Archive for the ‘Men Health’ Category

“No pain, no gain.” So say those working out to build up their muscles, and on a cellular level it is a pretty accurate description of how muscle mass increases. Exercise causes tears in muscle membrane and the healing process produces an increased amount of healthy muscle. Implicit in this scenario is the notion that muscle repair is an efficient and ongoing process in healthy individuals. However, the repair process is not well understood. New University of Iowa research into two types of muscular dystrophy now has opened the door on a muscle repair process and identified a protein that plays a critical role.

The protein, called dysferlin, is mutated in two distinct muscular dystrophies known as Miyoshi Myopathy and limb-girdle muscular dystrophy type 2b. The UI study suggests that in these diseases, the characteristic, progressive muscle degeneration is due to a faulty muscle-repair mechanism rather than an inherent weakness in the muscle’s structural integrity. The research findings reveal a totally new cellular cause of muscular dystrophy and may lead to many discoveries about normal muscle function and to therapies for muscle disorders.

The research team led by Kevin Campbell, Ph.D., the Roy J. Carver Chair of Physiology and Biophysics and interim head of the department, UI professor of neurology, and a Howard Hughes Medical Institute (HHMI) Investigator, studied the molecular consequences of losing dysferlin and discovered that without dysferlin muscles were unable to heal themselves.

The UI team genetically engineered mice to lack the dysferlin gene. Just like humans with Miyoshi Myopathy and limb-girdle muscular dystrophy type 2b, the mice developed a muscular dystrophy, which gets progressively worse with age. However, treadmill tests revealed that the muscles of mice that lack dysferlin were not much more susceptible to damage than the muscles of normal mice. This contrasts with most muscular dystrophies of known cause where genetic mutations weaken muscle membranes and make muscles more prone to damage.

“This told us that the dystrophies caused by dysferlin loss were very different in terms of how the disease process works compared to other dystrophies we have studied,” Campbell said. “We were gradually picking up clues that showed we had a different type of muscular dystrophy here.”

Most muscular dystrophy causing genetic mutations have been linked to disruption of a large protein complex that controls the structural integrity of muscle cells. The researchers found that dysferlin was not associated with this large protein complex. Rather, dysferlin is normally found throughout muscle plasma membrane and also in vesicles, which are small membrane bubbles that encapsulate important cellular substances and ferry them around cells. Vesicles also are important for moving membrane around in cells.

Previous studies have shown that resealing cell membranes requires the accumulation and fusing of vesicles to repair the damaged site.

Using an electron microscope to examine muscles lacking dysferlin, the UI team found that although vesicles gathered at damaged membrane sites, the membrane was not resealed. In contrast, the team discovered that when normal muscle is injured, visible “patches” form at the damaged sites, which seal the holes in the membrane. Chemicals that tag dysferlin proved that these “patches” were enriched with dysferlin and the patches appeared to be formed by the fusion of dysferlin-containing vesicles that traveled though the cell to the site of membrane damage.

The researchers then used a high-powered laser and a special dye to visualize the repair process in real time.

Under normal conditions, the dye is unable to penetrate muscle membrane. However, if the membrane is broken the dye can enter the muscle fiber where it fluoresces. Using the laser to damage a specific area of muscle membrane, the researchers could watch the fluorescence increase as the dye flowed into the muscle fiber.

“The more dye that entered, the more fluorescence we saw,” Campbell explained. “However, once the membrane was repaired, no more dye could enter and the level of fluorescence remained steady. Measuring the increase in fluorescence let us measure the amount of time that the membrane stayed open before repair sealed the membrane and prevented any more dye from entering.”

In the presence of calcium, normal membrane repaired itself in about a minute. In the absence of calcium, vesicles gathered at the damaged muscle membrane, but they did not fuse with each other or with the membrane and the membrane was not repaired. In muscle that lacked dysferlin, even in the presence of calcium, the damaged site was not repaired.

Campbell speculated that dysferlin, which contains calcium-binding regions, may be acting as a calcium sensor and that the repair system needs to sense the calcium in order to initiate the fusion and patching of the hole. Campbell added that purifying the protein and testing its properties should help pin down its role in the repair process.

The discovery of a muscle repair process and of dysferlin’s role raises many new questions. In particular, Campbell wonders what other proteins might be involved and whether defects in those components could be the cause of other muscular dystrophies.

“This work has described a new physiological mechanism in muscle and identified a component of this repair process,” Campbell said. “What is really exciting for me is the feeling that this is just a little hint of a much bigger picture.”

In addition to Campbell, the UI researchers included Dimple Bansal, a graduate student in Campbell’s laboratory and the lead author of the paper, Severine Groh, Ph.D., and Chien-Chang Chen, Ph.D., both UI post-doctoral researchers in physiology and biophysics and neurology, and Roger Williamson, M.D., UI professor of obstetrics and gynecology. Also part of the research team were Katsuya Miyake, Ph.D., a postdoctoral researcher, and Paul McNeil, Ph.D., a professor of cellular biology and anatomy at the Medical College of Georgia in Augusta, Ga., and Steven Vogel, Ph.D., at the Laboratory of Molecular Physiology at the National Institute of Alcohol Abuse and Alcoholism, Rockville, Md.

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Article adapted by MD Sports from original press release.
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Contact: Jennifer Brown
University of Iowa 

The study was funded by a grant from the Muscular Dystrophy Association.

University of Iowa Health Care describes the partnership between the UI Roy J. and Lucille A. Carver College of Medicine and UI Hospitals and Clinics and the patient care, medical education and research programs and services they provide.

