Archive for the ‘Legal Steroid Alternative’ Category

By studying the genes of a German child born with unusually well developed muscles, an international research team has discovered the first evidence that the gene whose loss makes “mighty mice” also controls muscle growth in people.

Writing in the June 24 issue of the New England Journal of Medicine, German neurologist Markus Schuelke, M.D., and the team show that the child’s extra-large muscles are due to an inherited mutation that effectively silences the myostatin gene, proving that its protein normally keeps muscle development in check in people.

People with muscle-wasting conditions such as muscular dystrophy, and others just wanting to “bulk up,” have eagerly followed work on myostatin, hoping for a way to counteract the protein’s effects in order to build or rebuild muscle mass. But while research with mice has continued to reveal myostatin’s role and the effects of interfering with it, no one knew whether any of the results would be relevant to humans.

“This is the first evidence that myostatin regulates muscle mass in people as it does in other animals,” says Se-Jin Lee, M.D., Ph.D., professor of molecular biology and genetics in the Institute for Basic Biomedical Sciences at Johns Hopkins and co-author on the study. “That gives us a great deal of hope that agents already known to block myostatin activity in mice may be able to increase muscle mass in humans, too.”

Lee and his team discovered in 1997 that knocking out the myostatin gene led to mice that were twice as muscular as their normal siblings, lending them the moniker “mighty mice.” Later, others showed that naturally bulky cattle, such as Belgian Blues, got their extra muscles from lack of myostatin, too.

An unusual opportunity to examine myostatin’s role in humans arose when Schuelke examined a newborn baby boy, almost five years ago, and was struck by the visible muscles on the infant’s upper legs and upper arms. When ultrasound proved that the muscles were roughly twice as large as other infants’, but otherwise normal, Schuelke realized that a naturally occurring mutation in the child’s myostatin gene might be the cause.

Sequencing the myostatin gene from the boy and his mother, who had been a professional athlete, revealed a single change in the building blocks of the gene’s DNA. Surprisingly, the change was not in the gene regions that correspond to the resulting protein, but in the intervening regions that are used only to create protein-making instructions, thus changing the gene’s protein-building message.

“The mutation caused the gene’s message, the messenger RNA, to be wrong,” says Hopkins

neurologist Kathryn Wagner, M.D., Ph.D., who tested the genetic mutation’s effect in laboratory studies. “If the message had been used to make a protein, it would be much shorter than it should be. But we think the process doesn’t even get that far; instead the cells just destroy the message.”

Co-authors from Wyeth Research, Cambridge, Mass., analyzed samples of the child’s blood for evidence of the myostatin protein and found none. “Both copies of the child’s myostatin gene have this mutation, so little if any of the myostatin protein is made,” says Schuelke. “As a result, he has about twice the muscle mass of other children.”

Completely lacking myostatin, the boy is stronger than other children his age, and fortunately has no signs of problems with his heart so far, Schuelke says. But he adds that it’s impossible to know whether the lack of myostatin in that crucial muscle might lead to problems as the boy gets older.

While other family members — the boy’s mother and her brother, father and grandfather — were also reported to have been usually strong, only the mother’s DNA was available for analysis along with her son’s. Schuelke discovered that only one copy of the mother’s myostatin gene had the mutation found in both copies of her son’s myostatin gene. (We have two copies of each gene; one inherited from the mother and one inherited from the father.)

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Article adapted by MD Sports Weblog from original press release.
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 Contact: Joanna Downer
Johns Hopkins Medical Institutions

 

The Johns Hopkins researchers were funded by the National Institutes of Health and the Muscular Dystrophy Association. The German researchers were funded by the parents’ self-help group (Helft dem muskelkranken Kind).

Authors on the paper are Schuekle, Christoph Hubner, Thomas Riebel and Wolfgang Komen of Charite, University Medical Center Berlin, Germany; Wagner and Lee of Johns Hopkins; Leslie Stolz and James Tobin of Wyeth Research, Cambridge, Ma.; and Thomas Braun of Martin-Luther-University, Halle-Wittenberg, Germany.

