Preworkout Protein Primer : Popping protein prior to training can do good things for hormones by Jerry Brainum

  One way that weight training enhances muscle growth is by stimulating the release of various anabolic hormones, such as testosterone and growth hormone. Along with another potentially anabolic hormone, insulin, they are profoundly affected by nutrition. For example, low-protein diets adversely affect the synthesis and release of insulinlike growth factor 1 (IGF-1), the active anabolic product of growth hormone. Without a large supply of amino acids, insulin has no anabolic activity at all. Conversely, the combination of high blood amino acids and insulin is quite anabolic.

  The latter effect has led to the development of postworkout recovery drinks consisting of a fast-acting protein, such as whey, and a rapidly absorbed source of carbohydrate. That nutrient combination provides the greatest release of insulin following training and promotes amino acid entry into muscle. It also promotes the rate-limiting enzyme required for glycogen, the main fuel in muscle that powers anaerobic exercise such as weight training. Glycogen itself is produced from carbohydrates, which is another reason to include simple carbs in a postworkout drink. Glycogen can also be synthesized from other sources, such as lactate or even protein, but the process isn’t nearly as efficient as it is with carbs.

  While the notion of taking a postworkout protein-and-carb drink is widely accepted by scientists as an efficient anabolic-response modifier in muscle, studies show that a preworkout protein-and-carb drink may work just as well or even better because of the increased blood flow into muscles that results from exercise. On the other hand, a pure protein drink may produce hypoglycemia, or low blood glucose, because of a heightened insulin release.

Taking in protein and carbs before training may also increase cortisol levels. Cortisol is a catabolic hormone released from the adrenal glands that is most often associated with muscle breakdown (although higher postworkout cortisol levels have a reverse effect in helping to supply energy for muscle recovery).

  The precise effects on anabolic hormones of having a protein drink prior to weight training remained speculative until recently.¹ Ten men, average age 23, all with at least five years of training experience, who’d taken no drugs or any supplements that would influence release of any type of anabolic hormone during exercise, participated in the study. Thirty minutes before training, one group took a protein drink containing 25 grams of whey and casein, and the other got a placebo. They all did sets of heavy one-rep squats, sets of 10-rep squats and four sets of 10-rep leg presses. They rested between sets two to three minutes.

  Both groups had a protein-and-carb recovery drink following the workout. The workout began three hours after the subjects ate a 500-calorie breakfast of 21 percent protein, 66 percent carb and 13 percent fat. The postworkout drink contained the same 25 grams of milk-derived protein as the preworkout drink, but it also included 50 grams of carbohydrate.

  The protein group showed lower levels of both GH and testosterone than the placebo group. The protein group, however, had higher blood insulin levels, but only during the first half of the workout, with a steady decline afterward until the subjects got the postworkout drink. The authors note that the elevated insulin produced by the preworkout protein drink likely led to decreased muscle breakdown and increased amino acid entry into muscle—in other words, a potent anabolic effect. The protein drink increased insulin to levels that would produce a maximal protein synthesis rate in muscle. The rapid release of amino acids from whey probably enhanced insulin’s anabolic activity.

  The lack of growth hormone response in the protein group isn’t surprising; past studies show that you get the highest release of GH during a preexercise fasting state. Any nutrients in the blood blunt the release of exercise-induced growth hormone. Milk proteins are rich in branched-chain amino acids and glutamate, both of which have potent GH-suppressing effects during exercise.

  The lower testosterone levels in the protein group were also expected. A high-protein diet is linked to lower levels of both total and free testosterone, as well as a decreased test response during exercise. That may result from a decreased testosterone synthesis, lowered secretion or increased clearance from the blood through its increased breakdown in the liver. On the other hand, since weight training promotes postworkout muscle protein synthesis, the lowered test level may merely reflect increased uptake into muscle, where the anabolic action is.

  Research shows that weight training enhances increased androgen cell receptors in muscle, and testosterone interacts with those receptors, explaining the relative paucity of the hormone in the blood after exercise. Postexercise nutrients may also divert blood from the muscles to the gastrointestinal tract, masking or diminishing testosterone blood levels. The preworkout protein drink, by increasing insulin release, promotes the activity of androgen muscle receptors.