 

Researchers in Purdue University’s School of Veterinary Medicine have discovered genetic and drug-treatment methods to arrest the type of muscle atrophy often caused by muscle disuse, as well as aging and diseases such as cancer.
The findings might eventually benefit people who have been injured or suffer from diseases that cause them to be bedridden and lose muscle mass, or sometimes limbs, due to atrophy, said Amber Pond, a research scientist in the school’s Department of Basic Medical Sciences.
“The weight loss and muscle wasting that occurs in patients with cancer or other diseases seriously compromises their well-being and is correlated with a poor chance for recovery,” Pond said. “In addition, muscle weakness caused by atrophy during aging can lead to serious falls and bone loss. Exercise is the most beneficial strategy to treat atrophy. However, many individuals are too ill to adequately participate in exercise programs.
“We’ve found a chemical ‘switch’ in the body that allows us to turn atrophy on, and, from that, we also have learned how to turn atrophy off.”
Findings based on the research, funded in large part by the American Heart Association, are detailed in a study available online today (Wednesday, May 24) in The FASEB Journal, published by the Federation of American Societies for Experimental Biology. The study will be in the journal’s print edition in July.
The research team found atrophy of skeletal muscle in mice could be inhibited with both gene therapy and drug treatment using astemizole (as-TEM-uh-zole), an antihistamine. This new insight has potential in many different areas of research, Pond said.
“We have discovered a direct link between atrophy and a protein in the skeletal muscle,” Pond said. “This led us to develop methods that would block the protein’s ability to cause atrophy. Through drug treatment, we were able to block atrophy, allowing muscle to retain 97 percent of its original fiber size in the face of atrophy.”
Astemizole, which was withdrawn from the market in 2000 because of its potential to cause serious cardiovascular problems, wouldn’t be suitable for use in humans, Pond said. The drug can be used in mice because it doesn’t affect their hearts to the same extent.
“Astemizole administration to humans poses too great a risk,” Pond said. “There’s a need for more study to avoid those side effects, but the key is that we found a protein capable of sensing muscle disuse and initiating atrophy.”
In the drug study, researchers used four groups of mice: a control group, a second group that was given astemizole, and two additional groups in which muscle atrophy was introduced. One of these two groups received astemizole while the second did not. Both of these groups were placed in cages constructed to elevate them so that they were unable to place any weight on their back legs.
“Use of the custom cages to produce atrophy was established in the ’80s for simulation of NASA space flight; you can’t mimic these effects on muscle and bone in cell culture,” said Kevin Hannon, associate professor of developmental anatomy and one of the study’s authors. “The mice were able to move around the cage and eat and drink on their own. We monitored their food and water intake and overall health and ensured that they were playing and eating normally.”
This method allowed the scientists to demonstrate the effects of skeletal muscle atrophy and investigate reasons for the link with the Merg1a protein. The Merg1a protein is a channel that normally passes a small electrical current across the cell.
The researchers implanted a gene into the skeletal muscle that resulted in a mutant form of this protein that combines with the normal protein and stops the current. The researchers found that the mutant protein would inhibit atrophy in mice whose ability to use their back legs was limited.
Because gene therapy is not yet a practical treatment option in humans, the researchers decided to go a step further and stop the function of the protein with astemizole, which is a known “Merg1a channel blocker.” The researchers found that the drug produced basically the same results as the gene therapy. In fact, muscle size increased in mice in the group that were given the drug without any other treatment.
“We are now looking at the differences in the structure of the heart and the skeleton to give us clues on how to specifically target muscles without the cardiac side effects,” Pond said.
###
This research also was partially supported by the U.S. Department of Agriculture and Purdue’s basic medical sciences department.
Writer: Maggie Morris, (765) 494-2432, maggiemorris@purdue.edu
Sources: Amber Pond, (765) 494-6185, pond@purdue.edu 
Kevin Hannon, (765) 494-5949, hannonk@purdue.edu
Related Web sites: 
Purdue School of Veterinary Medicine: http://www.vet.purdue.edu/ 

Researchers in Purdue University’s School of Veterinary Medicine have discovered genetic and drug-treatment methods to arrest the type of muscle atrophy often caused by muscle disuse, as well as aging and diseases such as cancer.

The findings might eventually benefit people who have been injured or suffer from diseases that cause them to be bedridden and lose muscle mass, or sometimes limbs, due to atrophy, said Amber Pond, a research scientist in the school’s Department of Basic Medical Sciences.

“The weight loss and muscle wasting that occurs in patients with cancer or other diseases seriously compromises their well-being and is correlated with a poor chance for recovery,” Pond said. “In addition, muscle weakness caused by atrophy during aging can lead to serious falls and bone loss. Exercise is the most beneficial strategy to treat atrophy. However, many individuals are too ill to adequately participate in exercise programs.

“We’ve found a chemical ‘switch’ in the body that allows us to turn atrophy on, and, from that, we also have learned how to turn atrophy off.”

Findings based on the research, funded in large part by the American Heart Association, are detailed in a study available online today (Wednesday, May 24) in The FASEB Journal, published by the Federation of American Societies for Experimental Biology. The study will be in the journal’s print edition in July.

The research team found atrophy of skeletal muscle in mice could be inhibited with both gene therapy and drug treatment using astemizole (as-TEM-uh-zole), an antihistamine. This new insight has potential in many different areas of research, Pond said.

“We have discovered a direct link between atrophy and a protein in the skeletal muscle,” Pond said. “This led us to develop methods that would block the protein’s ability to cause atrophy. Through drug treatment, we were able to block atrophy, allowing muscle to retain 97 percent of its original fiber size in the face of atrophy.”

Astemizole, which was withdrawn from the market in 2000 because of its potential to cause serious cardiovascular problems, wouldn’t be suitable for use in humans, Pond said. The drug can be used in mice because it doesn’t affect their hearts to the same extent.

“Astemizole administration to humans poses too great a risk,” Pond said. “There’s a need for more study to avoid those side effects, but the key is that we found a protein capable of sensing muscle disuse and initiating atrophy.”

In the drug study, researchers used four groups of mice: a control group, a second group that was given astemizole, and two additional groups in which muscle atrophy was introduced. One of these two groups received astemizole while the second did not. Both of these groups were placed in cages constructed to elevate them so that they were unable to place any weight on their back legs.

“Use of the custom cages to produce atrophy was established in the ’80s for simulation of NASA space flight; you can’t mimic these effects on muscle and bone in cell culture,” said Kevin Hannon, associate professor of developmental anatomy and one of the study’s authors. “The mice were able to move around the cage and eat and drink on their own. We monitored their food and water intake and overall health and ensured that they were playing and eating normally.”

This method allowed the scientists to demonstrate the effects of skeletal muscle atrophy and investigate reasons for the link with the Merg1a protein. The Merg1a protein is a channel that normally passes a small electrical current across the cell.

The researchers implanted a gene into the skeletal muscle that resulted in a mutant form of this protein that combines with the normal protein and stops the current. The researchers found that the mutant protein would inhibit atrophy in mice whose ability to use their back legs was limited.

Because gene therapy is not yet a practical treatment option in humans, the researchers decided to go a step further and stop the function of the protein with astemizole, which is a known “Merg1a channel blocker.” The researchers found that the drug produced basically the same results as the gene therapy. In fact, muscle size increased in mice in the group that were given the drug without any other treatment.

