Archive for the ‘Sports Injury’ Category

Researchers at The University of Auckland have shown for the first time that the mere presence of carbohydrate solution in the mouth immediately boosts muscle strength, even before it is swallowed.

The results suggest that a previously unknown neural pathway is activated when receptors in the mouth detect carbohydrate, stimulating parts of the brain that control muscle activity and producing an increase in muscle strength.

Previous research had shown that the presence of carbohydrate in the mouth can improve physical performance during prolonged activity, but the mechanism involved was not known and it was unclear whether a person must be fatigued for the effect to be seen.

“There appears to be a pathway in the brain that tells our muscles when energy is on the way,” says lead researcher Dr Nicholas Gant from the Department of Sport and Exercise Science.

“We have shown that carbohydrate in the mouth produces an immediate increase in neural drive to both fresh and fatigued muscle and that the size of the effect is unrelated to the amount of glucose in the blood or the extent of fatigue.”

The current research has been published in the journal Brain Research and has also captured the attention of New Scientist magazine.

In the first of two experiments, 16 healthy young men who had been doing biceps exercises for 11 minutes were given a carbohydrate solution to drink or an identically flavored energy-free placebo. Their biceps strength was measured before and immediately afterward, as was the activity of the brain pathway known to supply the biceps.

Around one second after swallowing the drink, neural activity increased by 30 percent and muscle strength two percent, with the effect lasting for around three minutes. The response was not related to the amount of glucose in the bloodstream or how fatigued the participants were.

“It might not sound like much, but a two percent increase in muscle strength is enormous, especially at the elite level. It’s the difference between winning an Olympic medal or not,” says co-author Dr Cathy Stinear.

As might be expected, a second boost in muscle strength was observed after 10 minutes when carbohydrate reached the bloodstream and muscles through digestion, but no additional boost in neural activity was seen at that time.

“Two quite distinct mechanisms are involved,” says Dr Stinear. “The first is the signal from the mouth via the brain that energy is about to be available and the second is when the carbohydrate actually reaches the muscles and provides that energy,” says Dr Stinear.

“The carbohydrate and placebo solutions used in the experiment were of identical flavor and sweetness, confirming that receptors in the mouth can process other sensory information aside from the basic taste qualities of food. The results suggest that detecting energy may be a sixth taste sense in humans,” says Dr Gant.

In the second experiment, 17 participants who had not been doing exercise and were not fatigued simply held one of the solutions in their mouths without swallowing. Measurements of the muscle between the thumb and index finger were taken while the muscle was either relaxed or active.

A similar, though smaller effect was observed as in the first experiment, with a nine percent increase in neural activity produced by the carbohydrate solution compared with placebo. This showed that the response is seen in both large powerful muscles and in smaller muscles responsible for fine hand movements.

“Together the results show that carbohydrate in the mouth activates the neural pathway whether or not muscles are fatigued. We were surprised by this, because we had expected that the response would be part of the brain’s sophisticated system for monitoring energy levels during exercise,” says Dr Stinear.

“Seeing the same effect in fresh muscle suggests that it’s more of a simple reflex – part of our basic wiring – and it appears that very ancient parts of the brain such as the brainstem are involved. Reflexive movements in response to touch, vision and hearing are well known but this is the first time that a reflex linking taste and muscle activity has been described,” she says.

Further research is required to determine the precise mechanisms involved and to learn more about the size of the effect on fresh versus fatigued muscle.

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Article adapted by MD Sports from original press release.
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Contact: Pauline Curtis
The University of Auckland

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“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.

Scientists may soon be able to influence muscle formation more easily as a result of research conducted in the National Institute of Arthritis and Musculoskeletal and Skin Diseases’ Laboratory of Muscle Biology. The researchers there and at institutions in California and Italy have found that inhibitors of the enzyme deacetylase can switch the pathway of muscle precursor cells (myoblasts) from simply reproducing themselves to becoming mature cells that form muscle fibers (myotubules).

It has been known for some time that deacetylase prevents the skeletal muscle gene from being expressed, which inhibits myoblasts from forming muscle. The research team has found that under certain conditions, deacetylase inhibitors (DIs) in myoblasts enhance muscle gene expression and muscle fiber formation.

