Thursday, October 31, 2013

Weight rebound after a low calorie diet: what works to prevent it? by Jerry Brainum


It's not that hard to lose excess body fat. All it takes is willpower and perseverance. No matter what type of diet that you choose, you need to consume less calories that you use through activity, including exercise.As to the best type of diet to use, there is no one size fits all formula, despite the plethora of diet books that claim the contrary. And the notion promulgated by some self-serving experts that "calories don't count," is also utter nonsense, since it goes against the physical principles of what causes weight, or more specifically, fat loss in the body. What you lose during a diet also makes a difference. The ideal is to lose excess body fat without sacrificing lean tissue, mainly muscle. When you lose muscle from extreme dieting, your resting metabolic rare declines, a scenario that favors rapid weight return. The primary cause of lost muscle mass from dieting is either too extreme a drop in calories, such as a starvation diet that doesn't supply sufficient protein to support lean mass maintenance, or a lack of exercise, especially resistance training.
    The truth is that 97 percent of those who go on a diet to lose body fat gain it all back. This is more likley to occur with more extreme diets, such as diets that feature a total daily caloric intake of under 1,000, or a diet that emphasizes zero carbohydrate intake. Such diets go against the natural grain of body metabolism, and the body reacts to such extreme measures by overcompensation, such as a reduction in thyroid hormone output that favors the regain of lost weight.
   But are there things you can do to prevent the return of lost body fat following a diet?  One way is to not try to go on a crash diet that is too low in calories. Instead aim for a more gradual weight-loss of about two pounds per week. This allows the body and the brain to adjust to the weight loss, and ensures greater long-term body compliance. The odds of maintaining lost weight following a crash diet are low, and only those with a zen-like degree of willpower are able to accomplish that goal.
    A newly published meta-analysis (an analysis of prior studies that is brought to a rational conclusion) examined various factors that may aid in keeping the weight off following a diet. The analysis looked at 20 studies involving 3,017 participants. The type of diets examined in the study were either low calorie, defined as 1,200 calories a day or less, and very low calorie, defined as 800 calories a day or less. The study noted that the main reasons for weight regain after a diet include adaptive thermogenesis, whereby the body adapts to a lower calorie intake, and increasing calories then results in weight gain; increased release of appetite-stimulating hormones, such as ghrelin; and simply a relapse in the same eating habits that produced excess fat in the first place.
    The study found that anti-obesity drugs seemed to help keep weight off after a diet. The study focused on two such drugs. Orlistat inhibits fat absorption, but has a high rate of side effects. The other drug mentioned was sibutramine, which reduces appetite, but also can cause heart problems. For that reason, it was removed from the market three years ago. But it still often shows up surreptitiously in various "fat-loss" supplements. In truth, perhaps the most effective fat-loss combination consisted of ephedrine and caffeine. This combination was so effective that it threatened the sale of more ineffectual diet drugs, leading to the eventual ban of ephedrine under the guise that it was toxic, which was nonsense. As such, current diet drugs are, in a word, crap, despite the finding of this new study.
   The study also suggested that meal replacements can aid the prevention of rebound weight gain. They are usually low in calories, and allow the dieter to know precisely what they are consuming in terms of calories and nutrient content. Most also are higher in protein, which helps to maintain lean mass, a key component of keeping the weight off.
   A high protein diet was also suggested as an effective tool for preventing weight- regain. High protein intake (at least 30% of total calories) not only helps maintain muscle mass through offsetting catabolic effects in muscle, but also increases feelings of satiety, thus helping to prevent overeating. Higher protein foods also produce a greater degree of diet-induced thermogenesis, which means greater resting calorie burn.
   Consumption of low glycemic index foods, or foods that do not overly stimulate a high blood glucose level or release of insulin, also can provide some advantages for those who want to prevent weight rebound effects. Low glycemic index foods are most often rich in fiber, which itself provides some satiety effects.
   Perhaps the most controversial aspect of this new nutrition meta-analysis is the suggestion that exercise doesn't aid in keeping weight off after a diet. Since exercise does burn calories, it's hard to understand how this could be so. On the other hand, some types of exercise result in a caloric compensation effect, in which the appitite is stimulated to a degree that results in not only a return of calories burned from exercise, but also additional calories. This, or course, favors rebound weight gain. However, this depends on what type of exercise you do. If your exercise consists solely of aerobics and stretching, the exercise will do little to prevent weight regain. But resistance exercise because if its greater involvement of larger muscle groups and higher muscle intensity level, does favor a higher resting metabolic rate. That, in turn, would help to prevent regaining lost fat.
   Finally, the meta-analysis found that fat-loss supplements don't help to prevent weight regain after a diet. Again, this seems contradictory, since most such supplements work by containing ingredients to both blunt appetite, as well as boost thermogenic effects, which would lead to greater calorie use at rest. But the truth is, despite the hyperbolic ads for such "fat loss" supplements, they provide only a minor adjunctive weight-loss effect. What this means is that the majority of fat loss comes from a combination of exercise and diet adjustments. The minimal thermogenic effects of the fat loss supplements  provide relatively minor effects, if any. Not only that, but many of the often exotic herbal ingredients of such fat loss supplements have little or no solid human research to prove their effectiveness. The only "proof" is often a few esoteric animal studies, which may or may not be applicable to human physiology.



Johansson, K, et al. Effects of anti-obesity drugs, diet, and exercise on weight-loss maintenance after a very low calorie diet or a low calorie diet: a systematic review and meta-analysis of randomized controlled trials. Am J Clin Nutr 2013: 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

 

 

