 continuous minutes, I wound up being threatened to get off the machine or else by an impatient bodybuilder. But I did make some gains on the program. I also recall interviewing a bodybuilder years ago named James Demelo. He also possessed incredible calf development, comparable to that seen on those with genetically-large calves. Yet, he told me that his calves weren’t always so impressive. When I asked him his secret for building such humongous calves, he replied.”My sets begin when others end.” What he meant by this was that he had built up a high tolerance to training pain, and often did sets of calves that featured high reps, but he had conditioned himself to train past the intense burning sensation in his calves that accompanied such intensive training.

A new study offers some hope for those with poor calf development. The study involved nine healthy men, who trained their calves three times a week for a month, doing standing calf raises for 4 sets of 50 reps. That’s a lot of reps, but that’s not the unusual aspect of this study. They did the calf raises either unrestrained or with a thigh cuff attached to their thighs. This cuff training is also known as “Occlusion training,” and various studies have shown that training this way appears to promote muscular growth, even when lighter weights are used. The theory is that occlusion training boosts levels of intramuscular anabolic hormones, including IGF-1 and testosterone. When training their calves with the cuff attached, the men showed a 26% increased calf blood filtration capacity, and a strength increase of 18%. There were no changes in the unrestricted leg. There was also no increase in muscle fatigue when using the cuff while training calves. The conclusion was that training in this manner increased the development of blood capillaries in the calves.  In practical terms, this means increased blood flow when training the calves, along with increased delivery of nutrients to the muscle. This combination of increased blood flow and muscle strength in the calves induced by the occlusion training may be just the ticket to wake up those stubborn calves. Only time will tell.

Short-term resistance training with blood flow restriction enhances microvascular filtration capacity of human calf muscles.Journal of Sports Sciences 2010: in press.

Learn which supplements work and which do not in my e-book, Natural Anabolics, available at jerrybrainum.com.

It’s no secret that ingesting carbohydrates improves exercise performance, particularly that related to exercise intensity levels and endurance. If you’ve ever viewed a long distance running event, such as a marathon, or cycling event, you probably have seen the results of athletes who didn’t ingest sufficient carbohydrates. Such athletes “bonk” or “hit the wall,” the use the idiomatic terms applied to such events. They simply run out of gas, and begin to resemble a drunk stumbling out of a bar at closing time, as their thigh muscles begin to fail them. In 1966, Swedish scientists developed what was later called carbohydrate loading. This involved  first a depletion, followed by a  higher than usual intake of carbs in the week prior to competition. In more recent years, the carb depletion phase has largely been abandoned in favor of just temporary overtraining for about three days, followed by complete rest along with increased carbs for another three days up to the event. This results in supercompensation of muscle and liver glycogen stores. Glycogen is the form of carbohydrate stored in the body, and consists of branched chains of glucose that can readily be converted into glucose, the type of sugar that circulates in the blood. Glycogen constitutes the major fuel source for both extended exercise, such as workouts lasting over an hour, as well as long distance running or cycling,although the latter also uses fat as a fuel late in the race.

In workouts lasting one hour or less, glycogen depletion is less of a major cause of fatigue. The major causes of fatigue during shorter workouts involve a drop in creatine stores in muscle, along with increased metabolic acidity, and an increase in phosphate levels in muscle. This mainly applies to anaerobic exercise, as is typified by bodybuilding workouts. Such workouts often involve a higher intensity level compared to aerobic training. Glycogen stores are not the limiting factor in shorter, more intense workouts because such workouts don’t usually result in significant glycogen depletion. The situation changes, however, when initial glycogen stores are lower, as occurs during a very low carb diet (under 50 grams of carbs daily). In that scenario, the lack of stored muscle glycogen can limit exercise intensity levels at the start of the diet. After about two weeks, the body adjusts to using other fuels, such as ketones from fat metabolism, and the feelings or training fatigue diminish.

Despite the fact that glycogen isn’t a limiting fatigue factor for short workouts under an hour, various studies still show that ingesting carbs seems to boost training intensity even under shorter training session conditions. One study, for example, found a 10% increase in training intensity when 45 grams of carbs were ingested immediately prior to exercise compared to a placebo.This is hard to understand, since it takes time to absorb and digest the ingested carbs, so the question arises: what causes the apparent ergogenic effect provided by carbs right before a workout?

Studies have revealed an interesting effect of carbs that goes beyond its being the primary substrate for glycogen synthesis in the body. It turns out that carbs interact with taste receptors in the mouth that relay messages to certain regions of the brain. Among the regions of the brain affected by carbs in the mouth are those that are involved in muscle performance, as well as fatigue sensations. Here’s the kicker: this effect occurs when carbs are just swished in the mouth like mouthwash, but aren’t swallowed. When researchers substituted artificial sweeteners for carbs, no ergogenic effect occurred. One study compared actual ingestion of carbs prior to training with just swishing the carbs in the mouth without swallowing the carbs. Ingesting the carbs resulted in a 2.3% training performance increase, while swishing without swallowing led to a 2.8% improvement. Thus merely swishing carbs without swallowing them prior to a workout lasting 30 minutes to one hour will result in a significant increase in training intensity with less perceived fatigue. In short, you will be able to train harder. This does not apply to workouts lasting more than an hour, in which actually swallowing the carbs will be more effective. This technique only works with carbs, and I suspect that simple carbs would be better for this purpose than more complex carbs. This is good news for those who are on low carb diets. It means you can get some of the energy benefits of carbs before training without actually ingesting the carbs.

Jeukendrup A, et al. Oral carbohydrate sensing and exercise performance.Curr Opin Clin Nutr Care 2010: in press.

Tired of being ripped off by the latest and greatest scientifically tested, doctor approved, used for centuries, anabolic supplement? Learn the truth in my e-book, Natural Anabolics, at jerrybrainum.com.