Knowledge of how DIs act against deacetylase is providing important insights on potential ways to correct problems that occur during embryonic muscle development. This research may also lead to methods to induce muscle growth, regeneration and repair in adults.

Simona Iezzi, Ph.D., and Vittorio Sartorelli, M.D., in the NIAMS Muscle Gene Expression Group, along with Pier Lorenzo Puri, M.D., at the Salk Institute for Biological Studies and other investigators at the University of Rome, exposed human and mouse myoblasts to DIs while they were dividing or after placement in a medium that stimulates myoblasts to become muscle cells. The researchers found that exposing dividing human and mouse myoblasts to a DI increased the levels of muscle proteins and led to a dramatic increase in the formation of muscle fibers. Similar experiments were done in developing mouse embryos, resulting in an increased number of somites (the regions of the embryo from which muscle cells are derived) and augmented expression of muscle genes.

Dr. Sartorelli’s group continues to investigate how the myoblasts are stimulated to fuse into myotubules. One theory is that the performance of poorly differentiated myoblasts is enhanced when they are recruited by cells with a good capacity to differentiate. Further research will be directed at discovering whether the cells that have been induced to form muscle will restore muscle function when transplanted into a mouse model of muscular dystrophy. In addition, the researchers at the NIAMS Muscle Gene Expression Group plan to expose adult muscle stem cells from a mouse model to DIs to understand their biology and their potential use as therapeutic tools.

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Article adapted by MD Sports from original press release.
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Contact: Judith Wortman
NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases

Iezzi S, Cossu G, Nervi C, Sartorelli V, Puri P. Stage-specific modulation of skeletal myogenesis by inhibitors of nuclear deacetylases. PNAS 2002;99(11):7757-7762.

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

Experts at The University of Nottingham are to investigate the effect of nutrients on muscle maintenance in the hope of determining better ways of keeping up our strength as we get old.

The researchers, based at the School of Graduate Entry Medicine and Health in Derby, want to know what sort of exercise we can take and what food we should eat to slow down the natural loss of skeletal muscle with ageing.

The team from the Department of Clinical Physiology, which has over 20 years experience in carrying out this type of metabolic study, need to recruit 16 healthy male volunteers in two specific age groups to help in it’s research.

Skeletal muscles make up about half of our body weight and are responsible for controlling movement and maintaining posture. However, at around 50 years of age our muscles begin to waste at approximately 0.5 per cent to one per cent a year. It means that an 80 year old may only have 70 per cent of the muscle of a 50 year old.

Since the strength of skeletal muscle is proportional to muscle size, such wasting makes it harder to carry out daily activities requiring strength, such as climbing stairs and leads to a loss of independence and an increased risk of falls and fractures.

In order for skeletal muscles to maintain their size, the large reservoirs of muscle protein require constant replenishment in the way of amino acids from protein contained within the food we eat. In fact, amino acids from our food act not only as the building blocks of muscle proteins but also actually ‘tell’ our muscle cells to build proteins.

Recent research from the clinical physiology team has shown that the cause of muscle wasting with ageing appears to be an attenuation of muscle building in response to protein feeding. In other words, as we age we lose the ability to covert the protein in the food we eat in to muscle tissue. The proposed research will investigate the mechanisms responsible for this deficit.

Dr Philip Atherton, who is currently recruiting volunteers, said: “I am really excited to be involved in this project because if we can determine ways to better maintain muscle mass as we age it will greatly benefit us all.”

The researchers are looking for 16 healthy, non-smoking, male volunteers aged 18 to 25 and 65 to 75.

Initially, the volunteers will undergo a health screening and then on a different day, under the supervision of a doctor, will be infused with an amino acid mixture to simulate feeding along with a ‘tagged’ amino acid that allows them to assess muscle building. To make these measures, blood samples will be taken from the arm and muscle biopsies from the thigh muscle under local anaesthesia. Volunteers will receive an honorarium to cover their expenses.

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Article adapted by MD Sports from original press release.
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Contact: Lindsay Brooke
University of Nottingham

 

The study will take place at The University of Nottingham’s Medical School which based at the City Hospital in Derby.

A University of Colorado at Boulder study of a space-age, low-gravity training machine used by several 2008 Olympic runners showed it reduced impacts on muscles and joints by nearly half when subjects ran at the equivalent of 50 percent of their body weight.