“We are now looking at the differences in the structure of the heart and the skeleton to give us clues on how to specifically target muscles without the cardiac side effects,” Pond said.

———————————–
Article adapted by MD Sports from original press release.
———————————–

Contact: Maggie Morris
Purdue University 

This research also was partially supported by the U.S. Department of Agriculture and Purdue’s basic medical sciences department.

Related Web sites: 
Purdue School of Veterinary Medicine: http://www.vet.purdue.edu/ 
FASEB Journal: http://www.fasebj.org/ 

University of Pittsburgh School of Medicine researchers have successfully used gene therapy to accelerate muscle regeneration in experimental animals with muscle damage, suggesting this technique may be a novel and effective approach for improving skeletal muscle healing, particularly for serious sports-related injuries. These findings are being presented at the American Society of Gene Therapy annual meeting in Baltimore, May 31 to June 4.

Skeletal muscle injuries are the most common injuries encountered in sports medicine. Although such injuries can heal spontaneously, scar tissue formation, or fibrosis, can significantly impede this process, resulting in incomplete functional recovery. Of particular concern are top athletes, who, when injured, need to recover fully as quickly as possible.
In this study, the Pitt researchers injected mice with a gene therapy vector containing myostatin propeptide–a protein that blocks the activity of the muscle-growth inhibitor myostatin–three weeks prior to experimentally damaging the mice’s skeletal muscles. Four weeks after skeletal muscle injury, the investigators observed an enhancement of muscle regeneration in the gene-therapy treated mice compared to the non-gene-therapy treated control mice. There also was significantly less fibrous scar tissue in the skeletal muscle of the gene-therapy treated mice compared to the control mice.
According to corresponding author Johnny Huard, Ph.D., the Henry J. Mankin Endowed Chair and Professor in Orthopaedic Surgery, University of Pittsburgh School of Medicine, and Director of the Stem Cell Research Center of Children’s Hospital of Pittsburgh, this approach offers a significant, long-lasting method for treating serious, sports-related muscle injuries.
“Based on our previous studies, we expect that gene-therapy treated cells will continue to overproduce myostatin propeptide for at least two years. Since the remodeling phase of skeletal muscle healing is a long-term process, we believe that prolonged expression of myostatin propeptide will continue to contribute to recovery of injured skeletal muscle by inducing an increase in muscle mass and minimizing fibrosis. This could significantly reduce the amount of time an athlete needs to recover and result in a more complete recovery,” he explained.
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Others involved in this study include, Jinhong Zhu, M.D., Yong Li, M.D., Ph.D., of the Growth and Development Laboratory, Children’s Hospital of Pittsburgh; and Chunping Qiao, M.D., and Xiao Xiao, M.D., Ph.D., of the Molecular Therapies Laboratory, department of orthopaedic surgery, University of Pittsburgh School of Medicine.
University of Pittsburgh School of Medicine researchers have successfully used gene therapy to accelerate muscle regeneration in experimental animals with muscle damage, suggesting this technique may be a novel and effective approach for improving skeletal muscle healing, particularly for serious sports-related injuries.
Skeletal muscle injuries are the most common injuries encountered in sports medicine. Although such injuries can heal spontaneously, scar tissue formation, or fibrosis, can significantly impede this process, resulting in incomplete functional recovery. Of particular concern are top athletes, who, when injured, need to recover fully as quickly as possible.
In this study, the Pitt researchers injected mice with a gene therapy vector containing myostatin propeptide–a protein that blocks the activity of the muscle-growth inhibitor myostatin–three weeks prior to experimentally damaging the mice’s skeletal muscles. Four weeks after skeletal muscle injury, the investigators observed an enhancement of muscle regeneration in the gene-therapy treated mice compared to the non-gene-therapy treated control mice. There also was significantly less fibrous scar tissue in the skeletal muscle of the gene-therapy treated mice compared to the control mice.
According to corresponding author Johnny Huard, Ph.D., the Henry J. Mankin Endowed Chair and Professor in Orthopaedic Surgery, University of Pittsburgh School of Medicine, and Director of the Stem Cell Research Center of Children’s Hospital of Pittsburgh, this approach offers a significant, long-lasting method for treating serious, sports-related muscle injuries.
“Based on our previous studies, we expect that gene-therapy treated cells will continue to overproduce myostatin propeptide for at least two years. Since the remodeling phase of skeletal muscle healing is a long-term process, we believe that prolonged expression of myostatin propeptide will continue to contribute to recovery of injured skeletal muscle by inducing an increase in muscle mass and minimizing fibrosis. This could significantly reduce the amount of time an athlete needs to recover and result in a more complete recovery,” he explained.
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Article adapted by MD Sports from original press release.
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Contact: Jim Swyers

Others involved in this study include, Jinhong Zhu, M.D., Yong Li, M.D., Ph.D., of the Growth and Development Laboratory, Children’s Hospital of Pittsburgh; and Chunping Qiao, M.D., and Xiao Xiao, M.D., Ph.D., of the Molecular Therapies Laboratory, department of orthopaedic surgery, University of Pittsburgh School of Medicine.

Cereal and non-fat milk is as good as a commercially-available sports drink in initiating post-exercise muscle recovery.

Background

This study compared the effects of ingesting cereal and nonfat milk (Cereal) and a carbohydrate-electrolyte sports drink (Drink) immediately following endurance exercise on muscle glycogen synthesis and the phosphorylation state of proteins controlling protein synthesis: Akt, mTOR, rpS6 and eIF4E.

Methods

Trained cyclists or triathletes (8 male: 28.0+/-1.6 yrs, 1.8+/-0.0 m, 75.4+/-3.2 kg, 61.0+/-1.6 ml O2 * kg-1 * min-1; 4 female: 25.3+/-1.7 yrs, 1.7+/-0.0 m, 66.9+/-4.6 kg, 46.4+/-1.2 mlO2 * kg-1 * min-1) completed two randomly-ordered trials serving as their own controls. After 2 hours of cycling at 60-65% VO2MAX, a biopsy from the vastus lateralis was obtained (Post0), then subjects consumed either Drink (78.5 g carbohydrate) or Cereal (77 g carbohydrate, 19.5 g protein and 2.7 g fat). Blood was drawn before and at the end of exercise, and at 15, 30 and 60 minutes after treatment. A second biopsy was taken 60 minutes after supplementation (Post60). Differences within and between treatments were tested using repeated measures ANOVA.