Saturday, October 26, 2013

Milk protein: Not for every body? by Jerry Brainum


For years, milk protein has consistently been rated the number one source of protein for anyone engaged in exercise or bodybuilding. The essential amino acid of content of milk protein is what's responsible for its high biological value. It is a rich source of branched-chain amino acids, often called "muscle amino acids" since they are metabolized in muscle, while other amino acids are metabolized in the liver. Of the two primary milk proteins, whey and casein, the whey portion (comprising 20% of native milk protein) is slightly richer in essential amino acids compared to the other protein in milk, casein (80% of milk protein). The two proteins also differ in their digestibility, with whey being absorbed rapidly, reaching a peak blood level of amino acids within an hour of ingestion. Casein provides a more sustained effect, since it tends to curdle in the stomach due to the presence of certain protein fractions. As such, the amino acids in casein are more gradually released, often for as long as seven hours. In terms of muscle protein synthesis, which is the underlying cornerstone of muscle hypertrophy or growth, whey tends to produce faster results because of its more rapid release of essential amino acids, which drive the muscle protein synthesis process. One amino acid in particular, leucine, appears to be the primary promoter of muscle protein synthesis through its stimulation effects on a protein called mTOR-1. When this protein is turned on by whey, a cascade ensues that results in upgraded muscle protein synthesis.
    Besides its effects on promoting muscle growth through increased muscle protein synthesis, milk protein also provides a number of valuable health benefits. This is due to the presence in milk protein of various smaller proteins called peptides. Research shows that these peptides may be active in the body, producing such beneficial effects as lowering elevated blood pressure, providing an immune boost, lowering inflammation, decreasing appetite.Milk protein also is great for maintaining lean mass under dieting conditions.
    But according to a new opinion paper, milk is not for every body, contrary to what those ubiquitous ads from the American Dairy Association have long touted. The authors of the paper assert that people who are obese have increased amounts of branched-chain amino acids, as well as glutamine in their blood. The increased presence of these amino acids promotes insulin release, exacerbating the already elevated insulin levels that are common with excess body fat. This tends to perpetuate obesity, since insulin promotes lipogenesis, or the synthesis of body fat, especially in the presence of excess calories or carbohydrates. In addition, the choronic elevation of insulin induced by the excess BCAA in the blood of the obese can cause destruction of the pancreatic cells that produce insulin, thus making a bad situation even worse. As evidence, the authors cite the common observation that people who've undergone a gastric bypass procedure (used to treat morbid obesity) show a significant drop in their blood levels of BCAA, along with weight-loss and improved insulin sensitivity. On the other hand, since this procedure results in a drastic drop in food intake, along with a concomitant decline in total caloric intake, you would expect to see a boost in insulin sensitivity and a loss of fat. The drop in BCAA may just be a bystander effect that is not crucial.
    The authors also note that in studies that have compared milk protein to meat, the milk protein has produced a greater release of insulin. Again, this effect is more related to the faster release of amino acids from milk protein, especially whey. In addition, the greater fat content in meat delays the digestion of its protein content, which results in a slower release of amino acids, and consequent blunted release of amino acids in comparison to milk protein.
    The authors of the paper also implicate leucine as a cause of obesity. They base this on studies in which rats on high fat diets were supplemented with leucine. They note that mTOR-1 is a promoter of fat accretion. This effect, however, is seen more frequently in animal studies, and is never seen when the studies involve human subjects. In addition, studies with humans show an opposite effect of leucine: a tendency to promote fat oxidation. Despite this, the authors suggest that over-stimulation of mTOR is a major cause of type-2 diabetes. Again, there is little or no human proof of this assertion. If it were true, those who chronically boost mTOR levels through consuming a high protein diet should all have type-2 diabetes, and obviously this isn't the case.
    Other studies show that in those who exercise, BCAA actually promotes fat oxidation. In  active people, BCAA promotes the synthesis of glycerol, a component of fat. This glycerol is stored in intramuscular fat as triglycerides. This intramuscular fat is a primary source of energy during exercise, and does not cause metabolic problems in those who are fit and active. In those who are sedentary, however, the intramuscular fat is not tapped into as much, and an increase is linked to muscular insulin resistance.
    The authors of the anti-milk paper also cite an in vitro or isolated cell study, in which exposing prostate  cells to milk protein increased the risk of prostate cancer by 32%. However,. this level of cellular exposure to milk protein never happens in the human body, a fact not mentioned by the authors. There is no evidence that consuming milk protein will cause cancer. They then note that restricting BCAA in fruit flies extends their lifespan. They suggest that it isn't calorie restriction, but instead BCAA restriction that is responsible for the extended  lifespans seen in caloric-restricted animals. This is so nonsensical that it's laughable. In fact, animal studies have shown that BCAA may be involved in life extension. There is, however, some truth to the fact that a lifelong promotion of mTOR stimulation may shorten lifespan for reasons too complex to discuss here.

Melnik, B, et al.Metabolic effects of milk protein intake strongly depend on pre-existing metabolic exercise status. Nut Metabol 2013;10:60.

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

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Wednesday, October 23, 2013

What exercises are best for the hamstring muscles? By Jerry Brainum

The terms "hamstrings" and "leg biceps" are often used to describe the muscle on the rear portion of the upper thighs. In fact, however, these terms are not anatomically correct. The hamstrings actually consist of three primary muscle groups, namely the semitendinosus (ST), semimembranosus (SM), and the biceps femoris (BF). Collectively, these three muscles produce the appearance of "leg biceps." Having well-developed hamstring development is vital to bodybuilding success because many competitors are weak in this area. They often show pronounced development of the frontal thigh muscles, often colloquially called "the Quads," but show a surprisingly deficient level of muscle bulk in the rear of their legs. This is most evident when the competitor does a side or rear body pose. The lack of development then becomes glaringly evident, and shows are often lost when this happens.
    Why would a bodybuilder show well-developed quads, but weak hamstrings? A lot has to do with the disproportionate level of strength between the front and rear thigh muscles. The frontal portion of the legs are far stronger, and are therefore capable of hoisting much heavier weight compared to the relatively weaker hamstrings. In addition, many bodybuilders pay far more attention to training their quads in comparison to their "hams," which often just get some cursory treatment following an intense quad workout. Such a scenario not only sets you up for a lack of overall thigh symmetry, but also sets the stage for a likely future hamstring injury. These injuries usually occur because of a lack of strength balance between the quads and the hams. Another frequent cause of injury, which is common in runners, is a hamstring tear or strain. This is caused by sudden stress imposed on tight hamstring muscles. In years past, athletes were often advised to warm-up their hamstrings with a stretching session. The object was to remove some of the "coldness" and muscle tightness in the hams so as to help prevent injury. A better way to warm-up the muscle is to do light activity first that involves the muscle, such as an easy jog or walk, followed by a brief stretching session.
    When it comes to training the hams, bodybuilders and others engaged in weight-training have a number of exercises to choose from. The most common exercises for this purpose include the following: leg curls, either standing or lying on a machine; stiff-legged deadlifts; good morning exercise, which involves placing a barbell across the shoulders, then bending forward;  and more specialized exercises, such as the glute-ham raise, which was popularized by the Russians years ago, and involves use of a special type of bench. Since the hamstring muscles attach at both the hips and behind the knees, bodybuilders are often advised to do exercises that involve both these muscle attachments to achieve complete development. In practical terms, this usually means doing a leg curl exercise and a standing stiff-legged deadlift, with the latter exercise working the hip attachment of the hamstrings. A variation of the stiff-legged deadlift is the Romanian deadlift, which is a more partial movement than the stiff-leg version.
    When bodybuilders train their hamstrings they are often targeting what they call "the leg biceps." Ostensibly, this refers to the biceps femoris. But, as noted above, the biceps femoris is only one of three hamstring muscles, and to get that massive, full appearance requires training all three muscles of the hamstrings. The salient question is: what are the best exercises for this purpose?
   A new study featured 12 trained men who did four of the most common hamstring exercises: leg curl, good morning, glute-ham, and Romanian deadlift. The muscle activity of the men was monitored while they did these exercises through the use of an electromyograph machine, which involves placing electrodes over the active muscles, which then transmit electrical activity elicited in the muscles by exercise to a computer. The primary finding of the study was that the semitendinosus muscle was the portion of the hamstrings most activated in the usual hamstring exercises. The maximum muscle stimulation of the hams was induced by the glute-ham and Romanian deadlift exercises. These were the only two exercises that significantly also trained the biceps femoris.
    If there is a practical implication from this study, it's that the old technique of combining a flexion exercise such as leg curls with a stretching movement, such as stiff-legged or Romanian dealifts, still makes sense. In fact, not doing both types of exercise means that you will never fully train the hamstrings, nor will you acheive the level of muscle density and strength possible in the hamstrings. As for the glute-ham exercise, that isn't available in many gyms, and is awkward to do until you get used to it. But if it's available, it could make a big difference in your hamstring development, especially if you follow it with stiff-legged or Romanian deadlifts.

   McAllister, MJ, et al. Muscle Activation during various hamstring exercises.J Str Cond Res 2013: 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.

 

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.

 

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

  
 
                                                      The Glute-Ham bench

Sunday, October 20, 2013

BODYBUILDING PHARMACOLOGY : MORE STEROID PROBLEMS BY JERRY BRAINUM

On May 7, 2009, L.A. Dodger outfielder Manny Ramirez was suspended for 50 games, losing $7.7 million in salary after he admitted to having used a substance called human chorionic gonadotropin, or HCG. A few ill-informed reporters noted that this meant the baseball star was caught using anabolic steroids, but HCG is not a steroid. It’s a protein-based hormone most associated with pregnancy and fertility. Many pregnancy tests work by detecting higher counts of HCG, since the substance rises early in pregnancy. At one point, HCG—along with an extreme diet only of 500 total daily calories—was touted as promoting bodyfat loss. The HCG diet plan is resurrected every few years, despite the absence of scientific evidence for its effectiveness.
The question: Why would a professional male athlete use the stuff? The answer: HCG is very similar to luteinizing hormone, which is secreted by the anterior pituitary gland. LH is involved in female fertility but also controls testosterone synthesis in the Leydig cells of the testes. Bodybuilders have injected HCG—it’s a protein, so it must be injected—to kick-start their own testosterone production after extended anabolic steroid regimens. Doctors also use it to treat men who have used steroids and have depressed testosterone levels after getting off the drugs.