*Under a licensing agreement between MetaMorphix Inc. and The Johns Hopkins University, Lee is entitled to a share of royalty received by the University on sales of products described in this article. Lee also is entitled to a share of sublicensing income from arrangements between MetaMorphix and American Home Products (Wyeth Ayerst Laboratories) and Cape Aquaculture Technologies. Lee and the University own MetaMorphix Inc. stock, which is subject to certain restrictions under University policy. Lee owns Cape Aquaculture Technologies stock, which is subject to certain restrictions under University policy. Lee has served as a paid consultant to MetaMorphix Inc. The terms of these arrangements are being managed by The Johns Hopkins University in accordance with its conflict of interest policies.

When given extra shots of the plant steroid brassinolide, plants “pump up” like major league baseball players do on steroids. Tracing brassinolide’s signal deep into the cell’s nucleus, researchers at the Salk Institute for Biological Studies have unraveled how the growth-boosting hormone accomplishes its job at the molecular level.The Salk researchers, led by Joanne Chory, a professor in the Plant Molecular and Cellular Biology Laboratory and a Howard Hughes Medical Institute investigator, published their findings in this week’s journal Nature.

“The steroid hormone brassinolide is central to plants’ growth. Without it, plants remain extreme dwarfs. If we are going to understand how plants grow, we need to understand the response pathway to this hormone,” says Chory. “This study clarifies what’s going on downstream in the nucleus when brassinolide signals a plant cell to grow.”

Brassinolide, a member of a family of plant hormones known as brassinosteroids, is a key element of plants’ response to light, enabling them to adjust growth to reach light or strengthen stems. Exploiting its potent growth-promoting properties could increase crop yields or enable growers to make plants more resistant to drought, pathogens, and cold weather.

Unfortunately, synthesizing brassinosteroids in the lab is complicated and expensive. But understanding how plant steroids work at the molecular level may one day lead to cheap and simple ways to bulk up crop harvests.

Likewise, since low brassinolide levels are associated with dwarfism, manipulating hormone levels during dormant seasons may allow growers to control the height of grasses, trees or other plants, thereby eliminating the need to constantly manicure gardens.

Based on earlier studies, the Salk researchers had developed a model that explained what happens inside a plant cell when brassinolide signals a plant cell to start growing.

But a model is just a model. Often evidence in favor of a particular model is indirect and could support multiple models. Describing the components of the signaling cascade that relays brassinolide’s message into a cell’s nucleus, postdoctoral researcher and lead author of the study Grégory Vert, now at the Centre national de la recherche scientifique (CNRS) in Montpellier, France, said, “All the players are old acquaintances and we knew from genetic studies that they were involved in this pathway. But when we revisited the old crew it became clear that we had to revise the original model.”

When brassinosteroids bind a receptor on the cell’s surface, an intracellular enzyme called BIN2 is inactivated by an unknown mechanism. Previously, investigators thought that inactivation of BIN2, which is a kinase, freed a second protein known as BES1 from entrapment in the cytoplasm, the watery compartment surrounding a cell’s nucleus, and allowed it to migrate or “shuttle” into the nucleus where it tweaked the activity of genes regulating plant growth.

A closer inspection, however, revealed that BIN2 resides in multiple compartments of a cell, including the nucleus, and it is there–not in the cytoplasm–that BIN2 meets up with BES1 and prevents it from activating growth genes. “All of a sudden the ‘BES1 shuttle model’ no longer made sense,” says Vert, adding that it took many carefully designed experiments to convince himself and others that it was time to retire the old model.

A new picture of how brassinosteroids stimulate plant growth now emerges based on those experiments: steroid hormones are still thought to inactivate BIN2 and reciprocally activate BES1, but instead of freeing BES1 to shuttle into the nucleus, it is now clear that the crucial activation step occurs in the nucleus where BES1 is already poised for action. Once released from BIN2 inhibition, BES1 associates with itself and other regulatory factors, and this modified form of BES1 binds to DNA, activating scores of target genes.