Results

At Post60, blood glucose was similar between treatments (Drink 6.1+/-0.3, Cereal 5.6+/-0.2 mmol/L, p<.05), but after Cereal, plasma insulin was significantly higher (Drink 123.1+/-11.8, Cereal 191.0+/-12.3 pmol/L, p<.05), and plasma lactate significantly lower (Drink 1.4+/-0.1, Cereal 1.00+/-0.1 mmol/L, p<.05). Except for higher phosphorylation of mTOR after Cereal, glycogen and muscle proteins were not statistically different between treatments. Significant Post0 to Post60 changes occurred in glycogen (Drink 52.4+/-7.0 to 58.6+/-6.9, Cereal 58.7+/-9.6 to 66.0+/-10.0 mumol/g, p<.05) and rpS6 (Drink 17.9+/-2.5 to 35.2+/-4.9, Cereal 18.6+/-2.2 to 35.4+/-4.4 %Std, p<.05) for each treatment, but only Cereal significantly affected glycogen synthase (Drink 66.6+/-6.9 to 64.9+/-6.9, Cereal 61.1+/-8.0 to 54.2+/-7.2%Std, p<.05), Akt (Drink 57.9+/-3.2 to 55.7+/-3.1, Cereal 53.2+/-4.1 to 60.5+/-3.7 %Std, p<.05) and mTOR (Drink 28.7+/-4.4 to 35.4+/-4.5, Cereal 23.0+/-3.1 to 42.2+/-2.5 %Std, p<.05). eIF4E was unchanged after both treatments.

Conclusion

These results suggest that Cereal is as good as a commercially-available sports drink in initiating post-exercise muscle recovery.

Author: Lynne Kammer, Zhenping Ding, Bei Wang, Daiske Hara, Yi-Hung Liao and John L. Ivy

Credits/Source: Journal of the International Society of Sports Nutrition 2009, 6:11

WESTCHESTER, Ill. – Athletes who get an extra amount of sleep are more likely to improve their performance in a game, according to a research abstract presented at the 21st Annual Meeting of the Associated Professional Sleep Societies (APSS).

The study, authored by Cheri Mah of Stanford University, was conducted on six healthy students on the Stanford men’s basketball team, who maintained their typical sleep-wake patterns for a two-week baseline followed by an extended sleep period in which they obtained as much extra sleep as possible. To assess improvements in athletic performance, the students were judged based on their sprint time and shooting percentages.

Significant improvements in athletic performance were observed, including faster sprint time and increased free-throws. Athletes also reported increased energy and improved mood during practices and games, as well as a decreased level of fatigue.

“Although much research has established the detrimental effects of sleep deprivation on cognitive function, mood and performance, relatively little research has investigated the effects of extra sleep over multiple nights on these variables, and even less on the specific relationship between extra sleep and athletic performance. This study illuminated this latter relationship and showed that obtaining extra sleep was associated with improvements in indicators of athletic performance and mood among members of the men’s basketball team.”

The amount of sleep a person gets affects his or her physical health, emotional well-being, mental abilities, productivity and performance. Recent studies associate lack of sleep with serious health problems such as an increased risk of depression, obesity, cardiovascular disease and diabetes.
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Article adapted by MD Sports from original press release.
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Contact: Jim Arcuri
American Academy of Sleep Medicine 

Experts recommend that adults get between seven and eight hours of sleep each night to maintain good health and optimum performance.

Persons who think they might be suffering from a sleep disorder are encouraged to consult with their primary care physician, who will refer them to a sleep specialist.

The annual SLEEP meeting brings together an international body of 5,000 leading researchers and clinicians in the field of sleep medicine to present and discuss new findings and medical developments related to sleep and sleep disorders.

More than 1,000 research abstracts will be presented at the SLEEP meeting, a joint venture of the American Academy of Sleep Medicine and the Sleep Research Society. The four-day scientific meeting will bring to light new findings that enhance the understanding of the processes of sleep and aid the diagnosis and treatment of sleep disorders such as insomnia, narcolepsy and sleep apnea.

ATHENS, Ohio – Men over 60 may be able to increase their strength by as much as 80 percent by performing intense weight training exercises, according to physiologists involved in studies of the health benefits of weight lifting. The researchers also have found that older men gain strength at the same rate as men in their 20s.

In a study of 18 men ages 60 to 75, Ohio University physiologists found that subjects who participated in a 16-week, high-intensity resistence training program on average were 50 percent to 80 percent stronger by the end of the study. None of the participants had engaged in weight lifting prior to the study. Researchers also observed improvements in the seniors’ muscle tone, aerobic capacity and cholesterol profile.

These are some of the latest findings from a decades-long examination of the impact of exercise on the health of men and women of all ages. When researchers compared the strength gains of the elderly participants in this study to findings from other studies they’ve done of college-age men, they found that changes in strength and muscle size were similar in both age groups. The findings were published in a recent issue of the Journal of Gerontology.

“There have been a number of research projects that have come out over the years that suggest there is no age limitation to getting stronger from resistance training,” said Robert Staron, co-author of this study and an associate professor of anatomy in the university’s College of Osteopathic Medicine. “It’s become obvious that it’s important to maintain a certain amount of muscle mass as we age.”

This new study also suggests that elderly men can handle heavy workloads over a long period of time. Participants – who all were in good health and closely monitored during testing and training – performed leg presses, half squats and leg extensions twice a week to exercise the lower body. When the men began the study, they were able to leg press about 375 pounds on average. After the 16-week period, they could take on about 600 pounds. Studies elsewhere have involved low-intensity exercises over a shorter term.

In addition to the increase in strength, researchers found that weight lifting had a beneficial impact on the participants’ cardiovascular system. Tests on an exercise treadmill showed that their bodies used oxygen more efficiently after weight training.

“The individuals run until they are completely exhausted, and it took longer for them to reach that point after resistance training,” Staron said.

Blood samples taken before and after weight training also showed favorable changes in participants’ overall cholesterol profiles, he said, including increases in HDL cholesterol levels and decreases in LDL cholesterol levels.

Losing muscle tone and strength is not uncommon for many senior citizens, Staron said, but this research suggests that a lack of physical exercise can contribute to the problem.