The implication is that Ramirez used HCG following an anabolic steroid regimen. Somehow, admitting to the use of HCG rather than steroids seems less severe, although there is little other reason for a healthy athlete to use it. The whole matter is moot, as the Los Angeles Times reported that Ramirez was suspended because his testostosterone-to-epitestosterone ratio was 4-to-1, 1-to-1 being the normal ratio. That means that he likely did use testosterone injections.
The steroids-in-sports issue is subject to heated controversy. In one corner you have a group that sees nothing wrong with using performance aids, noting that there are rarely any medical complications from their use among healthy athletes. That, of course, avoids the ethical issue: that using steroids and other so-called performance drugs is a blatant form of cheating and detracts from the nobility of being an athletic champion. On the other hand, no drug alone can produce a champion. Training, skill and genetic makeup all play prominent roles in determining who rules the athletic roost.

Indeed, if we were to literally follow the rule of no unfair advantage, we’d ban athletes born with certain genetic mutations from all sports competitions: those born minus genes that code for myostatin; those born with ACTN3 mutations; those with mutations in the ACE enzyme and so on. Although athletes with those mutations are without a doubt “natural,” they possess advantages over athletes not as genetically gifted.
Rare as they are, complications arising from steroid use do occur. Perhaps the primary problem in that regard is that some people may have occult medical problems that become evident following their use of steroids. Complications can range from cardiovascular disease to more benign conditions, such as hair loss and acne.

The medical literature often reports on case studies showing adverse effects of anabolic steroids, but no scientist in his or her right mind would think that a case study proves a cause-and-effect relationship between steroid use and medical complications. Rather, the studies are meant to alert physicians to potential problems. So what follow are a few recently reported case studies involving anabolic steroid use.
The connection between anabolic steroids and blood clotting is controversial. The majority of serious adverse effects, including a few deaths, have involved cardiovascular complications. Most heart attacks and strokes are initiated by a clot that occludes an artery in a heart with blood vessels already narrowed by atherosclerosis. A few body­builders have had minor heart attacks and strokes, although a direct cause and effect has never been established between those symptoms and anabolics. One study showed that high-dose testosterone injections increase hematocrit, or concentration of red blood cells.

1 Thicker blood increases the risk of internal clot formation and boosts the risk of stroke. The higher the dose of testosterone, the greater the effect on hematocrit. High doses can also raise blood pressure, lower protective high-density lipoprotein and adversely affect heart muscle structure. Those effects, however, are offset by the good nutrition and exercise practices of most bodybuilders and athletes, which explains why you rarely see them dropping dead from heart attacks or strokes.

But there can be exceptions. A 19-year-old bodybuilder showed up at a medical clinic with a significant swelling of his left leg.2 He was otherwise healthy and had no family history of abnormal clotting. Tests revealed that the swelling resulted from a clot, which was treated with anticoagulants. The same man returned to the clinic two years later, this time complaining of shortness of breath, chest pain and fever and spitting up blood. Those are signs of a pulmonary embolism, or a blood clot in the lung, which can rapidly prove fatal. He was again given anticoagulants but woke up in the morning with nausea and headache. That proved to be caused by a subdural hematoma, or blood clot on the brain. Further tests showed that he had a genetic deficiency of protein C, which protects against excess clotting.

It turned out that the bodybuilder used high doses of Dianabol. When asked how much he took, he replied, “Usually a handful”; it came in five-milligram tablets. That reminds me of the time I witnessed a well-known bodybuilder casually gulp down an entire bottle of Anavar following dinner by just pouring the pills into his mouth like candy. The point is, this guy wasn’t aware of his clotting problem, which was likely accentuated by his use of Dianabol. Fortunately, he received treatment in time and survived with no complications. Would he have had the pulmonary embolism without using steroids? Difficult to say, but the fact that he had no clotting problems prior to using the steroid does suggest some involvement.

Another case ended more tragically. An autopsy on a 29-year-old man found dead in his house discovered that he had used large doses of the anabolic steroids nandrolone, a.k.a. Durabolin, and testosterone.3 You recall the normal ratio of testosterone to epitestosterone is 1-to-1. This guy showed a 35-to-1 ratio. The cause of death proved to be rare: pulmonary peliosis, characterized by blood-filled cysts in his lungs, which resulted in massive internal hemorrhage and lung collapse.

An earlier case of pulmonary peliosis in a steroid user involved a hospitalized man given Anadrol long-term to treat anemia. (Anabolic steroids are no longer used to treat that particular condition, which is a complication of kidney failure.) Most cases of peliosis in steroid users occur in long-term users, such as hospitalized patients, and happen in the liver. Steroids have, however, been implicated in a few deaths of unhospitalized people, such as the Austrian professional bodybuilder who died several years ago of massive internal bleeding. While liver enzyme abnormalities are common in those on high-dose oral regimens, peliosis hepatitis, as the liver version of the disease is called, is rare.

Another case study links steroid use to multiorgan damage in a 24-year-old man who worked out regularly and didn’t drink alcohol.4 He did, however, inject himself three times a week with testosterone for two months prior to his reported symptoms. His diagnosis was acute pancreatitis, or inflammation of the pancreas, acute kidney failure and elevated blood calcium. Doctors attributed his problems to his very high blood calcium and his steroid use, although the precise amount of testosterone he injected wasn’t disclosed. Curiously, abnormal elevation of blood calcium is almost never observed in athletes who use anabolic steroids.

A recent report involving two young men, aged 21 and 30, attributed their acute kidney injury to their use of steroids and vitamins.

While liver and blood lipid abnormalities are common in those on high-dose steroid regimens, kidney problems are rare. A 1994 case study described a 26-year-old man who developed severe cholestasis—failure of bile circulation due to liver inflammation—and acute kidney injury after using a veterinary form of stanozol, or Winstrol. The swelling was thought to have caused his kidney problem. A 1999 report documented similar problems in another young man who used Dianabol. He recovered rapidly after being treated with a drug used to promote bile flow in his liver.

In the more recent cases the two men were also taking a veterinary supplement containing massive amounts of vitamins A, D and E. The extreme dose of vitamin D resulted in high blood calcium, which produces volume depletion and constriction of the blood vessels in the kidney and, often, kidney damage. Calcium deposits in the kidneys can lead to renal failure. While vitamin D is more often in short supply in most people’s diets, these guys were taking 17,500,000 units once a week. The suggested dose for vitamin D is between 2,000 and 4,000 units daily, and exposure to sun for 30 minutes can produce 10,000 units of D in the skin. No wonder they had kidney problems.

Despite the obvious cause of the men’s problems, the doctors writing the case study attributed their kidney problems to the excessive vitamin intake and anabolic steroids, though the steroids weren’t named. They appear to have based that conclusion on the few reports of kidney problems related to steroid use. Trouble is, most of the prior studies also involved liver problems, and none involved massive, possibly toxic, intake of fat-soluble vitamins. Anabolic steroids here were more than likely innocent bystanders.

