Archive for the ‘Runner’ Category

And it increases endurance to run a mile and decreases inflammation

The Salk Institute scientist who earlier discovered that enhancing the function of a single protein produced a mouse with an innate resistance to weight gain and the ability to run a mile without stopping has found new evidence that this protein and a related protein play central roles in the body’s complex journey to obesity and offer a new and specific metabolic approach to the treatment of obesity related disease such as Syndrome X (insulin resistance, hyperlipidemia and atherosclerosis).

Dr. Ronald M. Evans, a Howard Hughes Medical Investigator at The Salk Institute’s Gene Expression Laboratory, presented two new studies (date) at Experimental Biology 2005 in the scientific sessions of the American Society for Biochemistry and Molecular Biology. The studies focus on genes for two of the nuclear hormone receptors that control broad aspects of body physiology, including serving as molecular sensors for numerous fat soluble hormones, Vitamins A and D, and dietary lipids.

The first study focuses on the gene for PPARd, a master regulator that controls the ability of cells to burn fat. When the “delta switch” is turned on in adipose tissue, local metabolism is activated resulting in increased calorie burning. Increasing PPARd activity in muscle produces the “marathon mouse,” characterized by super-ability for long distance running. Marathon mice contain altered muscle composition, which doubles its physical endurance, enabling it to run an hour longer than a normal mouse. Marathon mice contain increased levels of slow twitch (type I) muscle fiber, which confers innate resistance to weight gain, even in the absence of exercise.

Additional work to be reported at Experimental Biology looks at another characteristic of PPARd: its role as a major regulator of inflammation. Coronary artery lesions or atherosclerosis are thought to be sites of inflammation. Dr. Evans found that activation of PPARd suppresses the inflammatory response in the artery, dramatically slowing down lesion progression. Combining the results of this new study with the original “marathon mouse” findings suggests that PPARd drugs could be effective in controlling atherosclerosis by limiting inflammation and at the same time promoting improved physical performance.

Dr. Evans says he is very excited about the therapeutic possibilities related to activation of the PPARd gene. He believes athletes, especially marathon runners, naturally change their muscle fibers in the same way as seen in the genetically engineered mice, increasing levels of fat-burning muscle fibers and thus building a type of metabolic ‘shield” that keeps them from gaining weight even when they are not exercising.

But athletes do it through long periods of intensive training, an approach unavailable to patients whose weight or medical problems prevent them from exercise. Dr. Evans believes activating the PPARd pathway with drugs (one such experimental drug already is in development to treat people with lipid metabolism) or genetic engineering would help enhance muscle strength, combat obesity, and protect against diabetes in these patients.

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Article adapted by MD Sports Weblog from original press release.
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Contact: Sarah Goodwin
Federation of American Societies for Experimental Biology

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 Weblog from original press release.
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Contact: Andrew McLaughlin
University of Bath

Whippets are bred for speed and have been clocked at speeds approaching 40 miles per hour over a 200-yard racing course. Scientists at the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health (NIH), have now discovered a genetic mutation that helps to explain why some whippets run even faster than others. Published in the open-access journal PLoS Genetics, their findings will make for a fascinating experiment in applied genetics and human nature: what will dog breeders do with this information, and what are the implications for human athletic performance?

A research team led by Elaine Ostrander, chief of the Cancer Genetics Branch in NHGRI’s Division of Intramural Research, reports that a mutation in a gene that codes for a muscle protein known as myostatin can increase muscle mass and enhance racing performance in whippets. Like humans, dogs have two copies of every gene, one inherited from their mother and the other from their father. Dr. Ostrander and colleagues found those whippets with one mutated copy of the myostatin (MTSN) gene and one normal copy to be more muscled than normal and are among the breed’s fastest racers. However, their research also showed that whippets with two mutated copies of the MTSN gene have a gross excess of muscle and are rarely found among competitive racers.

This is the first work to link athletic performance to a mutation in the myostatin gene, with Dr. Ostrander observing: “The potential to increase an athlete’s performance by disrupting MSTN either by natural or perhaps artificial means could change the face of competitive human and canine athletics.” However, the authors stress that: “Extreme caution should be exercised when acting upon these results because we do not know the consequences for overall health associated with myostatin mutations.”