  Other effects of the preworkout protein drink included a heightened postworkout energy expenditure that’s likely related to the higher energy requirements of muscle protein synthesis after the workout—which, by the way, is powered mainly by fat. The increased metabolic effect is also reflected in a higher resting energy expenditure two hours after the workout in the protein group. On the other hand, the lack of GH, coupled with the increased insulin release, also lowered postworkout fat oxidation.

  What it all points to is that a preworkout protein drink increases insulin levels during the workout, which in turn results in less muscle breakdown, higher amino acid entry into muscle and possibly greater testosterone uptake into muscle—in short, an anabolic environment conducive to muscular growth.

¹ Hulmi, J.J., et al. (2005). Protein ingestion prior to strength training affects blood hormones and metabolism. Med Sci Sports Exerc. 37:1990-1997.

©,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

The ultimate cause of death by Jerry Brainum

For years, I've read and heard about old people dying from "old age." That never made any sense to me, after all, you have to die from something, and dying from old age wasn't exactly a specific cause of death. Yet, there was no doubt that old people die, so something must be killing them. In most cases, the main killers are either cardiovascular disease or cancer. Both of them rise with age as the body's defenses gradually ebb with time. But then you have the cases of those people who manage to outwit the odds, and make it to 100 or over. Gerontologists, or those who study the science of aging, have analyzed such people, and found that they have a series of genetic anomalies that appear to protect them against the main killers, cardiovascular disease and cancer. They stay remarkable healthy until they reach about 105, then their health suddenly declines, and most die soon after reaching that age.The statistics show that 30% of them die from pneumonia,which in them is considered a failure of the immune system, since the same type of pneumonia would rarely kill a younger person. Fitness guru, Jack Lalanne made it to 95 in good health, but then succumbed to pneumonia. Dying from pneumonia is hardly "dying of old age."
     But what about the other 70% of very old people; what kills them? It's a salient question, since some scientists, such as the late Roy Walford, suggested that humans should live to at least 140. In reality, however, the oldest confirmed person on record was a French woman named Jean Calment, who died in 1997 at age 122. She was still drinking and smoking over the age of 100, strongly suggesting that her longevity was based on a lucky draw of the genetic cards.But again, what is the primary cause of death in old people that is often referred to as "dying of old age." The answer is systemic amyloidosis.
     Specifically, it has to do with transthyretin amyloidosis (TA). Transthyretin is normally good stuff. It's a protein that transports both thyroid hormones and vitamin A in the blood. But when the gene for transthyretin gets mutated, the protein that comprises it, known as amyloid, become misfolded and sticky. They tend to aggregate into long fibers that can accumulate inside blood vessels and other tissues in the body. They can damage organs, nerves, and heart tissue. In the brain, a form of amyloid called beta-amyloid is thought to be the primary cause of Alzheimer's disease.Beta-amyloid tends to form gummy sticky tendrils that interfere and eventually destroy nerve function. While there are several types of amyloid diseases that result from genetic mistakes, the type that affects older folks is known as senile systemic amyloidosis. Many cases of heart failure are actually caused by a build-up of amyloid protein in the heart muscle. There are about 27 proteins linked to amyloid formation. In the very old people, the build-up of amyloid causes death by clogging blood vessels, just as rust clogs old pipes. What isn't fully established is whether amyloidosis is a normal part of aging, or a pathological process.
    But what is known is that the oldest of the old die from the effects of excess amyloid in their bodies, which chokes off their organ function. Ironically., most of these people never get the most common amyloid-based disease, Alzheimer's, but instead die from the build-up of amyloid in their bodies. Their brain remains intact and normal. There are a number of drugs known to prevent the accumulation of excess amyloid in the body. The question now is whether supplying these drugs to very old people will prevent the most common immediate cause of death in people of advanced age, excess amyloid accumulation. If you could prevent such accumulation safely, would that extend lifespan to 140 or more? That is a question that remains to be answered.
    Update: a new drug has been introduced called tafamidis(Vyndaqel), which specifically targets transthyretin amyloidosis. It will be interesting to see if this drug is given to older people, and if it extends their life.