“Certainly, inactivity does play a role in contributing to the decrease in muscle mass,” Staron said. “If we can maintain a certain level of strength through exercise, our quality of life should be better as we age.”

Before beginning a weight lifting regimen, it’s a good idea to consult a physician, Staron advised, adding that it’s also important to learn proper weight lifting techniques. Staron and his colleagues now have turned their attention to how certain weight training routines impact young people.

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Article adapted by MD Sports from original press release.
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Contact: Andrea Gibson
Ohio University

Collaborators on this project are Fredrick Hagerman, Robert Hikida and Thomas Murray of the College of Osteopathic Medicine, former graduate student Seamus Walsh, Roger Gilders of the College of Health and Human Services, Kumika Toma of the College of Arts and Sciences and Kerry Ragg of the Student Health Service.

Research news from Journal of Mass Spectrometry

A new mass spectrometry test can help sports anti-drug doping officials to detect whether an athlete has used drugs that boost naturally occurring steroid levels. The test is more sensitive compared to previous alternatives, more capable of revealing specific suspicious chemical in the body, faster to perform, and could be run on standard drug-screening laboratory equipment. The new test is announced in a special issue of the Journal of Mass Spectrometry that concentrates on detecting drugs in sports.

One of the roles of the masculinising hormone testosterone is to increase muscle size and strength. Taking extra testosterone, or taking a chemical that the body can use to create extra testosterone, could therefore enhance an athlete’s performance. For this reason taking it is banned by the World Anti-Doping Agency (WADA).

The exact level of testosterone varies considerably between different people, so simply measuring total testosterone in an athlete’s urine can not show whether he or she has deliberately taken extra. There is, however, a second chemical in the body, epitestosterone, which is normally present in approximately equal proportions to testosterone. Comparing the ratio of testosterone to epitestosterone can then indicate whether testosterone or a precursor has been taken.

The problem is that it is not always easy to measure these two substances, particularly as they are only present in urine at very low concentrations.

A team of scientists the Sports Medicine Research and Testing Laboratory at the University of Utah have developed a test that makes use of liquid chromatography-tandem mass spectrometry. This method has incredibly high sensitivity (down to 1 ng/ml) and increases the power with which officials can search for both testosterone and epitestosterone within a sample.

“Our system means that we can determine the testosterone/epitestosterone ratio in a sample with greater confidence, and therefore be in a better position to spot doping violations without falsely accusing innocent athletes,” says lead investigator Dr Jonathan Danaceau.

“Not only is the test more sensitive, it is also faster to perform,” says colleague Scott Morrison.

“Having this sort of test available makes cheating harder and lets us take one more step towards enabling free and fair competition,” says Laboratory Director Dr Matthew Slawson.

This paper is part of a special issue for the Olympic Games from the Journal of Mass Spectrometry which focuses of drug use in sport. The issue is available free of charge online for one month at http://www.interscience.wiley.com/journal/jms. The other articles publishing in this issue are:

 

  • History of Mass Spectrometry at Olympic Games (DOI: 10.1002/jms.1445)
  • Nutritional supplements cross-contaminated and faked with doping substances (DOI: 10.1002/jms.1452)
  • Hair analysis of anabolic steroids in connection with doping control results from horse samples (DOI: 10.1002/jms.1446)
  • Mass spectrometric determination of Gonadotrophin releasing hormone (GnRH) in human urine for doping control purposes by means of LC-ESI-MS/MS (DOI: 10.1002/jms.1438)
  • Liquid chromatographic-mass spectrometric analysis of glucuronide-conjugated anabolic steroid metabolites: method validation and inter-laboratory comparison (DOI: 10.1002/jms.1434)
  • Mass Spectrometry of Selective Androgen Receptor Modulators (DOI: 10.1002/jms.1438)
  • Can glycans unveil the origin of glycoprotein hormones? – human chorionic gonadotropin as an example (DOI: 10.1002/jms.1448)
  • A High-Throughput Multicomponent Screening Method for Diuretics, Masking Agents, Central Nervous System Stimulants and Opiates in Human Urine by UPLC-MS/MS (DOI: 10.1002/jms.1436)
  • The application of carbon isotope ratio mass spectrometry to doping control (DOI: 10.1002/jms.1437)
  • Identification of zinc-alpha-2-glycoprotein binding to clone ae7a5 anti-human epo antibody by means of nano-hplc and high-resolution highmass accuracy esi-ms/ms (DOI: 10.1002/jms.1444)
  • Low LC-MS/MS Detection of Glycopeptides Released from pmol Levels of Recombinant Erythropoietin using Nanoflow HPLC-Chip Electrospray Ionization (DOI: 10.1002/jms.1439)
  • Introduction of HPLC/Orbitrap mass spectrometry as screening method for doping control (DOI: 10.1002/jms.1447)

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Article adapted by MD Sports from original press release.
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Contact: Jennifer Beal
Wiley-Blackwell

University Park, Pa. — Girls and boys are now equally caught up in the social pressure for a muscular body image currently lauded in popular culture. A Penn State researcher contends those pressures are leading girls and boys down unhealthy avenues such as the misuse of anabolic steroids.

“Young girls have always had to struggle against the media stereotypes of stick-thin models or voluptuous sexuality, but with the rising popularity of women sports, girls are bombarded with buffed body images,” says Dr. Charles Yesalis, professor of health policy and administration, and exercise and sports science at Penn State, and editor of the newest edition of the book “Anabolic Steroids in Sports and Exercise.” “Now, young boys face pop culture musclemen like The Rock and Steve Austin, given the influence of professional wrestling shows.”

“The current film ‘Charlie’s Angels’ sports karate-kicking women in cool clothes,” he added. “Today’s children look with envy at the physiques of actors Arnold Schwarzenegger, Jean-Claude Van Damme, Wesley Snipes, and Linda Hamilton, whose roles call for a muscular build. Hollywood stars are openly taking Human Growth Hormone (HGH) injections to combat aging.”

In addition, children are entering competitive sports at younger ages and many working families have children signed up in two or three sports. Parents, coaches and young athletes are facing growing violence in amateur athletics. The pressure to win at all costs continues to weigh heavily on children, Yesalis notes.

The concern is that many youths will take shortcuts to achieving a muscular build by using anabolic steroids. Female athletes also are pressured to achieve low body fat to excel in their sport. The Penn State researcher has seen evidence that the pressures are reaching down to young children. For example, the book cites figures from the Monitoring The Future Study, a national-level epidemiological survey conducted annually since 1975. Approximately 50,000 8th, 10th and 12 graders are surveyed each year.