While recent headlines about steroid use in sports have focused on baseball, football has been linked to steroid use for years. When you compare the size of today’s pro football players with those of years past, you have to wonder what’s going on. I was asked to give a talk to pro players at a meeting of the National Football League Players Association 22 years ago. My talk was on the topic of how to build muscle without using drugs. After my presentation, though, the players gathered around to ask me about “the best steroid cycles.” They all claimed not to want to use drugs, but since most were linemen, they felt the drugs were a necessary evil for the size they needed to successfully compete.

A recent study surveyed 2,552 retired football players about their competitive use of anabolic steroids.6 Of the responding players, 9.1 percent reported having used steroids. As I found, most were line players, with 16.3 percent of offensive-line and 14.8 percent of defensive-line players using. The retired pros reported a variety of musculoskeletal injuries that they linked to drugs, including disk herniations, knee injuries, elbow injuries, neck injuries, spine injuries and foot, toe and ankle injuries. Interestingly, none reported any connection between steroid use and tendon injuries. Prior studies involving animals had shown that steroids may adversely affect tendon function.

Perhaps the most famous case of a pro football player and steroids was that of Lyle Alzado. Alzado was a ferocious lineman—his famous line was, “If King Kong and me went into an alley, only one of us would come out, and it wouldn’t be the f—in’ monkey.” Years ago he wasted away from the effects of a brain tumor. Alzado attributed his disease to his 26 years of using anabolic steroids without a break. Privately, however, he felt that the tumor got legs from his use of growth hormone, which he added to his regimen when he returned to football at age 40. While some studies do implicate growth hormone in brain tumors, the effect is more theoretical than actual. Children with GH deficiency are treated with GH for years and have no increased incidence of brain tumors.

I suspect that most football injuries stem from the violence inherent in the sport itself rather than from any particular drug use. Few pro football players retire without some kind of chronic injury. On the other hand, a good case can be made for the notorious “’roid rage” shown by some players, such as one guy with the same initials as a popular fruit juice.


References
1 Coviello, A.D., et al. (2008). Effects of graded doses of testosterone on erythropoiesis in healthy young and older men. J Clin Endocrin Metab. 93:914-919.
2 Alhadad, A., et al. (2008). Pulmonary embolism associated with protein C deficiency and abuse of anabolic-androgen steroids. Clin Appl Thromb Hemost. In press.
3 Vougiouklakis, T., et al. (2009). First case of fatal pulmonary peliosis without any other organ involvement in a young testosterone-abusing male. Foren Sci Int. 186(1-3):e13-6.
4 Samaha, A., et al. (2008). Multi-organ damage induced by anabolic steroid supplements: A case report and literature review. J Med Care Reports. 2:340.
5 Daher, E.F., et al. (2009). Acute kidney injury due to anabolic steroid and vitamin supplement abuse: Report of two cases and a literature review. Int Urol Nephrol. 41(3):717-23.
6 Horn, S., et al. (2009). Self-reported anabolic-androgenic steroid use and musculoskeletal injuries. Am J Phys Rehabil. 88:192-200.

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


©,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.

 

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.

 

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

 

Saturday, October 19, 2013

Can garlic help you lose body fat? By Jerry Brainum

With all the exotic ingredients used in many of the current fat-loss supplements, it's easy to overlook some common ingredients that may be even more effective than the fancy stuff thrown into the list of "proprietary" ingredients on the labels of top-selling weight-loss products. A good example of this is garlic. The health advantages of garlic are enormous.Studies have shown that sulfur compounds found in the "stinking rose" appear to offer preventive effects against the onset of the two major killers: cardiovascular disease and cancer. In fact, one way that garlic compounds accomplish this is by upgrading the synthesis of nitric oxide in the body. But that is another story. Let's focus on how garlic can be used to help shed excess body fat.
    In a recent study that used mice as subjects, the effects of garlic to prevent the onset of obesity in the rodents was tested. The study involved a type of mouse bred to mimic human obesity. These mice were fed a 45% high fat diet for two months to induce obesity. They then continued on the high fat diet, but the diet was supplemented with either 2% or 5% garlic for another seven weeks.Consuming the garlic reduced the weight of the mice, but more importantly it also lowered the fat stores of the rodents, despite the high fat intake.Garlic also lowered the fat content in the blood and in the liver of the mice.Further investigation revealed that garlic had altered genes involved in body fat synthesis. Not only that, but garlic increased the activity of thermogenic proteins called uncoupling proteins that convert calories into heat in the liver, muscles, and body fat. Garlic also upgraded the activity of a protein called AMPK, which acts as an energy sensor in the body. When AMPK is stimulated,fat oxidation is increased in muscle.
      There are two obvious problems with the findings of this study. The first is that the study involved mice. Much of the thermogenic activity in the mice occurred in brown adipose tissue (BAT). Unfortunately, BAT is not as active in humans as it is in mice, although recent evidence suggests that it may be more active in some people than it is in others. Those with active BAT are people who seem to be able to eat whatever they want to, yet never get fat. In contrast,. those who get fat easily usually show a deficient thermogenic response, as in no BAT activity. The whole idea behind most fat-loss supplements is to boost thermogenic activity, not by increasing BAT, but rather by boosting the output of epinephrine and norepinephrine, which promote release of stored fat in fat cells. The other problem with the study was the level of garlic intake. Most people do not consume 2-5% of their diets as garlic. However, those who habitually eat a "Mediterranean" style diet probably do either match or approach this level of garlic intake. It's no coincidence that those who do eat in  this manner are rarely obese.
Soon-Lee, M, et al. Reduction of body weight by dietary garlic is associated with an increase of uncoupling protein mRNA expression and activation of AMP-activated protein kinase in diet-induced obese mice.J Nutr 2011:141:1947-53

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EAT TO GROW : Fat-Burning Firepower Do branched-chain amino acids help blast away fat? by Jerry Brainum

The branched-chain amino acids—leucine, valine and isoleucine—are essential amino acids, meaning they cannot be synthesized in the human body and so must be supplied in the diet. Recent studies show that leucine is particularly important for muscle protein synthesis, since it activates a number of other substances that play vital roles in the process.

While other amino acids are metabolized primarily in the liver, the branched-chain amino acids (BCAAs) are unique in that the major portion of their metabolism occurs in muscle. Under low-calorie conditions, especially when there’s not enough protein in the diet, cortisol is released in a stress-related response. In muscle, cortisol promotes the breakdown of amino acids—the branched-chain aminos.
Based on that finding, some have suggested that taking supplemental BCAAs provides anticatabolic effects in hard-training athletes. In that scenario, the supplemental BCAAs are sacrificed instead of the existing BCAAs in muscle, thereby sparing the muscle. Besides interacting with cortisol, BCAAs also promote testosterone release to some extent, especially if taken prior to intense exercise. Testosterone is an anabolic hormone, directly opposing the catabolic activities of cortisol.

A study presented at the 2005 meeting of the American College of Sports Medicine highlighted another beneficial effect of BCAA supplements that has particular relevance for those on low-carbohydrate diets.1 A major problem with low-carb diets is the depletion of readily available energy substrates, such as glycogen, which is the primary fuel that powers anaerobic exercise, such as weight training. The primary source of glycogen in the diet is carbohydrate.

Glycogen promotes the production of substances important in the synthesis of ATP, the immediate source of energy for muscular contraction. One such substance is oxaloacetate. Without it the cycle that normally produces ATP just doesn’t function well, leading to a drop in energy and training intensity.

But an intermediate substance called succinyl coenzyme-A (SCA) enhances oxaloacetate availability. That’s where BCAAs enter the picture, since they directly increase SCA. The new study hypothesized that the energy-promoting effect of BCAAs was so potent that it could even overcome the effects of carbohydrate depletion.

