Friday, December 28, 2012

Feeding the Female Athlete:Nutritional requirements for strength-training women by Jerry Brainum


A recently published comprehensive review examined the nutritional requirements of women who regularly engaged in bodybuilding, powerlifting and/or weightlifting. While many of their nutritional requirements are similar to those of men, there are a few notable differences.
    Women often initially show greater strength gains because they’re usually weaker than men at the start of a training program. Another obvious difference between the sexes is the ultimate degree of attainable muscle size. Because of both structural and hormonal differences, the average man can develop far larger muscles than the average woman. That’s most often attributed to men’s higher level of testosterone. Women won’t develop a masculine body shape—unless, of course, they use testosterone-based drugs and other anabolic substances associated with muscle bulk. (The fact that women respond to such drugs is evident from the appearance of some competitive female bodybuilders, whose muscular size far exceeds what could be developed through natural means.) Women who choose the natural route can still attain a significant loss of bodyfat and muscular definition, though it’s admittedly an uphill battle in comparison to males because a woman’s hormonal profile—higher estrogen, lower testosterone—tends to favor fat accretion, especially in the lower body and just under the skin.
    From the standpoint of exercise metabolism, women show a clear superiority in fat use over men—again, likely the result of higher estrogen. When engaged in exercise, women can tap into fat stores more efficiently and rapidly than men. The performance gap between men and women is far less significant in endurance than strength sports.
     Women store higher levels of fat in muscle, known as intramuscular triglyceride. IMTG is believed to be related to a woman’s higher percentage of slow-twitch muscle fibers, also known as “endurance” fibers, which preferentially burn more fat during activity and at rest. Studies of endurance exercise show that women tap into IMTG at greater levels than men.
    The greater use of fat spares muscle glycogen, which is stored carbohydrate, an effect that extends to weight training, with women using more fat and less glycogen. It’s attributed to a lower activity of the glycolytic enzymes in muscle that activate muscle glycogen breakdown, which may be due to higher estrogen levels.
     Because of their concern with appearance, many women overly restrict calorie intake, which some studies show can work against elite female athletes. Overly restricting calories leads to a lower metabolic rate, which paradoxically increases bodyfat levels. A low energy intake also leads to fatigue, irritation and decreased performance—as it does in men.
     Women who don’t eat enough show decreased thyroid hormone activity, which not only depresses fat losses but also results in lower energy. Bone mass, fertility and creatine replenishment in muscle are also adversely affected. Not consuming enough food increases the risks of nutrient deficiencies.
Since weight training increases resting metabolic rate for up to 36 hours, women should get most of their calories before and after training. That keeps calories from shifting to bodyfat stores. From a practical standpoint, women engaged in weight training need to eat 39 to 44 calories per kilogram of bodyweight daily. Health and energy problems occur if an active woman’s total daily calories drop below 1,800.
     Studies confirm that women handle carbohydrates differently than men. Women not only use less glycogen during training but also synthesize less after a workout. To synthesize more glycogen following training, a woman must take in up to eight grams of carbohydrate per kilogram of bodyweight. That much carb, however, would use up a large percentage of her daily calories.
    Women do need carbohydrates for purposes of glycogen replenishment following training, but they don’t need to eat like endurance athletes. The best type of carbs are those with a low-glycemic rating, meaning that they provide a slower delivery of carbs into the body, favoring less fat synthesis. Foods high in fiber have lower glycemic index numbers—fruits, vegetables, brown rice, whole-grain breads, oatmeal, beans, legumes and sweet potatoes. Cruciferous vegetables, such as broccoli, brussels sprouts, kale, cabbage and bok choy, are particularly beneficial for women because they contain natural elements that lower excessive estrogen levels, thus helping women lose superfluous water and fat.