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Article adapted by MD Sports Weblog from original press release.
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Contact: Johanna Dehlinger
Public Library of Science

CITATION: Mosher DS, Quignon P, Bustamante CD, Sutter NB, Mellersh CS, et al. (2007) A Mutation in the Myostatin Gene Increases Muscle Mass and Enhances Racing Performance in Heterozygote Dogs. PLoS Genet. doi:10.1371/journal.pgen.0030079.eor
 

Energy bars, touted for improving athletic performance while providing the right combination of essential nutrients, may not always give endurance athletes the boost they expect.An Ohio State University researcher compared two popular energy bars and found that one of the bars didn’t give the moderate increase in blood sugar known to enhance performance in endurance athletes. Instead, its effect was much like a candy bar – giving a big rush of sugar to the blood, followed by a sharp decline.

“Theoretically, energy bars produce more moderate increases and decreases in blood sugar levels than a typical candy bar,” said Steve Hertzler, an associate professor of medical dietetics at Ohio State. “But these claims aren’t necessarily valid.” His study appears in a recent issue of the Journal of the American Dietetic Association.

Hertzler wanted to know how energy bars affected blood glucose levels. Glucose is a sugar that provides energy to the body’s cells – for example, red-blood cells and most parts of the brain derive most of their energy from glucose.

“Athletes – especially those involved in endurance sports – want to enhance performance, and energy bars claim to help keep blood sugar levels at a moderate level,” Hertzler said.

Volunteers had to fast for at least 12 hours before taking part in each of four experiments. Then, they ate one of four experimental “meals” consisting of either four slices of white bread; a Snickers bar; an Ironman PR Bar; or a PowerBar. Each experimental meal provided the same amount of carbohydrates (50 grams.)

Hertzler then tested the effects these foods had on blood glucose levels at 15-minute intervals for up to two hours after each experimental meal. The volunteers had to wait at least 24 hours between each experimental meal.

Hertzler measured each subject’s blood samples for glucose levels, to determine which food most raised blood sugar levels.

Both energy bars caused blood glucose levels to peak at 30 minutes, while levels peaked at 45 minutes after the bread and candy bar were consumed. Blood glucose levels declined steadily throughout the duration of testing for all foods but the Ironman PR Bar. This bar caused blood glucose rates to remain fairly steady, probably because of the moderate carbohydrate level of the bar, according to Hertzler.

“Though blood glucose rates peaked at 30 minutes with both bars, the high-carbohydrate energy bar – the PowerBar – caused a much sharper decline,” Hertzler said. “In fact, the decline was sharper than with the candy bar.” Much of the energy derived from the bread and the candy bar came from carbohydrate and the same was true for the PowerBar. While the bar is low in protein and fat, more than 70 percent of it is made up of carbohydrate (such as high-fructose corn syrup; oat bran; and brown rice). In contrast, 40 percent of the Ironman PR is comprised of carbohydrate (high fructose corn syrup and fructose.) The rest of the bar was comprised of 30 percent fat and 30 percent protein.

“The composition of this bar may have been responsible for the diminished blood glucose response,” Hertzler said. “Athletes involved in short-duration events who want a quick energy boost should eat a high-carbohydrate energy bar or a candy bar,” he suggests. “However, endurance athletes would do well to consume an energy bar with a moderate carbohydrate level.”

Hertzler conducted this study while at Kent State University in Kent, Ohio. He is continuing similar research at Ohio State.

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Article adapted by MD Sports Weblog from original press release.
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Contact: Steve Hertzler
Ohio State University

Editor’s note: This research was funded by a grant from Kent State University. The researcher received no funding from either energy bar manufacturer.

Female athletes often lose their menstrual cycle when training strenuously, but researchers have long speculated on whether this infertility was due to low body fat, low weight or exercise itself. Now, researchers have shown that the cause of athletic amenorrhea is more likely a negative energy balance caused by increasing exercise without increasing food intake.”A growing proportion of women are susceptible to losing their menstrual cycle when exercising strenuously,” says Dr. Nancy I. Williams, assistant professor of kineseology and physiology at Penn State. “If women go six to 12 months without having a menstrual cycle, they could show bone loss. Bone densities in some long distance runners who have gone for a prolonged time period without having normal menstrual cycles can be very low.”

In studies done with monkeys, which show menstrual cyclicity much like women, researchers showed that low energy availability associated with strenuous exercise training plays an important role in causing exercise-induced amenorrhea. These researchers, working at the University of Pittsburgh, published findings in the Journal of Clinical Endocrinology and Metabolism showing that exercise-induced amenorrhea was reversible in the monkeys by increasing food intake while the monkeys still exercised.

Williams worked with Judy L. Cameron, associate professor of psychiatry and cell biology and physiology at the University of Pittsburgh. Dana L. Helmreich and David B. Parfitt, then graduate students, and Anne Caston-Balderrama, at that time a post-doctoral fellow at the University of Pittsburgh, were also part of the research team. The researchers decided to look at an animal model to understand the causes of exercise-induced amenorrhea because it is difficult to closely control factors, such as eating habits and exercise, when studying humans. They chose cynomolgus monkeys because, like humans, they have a menstrual cycle of 28 days, ovulate in mid-cycle and show monthly periods of menses.