Referring to the work of Vert and other members of the brassinosteroid team, Chory says, “The old model may be out, but Greg’s new studies, together with those of former postdocs, Yanhai Yin and Zhiyong Wang, have allowed us to unravel the nuclear events controlling brassinosteroid responses at the genomic level. This turns our attention to the last mystery: the gap in our understanding of the events between steroid binding at the cell surface and these nuclear mechanisms.”

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Article adapted by MD Sports Weblog from original press release.
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Contact: Gina Kirchweger
Salk Institute

The Salk Institute for Biological Studies in La Jolla, California, is an independent nonprofit organization dedicated to fundamental discoveries in the life sciences, the improvement of human health and the training of future generations of researchers. Jonas Salk, M.D., whose polio vaccine all but eradicated the crippling disease poliomyelitis in 1955, opened the Institute in 1965 with a gift of land from the City of San Diego and the financial support of the March of Dimes.

Lower muscle mass and an increase in body fat are common consequences of growing older.

While exercise is a proven way to prevent the loss of muscle mass, a new study led by McMaster researcher Dr. Mark Tarnopolsky shows that taking a combination of creatine monohydrate (CrM) and conjugated linoleic acid (CLA) in addition to resistance exercise training provides even greater benefits.

The study to be published on Oct. 3 in PLoS One, an international, peer-reviewed online journal of the Public Library of Science, involved 19 men and 20 women who were 65 years or older and took part in a six-month program of regular resistance exercise training.

In the randomized double blind trial, some of the participants were given a daily supplement of creatine (a naturally produced compound that supplies energy to muscles) and linoleic acid (a naturally occurring fatty acid), while others were given a placebo. All participants took part in the same exercise program.

The exercise training resulted in improvements of functional ability and strength in all participants, but those taking the CrM and CLA showed even greater gains in muscle endurance, an increase in fat-free mass and a decrease in the percentage of body fat.

“This data confirms that supervised resistance exercise training is safe and effective for increasing strength and function in older adults and that a combination of CrM and CLA can enhance some of the beneficial effects of training over a six month period,” said Tarnopolsky, a professor of pediatrics and medicine.

This study provides functional outcomes that build on an earlier mechanistic study co-led by Tarnopolsky and Dr. S. Melov at the Buck Institute of Age Research, published in PLoS One this year, which provided evidence that six months of resistance exercise reversed some of the muscle gene expression abnormalities associated with the aging process.

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Article adapted by MD Sports Weblog from original press release.
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Contact: Veronica McGuire
McMaster University

Myostatin (MSTN) is a transforming growth factor-ß (TGF-ß) family member that plays a critical role in regulating skeletal muscle mass [1]. Mice engineered to carry a deletion of the Mstn gene have about a doubling of skeletal muscle mass throughout the body as a result of a combination of muscle fiber hyperplasia and hypertrophy [2]. Moreover, loss of myostatin activity resulting either from postnatal inactivation of the Mstn gene [3], [4] or following administration of various myostatin inhibitors to wild type adult mice [5][7] can also lead to significant muscle growth. Hence, myostatin appears to play as least two distinct roles, one to regulate the number of muscle fibers that are formed during development and a second to regulate growth of muscle fibers postnatally. The function of myostatin appears to have been conserved across species, as inactivating mutations in the myostatin gene have been demonstrated to cause increased muscling in cattle [8][11] , sheep [12], dogs [13] and humans [14]. As a result, there has been considerable effort directed at developing strategies to modulate myostatin activity in clinical settings where enhancing muscle growth may be beneficial. In this regard, loss of myostatin activity has been demonstrated to improve muscle mass and function in dystrophic mice [15][17] and to have beneficial effects on fat and glucose metabolism in mouse models of obesity and type II diabetes [18].