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

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

Another DMAA horror story

It appears that the days of DMAA are numbered. The Food and Drug Administration (FDA) recently sent out a warning letter to several companies whose products contain DMAA. This was shortly followed by a rash of class action lawsuits filed against these same companies. Many of the companies have voluntarily removed DMAA from their products, but other companies, particularly one, still insists that DMAA is a natural substance that falls under the aegis of the DHSA law of 1994. This means that if it exists naturally in food, it's allowable in supplements.The entire basis for the natural source of DMAA stems from a single study published in a now defunct Chinese journal in 1996. That study found a content of 0.7% DMAA in a sample of geranium oil.They did not, however, perform a confirmatory test, which would have involved comparing the substance that they found in the geranium oil to an actual sample of DMAA. As such, the finding that DMAA exists naturally in germanium is open to question.
    But it isn't really. A number of analytical studies have examined various samples of geranium oil for the presence of DMAA, and none, not one, has ever detected the presence of DMAA in those samples. This has led to the notion that DMAA never actually existed in geranium oil, but was added to supplements. This is a problem, since DMAA is an old drug, originally used as a nasal decongestant. If it's added to supplements, that makes it illegal. Canada banned DMAA soon after the updated analytical tests were published. One of the companies that sells a DMAA product has countered the extensive criticism of  DMAA by sponsoring a series of studies to test for the safety of supplements containing DMAA in suggested doses. These studies show that other than a slight rise in blood pressure, DMAA appears to be safe when used as directed. But the death of two army recruits who allegedly suffered fatal strokes after using a DMAA supplement, renewed the attacks on DMAA, and led to the FDA action. In the meantime, the company that sponsored the safety studies of DMAA has announced that they have another study that will prove that DMAA is indeed found naturally in geranium oil. But they have not yet released the study.
     The real question is how safe is DMAA, and does it deserve to suffer the fate of previous supplements, such as ephedrine, which was wrongfully removed from market sales because of questionable safety concerns. Besides the deaths of the two soldiers, a number of adverse reports have been published related to the use of DMAA in New Zealand as a "party drug." One such report was of a user who suffered a stroke after ingesting DMAA. Other side effects have included panic attacks, seizures,and stress-induced cardiomyopathy. But these cases may have involved people who used larger doses than the suggested supplemental dose of DMAA. The case of the guy who had the stress-induced cardiomyopathy is a good example.
     This involved a 24-year-old man who showed up at a hospital emergency room soon after ingesting a popular bodybuilding supplement called "Jack3D" that contained DMAA and several other common bodybuilding ingredients, such as creatine, beta-alanine, and arginine. It also contained caffeine, which can have similar effects to that of DMAA. In fact, the strength of DMAA has been compared to what happens when you drink 3-4 cups of strong coffee.While the guy had a viral illness a month earlier, he also had no signs or history of cardiovascular disease. But when he arrived at the ER, his symptoms included a headache, heart palpitations,nausea, vomiting, and chest pain.He was also heavily sweating, with elevated heart rate and blood pressure.A chest X-ray showed signs of pulmonary edema, or fluid in the lungs. A urine test proved negative for cocaine usage. But his heart ejection fraction was below 20. Normal is 55 or above, and a low reading suggests heart failure.
      The official diagnosis was for Takotsubo cardiomyopathy, a form of heart failure. But a month after leaving the hospital, he showed a normal ejection fraction reading. It turned out that the man worked for a distributor of the company that sells Jack3D. He had customized his Jack3D supplement by adding more DMAA, 1.5 times more than was contained in the product. A report published in 1950 said that DMAA has a more potent level of toxicity than ephedrine, but less than amphetamine. The report, which was related to the use of DMAA in nasal decongestants, suggested that because of the frequent side effects associated with its use, products containing DMAA should be removed from the market, and that's just what the drug companies did--20 years later.
     So, is the FDA justified in its actions against DMAA? There have been 42 adverse reports sent to the FDA about DMAA. But the fact that DMAA is a drug, and is added to supplements under the guise that it's found naturally in geranium oil, does mean that its presence in over the counter supplements is a violation of the law, and that means that the FDA was correct in its decision about DMAA.

  

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.

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

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

Future Shock by Jerry Brainum

 

   Martin Mesomorph turned on his holoviewer and was immediately face-to-face with President Arnold Schwarzenegger, or at least a lifelike holographic image of the president and erstwhile multi-Mr. Olympia winner. Schwarzenegger was promising the people that he would terminate the foreign interests who had used their hefty oil-based cash flow to buy most of the real estate in the United States. The former oil barons had to do something, since their energy stranglehold on the world had ended with the advent of hydrogen-powered vehicles. Martin himself owned a hydrogen-powered Hummer.