The MTF data shows that during the 1990s, anabolic steroid use among 12 graders –both boys and girls – rose to an all-time high with more than 500,000 adolescents having cycled – an episode of use of 6 to 12 weeks – during their lifetime. And the percentage of girls alone doubled in the same period.

A 1998 study of 965 youngsters at four Massachusetts middle schools found that 2.7 percent admitted to taking illegal steroids for better sports performance. That included some boys and girls as young as 10 years old. “This year’s Olympic doping scandals and the epidemic of anabolic steroids in professional baseball just glorify and justify steroids to impressionable youths,” Yesalis notes. “The use of anabolic steroids has cascaded down from the Olympic, professional and college levels to high schools and junior high schools and now middle schools for athletes and non-athletes alike. ”

“Anabolic steroids are made to order for a female wanting to attain a lean athletic body. While most drug abuse has outcomes that tend to discourage use, females who use anabolic steroids may experience a decrease in body fat, increased muscle size and strength, and enhanced sports performance,” he says.

Girls and boys misusing anabolic steroids may win approval and rewards from parents, coaches and peers, but don’t realize there are long-term negative effects on their health, particularly girls, according to Yesalis. Young girls face potential permanent side effects of male hair growth or baldness, deepening of the voice, the enlargement of the clitoris as well as the known risks of heart and liver diseases.

Published by Human Kinetics, the book incorporates the latest research, experience and insights of 15 experts on the scientific, clinical, historical, legal and other aspects of steroid abuse and drug testing. New information looks at the effects of steroids on health, particularly that of women.

This year, trials of East German doctors, coaches and officials reveal records of systematic doping of young athletes without their own or parents’ knowledge. In 1974, officials’ plan to turn the tiny Communist nation into a superpower in sports included giving performance-enhancing drugs to all competing athletes including children as young as 10 years old. The indictments included 142 former East German athletes who now complain of health problems. In media reports, several female athletes report incidents of miscarriages, liver tumor, gynecological problems and enlarged heart, all showing up decades after the steroid misuse.

“Our society’s current strategy for dealing with the abuse of anabolic steroids in sport primarily involves testing, law enforcement and education,” Yesalis says. “But our efforts to deal with this problem have not been very successful. Unless we deal with the social environment that rewards winning at all costs and an unrealistic physical appearance, we won’t even begin to address the problem.”

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Article adapted by MD Sports Weblog from original press release.
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Contact: Vicki Fong
Penn State

New study dispels belief that increasing the hormone level improves the sexual function

Bethesda, Md.— The American Journal of Physiology: Endocrinology and Metabolism, one of the 14 peer-reviewed journals published by the American Physiological Society (APS), spotlights recent research findings designed to improve and understand human well-being and health. A study in the December edition examines how different doses of testosterone affect body composition, muscle size, strength, and sexual functions.

Background

Testosterone regulates many physiological processes, including muscle protein metabolism, some aspects of sexual and cognitive functions, secondary sex characteristics, erythropoiesis, plasma lipids, and bone metabolism. However, testosterone dose dependency of various hormonal dependent functions has not been well understood in the scientific community. Previous studies reveal that administration of replacement doses of testosterone to hypogonadal men and of supraphysiological doses to eugonadal men increases fat-free mass, muscle size, and strength. Conversely, suppression of endogenous testosterone concentrations is associated with loss of fat-free mass and a decrease in fractional muscle protein synthesis.

What is not known is whether testosterone effects on the muscle are dose dependent, or the nature of the testosterone dose-response relationships. Animal studies suggest that different androgen-dependent processes have different androgen dose-response relationships. Sexual function in male mammals is maintained at serum testosterone concentrations that are at the lower end of the male range. However, it is not known whether the low normal testosterone levels that normalize sexual function are sufficient to maintain muscle mass and strength, or whether the higher testosterone concentrations required to maintain muscle mass and strength might adversely affect plasma lipids, hemoglobin levels, and the prostate.

The Study

The primary objective of this study was to determine the dose dependency of testosterone’s effects on fat-free mass and muscle performance. The authors hypothesized that changes in circulating testosterone concentrations would be associated with dose-dependent changes in fat-free mass, muscle strength, and power in conformity with a single linear dose-response relationship, and that the dose requirements for maintaining other androgen-dependent processes would be different.

Young men were treated with a long-acting gonadotropin-releasing hormone (GnRH) agonist to suppress endogenous testosterone secretion, and concomitantly also with one of five testosterone-dose regimens to create different levels of serum testosterone concentrations extending from subphysiological to the supraphysiological range. The lowest testosterone dose, 25 mg weekly, was selected because this dose had been shown to maintain sexual function in GnRH antagonist-treated men. The selection of the 600-mg weekly dose was based on the consideration that this was the highest dose that had been safely administered to men in controlled studies.

The authors of the study, “Testosterone Dose-Response Relationships in Healthy Young Men” are Shalender Bhasin, Linda Woodhouse, Connie Dzekov, Jeanne Dzekov, Indrani Sinha-Hikim, Ruoquing Shen, and Atam B. Singh, all from the Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA; Richard Casaburi, Dimple Bhasin, Nancy Berman, Rachelle Bross and Jeffrey Phillips, from the Harbor-University of California Los Angeles Medical Center, Torrance, CA; Xianghong Chen and Kevin E. Yarasheski at the Biomedical Mass Spectrometric Research Resource, Department of Internal Medicine, Washington University, School of Medicine, St. Louis, Missouri, Lynne Magliano and Thomas W. Storer, from the Laboratory for Exercise Sciences, El Camino College, El Camino, CA.

Protocol

This was a double-blind, randomized study consisting of a four-week control period, a 20-week treatment period, and a 16-week recovery period. The participants were healthy men, 18-35 years of age, with prior weight-lifting experience and normal testosterone levels. These men had not used any anabolic agents and had not participated in competitive sports events in the preceding year, and they were not planning to participate in competitive events in the following year. The participants were asked not to undertake strength training or moderate-to-heavy endurance exercise during the study. These instructions were reinforced every four weeks.