The study featured seven men who depleted their existing glycogen stores through exercise and lack of food. Then one group took 300 milligrams per kilogram (2.2 pounds) of BCAAs, while the other group got a placebo. After that the men rode exercise bikes to exhaustion. Those in the BCAA group showed higher blood glucose levels than the placebo group. The BCAA group also appeared to more readily burn fat during exercise. The increased fat availability, coupled with the higher glucose levels, overcame the normal negative effects of glycogen depletion during exercise.

1 Adolpho, T., et al. (2005). Influence of branched-chain amino acid supplementation on free fatty acid oxidation during endurance exercise after muscle glycogen depletion. Med Sci Sports Exer. 37:S349.

  
©,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.

 

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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.

 

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.

 


 

TRAIN TO GAIN : Catabolic Conclusions When to do aerobics so you don’t lose muscle by Jerry Brainum

Researchers have arrived at contradictory conclusions concerning the effect of combining aerobic exercise and weight training. Most studies, however, show that using a program that features both types of exercise results in blunted muscular strength and size gains. The reason: Aerobics and weight training lead to physiological changes in muscle structure that more or less cancel each other out.

For example, weight training leads to increased muscle contractile protein synthesis, resulting in greater strength gains. Aerobic exercise blocks that effect. Weight training doesn’t affect mitochondria, the structures in cells where energy is produced and fat is oxidized. Aerobics increases both blood delivery to muscle (providing oxygen to spark energy production) and mitochondrial activity.

To develop maximum fitness and a favorable body composition, you need to do both kinds of exercise. The question is how to incorporate aerobics with weight training without sacrificing hard-earned muscle.

A new study provides some hints.1 It featured 16 men who were divided into two groups, each employing a different style of aerobic exercise. One group did high-intensity interval training, characterized by alternating periods of high- and low-intensity exercise. The other group did the usual style of steady-state aerobics, using the same level of intensity throughout the workout. The aerobic sessions lasted about 40 minutes.

After completing the aerobic exercise, the subjects did a weight workout consisting of bench presses and leg presses, four sets of each with a weight equal to 75 percent of their one-rep maximums. The men rested various lengths of time after the aerobics—four, eight or 24 hours. Leg press strength was compromised four and eight hours after aerobics but not 24 hours. Since the aerobics consisted of stationary cycling, only lower-body strength was affected.

The study confirms conventional bodybuilding practice that training legs on the same day you do any type of aerobics affecting the leg muscles will adversely affect leg strength. The obvious solution is to wait a day after doing aerobics to train your legs.

1 Sporer, B.C., et al. (2003). Effects of aerobic exercise on strength performance following various periods of recovery. J Strength Cond Res. 17:638-44.

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©,2017 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

 

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EAT TO GROW : Cardio Combo Plant sterols and exercise can synergize for heart protection by Jerry Brainum

Plants do not synthesize cholesterol. The plant versions of cholesterol are substances collectively known as plant sterols, such as lathosterol, campesterol and beta-sitosterol. They’re structurally similar to cholesterol, and studies show that they can displace cholesterol in the human body. So taking them in will promote the excretion of the cholesterol you get from food, which would have the effect of reducing cardiovascular disease.

What if you combined plant-sterol intake with aerobic exercise, which also has established credentials for cardiovascular protection? Would the combination be more effective than either alone?

That was the focus of a recent study.1 It lasted eight weeks and featured 84 human subjects randomly assigned to one of four groups: 1) combination of sterols and exercise; 2) exercise; 3) sterols alone; 4) control, no exercise or sterols. The sterols-alone group decreased total blood cholesterol by 8.2 percent compared to starting measurements. The plant sterols also lowered low-density-lipoprotein (LDL) cholesterol, elevated levels of which are a risk factor for cardiovascular disease.

Exercise alone increased beneficial high-density-lipoprotein (HDL) cholesterol by 7.5 percent, while decreasing blood triglycerides, or fat, by 13.3 percent from baseline. Bodyfat levels in those subjects also declined an average of 3.9 percent from the aerobic exercise after eight weeks. The big news, however, is that the combination of plant sterols and aerobic exercise worked better in lowering all cardiovascular risk factors than either intervention alone.

Plant sterols were at one time promoted as “testosterone precursors.” That was based on two things. First, the raw material for testosterone synthesis in the body is cholesterol, which is converted through several enzymatic steps into testosterone. But the human body cannot do the same conversion for plant sterols because it lacks the necessary enzyme. It can, however, be done under lab conditions. The second reason for promoting plant sterols as testosterone boosters was the similarity in name between “sterols” and “steroids.” In reality, that similarity was all the two substances had in common, other than being similar in structure to cholesterol.

Besides being useful for the prevention of cardiovascular disease, plant sterols can help prevent prostate gland enlargement. In fact, the active ingredients in saw palmetto, which is often used to prevent prostate problems, are various plant sterols.

On the negative side animal-based studies and a few human studies have linked a heavy intake of plant sterols to lowered testosterone levels. That likely has something to do with displacing cholesterol in reactions where cholesterol is used to synthesize testosterone in the body. The good news, though, is that you would need to ingest megadoses of plant sterols to induce any type of testosterone-inhibiting activity.

1 Varady, K.A., et al. (2004). Plant sterols and endurance training combine to favorably alter plasma lipid profiles in previously sedentary hypercholesterolemic adults after eight weeks. Am J Clin Nutr. 80:1159-66.

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TRAIN TO GAIN : Pump Up Heart Health Weight training does it! by Jerry Brainum

Most physicians tell patients that the best way to prevent cardiovascular disease is to exercise and follow a proper diet. For years the party line on diet mandated a drastic reduction in fat intake, with no specific suggestions for what type of fat to reduce. Later, saturated fat was indicted as the evil one that promoted cardiovascular disease.

Continuing research clearly shows that not all fats are created equal. What we now call the “good fats” include monounsaturated fat, such as that found in olive oil, and omega-3 fats, which are found in fatty fish and flaxseed. Such fats not only aren’t bad for the heart but appear to protect against cardiovascular disease as well.

A similar change has occurred in the way health professionals view exercise. While in the past most doctors believed that only aerobic exercise offered any benefits, recent research has shown that weight training can also provide significant preventive effects. A recent study published in the prestigious Journal of the American Medical Association is typical of the newer research.1

The study was part of a larger look at the health habits of 44,452 American health professionals who were monitored every two years to assess potential cardiovascular risk factors. In the follow-up, running, weight training and rowing exercise were inversely related to cardiovascular disease. Specifically, men who ran an hour or more each week showed a 42 percent risk reduction compared to inactive men. Men lifting weights 30 minutes or more each week showed a 23 percent risk reduction over men who didn’t lift weights. Rowing for one hour or more each week led to an 18 percent risk reduction compared to men who didn’t row. Just walking 30 minutes a day resulted in an 18 percent risk reduction.

But the most interesting finding of this study, besides the fact that weight training had positive cardiovascular-protective benefits, was that the most important aspect of exercise was intensity. Cardiovascular risk dropped as exercise intensity rose. Thus, according to this latest study, training harder is more important for cardiovascular health than training longer.

1 Tanasescu, M., et al. (2000). Exercise type and intensity in relation to coronary heart disease in man. JAMA. 288:1994-2000.

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TRAIN TO GAIN : Set-ing Your Hormone Zone Sets, reps and hormones by Jerry Brainum

While some bodybuilders do as few as four sets per muscle group, others do 20 or more. Those in the latter category often resort to a little chemical help, such as anabolic steroids, that makes for more complete recovery and thus compensates to a certain extent for gross overtraining. Still, I’d venture to guess that if you asked many bodybuilders for a scientific rationale for their training procedures, most wouldn’t have a sensible answer. Their rationale would be something like, “It just feels right.”