“It is difficult to obtain rigorous control in human studies, short of locking people up,” says Williams.

Previous cross-sectional studies and short-term studies in humans had shown a correlation between changes in energy availability and changes in the menstrual cycle, but those studies were not definitive.

There was also some indication that metabolic states experienced by strenuously exercising women were similar to those in chronically calorie restricted people. However, whether the increased energy utilization which occurs with exercise or some other effect of exercise caused exercise-induced reproductive dysfunction was unknown.

“The idea that exercise or something about exercise is harmful to females was not definitively ruled out,” says Williams. “That exercise itself is harmful would be a dangerous message to put out there. We needed to look at what it was about exercise that caused amenorrhea, what it was that suppresses ovulation. To do that, we needed a carefully controlled study.”

After the researchers monitored normal menstrual cycles in eight monkeys for a few months, they trained the monkeys to run on treadmills, slowly increasing their daily training schedule to about six miles per day. Throughout the training period the amount of food provided remained the standard amount for a normal 4.5 to 7.5 pound monkey, although the researchers note that some monkeys did not finish all of their food all of the time.

The researchers found that during the study “there were no significant changes in body weight or caloric intake over the course of training and the development of amenorrhea.” While body weight did not change, there were indications of an adaptation in energy expenditure. That is, the monkeys’ metabolic hormones also changed, with a 20 percent drop in circulating thyroid hormone, suggesting that the suppression of ovulation is more closely related to negative energy balance than to a decrease in body weight.

To seal the conclusion that a negative energy balance was the key to exercise-induced amenorrhea, the researchers took four of the previous eight monkeys and, while keeping them on the same exercise program, provided them with more food than they were used to. All the monkeys eventually resumed normal menstrual cycles. However, those monkeys who increased their food consumption most rapidly and consumed the most additional food, resumed ovulation within as little as 12 to 16 days while those who increased their caloric intake more slowly, took almost two months to resume ovulation.

Williams is now conducting studies on women who agree to exercise and eat according to a prescribed regimen for four to six months. She is concerned because recreational exercisers have the first signs of ovulatory suppression and may easily be thrust into amenorrhea if energy availability declines. Many women that exercise also restrict their calories, consciously or unconsciously.

“Our goal is to test whether practical guidelines can be developed regarding the optimal balance between calories of food taken in and calories expended through exercise in order to maintain ovulation and regular menstrual cycles,” says Williams. “This would then ensure that estrogen levels were also maintained at healthy levels. This is important because estrogen is a key hormone in the body for many physiological systems, influencing bone strength and cardiovascular health, not just reproduction.”

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Article adapted by MD Sports Weblog from original press release.
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Contact: A’ndrea Elyse Messer
Penn State

The old adage “use it or lose it” is truer than ever. People who maintain a vigorously active lifestyle as they age gain less weight than people who exercise at more moderate levels, according to a first-of-its-kind study that tracked a large group of runners who kept the same exercise regimen as they grew older. The study also found that maintaining exercise with age is particularly effective in preventing extreme weight gain, which is associated with high blood pressure, high cholesterol, diabetes, and other diseases.

The study, conducted by Paul Williams of the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab), followed 6,119 men and 2,221 women who maintained their weekly running mileage (to within three miles per week) over a seven-year period. On average, the men and women who ran over 30 miles per week gained half the weight of those who ran less than 15 miles per week.

“To my knowledge, this is the only study of its type,” says Williams, a staff scientist in Berkeley Lab’s Life Sciences Division. “Other studies have tracked exercise over time, but the majority of people will have changed their exercise habits considerably.”

The research is the latest report from the National Runners’ Health Study, a 20-year research initiative started by Williams that includes more than 120,000 runners. It appears in the May issue of the journal Medicine and Science in Sports and Exercise.

Specifically, between the time subjects entered the study and when they were re-contacted seven years later, 25-to-34-year-old men gained 1.4 pounds annually if they ran less than 15 miles per week. In addition, male runners gained 0.8 pounds annually if they ran between 15 and 30 miles per week, and 0.6 pounds annually if they ran more than 30 miles per week.

This trend is mirrored in women. Women between the ages of 18 and 25 gained about two pounds annually if they ran less than 15 miles per week, 1.4 pounds annually if they ran 15 to 30 miles per week, and slightly more than three-quarters of a pound annually if they ran more than 30 miles per week. Other benefits to running more miles each week included fewer inches gained around the waist in both men and women, and fewer added inches to the hips in women.