Myostatin is synthesized as a precursor protein that undergoes proteolytic processing to generate an N-terminal propeptide and a C-terminal dimer, which is the biologically active species. Following proteolytic processing, the propeptide remains bound to the C-terminal dimer and maintains it in an inactive, latent complex [6], [19], [20], which represents one of the major forms of myostatin that circulates in the blood [21], [22]. In addition to the propeptide, other binding proteins are capable of regulating myostatin activity in vitro, including follistatin [19], [21], FLRG [22], and Gasp-1 [23]. We previously showed that follistatin can also block myostatin activity in vivo; specifically, we showed that follistatin can ameliorate the cachexia induced by high level expression of myostatin in nude mice [21] and that transgenic mice expressing follistatin in muscle have dramatic increases in muscle mass [19]. Here, I show that overexpression of follistatin can also cause substantial muscle growth in mice lacking myostatin, demonstrating that other TGF-ß related ligands normally cooperate with myostatin to suppress muscle growth and that the capacity for enhancing muscle growth by targeting this signaling pathway is much larger than previously appreciated.

Results

Increased muscle mass in transgenic mice expressing FLRG

Previous studies have identified several proteins that are normally found in a complex with myostatin in the blood [22], [23]. One of these is the follistatin related protein, FLRG, which has been demonstrated to be capable of inhibiting myostatin activity in vitro. To determine whether FLRG can also inhibit myostatin activity in vivo, I generated a construct in which the FLRG coding sequence was placed downstream of a myosin light chain promoter/enhancer. From pronuclear injections of this construct, a total of four transgenic mouse lines (Z111A, Z111B, Z116A, and Z116B) were obtained containing independently segregating insertion sites. Each of these four transgenic lines was backcrossed at least 6 times to C57 BL/6 mice prior to analysis in order to control for genetic background effects. Northern analysis revealed that in three of these lines the transgene was expressed in skeletal muscles but not in any of the non-skeletal muscle tissues examined (Figure 1); in the fourth line, Z111B, the expression of the transgene was below the level of detection in these blots. As shown in Table 1, all four lines exhibited significant increases in muscle weights compared to wild type control mice. These increases were observed in all four muscles that were examined as well as in both sexes. Moreover, the rank order of magnitude of these increases correlated with the rank order of expression levels of the transgene; in the highest-expressing line, Z116A, muscle weights were increased by 57–81% in females and 87–116% in males compared to wild type mice. Hence, FLRG is capable of increasing muscle growth in a dose-dependent manner when expressed as a transgene in skeletal muscle.

The research was funded by grants from the NIH and the Muscular Dystrophy Association and by a gift from Merck Research Laboratories.

See http://www.jhu.edu/sejinlee/%20for%20more%20information for more information.
Citation: Lee S-J (2007) Quadrupling Muscle Mass in Mice by Targeting TGF-ß Signaling Pathways. PLoS ONE 2(8): e789. doi:10.1371/journal.pone.0000789

LINK TO THE PUBLISHED ARTICLE http://www.plosone.org/doi/pone.0000789

Source: Nick Zagorski
Johns Hopkins Medical Institutions

The serious athlete knows better than to rely just on a famous cereal to provide additional energy in preparation of a sporting event. Supplements have assumed an important role in today’s training regimen. Some – such as anabolic steroids — have been deemed illegal by most sports authorities. Others – such as caffeine and creatine — are controversial yet presently allowed.Background
Caffeine, the primary ingredient of coffee, is used as a central nervous system stimulant, diuretic, circulatory and respiratory stimulant, and as an adjunct in the treatment of headaches. Evidence shows that caffeine intensifies muscle contractions, masks the discomfort of physical exertion, and even speeds up the use of the muscles’ short-term fuel stores. Some exercise physiologists believe that caffeine might improve performance by increasing fat oxidation and conserving muscle glycogen.