Sixty-one eligible men were randomly assigned to one of five groups. All received monthly injections of a long-acting GnRH agonist to suppress endogenous testosterone production. In addition, group 1 received 25 mg of testosterone enanthate intramuscularly weekly; group 2, 50 mg testosterone enanthate; group 3, 125 mg testosterone enanthate; group 4, 300 mg testosterone enanthate; and group 5, 600 mg testosterone enanthate. Twelve men were assigned to group 1, 12 to group 2, 12 to group 3, 12 to group 4, and 13 to group 5.

Nutritional Intake

Energy and protein intakes were standardized at 36 kcal/kg. The standardized diet was initiated two weeks before treatment started; dietary instructions were reinforced every four weeks. The nutritional intake was verified by analysis of three-day food records and 24-hour food recalls every four weeks.

Outcome Measures

Body composition and muscle performance were assessed at baseline and during week 20. Fat-free mass and fat mass were measured by underwater weighing and dual-energy X-ray absorptiometry. Total thigh muscle and quadriceps muscle volumes were measured by MRI scanning.

For estimation of total body water, the men ingested 10 g of 2H2O, and plasma samples were drawn at 0, 120, 180, and 240 min. A measurement of 2H abundance in plasma was made by nuclear magnetic resonance spectroscopy, with a correction factor of 0.985 for exchangeable hydrogen. Another measure of bilateral leg press strength was taken by use of the one-repetition maximum (1-RM) method. A seated leg press exercise with pneumatic resistance was used for this purpose. Subjects performed 5-10 min of leg cycling and stretching warm-up and received instruction and practice in lifting mechanics before performing progressive warm-up lifts leading to the 1-RM. Seat position and the ensuing knee and hip angles, as well as foot placement, were measured and recorded for use in subsequent testing. To ensure reliability in this highly effort-dependent test, the 1-RM score was reassessed within seven days, but not sooner than two days, after the first evaluation. If duplicate scores were within five percent, the higher of the two values was accepted as the strength score. If the two tests differed by greater than five percent, additional studies were conducted.

Sexual function was assessed by daily logs of sexual activity and desire that were maintained for seven consecutive days at baseline and during treatment by use of a published instrument. Spatial cognition was assessed by a computerized checkerboard test and mood by Hamilton’s depression and Young’s mania scales.

Adverse experiences, blood counts and chemistries, prostate-specific antigen (PSA), plasma lipids, total and free testosterone, luteinizing hormone (LH), sex steroid-binding globulin (SHBG), and insulin-like growth factor I (IGF-I) levels were measured periodically during control and treatment periods. Serum total testosterone was measured by an immunoassay.

Results

Of 61 men enrolled, 54 completed the study: 12 in group 1, 8 in group 2, 11 in group 3, 10 in group 4, and 13 in group 5. One man discontinued treatment because of acne; other subjects were unable to meet the demands of the protocol. The five groups did not significantly differ with respect to their baseline characteristics. Key findings included:

– Compliance: All evaluable subjects received 100percent of their GnRH agonist injections, and only one man in the 125-mg group missed one testosterone injection.

– Nutritional intake: Daily energy intake and proportion of calories derived from protein, carbohydrate, and fat were not significantly different among the five groups at baseline. There was no significant change in daily caloric, protein, carbohydrate, or fat intake in any group during treatment.

– Hormone levels: Serum total and free testosterone levels, measured during week 16, one week after the previous injection, were linearly dependent on the testosterone dose (P = 0.0001). Serum total and free testosterone concentrations decreased from baseline in men receiving the 25- and 50-mg doses and increased at 300- and 600-mg doses. Serum LH levels were suppressed in all groups. Serum SHBG levels decreased dose dependently at the 300- and 600-mg doses but did not change in other groups. Serum IGF-I concentrations increased dose dependently at the 300- and 600-mg doses.

– Body composition: Fat-free mass, measured by underwater weighing, did not change significantly in men receiving the 25- or 50-mg testosterone dose, but it increased dose dependently at higher doses. The changes in fat-free mass were highly dependent on testosterone dose (P = 0.0001) and correlated with log total testosterone concentrations during treatment (r = 0.73, P = 0.0001). Fat mass, measured by underwater weighing, increased significantly in men receiving the 25- and 50-mg doses, but did not change in men receiving the higher doses of testosterone. There was an inverse correlation between change in fat mass by underwater weighing and log testosterone concentrations.

– Muscle size: The thigh muscle volume and quadriceps muscle volume did not significantly change in men receiving the 25- or 50-mg doses but increased dose-dependently at higher doses of testosterone. The changes in thigh muscle and quadriceps muscle volumes correlated with log testosterone levels during treatment.

– Muscle performance: The leg press strength did not change significantly in the 25- and 125-mg-dose groups but increased significantly in those receiving the 50-, 300-, and 600-mg doses. Leg power did not change significantly in men receiving the 25-, 50-, and 125-mg doses of testosterone weekly, but it increased significantly in those receiving the 300- and 600-mg doses. The increase in leg power correlated with log testosterone concentrations and changes in fat-free mass and muscle strength.

– Behavioral measures: The scores for sexual activity and sexual desire measured by daily logs did not change significantly at any dose. Similarly, visual-spatial cognition and did not change significantly in any group.

– Adverse experiences and safety measures: Hemoglobin levels decreased significantly in men receiving the 50-mg dose but increased at the 600-mg dose; the changes in hemoglobin were positively correlated with testosterone concentrations. Changes in plasma HDL cholesterol, in contrast, were negatively dependent on testosterone dose and correlated with testosterone concentrations. Total cholesterol, plasma low-density lipoprotein cholesterol, and triglyceride levels did not change significantly at any dose. Serum PSA, creatinine, bilirubin, alanine aminotransferase, and alkaline phosphatase did not change significantly in any group, but aspartate aminotransferase decreased significantly in the 25-mg group. Two men in the 25-mg group, five in the 50-mg group, three in the 125-mg group, seven in the 300-mg group, and two in the 600-mg group developed acne. One man receiving the 50-mg dose reported decreased ability to achieve erections.

Discussion

The researchers found that GnRH agonist administration suppressed endogenous LH and testosterone secretion. Therefore, circulating testosterone concentrations during treatment were proportional to the administered dose of testosterone enanthate. This strategy of combined administration of GnRH agonist and graded doses of testosterone enanthate was effective in establishing different levels of serum testosterone concentrations among the five treatment groups. The different levels of circulating testosterone concentrations created by this regimen were associated with dose- and concentration-dependent changes in fat-free mass, fat mass, thigh and quadriceps muscle volume, muscle strength, leg power, hemoglobin, circulating IGF-I, and plasma HDL cholesterol.