“As these runners aged, the benefits of exercise were not in the changes they saw in their bodies, but how they didn’t change like the people around them,” says Williams.

Although growing older and gaining weight is something of a package deal, it isn’t the same in everyone. The lucky few remain lean as they age, most people pack on several pounds, and some people become obese. The latter group is particularly at risk for high blood pressure, high cholesterol, and diabetes. Fortunately, Williams’ results show that maintaining exercise can combat such extreme weight gain.

“Getting people to commit to a vigorously active lifestyle while young and lean will go a long way to reducing the obesity epidemic in this country,” says Williams.

Another paper published in the November 2006 issue of the journal Obesity by Williams and Paul Thompson of Hartford (CT) Hospital found that runners who increased their running mileage gained less weight than those who remained sedentary, and runners that quit running became fatter.

“The time to think about exercise is before you think you need it,” says Williams. “The medical journals are full of reports on how difficult it is to regain the slenderness of youth. The trick is not to get fat.”

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Article adapted by MD Sports Weblog from original press release.
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Contact: Dan Krotz
DOE/Lawrence Berkeley National Laboratory

Williams’ research was funded by the National Heart, Lung and Blood Institute. The study in the May issue of the journal Medicine and Science in Sports and Exercise is entitled Maintaining Vigorous Activity Attenuates 7-yr Weight Gain in 8,340 Runners.

Trained runners who severely limit the amount of fat in their diets may be suppressing their immune system and increasing their susceptibility to infections and inflammation, a University at Buffalo study has shown.In findings presented here today (May 22, 1999) at the fourth International Society for Exercise and Immunology Symposium, lead author Jaya T. Venkatraman, Ph.D., reported that running 40 miles per week on a diet composed of approximately 17 percent fat compromised the runners’ immune response.

The medium and high-fat diets, composed of approximately 32 and 41 percent fat respectively, left the immune system intact, and enhanced certain components, the findings showed.

“The data suggest that higher-fat diets may lower the proinflammatory cytokines, free radicals and hormones, and may enhance the levels of anti-inflammatory cytokines,” Venkatraman said.

Venkatraman is an associate professor of nutrition in the Department of Physical Therapy, Exercise and Nutrition Sciences in the UB School of Health Related Professions.

Earlier studies published by a UB research group headed by David Pendergast, Ed.D., professor of physiology and biophysics, reported that competitive runners who increased the proportion of fat in their diets improved their endurance with no negative effect on weight, body composition, blood pressure, pulse rate or total cholesterol. (See editor’s note)

However, since a high level of fat was thought to be immunosuppressive, the researchers sought to determine if increasing dietary fat would compromise various elements of the immune system, while improving performance.

“In general, moderate levels of exercise are known to enhance the immune system,” said Venkatraman. “But high-intensity exercise and endurance exercise produce excess levels of free radicals, which may place stress on the immune system.

“Since we have shown that athletes perform better on a higher-fat diet than on a low-fat diet, it was important to determine if the higher-fat diet would further compromise the immune system,” she said. “We found that it did not, but the very-low-fat diet did.”

The study involved six female and eight male competitive runners who trained at 40 miles a week and were part of a larger performance study. They spent a month on their normal diets, followed by a month each on diets composed of approximately 17 percent, 32 percent and 41 percent fat. Protein remained stable at 15 percent and carbohydrates made up the difference.

The immune status of the runners was obtained by analyzing concentrations of essential components of the immune system — leukocytes, cytokines and plasma cortisol — in blood samples taken before and after an endurance exercise test. The tests were conducted at the end of each four-week diet period.

Results showed that natural killer cells, a type of leukocyte and one of the body’s defense mechanisms marshaled to fight infection, were more than doubled in runners after the high-fat diet, compared to the low-fat regimen. Levels of PGE2, inflammation-causing prostaglandins, increased after the endurance test and were higher when the runners were on the low-fat diet.

This study is part of a larger investigation to determine the effects of dietary fat on performance, biochemical and nutritional status, and plasma lipids and lipoprotein profiles in distance runners being conducted by a study group composed of — in addition to Venkatraman and Pendergast — Peter Horvath, Ph.D., associate professor in the UB Department of Physical Therapy, Exercise and Nutrition Sciences, and John Leddy, M.D., clinical professor of orthopaedics and associate director of the UB Sports Medicine Institute.

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Article adapted by MD Sports Weblog from original press release.
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Contact: Lois Baker
University at Buffalo