Creatine is used by athletes to increase lean body mass and improve performance in single and repetitive high-intensity, short-duration exercise tasks such as weightlifting, sprinting, and cycling. It is a popular nutritional supplement that is used by physically active people – from recreational exercisers to Olympic and professional athletes. According to a recent survey, 28 percent of athletes in an NCAA Division IA program reported using creatine. The creatine that is normally present in human muscle may come from two potential sources: dietary (animal flesh) and internally manufactured.

The purpose of creatine supplementation is to increase either total creatine stores or phosphocreatine (PCr) stores within muscle. Supplementation increases the rate of resynthesis of creatine phosphate following exercise. Various studies have shown increased muscle PCr levels after supplementing with 20-30 grams of creatine monohydrate daily.

Creatine supplementation has also been known to shorten relaxation time during intermittent maximal iosometric muscle contraction. This shortened time, coupled with a creatine loaded muscle facilitates calcium absorption into the sarcoplasmic reticulum (the endoplasmic reticulum of skeletal and cardiac muscle). However, some believe that caffeine intake enhances calcium release from the sarcoplasmic reticulum.

The Study
This has lead a research team from Belgium to suggest that the combined effects of creatine and caffeine supplementation may be counterproductive to creatine’s effect on muscle relaxation time. The authors of the study, “Opposite Actions of Caffeine and Creatine on Muscle Relaxation Time in Humans” are P. Hespel, B. Op ‘T Eijnde, and M. Van Leemputte, all from the Department of Kinesiology, Katholieke Universiteit Leuven, Leuven, Belgium. Their findings appear in the February 2002 edition of the Journal of Applied Physiology.

Methodology
Ten physical education students (nine men and one woman) participated in the study. They were told to abstain from medication and caffeine intake one week prior to the experiment. The subjects were additionally asked to avoid changes in their level of physical activity and diet during the 25-week duration of the study. In this double blind experiment, the subjects performed the exercise test before and after creatine supplementation, short-term caffeine intake, creatine supplementation in the short term, acute caffeine intake, or a placebo.

This study required the random assignment of the students into five experimental protocols, each lasting eight days. Three elements were measured during an experiment consisting of 30 intermittent contractions of quadriceps entailing two seconds of stimulation and two seconds of rest. Measurements included maximum torque (Tmax), contraction time (CT) from 0.25 to 0.75 of Tmax, and relaxation time (RT) from 0.75 to 0.25 of max.

Results
Key findings of this study included:

· a confirmation of the fact that oral creatine supplementation shortens muscle relaxation time in humans: relation time was reduced by five percent and was significantly shorter than after the placebo;

· discovery that the intake of caffeine, combined with a daily creatine supplement, counteracted the beneficial effects of creatine intake on relaxation time and fatigue enhanced this inhibitory effect; and

· the observation that caffeine reduces the functional capacity of sacroplasmic reticulum calcium ATPase.

Conclusion The researchers believe that the findings from this experiment offer indirect evidence that suggests that facilitation of muscle relaxation may be important to the ergogenic action of creatine supplementation as well as power production during sprint exercises.

However, for the athlete in training, the key finding is that sustained caffeine intake, over a three-day period, negates the benefits of creatine supplements.

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Article adapted by MD Only Sports Weblog from original press release.
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Contact: Donna Krupa
American Physiological Society

We could not survive without hormones. They are among the most common and vital chemical messengers in the body. From head to toe, each moment of life, they signal cells to perform tasks that range from the ordinary to the extraordinary. Among their many roles, hormones help regulate body temperature, blood pressure, and blood sugar levels. In childhood, they help us “grow up.” In the teen years, they are the driving force behind puberty.

What Is A Hormone?

Hormones are powerful chemicals that help keep our bodies working normally. The term hormone is derived from the Greek word, hormo, which means to set in motion. And that’s precisely what hormones do in the body. They stimulate, regulate, and control the function of various tissues and organs. Made by specialized groups of cells within structures called glands, hormones are involved in almost every biological process including sexual reproduction, growth, metabolism, and immune function. These glands, including the pituitary, thyroid, adrenals, ovaries, and testes, release various hormones into the body as needed.