While so-called instinctive training does have merit in that different exercise routines affect people differently, you can’t escape science. Don’t believe me? Step off a tall building and see if your “instinctive” belief that you can fly prevents you from getting up close and personal with a slab of concrete.

Exercise scientists have recently published a raft of interesting studies that have more practical value than the usual fare published in science journals. One such study examined the hormonal effects of using various set and rep protocols.1

Such information is relevant to those seeking gains in muscular size and strength because exercise affects the flow of various anabolic hormones, such as growth hormone, testosterone and, from a catabolic standpoint, cortisol. The connection between exercise and hormones is evident when you consider that intense weight training increases the number of androgen receptor sites in muscle, which in turn creates a greater connection between testosterone and muscle. Testosterone promotes muscle growth, as looking at any anabolic steroid user will tell you. That also explains why using steroids without exercise doesn’t work well for adding muscle mass—because of the limited number of androgen receptor sites available in those who don’t work out.

The study featured 11 young men, average age 23, all of whom had two to eight years of training experience, although none were competitive athletes. The subjects were divided into three groups that used different training protocols:
  1. Maximum strength (MS). This group used weights that allowed an average of five reps per set, lifting 88 percent of maximum weight for one rep, with three minutes of rest after each set.
  2. Muscular hypertrophy (MH). This group used a plan designed to promote optimal muscle gains. It involved weights that allowed 10 reps per set at 75 percent of one-rep-maximum weight, with two minutes of rest after each set. The MH and the MS routines used two, four and six sets per exercise.
  3. Strength endurance (SE). This group used weights that were 60 percent of one-rep maximum for 15 reps per set, with one minute of rest after each set. They did two or four sets per exercise. Even four sets with this protocol proved difficult for the subjects, and all refused to do six sets.
All three groups did four exercises: bench presses, lat pulldowns, squats and overhead presses. To meet the rep goals, they dropped the weight on each set after the first. All subjects trained at the same time each day to avoid any time-related hormonal influences.

Varying the number of sets in the MS protocol had no effect on any hormones, but in the MH and SE groups growth hormone and cortisol were higher after four sets rather than two. Both growth hormone and cortisol rose higher in the SE and MH groups than in the MS subjects but were higher in the MH subjects only after they did four and six sets. The SE produced the highest growth hormone release of all three routines—surprising, since it featured the lightest weights.

The study shows that higher hormone levels may not play a role in gains during a heavy strength program, but lifting heavy produces gains through other means, such as increased intracellular growth mechanisms and higher maximum neural activation of muscles. That’s noticeable with many Olympic lifters, who are undoubtedly strong but not necessarily heavily muscled.

The study confirmed past observations that doing more sets increases the secretion of both growth hormone and cortisol, though it did not affect testosterone release. It also showed that doing two sets led to a growth hormone release without an accompanying increase in cortisol. When the sets increased to four, both GH and cortisol increased, but the GH release was great enough to offset the catabolic effects of the cortisol.

Another interesting finding was that there appears to be a ceiling to the extent of hormonal release during weight training. Six sets didn’t promote any more hormone release than four sets per exercise. GH was higher during the strength endurance protocol than it was during the muscular hypertrophy protocol, an effect thought to occur from extended low tension, or stress, during the higher reps on the endurance routine.

Based on this study, it isn’t necessary to do more than four sets per exercise for optimum hormone release. That information applies to trainees not using any type of anabolic drug, as drugs could enable them to train past that four-set limit and still show considerable muscular progress.

Now that we have a good idea of how many sets to do per exercise to promote maximum hormone secretion, the next study should examine the total number of sets per muscle group that works best for that purpose and the optimum training frequency.

1 Smillios, I., et al. (2003). Hormonal responses after various resistance exercise protocols. Med Sci Sports Exer. 35:644-654.

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Wednesday, October 16, 2013

Why you shouldn't consider running a marathon unless you're in great shape by Jerry Brainum


Back in the early 70s, America was enthralled with a running craze. Or more specifically, a jogging craze. Just about everywhere you looked, people had laced up their Adidas or Rebok running shoes, and were hitting the roads. Numerous books extolled the many benefits associated with jogging, such as fat loss and improved cardiovascular health. Some even hinted that regular jogging held the key to an extended lifespan. Even the regulars at Gold's Gym got pulled in. I recall running in a park near the gym in the late 70s. I often ran with the famous Mentzer brothers, Mike and Ray. On one occasion, after a late night workout, I ran with my friend and training partner, Bill Grant, a Mr.America and Mr.World winner. We were stopped by the police who couldn't understand why a white guy and a black guy would be running down the street at 2 a.m. 
   At the height of the running craze, a pathologist from Inglewood, California named Thomas Bassler declared that anyone who followed the "running lifestyle" that included no smoking and no junk food eating, and who could complete a marathon in under four hours was immune from having a heart attack. This statement by a physician caused even more people to get involved in the running craze. Perhaps the most popular book related to running at the time was aptly titled The Complete Book of Running. It was written by Jim Fixx, whose enthusiasm for running was clearly infectious. Fixx had led an unhealthy lifestyle, being overweight, sedentary, and an avowed junk food water until age 35, when he began running. His father had died of cardiovascular disease at 42, so Fixx had some clear motivation to start exercising. But what he didn't know was that he also possessed an enlarged heart that put him at greater risk of having a heart attack. He also felt that exercise was more important than diet. Fixx, the champion of running, died of a heart attack at 52 while engaged in his favorite activity. An autopsy revealed that one of his coronary arteries was 95% blocked, while two others were 85% and 70% blocked respectively. His death made many people question the "heart attack immunity theory" suggested by Dr.Bassler.
    While the jogging craze eventually abated, the zeal for long distance running seems to have increased over the years. For many, the ability to complete the 26 mile, 385 yard course of a marathon race represents a personal victory. It makes them feel that they can do anything if they persevere and set their mind to it.  But the truth is that many people are not fully prepared to undergo the rigors of a marathon race, and the stress it imposes on the body, particularly the heart.
    Even experienced marathon runners could be at risk if they are unaware of certain underlying cardiovascular conditions. A good example of this is the case of U.S Congressman, Goodloe Byron. Byron died of a heart attack while jogging in 1978. He was only 49 at the time. Prior to that unfortunate event, Byron had completed running six Boston Marathons with a best time of 3:28:40, and hadn't smoked for over 25 years. This, of course, met Dr.Bassler's criteria for heart attack immunity. But a series of prior treadmill stress tests on Byron had revealed that he likely suffered from atherosclerosis. His last test revealed outright cardiovascular disease, and he was advised not to run, which he ignored.
    In a new study of amateur marathon runners who had competed in a Canadian marathon, tests done before and after the race revealed that half the runners showed potentially severe heart defects related to heart muscle injury incurred from running the race. The subjects were 20 runners, with an age range of 18 to 60, none of whom showed any prior cardiovascular disease, or were on any drugs used to treat cardiovascular disease. The runners were tested and observed for six to eight weeks prior to the race, and also on the day of the race. They were again tested 48 hours after competing the marathon. These tests revealed that half the runners showed a decrease in the function of the left and right ventricles of their hearts. Some of them also showed edema or swelling of the heart muscle, as well as reduced blood flow. Those with lower fitness and less training were more prone to show these disturbances in heart function.
   The good news is that the effects are transient. All the runners showed that the changes induced in heart function returned to normal within three months. But this study does also suggest that if you contemplate running a marathon, follow the Boy Scout creed and be prepared. Training for just a few weeks isn't enough. It takes at least 6-8 months or more to properly prepare for running a marathon. In addition, the damage imposed on joints and heart function can take at least three months to recuperate after a marathon. Competing in another long distance race within that time is not just foolish, but could be life threatening for some. Perhaps those seeking to prove something to themselves would be well advised to seek a safer pursuit to boost their self-esteem.
    In reality, however, emerging research is showing that long-term participation in long distance running events can reverse the benefits of exercise on heart function. This, of course, is the converse of what Dr.Bassler proposed in the 1970s. The new studies suggest that those who regularly engage in long distance running have a higher incidence of heart rhythm defects. In some cases, these disturbances in heart rhythm can result in sudden death. Studies show that participation in long distance running raises the risk of atrial fibrillation, a common heart rhythm disturbance, 5-10-fold. In addition, veteran marathon runners show increased calcium deposits in their coronary arteries, a harbinger of atherosclerosis.Jogging at a rapid pace  more than 4 hours a week causes the loss of all exercise-related heart benefits.
   The increase in heart rhythm disturbances seen in long distance runners may result from an increase of scar tissue (fibrosis) in the heart, which sets the state for aberrant heart rhythms, especially atrial fibrillation. Ultramarathon runners (50 mile or more runs) show levels of the adrenal hormone, aldosterone, that are 5-times higher than normal. This is significant because elevated chronic aldosterone levels are associated with cardiac fibrosis. Running long distances also boosts levels of inflammatory cytokines, immune system chemicals that can damage the heart. While endurance athletes show a heightened parasympathetic response, which results in their typically very low resting heartbeats, it also sets them up for possible heart rhythm problems later on.
   It is perhaps important to consider what happened to Pheidippides (portrayed by Steve Reeves in the 1959 film, The Giant of Marathon),  the Athenian man said to be the inspiration for the marathon race. He ran 25 miles, then promptly dropped dead. Enough said.