Serum PSA levels, sexual desire and activity, and spatial cognition did not change significantly at any dose. The changes in fat-free mass, muscle volume, leg press strength and power, hemoglobin, and IGF-I were positively correlated, whereas changes in plasma HDL cholesterol and fat mass were negatively correlated with testosterone dose and total and free testosterone concentrations during treatment.

There were no significant changes in overall sexual activity or sexual desire in any group, including those receiving the 25-mg dose. Testosterone replacement of hypogonadal men improves frequency of sexual acts and fantasies, sexual desire, and response to visual erotic stimuli. The data demonstrate that serum testosterone concentrations at the lower end of male range can maintain some aspects of sexual function.

Conclusions

This study demonstrates that an increase in circulating testosterone concentrations results in dose-dependent increases in fat-free mass, muscle size, strength, and power. The relationships between circulating testosterone concentrations and changes in fat-free mass and muscle size conform to a single log-linear dose-response curve. The data do not support the notion of two separate dose-response curves reflecting two independent mechanisms of testosterone action on the muscle.

In addition, the study could not determine if responsiveness to testosterone is attenuated in older men. Testosterone dose-response relationships might be modulated by other muscle growth regulators, such as nutritional status, exercise and activity level, glucocorticoids, thyroid hormones, and endogenous growth hormone secretory status. Serum PSA levels decrease after androgen withdrawal, and testosterone replacement of hypogonadal men increases PSA levels into the normal range.

The data demonstrate that different androgen-dependent body functions respond differently to different testosterone dose-response relationships. Some aspects of sexual function and spatial cognition, and PSA levels, were maintained by relatively low doses of testosterone in GnRH agonist-treated men and did not increase further with administration of higher doses of testosterone. In contrast, graded doses of testosterone were associated with dose and testosterone concentration-dependent changes in fat-free mass, fat mass, muscle volume, leg press strength and power, hemoglobin, IGF-I, and plasma HDL cholesterol.

Testosterone doses associated with significant gains in fat-free mass, muscle size, and strength were associated with significant reductions in plasma HDL concentrations. Further studies are needed to determine whether clinically significant anabolic effects of testosterone can be achieved without adversely affecting cardiovascular risk. Selective androgen receptor modulators that preferentially augment muscle mass and strength, but only minimally affect prostate and cardiovascular risk factors, are desirable.

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

Source: American Journal of Physiology: Endocrinology and Metabolism, December 2001

The American Physiological Society (APS) was founded in 1887 to foster basic and applied science, much of it relating to human health. The Bethesda, MD-based Society has more than 10,000 members and publishes 3,800 articles in its 14 peer-reviewed journals every year.

Genetic research into athletic ability should be encouraged for its potential benefits in both sport and public health, a leading group of scientists meeting at the University of Bath said today.

Genetic research into athletic ability should be encouraged for its potential benefits in both sport and public health, a leading group of scientists meeting at the University of Bath said today.

However, ethical concerns, such as whether seeking information about differences between ethnic groups could be perceived as racist research, need to be properly addressed, they warn.

Their recommendations are published in a ‘position stand’ on genetic research and testing launched at the British Association of Sport & Exercise Sciences annual meeting today.

They call for more genetic research in the sport and exercise sciences because of the anticipated benefits for public health, but want researchers to take a more active role in debating the implications of their work with the public.

“If a powerful muscle growth gene was identified, on the one hand this could help develop training programmes that increase muscle size and strength in athletes, but even more importantly the knowledge could be used to develop exercise programmes or drugs to combat muscle wasting in old age,” said Dr Alun Williams from Manchester Metropolitan University, one of the report’s authors.

“We, as scientists investigating genetics, acknowledge a public concern about some genetic research and we believe scientists need to engage in public in debates about the potential benefits of their research.

“Research into the athletic success of East African distance runners or sprinters of West African ancestry might be perceived as unethical.

“But understanding the limits of human exercise capacity in sport could lead to the development of treatments for a range of diseases like cancer and cardiovascular disease.”

The potential applications of genetic testing in sport and exercise also raise some ethical concerns, for example in identifying potential athletic ability before birth.

An Australian company already offers the first genetic performance test (for the ACTN3 gene) which has been linked to sprint and power performance.

The report authors are sceptical about whether this test is useful but anticipate that more advanced versions of these tests will be available in future.

“We are not yet at a point where we can identify a potential future Olympic champion from genetic tests but we may not be very far away,” said Dr Williams, who wrote the report with Drs Henning Wackerhage (Aberdeen University), Andy Miah (University of Paisley), Roger Harris (University of Chichester) and Hugh Montgomery (University College London).

They highlight two dangers of genetic performance tests. Firstly, genetic performance tests might later be linked to disease. For example, a muscle growth gene may later be linked to cancer growth.

“Not all people may want to know, while young that they are at increased risk of cancer by early middle age, but they might inadvertently become aware of that just because they had a ‘sport gene’ test,” said Dr Williams.

Secondly, genetic performance tests can be performed even before birth and this may lead to the selection of foetuses or to abortions based on athletic potential.

The report recommends genetic counselling and that the testing should be confined to mature individuals who fully understand the relevant issues.

Genetic tests might also be used to screen for health risks during sport such as genes that are linked to sudden cardiac death.

Genetic tests for sudden cardiac death are already available but the report recommends that such testing should not be enforced on athletes.

Problems with mandatory testing are highlighted by the case of the basketball player Eddy Curry, who had an irregular heart beat.

Curry was asked by his club, the Chicago Bulls, to perform a predictive genetic test for a heart condition. The athlete refused and was traded to the New York Knicks who did not make such a demand.

In future, genetic tests might be used to identify those that respond with the biggest drop in cholesterol, blood pressure or glucose to exercise.

In a personalised medicine approach, such tests could be used to select subjects for therapeutic exercise programmes but scientists are concerned that this might undermine the ‘exercise for all’ message that already seems difficult to get across to the public.

The authors say that genetic testing might also be used to detect gene doping, which may be a real threat by the time of the London Olympics in 2012, or to show that positive doping tests are the result of a genetic mutation in an athlete.

The report recommends that genetic testing should be used for anti-doping testing as long as the genetic samples are destroyed after testing.

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Article adapted by MD Sports from original press release.
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Contact: Andrew McLaughlin
University of Bath