     Studies show that men burn more protein during training than women do. Women’s higher use of fat during exercise may provide a sparing effect on protein, as well as glycogen. On the other hand, studies also show that women are less efficient than men in promoting muscle protein synthesis after training. That points to a need to get more protein at that critical time. For building lean mass, women are advised to eat small amounts of high-quality, rapidly digested protein with some carbohydrate before and after exercise and between meals to maintain an optimal anabolic metabolic environment.
    Women are also advised to ignore the myths about high-protein diets, among them that eating a lot of protein leads to bone loss and osteoporosis. Studies show an opposite effect: A higher protein intake promotes bone mass. Some high-protein foods also provide nutrients essential to bone formation and maintenance, such as calcium, magnesium and vitamin D.
     Some women espouse vegetarianism in the belief that it’s both healthier than eating meat and favors less bodyfat. While it’s indeed possible to maintain health while forgoing animal proteins, that’s not ideal for bodybuilding. Women need to pay special attention to iron intake, since they’re more at risk for anemia. Meat contains the most easily absorbed source of iron, heme iron, while the iron contained in plant sources often isn’t as available, due to iron-blocking substances in plants, such as oxalate and phytate. Animal proteins also provide such vital nutrients as B-complex vitamins and minerals. Women who are worried about the fat content of meat can take a high-quality protein supplement such as whey and/or casein, which will be devoid of fat and carbs.
    Some women may also be overly concerned about fat, thinking that eating fat promotes bodyfat. A suitable fat intake helps replenish the intramuscular fat stores that women tap into during exercise, which also spares their limited muscle glycogen stores. Women should get 30 percent of their daily calorie requirement from fat to replenish depleted IMTG stores. If they don’t get enough dietary fat, those muscle fat stores can remain depleted for two days after training, adversely affecting exercise ability.
     Dietary fat is also required to maintain sex hormone function in women, just as it is in men. If a woman doesn’t eat enough fat, she’ll likely experience menstrual disturbances. Getting less than 15 percent of calories from fat also increases the risk of an essential fatty acid deficiency, which can result in diminished fat burning in addition to serious health problems.
   Dietary fats should come from lean protein foods, nuts, seeds, fatty fish such as salmon (or fish oil supplements for omega-3 if you hate eating fish), as well as flaxseed, safflower, canola and extra-virgin olive oils. Avoid trans fats—also known as partially hydrogenated fats—which favor bodyfat, cancer and cardiovascular disease, in addition to amino acid loss in muscle. Eating healthful fats permits a lower carb intake, favoring better body composition for female strength athletes.
    Women respond to most supplements like men. Creatine works well, although it doesn’t block protein oxidation as it does in men. It’s a moot point, though, since women burn less protein than men during exercise anyway. Women should also avoid all types of testosterone-boosting supplements, including the estrogen blockers. Such supplements are great for men, but in women they can create serious hormonal disturbances.
    DHEA acts as a hormone precursor in both men and women. In men it tends to convert into estrogen, but in women it always converts into testosterone. While that initially sounds good for female strength athletes, many of them have developed serious cases of acne when taking DHEA. That’s not so surprising if you consider that the DHEA spurt in teenagers of both sexes is what causes acne. A form of DHEA that doesn’t convert into sex hormones, 7-keto DHEA, is also available in supplement form. It may help prevent dieting plateaus by maintaining thyroid output, but it’s free of the adverse effects associated with regular DHEA.
Add it up, and it’s clear that women strength athletes should reduce carbohydrate intake in favor of “good” fat sources while increasing their protein, especially after training. Doing so ensures great progress while maintaining energy and health.   