Larose, E, et al. Transient myocardial tissue and function changes during a marathon in less fit marathon runners. Can J Cardiol 2013;1269-73.

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Sunday, October 13, 2013

Does ingesting carbs after a workout build more muscle when added to protein? by Jerry Brainum


In recent years a popular sports nutrition concept has been that of nutrient timing. This concept suggests that when you consume certain nutrients in proximity to a workout can alter the results you get in terms of added muscle mass and strength. This is most often related to ingesting a fast-acting protein source, such as whey, with a high glycemic index carbohydrate, or a carbohydrate source that is quickly digested and absorbed. The principle behind this is that a rapidly absorbed protein such as whey, or even amino acids, will promote a more efficient  level of muscle protein synthesis, the cornerstone of muscular hypertrophy gains. The carbohydrates enter the picture because carbs are considered the most potent nutrient stimulator of insulin. While insulin has several functions in the body, in this sense a greater insulin release is sought because the extra insulin produced following a workout is thought to work in concert with essential amino acids, especially the branched-chain amino acid, leucine, to promote a greater level of muscle protein synthesis compared to consuming just protein alone.
    While it makes sense, this notion of adding a simple carb to a fast-acting protein source is theoretical.Some studies show a definite effect when protein is combined with carbs, while others show little or no effect. Indeed, recent studies suggest that consuming the correct amount of essential amino acids following a workout (about 8-10 grams, obtainable from 20-25 grams of whey protein) maximally promotes the muscle protein synthesis process alone, and added carbs do not add to this process.
    A lot of the confusion concerning the utility of a post-workout protein/carb drink accrues from a lack of understanding about insulin. Insulin is more related to a prevention of muscle protein breakdown, rather than simulating muscle protein synthesis. This, however, is an important consideration when you realize that muscle growth is the result of a balance between muscle protein synthesis and muscle protein breakdown, with growth featuring a greater activity of muscle protein synthesis. But blunting muscle protein breakdown pushes the metabolic scale towards more anabolic effects in muscle by favoring muscle protein synthesis. In that respect, insulin does help build muscle. The mistake often made about insulin is in relation to how much is required to affect muscle anabolic effects.
   It turns out that only slight elevations of insulin above basal levels are all that's required to blunt muscle catabolic effects. Just consuming protein alone is enough to elicit a release of insulin that is sufficient to interact with the ingested amino acids in promoting muscle protein synthesis. Leucine alone is known to promote the release of insulin. This explains the recent studies showing that protein alone is enough to boost muscle protein synthesis following training. Indeed, one study showed that boosting insulin levels 30-times above fasting level did not further boost muscle protein synthesis if blood levels of amino acids were high. Just consuming protein alone, especially whey, which is rich in leucine, is enough to boost insulin levels 2-3-fold above resting levels. This level of insulin alone is enough to provide the anti-catabolic effects of insulin following exercise. Other studies show that adding 30 or 90 grams of carbs to 20 grams of protein does not boost muscle protein synthesis to a greater degree, despite the fact that 90 grams of carbs promotes a greater insulin release compared to 30 grams. The level of insulin release required to boost muscle protein synthesis beyond this level can only be achieved injecting insulin, which would allow superphysiological levels of insulin to exist in the blood, far higher levels than can ever be reached through ingesting any amount of carbohydrates.
     But there are other reasons to add fast-acting carbs after a workout, even if it doesn't affect muscle protein synthesis. Carbs are still the best way to replenish depleted muscle glycogen levels. Glycogen repletion is required for complete muscle repair, and also serves as the primary energy source for anaerobic workouts such as occurs in bodybuilding. The enzymes that convert ingested carbs into glycogen are primed following training, and it's advisable to take advantage of this by consuming carbs within 2 hours following training. It fact, the timing for carb intake after training is even more critical than it is for protein intake. The muscle protein synthesis process continues for 24-48 hours following training. But the heightened glycogen-replenishing enzymes only last for 2 hours after a workout.In addition, the combination of protein and carbs will blunt cortisol release, as well as lower levels of AMPK, both of which interfere with muscle protein synthesis after training.
     