Levels of some hormones like parathyroid hormone, which helps regulate calcium levels in the blood and bone, actually increase as a normal part of aging and may be involved in bone loss leading to osteoporosis. But the levels of a number of other hormones, such as testosterone in men and estrogen in women, tend to decrease over time. In other cases, the body may fail to make enough of a hormone due to diseases and disorders that can develop at any age. When this occurs, hormone supplements—pills, shots, topical (rub-on) gels, and medicated skin patches—may be prescribed.

How Hormones Work

Most hormones exist in very low concentrations in the bloodstream. Each hormone molecule travels through the blood until it reaches a cell with a receptor that it matches. Then, the hormone molecule latches onto the receptor and sends a signal into the cell. These signals may instruct the cell to multiply, to make proteins or enzymes, or to perform other vital tasks. Some hormones can even stimulate a cell to release other hormones. However, no single hormone affects all cells in the same way. One hormone, for example, may stimulate a cell to perform one task, while the same hormone can have an entirely different influence over another cell. The response of some cells to hormonal stimulation also may change throughout life.

DHEA

Dehydroepiandrosterone or DHEA is made from cholesterol by the adrenal glands, which sit on top of each kidney. Production of this substance peaks in the mid-20s, and gradually declines with age in most people. What this drop means or how it affects the aging process, if at all, is unclear. In fact, scientists are somewhat mystified by DHEA and have not fully sorted out what it does in the body. However, researchers do know that the body converts DHEA into two hormones that are known to affect us in many ways: estrogen and testosterone.

Human Growth Hormone

Human growth hormone (hGH) is made by the pituitary gland, a pea-sized structure located at the base of the brain. It is important for normal development and maintenance of tissues and organs and is especially important for normal growth in children.

Studies have shown that injections of supplemental hGH are helpful to certain people. Sometimes children are unusually short because their bodies do not make enough  GH. When they receive injections of this hormone, their growth improves. Young adults who have no pituitary gland (because of surgery for a pituitary tumor, for example) cannot make the hormone and they become obese. When they are given hGH, they lose weight.

Like some other hormones, blood levels of hGH often decrease as people age.Although there is no conclusive evidence that hGH can prevent aging, some people spend a great deal of money on supplements. These supplements are claimed by some to increase muscle, decrease fat, and to boost an individual’s stamina and sense of well being. Shots—the only proven way of getting the body to make use of supplemental hGH—can cost more than $15,000 a year. They are available only by prescription and should be given by a doctor. Some dietary supplements, known as human growth hormone releasers, are marketed as a low-cost alternative to hGH shots. But claims that these over-the-counter products retard the aging process need to be examined. While some studies have shown that supplemental hGH does increase muscle mass, it seems to have less impact on muscle strength or function in older adults.

Testosterone

Ask an average man about testosterone, and he might tell you that this hormone helps transform a boy into a man. Or, he might tell that you that it has something to do with sex drive.   Or, if he has read news stories in recent years, he might mention male menopause, a condition thought to be caused by diminishing testosterone levels in aging men.

Testosterone is indeed a vital sex hormone that plays an important role in puberty. In men, testosterone not only regulates sex drive (libido), it also helps regulate bone mass, fat distribution, muscle mass and strength, and the production of red blood cells and sperm.But contrary to what some people believe, testosterone isn’t exclusively a male hormone.  

Women produce small amounts of it in their bodies as well. In men, testosterone is produced in the testes, the reproductive glands that also produce sperm. The amount of testosterone produced in the testes is regulated by the hypothalamus and the pituitary gland.