Volek, J.S., et al. (2006). Nutritional aspects of women strength athletes. British J Sports Med. 40:742-48.




©,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.

 

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Wednesday, December 19, 2012

Muscle Destruction From Steroids, and how Nolvadex really works by Jerry Brainum


Anabolic steroids are synthetic, structurally modified versions of testosterone. They are termed “anabolics” because they provoke reactions in muscle and other tissues that result in either growth or stabilization of the tissues. Anabolic steroids have legitimate medical uses, such as preventing excessive tissue breakdown. Athletic use of steroids, however, is far more publicized than their medical applications. Bodybuilders and other athletes who use anabolic steroids often self-medicate with dosages far above what medical treatment requires. In line with the adage “Only the dose determines the poison,” those using large doses of steroids or several of the drugs simultaneously can be subject to systemic side effects: liver problems, negative changes in blood lipids and heart structure, fluid retention, gynecomastia in males, virilism in women, inhibition of testosterone production and possible adverse behavioral changes in susceptible individuals.
     While all of those side effects are possible in theory, in reality they rarely occur. Athletes monitor themselves for adverse effects, although rarely under the care of a physician. They use other drugs to mitigate some of the side effects of large doses, such as estrogen-blocking drugs to prevent estrogen-related side effects.
      Idiosyncratic reactions, however, are always possible. That means some steroid users experience unusual or rare side effects. Why that happens is unknown but probably has something to do with genetics or individual susceptibility. One recent case study illustrates the point.
      A 39-year-old previously healthy amateur bodybuilder reported to an emergency room with excruciating pain and inability to move his right shoulder after an injection of steroids in that shoulder, which was followed by a shoulder workout on the same day.1 He trained five days a week and had done so for the previous eight years. For the past seven years he had also used anabolic steroids. Deploying a 23-gauge needle and sterile technique, he injected steroids into his shoulder four times a week. He denied doing any type of abrupt overstretching exercise that could have caused a severe muscle strain.
    The physical exam showed that his right deltoid was swollen and tense, with the skin around it red, tender and warm. He had no apparent bruising and no fever. The picture became clearer when blood tests revealed a creatine kinase enzyme level of 18,200—normal is below 195. Creatine kinase is an enzyme that adds a phosphate to creatine in muscle, thereby helping the muscle store creatine. When muscle is damaged, even with intense exercise, CK is released from the muscle into the blood. Having large amounts in the blood point to severe muscle damage. Because the bodybuilder’s blood potassium, also released by damaged muscle, was high, the diagnosis was rhabdomyolysis, which means massive muscle destruction.
     Rhabdomyolysis can have several causes, among them toxic reactions, lack of blood flow to muscle, infections and inflammation. One type, which is called exertional rhabdomyolysis, occurs when muscle cells are damaged by unaccustomed exercise. For example, untrained persons who exercise in hot, humid weather can develop it, but it can also occur in well-trained athletes. Switching to a new mode of intense training without preparation can bring it on. A few cases have occurred in bodybuilders who abruptly began high-rep—100 reps or more per set—training regimens, particularly in hot weather without drinking adequate fluids.
     Destruction of the muscle cell membrane causes the leakage of intramuscular materials, such as CK, minerals and other enzymes. In severe cases myoglobin, the oxygen-carrying protein in muscle, is also released in large amounts and can crystallize in the kidneys. That blocks the kidneys’ filtering units and rapidly induces kidney failure. Without immediate treatment, death follows.
    Several cases of exercise- or drug-related rhabdomyolysis in long-distance runners, football players and military personnel have been reported in the medical literature. One published case study involved a 25-year-old male professional dancer who showed up at a hospital complaining about severe thigh and calf pain.
     The pain began after he engaged in a 45-minute aerobic workout on a cross-training machine. He experienced severe muscle cramps and a day later showed up at the hospital. He was given an anti-inflammatory drug but returned two days later, still in severe pain. Tests revealed a high CK level, which led to a diagnosis of rhabdomyolysis. He received intravenous fluids and buffers such as potassium bicarbonate to alkalinize his blood and prevent myoglobin precipitation in the kidneys. He received cortisone to relieve inflammation, Valium to relax his muscles and Tylenol for pain.
     The dancer had used two steroid drugs, Winstrol and Primabolan, four ampoules each a week apart. Before his pain set in, he’d used only one ampoule of Primobolan a few days before, injecting it into his thigh. His treatment proved successful, and he was released from the hospital.
     Reports involving bodybuilders have been sporadic and may have been written off as severe muscle strains. One 40-year-old bodybuilder who initially denied using any anabolic steroid or other drugs suffered rhabdomyolysis in his biceps. In fact, he’d also injected Winstrol into the affected shoulder, leading the attending physicians to suspect that the injection itself had caused the localized rhabdomyolysis. The doctors suggested that he might have had a toxic reaction to the drug—a not unwarranted assumption, as most forms of injectable Winstrol are veterinary versions not subject to the same quality control as drugs slated for human use. A more likely possibility is that the bodybuilder had a compartment syndrome, the name given to a swelling of the fascia that surrounds muscle. Usually occurring in the calf, it’s rare in the shoulders because of the higher mobility of the shoulder and its attendant fascia. Only three previous cases were reported in the medical literature, and they involved drug overdoses or intoxication after minor trauma.
    The analysis was that the bodybuilder suffered increased compartment syndrome due to the injected fluid, causing a blood clot, which decreased the elasticity in the shoulder fascia. Compounded by the bodybuilder’s growing shoulder muscle mass, those factors increased the intracompartmental pressure. The shoulder workout that followed amplified the effect of limited blood flow, which resulted in the characteristic muscle breakdown. His treatment proved successful, and he returned to normal training with no evidence of kidney problems.