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Friday, October 11, 2013

Does a high protein diet decrease muscle endurance? by Jerry Brainum


Even those who profess to know nothing at all about nutrition still seem to be aware of the importance of consuming a high protein diet in order to build muscle. Many mistakenly believe that the need for increased protein is related to muscles being made out of protein. In fact, muscle tissue is only 22 percent protein. The majority of muscle, similarly to other body tissues, is composed mainly of water. You don't have to have a physiology degree to know that consuming a lot of water won't build big muscles. The structural and contractile proteins in muscle are what determines muscular size and strength (with strength also having a neural component). Until recently, many nutrition authorities advised those engaged in weight-training that their requirement for protein was the same as a person who did nothing more strenuous than changing the channels on a TV. This seemed intuitively wrong, and it turned out that it was. The requirement for dietary protein does indeed increase for those seeking added muscle mass.
    It's still a matter of debate, however, as to just how much extra protein is needed to build muscle. The consensus of published research puts the range as between 1.6 and 2.7 grams of protein per kilogram of bodyweight. In reality, most competitive bodybuilders consume far more protein than this recommended range. According to the scientists, excess protein will simply be oxidized in the liver, thus not contributing to muscle building progress. On the other hand, other research has shown that protein requirements increase for anyone under dieting or caloric restriction regimes. If you lower your total calorie or carbohydrate intake, you need to boost protein intake to prevent the loss of excess lean mass, which includes muscle. A loss of muscle from excessive dieting results in a lowered resting metabolic rate, which practically ensures the regain of lost weight. Indeed, a just published review of the protein needs of those engaged in weight-training under calorie-restricted conditions concluded that the range of protein needed is between 2.3 to 3.1 grams per kilogram of fat-free mass. The less calories consumed, the greater the need for a higher protein intake to preserve muscle tissue.
    Various critiques have been offered over the years about consuming a high protein diet. These range from a higher protein diet promoting dehydration (possible, but never happens in the real world); loss of calcium (only if pure protein minus phosphate, a common mineral in high protein foods is consumed); and perhaps the silliest of all: a high protein diet can make you fat. The latter effect is based on the fact that that a gram of protein contains four calories, and excess calories from any source can be converted into body fat. The problem with this is that in those who are active and exercise, any excess protein is not converted into fat, but is rather oxidized in the liver. Certain amino acids can be converted into glucose, but recent research shows this conversion produces only small amounts of glucose, much less than previously believed.
    One of the most outrageous critiques of a high protein diet was recently published by a group of Japanese researchers. This involved a study in which mice were provided a high protein diet starting at 8 weeks of age, then followed for 20 to 50 weeks. During this time, the mice engaged in endurance exercise, presumably running on mouse-sized treadmills. The mice were closely watched for any changes in mitochondrial function and muscular endurance. The mitochondria are cell structures where energy is produced as ATP, and fat is oxidized. They are closely associated with endurance, and endurance exercise is known to boost the number of mitochondria in cells.
    In the new mouse study, some of the mice consumed a high protein diet, while others consumed normal mouse chow. At the end of 50 weeks, the high protein mice showed a decreased number of mitochondria, less mitochondrial activity, along with reduced running distance.The high protein mice did also show greater muscle mass and grip power compared to their normal eating littermates. The study authors suggest that these negative changes in mitochondria number and function, as well as the loss of endurance in the high protein mice, resulted from the high protein intake stimulating a protein called mTOR. This protein, which is stimulated by amino acids, particularly the branched-chain amino acid, leucine, sets into motion a cascade that culminates in increased muscle protein synthesis. When you lift weights and consume a high protein diet, you promote the activity of mTOR. This results in bigger and stronger muscles. Recent research even shows that anabolic steroids produce their notable effects in muscle through this same mechanism.
    When you engage in endurance exercise, another protein, called AMPK is increased. This protein is also increased under low calorie intake, or low carb intake. In the body, AMPK acts as an energy sensor, boosting glucose uptake into muscle and also promoting fat oxidation in muscle. But AMPK also blocks the activity of mTOR. This is the basis of the long-held notion that doing endurance or aerobic exercise leads to either a loss of muscle mass, or a prevention of muscle mass gains. In the study with the mice, the high protein diet led to a dominant mTOR effect, while AMPK levels remained stable. This, in turn, led to reduced mitochondrial activity in the rodents, although they gained muscle mass. Based on this result, the Japanese researchers suggest that consuming a high protein diet will lead to a loss of muscle endurance.
   The problem with this, however, is first, what occurs in mice isn't necessarily replicated in humans.In fact, recent evidence shows that weight-training is capable of boosting mitochondrial activity, and also boosts the levels of a protein called PGC-1A, which stimulates the development of new mitochondria. Several nutrients, including resveratrol, also are known to boost the activity of PGC-1A. There is no human evidence that consuming a chronic high protein diet will adversely affect muscular endurance. Indeed, endurance athletes are advised to consume more protein than even strength athletes because some of the protein can be used for energy, and also to help repair damaged muscle tissue that is common after long distance running events.Some evidence does show that doing an extensive amount of aerobic exercise following a weight-training routine may interfere with muscle and strength gains through the AMPK mechanism. However, this only pertains to aerobic sessions that are over one hour in length. Shorter sessions have little or no effect on muscle growth. There is one exception to this, however. If you engage in intense aerobic activity under zero carbohydrate conditions, there is an outside chance that you may sacrifice some muscle because of elevated cortisol levels that may result.But even in this instance, a higher protein intake will act as a buffer against muscle loss, especially the branched-chain amino acids and a leucine metabolite called HMB.

Mitsuishi, M, et al. Dietary protein decreases exercise endurance through rapamycin-sensitive suppression of muscle mitochondria.Am J Physiol Endocrin Metabol 2013: in press

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

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Tuesday, October 8, 2013

NAC: a new treatment for mental illness? by Jerry Brainum

N-acetyl cysteine, or NAC, is an antioxidant available in supplement form. Its major use is to act as a direct precursor in the body for the synthesis of glutathione, a major endogenous, or built-in antioxidant. In the liver, glutathione provides extensive detoxifying actions. A depletion of glutathione, which can occur with the ingestion of the amanita phalloides or "death cap" mushroom, or by ingesting an overdose of the common pain reliever, acetaminophen (Tylenol) can cause liver failure. In hospital settings, intravenous NAC is often used to treat liver glutathione depletion. Glutathione is also used to help degrade anabolic steroid drugs, and prevent the liver inflammation that would otherwise result from heavy steroid usage. Glutathione, which consists of three bonded amino acids, glutamic acid, glycine, and cysteine, is also available in supplement form, but it's useless when taken orally because it's degraded in the stomach into its constituent three amino acids. Cysteine is considered the major nutrient precursor for glutathione synthesis, and NAC is a more absorbable form of the amino acid.
    From an exercise perspective, the findings about NAC supplementation are mixed. Some studies show that it helps prevent muscle fatigue, and may even block catabolic effects in muscle that can occur with intensive training.One study found that intravenous administration of NAC increased the time to exercise exhaustion by 26.3 percent. More recent studies, however, question the use of NAC just prior to or immediately following exercise because of an interference with the beneficial effects of reactive oxygen species or ROS, which are also produced during exercise. These are by-products of oxygen metabolism that were previously thought to have only negative health effects. Recent research suggests that ROS can produce some beneficial effects related to exercise adaptation processes. Taking NAC too close to exercise may negate these beneficial effects. Not all studies have found this, however, and it's still a matter of debate among scientists.
   Other research has found a new role for NAC. This involves the treatment of mental illness and addictions. Most current psychiatric drugs work through interaction with brain neurotransmitters, which are amino acid-based substances that transmit nerve signals in the brain. Having too low or too high a level of these neurotransmitters can produce symptoms of mental illness, including schizophrenia, depression, and bipolar illness. The current drugs work by modulating the activity of these neurotransmitters, which may or may not relieve disease symptoms. One problem with the drugs is that they are replete with an extensive list of possible side effects.But it turns out that there is another pathway involved in mental illness. This involves an out-of-control level of both inflammation and oxidative stress in the brain.
     Excess inflammation and oxidative stress in the brain produce damage by reducing proteins that stimulate neural growth, such as brain-derived neurotrophic factor. This proteins are involved in brain repair, and when in short supply, lead to brain damage. Extensive inflammation in the brain also promotes the death of neurons, leading to diseases such as Alzheimer's and Parkinson's diseases. Excess oxidation damages cellular mitochondria in the brain, leading to cell death, since the mitochondria are the sources of energy production in cells, including brain cells.
    Preliminary studies with NAC show that it appears to relieve the symptoms of mental illness through a lowering of both excess inflammation and oxidation effects. It has been shown to reduce the depressive phase of bipolar illness. Other studies show that it reduces cravings for cocaine, marijuana, and even cigarette smoking. The only side effect thus far has been nausea when excessive doses of NAC are provided. Besides NAC, several other nutrients have also shown potential to treat most forms of mental illness because of their anti-inflammatory and anti-oxidant properties. These include omega-3 fatty acids, as found in fish oil. Aspirin and statin drugs also appear capable of reducing brain inflammation. Some studies show that intravenous glutathione appears to offer remarkable protective effects against the progression of Parkinson's disease.
    The usual dose of oral NAC is 600 milligrams, taken twice daily. Besides its positive effects against mental illness, NAC may also alleviate another epidemic condition, non-alcoholic fatty liver, which is linked to insulin insensitivity,  the onset of the metabolic syndrome and subsequent cardiovascular disease and diabetes.

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

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