The new study has implications for both competitive runners rehabilitating from injuries and for ordinary people returning from knee and hip surgeries, according to Associate Professor Rodger Kram of CU-Boulder’s integrative physiology department.

Known as the “G-Trainer,” the machine consists of a treadmill surrounded by an inflatable plastic chamber that encases the lower body of the runner, said Kram. Air pumped into the chamber increases the pressure and effectively reduces the weight of runners, who are sealed in the machine at the waist in a donut-shaped device with a special zipper and “literally lifted up by their padded neoprene shorts,” he said.

Published in the August issue of the Journal of Applied Biomechanics, the study is the first to quantify the effects of running in the G-Trainer, built by Alter-G Inc. of Menlo Park, Calif., using technology developed at NASA’s Ames Research Center in California. The paper was authored by Kram and former CU-Boulder doctoral student Alena Grabowski, now a postdoctoral researcher at the Massachusetts Institute of Technology.

Although G-Trainers have been used in some sports clinics and college and professional sports training rooms since 2006, the new study is the first scientific analysis of the device as a training tool for running, said Grabowski.

“The idea was to measure which levels of weight support and speeds give us the best combination of aerobic workout while reducing the impact on joints,” said Kram. “We showed that a person can run faster in the G-Trainer at a lower weight and still get substantial aerobic benefits while maintaining good neuromuscular coordination.”

The results indicated a subject running at the equivalent of half their weight in the G-Trainer at about 10 feet per second, for example — the equivalent of a seven-minute mile — decreased the “peak” force resulting from heel impact by 44 percent, said Grabowski. That is important, she said, because each foot impact at high speed can jar the body with a force equal to twice a runner’s weight.

Several former CU track athletes participating in the 2008 Olympics in Beijing have used the machine, said Kram. Alumna Kara Goucher, who will be running the 5,000- and 10,000-meter races in Beijing, has used the one in Kram’s CU-Boulder lab and one in Eugene, Ore., for rehabilitation, and former CU All-American and Olympic marathoner Dathan Ritzenhein also uses a G-Trainer in his home in Oregon. Other current CU track athletes who have been injured have tried the machine in Kram’s lab and found it helpful to maintain their fitness as they recovered, Kram said.

For the study, the researchers retrofitted the G-Trainer with a force-measuring treadmill invented by Kram’s team that charts vertical and horizontal stress load on each foot during locomotion, measuring the variation of biomechanical forces on the legs during running. Ten subjects each ran at three different speeds at various reduced weights, with each run lasting seven minutes. The researchers also measured oxygen consumption during each test, Kram said.

Grabowski likened the effect of the G-Trainer on a runner to pressurized air pushing on the cork of a bottle. “If you can decrease the intensity of these peak forces during running, then you probably will decrease the risk of injury to the runner.”

The G-Trainer is a spinoff of technology originally developed by Rob Whalen, who conceived the idea while working at NASA Ames as a National Research Council fellow to help astronauts maintain fitness during prolonged space flight. While the NASA technology was designed to effectively increase the weight of the astronauts to stem muscle atrophy and bone loss in low-gravity conditions, the G-Trainer reverses the process, said Grabowski.

In the past, sports trainers and researchers have used climbing harnesses over treadmills or flotation devices in deep-water swimming pools to help support the weight of subjects, said Kram. Harnesses are cumbersome, while pool exercises don’t provide sufficient aerobic stimulation and biomechanical loading on the legs, he said.

Marathon world-record holder Paula Radcliffe of Great Britain is currently using a G-Trainer in her high-altitude training base in Font-Remeu, France. Radcliffe is trying to stay in top running shape while recovering from a stress fracture in her femur in time for the 2008 Olympic women’s marathon on Aug. 17, according to the London Telegraph.

Kram and Grabowski have begun a follow-up study of walking using the G-Trainer. By studying subjects walking at various weights and speeds in the machine, the researchers should be able to quantify its effectiveness as a rehabilitation device for people recovering from surgeries, stress fractures and other lower body injuries, Kram said.

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Article adapted by MD Sports from original press release.
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Contact: Rodger Kram
University of Colorado at Boulder