                                                 How Nolvadex Really Works

Tamoxifen citrate, or Nolvadex, is used to treat breast cancer, particularly in older women who have estrogen-sensitive breast cancer; 70 to 80 percent of all breast cancers are estrogen-sensitive. For years it’s also been used by male bodybuilders on anabolic steroids to help prevent gynecomastia, or the formation of male breast tissue.
    Gyno is caused by an imbalance between estrogen and testosterone, favoring increased estrogen. The steroid drugs convert into estrogen through the actions of aromatase, an enzyme found throughout the body. The usual practice for preventing estrogen-related side effects, which include excess water and fat retention, is to take drugs that either interfere with aromatase activity, such as Arimidex, or block estrogen cell receptors, such as Nolvadex.
     Nolvadex is the older of the two “estrogen solutions,” and most athletes looking to lower estrogen now rely on aromatase-inhibitors because of the notion that they’re more reliable in diminishing estrogen. Nolvadex is also thought to interfere with the activity of growth hormone and its anabolic product, insulinlike growth factor 1. On the other hand, lowering estrogen too much, which is possible with extended use of aromatase inhibitors, may interfere with the anabolic reactions involving androgen receptors and testosterone.
Nolvadex is structurally similar to estrogen and can bind to estrogen cell receptors, thereby blocking estrogen from binding to them. If estrogen cannot interact with its cellular receptors, it cannot exert biological activity and becomes inert. Nolvadex also interferes with the negative feedback signal sent by circulating estrogen in the blood to the pituitary gland. That results in blunting release of gonadatropins, including luteinizing hormone, which controls testosterone synthesis at the Leydig cells in the testes. The reduced estrogen-feedback signal induced by Nolvadex results in greater release of luteinizing hormone and higher blood testosterone. One author has noted that using 20 milligrams of Nolvadex daily—a standard bodybuilding dose—can raise blood testosterone by 150 percent. On the other hand, Nolvadex has both agonist and antagonist properties. That is, when used in high doses for extended times, it may act more like an estrogen agonist. Animal studies show that extended use of Nolvadex interferes with the activity of two testicular enzymes involved in testosterone synthesis, although that hasn’t been confirmed in human studies.
    What’s interesting about Nolvadex is that recent research that directly compared it to the newer and supposedly more effective aromatase-inhibiting drugs found that Nolvadex appears to be more effective in preventing gynecomastia and other estrogen-related effects in men. How can that be?
    A study presented at a scientific conference related to breast cancer research may provide the answer. Researchers from the famed Mayo Clinic explained that Nolvadex isn’t active but is rather like a pro-hormone. In the liver, enzymes convert Nolvadex into two metabolites that are the effective versions of the drug, endoxifen and 4-hydroxytamoxifen. The study sought to explain why using Nolvadex helps some women with breast cancer but not in others. The researchers found that an enzyme system in the liver called CYP2D6 must convert Nolvadex into its active metabolites in order for the drug to work. In some women that system isn’t as active, which means that they don’t convert the Nolvadex into its most active metabolite, endoxifen. For them Nolvadex doesn’t effectively treat breast cancer.
     Most surprising, however, was the finding that endoxifen didn’t just block the estrogen cell receptor, as was previously supposed, but actually degraded it. No receptor means no estrogen cell activity. So drug researchers are now at work producing a direct endoxifen drug, since that’s the actual active form of Nolvadex. The direct form won’t depend on liver enzymes to become active.
     While this study involved in vitro, or isolated-cell, protocols, there is no reason to believe that the results don’t apply to men. The findings explain why Nolvadex works better in preventing estrogen-related side effects in some men more than others. In addition, the fact that this active metabolite of Nolvadex actually degrades estrogen receptors explains why the head-to-head studies comparing Nolvadex to aromatase inhibitors showed Nolvadex to be superior in preventing estrogen-related side effects in men. A notable bonus: Nolvadex is far less expensive than most aromatase inhibitors.
References
1 Farkash, U., et al. (2009). Rhabdomyolysis of the deltoid muscle in a bodybuilder using anabolic-androgenic steroids: A case report. J Athlet Training. 44:98-100.
2 Adamson, R., et al. (2005). Anabolic steroid-induced rhabdomyolysis. Hosp Med. 66:362.