   While watching the news broadcast of President Schwarzenegger’s speech, Martin looked at a reflection of himself in a mirror across the room. He marveled at his own physique, with his 23-inch arms and 22-inch, well-defined calves. At a height of 6’, Martin carried 325 pounds of solid muscle, with a bodyfat level of a mere 5 percent. Martin was in the midst of training for the International Galaxy bodybuilding show, the premier professional bodybuilding contest. The Galaxy contest had superseded the old Mr. Olympia event that Arnold had won so long ago.
Just a few years earlier Martin had been an average competitor, hardly good enough to compete in a national contest, much less an international professional event. Even though he indulged in the gamut of available anabolic drugs, it seemed he didn’t have the genes to compete with the big boys at the pro level.

   Then Martin discovered gene doping. The first thing he used was an injected form of the gene for insulinlike growth factor-1 (IGF-1). Although the therapy had been developed solely for use in treating muscle-wasting diseases, such as muscular dystrophy, athletes had jumped at the chance to use gene therapy for athletic enhancement. In fact, the last Olympic games said to be untainted by gene doping was way back in 2004, at the Summer Games in Athens. A short time later gene doping made its way into sports.

   Martin responded spectacularly to the IGF-1 gene therapy. His bodyweight rose from 240 pounds to more than 300, and the gain was all muscle. He soon added other gene therapies. One was a highly active cleavage product of IGF-1 called mechano-growth factor. Although he wasn’t blessed with great calf development, when Martin injected the MGF gene into his calves, they grew to massive proportions overnight.

   Dieting used to be difficult for Martin. Those low-carb plans made him dream about ice cream and pizza orgies. The days of hunger, however, ended with the advent of the new fat-burning drugs. One worked by inhibiting the gene for an enzyme called acetyl coenzyme-A carboxylase, which synthesized another chemical called malonyl-coenzyme A. Now Martin burned fat 24 hours a day. He was burning fat as he listened to Arnold once again thank everyone for the grass-roots campaign that had led to the constitutional amendment permitting him to run for president.
Martin’s reverie was broken by the sound of his phone ringing. His doctor was calling. “Martin, your tests came back, and I have some bad news for you.”

   While the above scenario may seem farfetched, most scientists who monitor the athletic-drug world say that gene doping is just around the corner. Drug use in sports has long been a cat-and-mouse game, with many athletes seeking performance-boosting substances that can’t be detected and sports authorities trying to keep pace by developing new tests to find them. The great concerns about gene doping are that there isn’t any known way to detect it and that detection tests won’t be available for the foreseeable future—if ever.

   Gene doping involves the insertion of artificial genes into muscle cells.1 An inserted gene then produces RNA, which dictates the synthesis of specific proteins by the cell. At present the most familiar technique for manipulating genes involves a protein, myostatin. Discovered in 1997, myostatin inhibits muscle growth. Animals born without genes that code for it usually show unprecedented muscular size, with a concomitant lack of bodyfat. Scientists then tested how myostatin works—in animals—by breeding special “knockout-gene” rats, in which the genes that code for myostatin were knocked out. As expected, the rats showed muscles about two to three times the size of normal rats.

   The New England Journal of Medicine recently described a five-year-old German boy who was born without myostatin genes. His mother, a track athlete, has only one gene for myostatin, which makes her look exceptionally muscular. But her son is something else. At the tender age of five he already shows signs of unusual muscle mass and strength. In all other ways, however, he appears completely normal. Is he a future Mr. Olympia or some other world-class athlete?

   To answer that question, consider how myostatin works. Special stem cells called satellite cells are normally recruited after muscle injury (including that induced by exercise) and contribute nuclei that result in the thickening of existing muscle cells by adding a buffer to them. We recognize this as added muscle size. The satellite cells are stimulated primarily by locally produced—that is, produced in the muscle itself—insulinlike growth factor 1 (IGF-1). Myostatin works by blocking satellite-cell function, and that inhibits muscle growth. Get rid of the myostatin, and you get rid of the impediment to muscle growth.

   Some scientists think that the supply of satellite cells is finite. Indeed, one reason for the weakness and loss of muscle that accompanies aging is that the body somehow loses the ability to adequately recruit satellite cells for muscle recovery. One scientist has suggested that since the German child produces no myostatin, he may exhaust all his satellite cells by about age 30. What happens after that is anyone’s guess.