As men age, their testes often produce somewhat less testosterone than they did during adolescence and early adulthood, when productionof this hormone peaks. In fact, many of the changes that take place in older men often are incorrectly blamed on decreasing testosterone levels. Some men who have erectile difficulty (impotence), for instance, may be tempted to blame this problem on lowered testosterone. However, in many cases, erectile difficulties are due to circulatory problems, not low  testosterone. Still, some men may be helped by testosterone supplementation. For these few men who have extreme deficiencies, testosterone therapy in the form of patches, injections, or topical gels may offer substantial benefit.

Testosterone products may help a man with exceptionally low testosterone levels maintain strong muscles and bones, and increase sex drive. However, what effects testosterone replacement may have in healthy older men without these extreme deficiencies requires more research.The NIA is investigating the role of testosterone therapy in delaying or preventing frailty. Results from preliminary studies involving small groups of men have been inconclusive, and it remains unclear to what degree supplementation of this hormone can sharpen memory or help men maintain stout muscles, sturdy bones, and robust sexual activity.

Many other questions remain about the use of this hormone in late life. It is unclear, for example, whether men who are at the lower end of the normal range of testosterone production would benefit from supplementation.Some investigators are also concerned about the long-term harmful effects that supplemental testosterone might have on the aging body. While some epidemiologic studies suggest that higher levels of testosterone are not associated with the higher incidence of prostate cancer, it is not yet known if testosterone therapy increases the risk of such cancer, the second leading cause of cancer death among men.

The bottom line: Although some older men who have tried testosterone therapy report feeling more energetic or younger, testosterone supplementation remains a scientifically unproven method for preventing or relieving any physical and psychological changes that men with normal testosterone levels may experience as they get older. The NIA is expanding its research to gather more evidence on the risks and benefits of testosterone supplementation in aging men with low testosterone levels.

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Article adapted by MD Only Sports Weblog from original press release.
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Source:  National Institute on Aging

If you decide to make the choice to begin bodybuilding, it is good to keep in mind not to become too overzealous and burn itself out too quickly, or even worse, injure yourself. Someone beginning bodybuilding should take it as a gradual process that will eventually lead to more experienced exercise routines.

Below are some suggestions and tip’s for bodybuilding beginners if that is what you choose to pursue.

Diet And Bodybuilding

One of the most important aspects for beginning bodybuilders is diet. If you keep eating fast food or other kinds of junk food you cannot have any expectations to be successful at this sport. When it comes to sculpting your body discipline is one of the main necessities. That is why it is recommended by trainers that you start to consume primarily meat, nuts, fish, grain and milk. Foods such as these are low in fat, as well as high in protein that will assist in helping build muscle as well as increase your metabolism.

Your Workout Routine

Concerning your workout regimen, starting off slowly is important for beginners in this sport. Beginners in this activity in the beginning come to the realization that even though they really want to look as if they have the same physique as bodybuilders on the cover of magazines, or on TV, it is a work in progress. Bodybuilding beginners should start with two sets of repetitions with roughly a minute of rest in between.

They should do this for roughly 45 minutes, 4 days a week. After four weeks have passed, after allowing a body and a time to build itself up, at that point the bodybuilder can start to move gradually up to 60 minutes of a workout while doing three sets of repetitions with roughly a minute of rest in between. At approximately this point, their body should slowly start to change, muscle should be gained and fat should be lost.

Along with exercise and diet, rest is equally important with bodybuilding beginners. This is vitally important, as the individuals muscles need to grow during this period. At a minimum six to eight hours of sleep is recommended per night.

Whatever Your Desires and Goals Are

Whether you want to get into bodybuilding for competitive reasons or for your own personal achievement, it is essential for beginners in this sport to be on a gradual process. Making sure that proper rest, diet and exercise are accomplished is important to physical success. At first do not concern yourself about looking like a bodybuilder immediately; focus on a workout plan that will work for your specific body type as well as your specific goals.

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Author Resource:- Listen to Corbin Newlyn as he shares his insights as an expert author and an avid writer in the field of bodybuilding. If you would like to learn more go to Bodybuilding Advice and at Female Bodybuilding tips.

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