 
 ©,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

 

Monday, December 3, 2012

Growth Hormone Muscle Zone by Jerry Brainum


Bodybuilders and other athletes speak of growth hormone with hushed reverence. Many think that GH is what’s primarily responsible for the massive physiques that dominate professional bodybuilding today and that seem to dwarf those of a generation ago.
    While it’s true that GH is one of three primary anabolic hormones in the body (the others being testosterone and insulin), it’s also true that GH is shrouded by myth. Take the notion that using a pharmaceutical form of GH enables you to eat as many as 10,000 calories a day yet lose appreciable levels of bodyfat simultaneously. Another idea is that GH promotes hyperplasia, or a splitting of muscle fibers into new fibers—a property that other anaboliic hormones don’t have.
    The reality about GH is not quite so dramatic. The only drug-tested Mr. Olympia occurred in Chicago back in 1990. Several of the competitors told me, off the record, that they planned to circumvent that year’s drug prohibition by using large amounts of GH. Then, as now, there was no official test to show that an athlete was injecting GH. The competitors figured that GH provided little or no actual anabolic or muscle-building effects by itself but did pack a punch when used with anabolic steroids. When the steroids were eliminated a few weeks before the contest, GH froze the muscle size produced by the earlier drug cycles and kept delivering fat-loss benefits.
     That makes a lot of sense because GH is a survival hormone. Among its many functions is that it preserves lean mass, mainly muscle, by promoting the use of bodyfat as fuel. GH also comes into play as a counter-regulatory hormone to insulin. When insulin lowers blood glucose, GH and other hormones prevent the levels from dropping too low. The antagonist effect of GH against insulin is so potent that many researchers believe that large doses of it promote insulin insensitivity, thus increasing the chance for diabetes. More recent studies, however, show that normal levels of GH, such as that induced by exercise, help prevent both metabolic syndrome and diabetes by cutting visceral, or deep-lying, abdominal fat.
     The anabolic reputation of GH has also fostered a large response from the food supplement industry. Most GH supplements on the market are based on various combinations of amino acids. Whether aminos actually promote a GH response depends on how and when they’re used. Intravenous administration of the amino acid arginine in 30-gram doses promotes significant GH release unless you’re deficient in the hormone or have defective hormone release mechanisms.
    When it’s taken orally, however, the scenario changes. Arginine goes to the liver, where it encounters the enzyme arginase, which degrades it. You could get around the formidable enzymatic barrier by increasing the oral dose, but then you’d probably have to deal with nausea. Besides, when you take arginine prior to weight training, it has the paradoxical effect of blunting GH release.
     Several studies have shown that a drug form of GH combined with exercise offers no advantages over exercise alone. On the other hand, the GH release produced by exercise does offer several significant effects for bodybuilding purposes. An increase in GH, coupled with the rise in other anabolic hormones, improves muscle protein synthesis. That translates into increased muscle size and strength. The actual anabolic effector is insulinlike growth factor 1, which is produced in the liver under the stimulation of GH release.
The IGF-1 produced in the liver is used throughout the body. IGF-1 is also produced locally in trained muscle, often as a result of damage from intense exercise. That IGF-1 is used for muscle repair and promotes the activity of muscle stem cells, or satellite cells. Locally produced IGF-1 is further spliced into two variants in muscle, with one being the mechano growth factor, or MGF, probably the most anabolic substance of all because it directly controls the activity of muscle satellite cells. MGF is so potent that it can resuscitate dying satellite cells in older animals and people.