   Several muscle diseases are the result of birth defects involving the lack of essential muscle proteins, such as dynorphin in some forms of muscular dystrophy, that lead to extensive muscle weakness. To combat it, one form of gene therapy injects an IGF-1 gene directly into muscle. To get into the muscle, the gene must be packaged with a vector, or delivery vehicle—typically an inactive virus, which shunts the IGF-1 gene into the muscle cell. The cell then starts pumping out IGF-1, which in turn promotes the activity of satellite cells. If it all works out, you wind up with bigger and stronger muscles.

   A study with mice showed that IGF-1 gene therapy worked perfectly, with the treated mice experiencing gains in muscle size that amounted to hypertrophy, or growth, two to three times normal. Injecting the gene for mechano-growth factor, which is a derived form of IGF-1, made the mice double their muscle size in only three weeks.

   Gene therapy uses a magic bullet approach to seek and destroy cancer cells. It may also enable the body to produce substances that are in short supply due to illness or aging. For example, hormones can theoretically be boosted by gene therapy. People born with defective genes that amount to biological time bombs could perhaps have their defective genes replaced.


   While it all sounds great and one day will likely change the face of medicine, it is new, and all of its ramifications are unknown. The possible dangers of gene therapy became evident in a case reported in 1998: An 18-year-old patient with a rare type of liver disorder—not life threatening—was offered the chance to serve as a human experiment in gene therapy to treat the condition. The patient readily agreed, but he died from multiple organ failure.


   Several possible gene therapies appear attractive to athletes, despite the dangers. One involves injected gene-encoded viruses for erythropoietin. EPO increases the volume of red blood cells, which in turn, increase oxygen delivery to cells. Blood doping was based on increasing the number of red blood cells. It was superseded by using recombinant-DNA drugs based on EPO. Use of the technique was popular with all types of endurance athletes and led to a scandal at the 1998 Tour de France, when an entire team was found to be using EPO-based drugs.


   Gene therapy for EPO, however, cannot be detected. In a 1997 study mice and monkeys got EPO gene therapy that resulted in an 81 percent increase in the level of hemoglobin, the protein that carries oxygen in the blood. But the animals’ blood got so thick from all those new blood cells that they had to have their blood diluted to prevent heart failure and stroke.

One advantage of injecting the IGF-1 gene is that it stays localized to the muscle. The problem with systemic IGF-1 is that it stimulates all types of cellular growth, including cancer. Keeping it sequestered in muscle should prevent that problem, but scientists remain uncertain of the ramifications of injecting what amounts to an IGF-1 production plant in muscle.


   Another type of gene therapy with potential athletic uses is the gene for vascular endothelial growth factor. That gene is inserted into the body with the same virus that causes the common cold; the activity of the virus is blocked. VEGF works by promoting the growth of new blood vessels, which means increased blood and oxygen delivery to muscles, lungs, liver and other tissues. On the other hand, cancer cells also spread throughout the body by promoting the production of new blood vessels. Will overproducing VEGF promote cancer? Who knows?


   Two other growth factors linked to increased muscle-satellite-cell activity—fibroblast and hepato—are candidates for gene therapy. Another therapeutic idea is to manipulate genes that lead to muscle catabolism, such as the ones for myostatin and a protein called ubiquitin. Blocking them alone would lead to considerable muscular growth. Deleting the gene for cytosolic phospholipase A-2 also promotes increased muscle growth.2


   Make no mistake: Gene therapy is the wave of the future in sports doping. You’ll know when it’s here by the number of world records that fall and by the appearance of athletes who use the growth-promoting gene therapies, such as those involving IGF-1 genes. The unanswered question is the fate of the athletes who turn themselves into human clinical experiments. Perhaps those contemplating using gene therapy might pause to consider the classic case of an experiment gone wrong: Dr. Jekyll and Mr. Hyde. Or better yet, Mary Shelley’s Frankenstein.

References

1 Unal, M., et al. (2004). Gene doping in sports. Sports Med. 34:357-62.
2 Haq, S., et al. (2004). Deletion of cytosolic phospholipase A2 promotes striated muscle growth. Nature Medicine. 9:944-51.

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

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