     If providing GH alone doesn’t do much for muscle growth, and considering that IGF-1 and MGF are the primary anabolic growth factors in muscle, why be concerned about promoting GH release through exercise?
One reason is the size-and-strength synergy of GH, testosterone and insulin. Each hormone appears to potentiate the anabolic effects of the others. They’re synergistic in another sense too. A high level of GH offsets the possible side effects of other anabolic hormones. For example, by itself insulin is the greatest promoter of increased bodyfat synthesis. It also lowers blood glucose, leading to a loss of training energy and increased fatigue. GH and, to a lesser extent, testosterone counteract insulin’s bad side.
Of the three major anabolic hormones, GH provides the most potent fat mobilization, especially for people on low-carbohydrate diets who exercise. GH is secreted most substantially when blood glucose and fat levels are lower and amino levels are higher—conditions typical of people on low-carb diets.
     One reason it’s so hard for people who have a lot of bodyfat to lose weight is that they usually have higher resting insulin levels. That opposes GH release. When they begin to exercise, their normal GH release response is also blunted, making fat loss an arduous process. The good news is research showing that losing bodyfat through regular diet and exercise normalizes the GH response to exercise.
    Another reason you want to promote a GH response during exercise is that GH is uniquely useful for preserving and repairing connective tissue, such as ligaments and tendons. Anyone who’s lifted for any length of time knows well the training setbacks caused by connective-tissue injuries. Connective tissue, unlike muscle, has a poor blood supply, so healing injuries can take weeks or even months. GH strengthens and repairs connective tissue, accelerates its healing and prevents the damage from occurring in the first place.
That helps explain why so many world-class athletes use GH, even if they aren’t interested in building massive muscles. GH helps them recuperate from intense training and protects connective tissue from injury.
GH’s role in protecting connective tissue also applies to people as they age. Most forms of joint pain involve connective tissue and often appear when GH levels drop with aging. Paradoxically, injecting large doses of GH causes joint pain in many people through an overgrowth of tissue.
     One interesting aspect of exercise and GH is that normally when large amounts of GH enter the blood, the brain’s feedback system blunts release of the hormone that releases GH. Yet with continued exercise, the body overcomes the feedback.
     As to what precisely sets off GH release during exercise, scientists still aren’t sure. There are, however, several candidates.One theory is that exercise-induced muscle tension provides a neural effect, leading to a GH release. Another popular hypothesis is that nitric oxide stimulates GH release during exercise. Studies show that NO does potently promote GH release, but they involved isolated cells, and whether the effect occurs in a living human body is still speculative.The most popular explanation is that the hydrogen ions, or acid produced in muscle, relay a chemical message to the brain that results in a heightened GH response. When subjects take antacids, such as sodium bicarbonate, during exercise, the GH release is blunted.
That raises the question of whether using supplements that reduce muscle acidity, such as beta-alanine, would reduce GH release. The answer is no; supplements work in the muscle, and the acid feedback mechanism that stimulates GH release occurs in the blood.Thus, ingesting sodium bicarbonate, or baking soda, which has an alkalizing effect on blood acidity, would likely blunt GH release if ingested prior to physical activity.
    So what type of exercise promotes the greatest GH release? The short answer is the kind that’s brief, hard and intense. Lifting weights would get more results than most aerobic workouts. To get a GH response from aerobics requires passing what exercise scientists refer to as the lactate threshold—when lactic acid appears in the muscle. That event signals a change from aerobic to anaerobic exercise metabolism. While doing high-intensity aerobics, such as interval training, promotes higher GH release, it also lowers the fat oxidation that occurs during lower-intensity aerobics. Interestingly, doing high-intensity aerobics increases resting pulse amplitude of GH release, meaning that you burn more fat at rest. That may help explain why interval training leads to greater fat loss than conventional steady-state aerobics.
    Early studies suggested that you can achieve the greatest GH response from exercise that you do several times a day. More recent studies, however, demonstrate that you get the greatest effect from the initial workout, with workouts done later on the same day leading to blunted GH release. That’s because the workout stimulates higher blood lipids, which persist for several hours afterward. Higher blood fat blunts further GH release during exercise.1
    The more muscle you use during an exercise, the greater the release of GH. So training larger muscle groups, such as the legs and back, produces a far greater GH release than training smaller muscle areas, such as arms or shoulders. Aerobic equipment that involves both upper- and lower-body muscles simultaneously stimulates higher GH levels than lower-body-only exercises or machines.
    One reason exercise promotes GH release is that it usually raises core body temperature. GH regulates body temperature and helps prevent overheating during exercise. Conversely, exercising in the cold inhibits the release of GH.2 So, for example, rowers have higher levels of GH than swimmers, whose core temperature goes down because they’re in the water.
    Eating a high-fat meal prior to training blunts GH release. So will eating carbs, but to a lesser extent.3 Some studies show that having a protein-and-carb drink before and after training leads to a greater GH release, though other studies haven’t substantiated that. Using asthma drugs in the category of beta-2 agonists also blunts GH release during exercise—that includes the drug clenbuterol. Researchers think that’s because the drugs increase the release of somatostatin, a protein that blocks GH. Even not drinking enough water during training blunts GH release.4
     GH response is greater when you do multiple sets than when you do single sets. One study showed a greater GH response among exercisers doing four sets than those doing two, but doing six had no further effect. Another study showed that doing forced reps increased GH release.
Doing a high-rep set at the end of a series of heavier sets also produces a much greater GH release, as does resting one minute or less between sets. Lowering the weight (eccentric or negative reps) produces greater GH release than raising the weight.5
   Since most scientists agree that GH and IGF-1 drop precipitously with age and that the lack of those hormones produces many symptoms associated with aging, continuing to engage in exercise known to elicit the greatest GH response can produce a reliable antiaging affect. It’s likely that the true advantages of weight training will manifest themselves in the realm of longevity and quality of life.

References
1 Stokes, K., et al. Human growth hormone responses to repeated bouts of sprint exercise with different recovery periods between bouts.J App Physiol. In press.
2 Wheldon, A., et al. (2006). Exercising in the cold inhibits growth hormone secretion by reducing the rise in core temperature. Growth Hor IGF-1 Res.16:125-31.
3 Cappon, C.P., et al. (1993). Acute effects of high-fat and high-glucose meals on the growth hormone response to exercise. J Clin Endocrin Metabol. 76:1418-22.
4 Peyreigne, C., et al. (2001). Effect of hydration on exercise-induced growth hormone response. Eur J Endrocrin. 145:445-50.
5 Kraemer, W.J., et al. (2005). Hormonal responses and adaptations to resistance exercise and training.Sports Med. 35:339-61.
 




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

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

 

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

 

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

 

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