Archive for the ‘Fat Loss’ 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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Women who walked two or more hours a week or who usually walked at a brisk pace (3 miles per hour or faster) had a significantly lower risk of stroke than women who didn’t walk, according to a large, long-term study reported in Stroke: Journal of the American Heart Association.

The risks were lower for total stroke, clot-related (ischemic) stroke and bleeding (hemorrhagic) stroke, researchers said.

Compared to women who didn’t walk:

  • Women who usually walked at a brisk pace had a 37 percent lower risk of any type of stroke and those who walked two or more hours a week had a 30 percent lower risk of any type of stroke.
  • Women who typically walked at a brisk pace had a 68 percent lower risk of hemorrhagic stroke and those who walked two or more hours a week had a 57 percent lower risk of hemorrhagic stroke.
  • Women who usually walked at a brisk pace had a 25 percent lower risk of ischemic stroke and those who usually walked more than two hours a week had a 21 percent lower risk of ischemic stroke — both “borderline significant,” according to researchers.

“Physical activity, including regular walking, is an important modifiable behavior for stroke prevention,” said Jacob R. Sattelmair, M.Sc., lead author and doctoral candidate in epidemiology at Harvard School of Public Health in Boston, Mass. “Physical activity is essential to promoting cardiovascular health and reducing risk of cardiovascular disease, and walking is one way of achieving physical activity.”

More physically active people generally have a lower risk of stroke than the least active, with more-active persons having a 25 percent to 30 percent lower risk for all strokes, according to previous studies.

“Though the exact relationship among different types of physical activity and different stroke
subtypes remains unclear, the results of this specific study indicate that walking, in particular, is associated with lower risk of stroke,” Sattelmair said.

Researchers followed 39,315 U.S. female health professionals (average age 54, predominantly white) participating in the Women’s Health Study. Every two to three years, participants reported their leisure-time physical activity during the past year — specifically time spent walking or hiking, jogging, running, biking, doing aerobic exercise/aerobic dance, using exercise machines, playing tennis/squash/racquetball, swimming, doing yoga and stretching/toning. No household, occupational activity or sedentary behaviors were assessed.

They also reported their usual walking pace as no walking, casual (about 2 mph), normal (2.9 mph), brisk (3.9 mph) or very brisk (4 mph).

Sattelmair noted that walking pace can be assessed objectively or in terms of the level of exertion, using a heart rate monitor, self-perceived exertion, “or a crude estimate such as the ‘talk test’ – wherein, for a brisk pace, you should be able to talk but not able to sing. If you cannot talk, slow down a bit. If you can sing, walk a bit faster.”

During 11.9 years of follow-up, 579 women had a stroke (473 were ischemic, 102 were hemorrhagic and four were of unknown type).

The women who were most active in their leisure time activities were 17 percent less likely to have any type of stroke compared to the least-active women.

Researchers didn’t find a link between vigorous activity and reduced stroke risk. The reason is unclear, but they suspect that too few women reported vigorous activity in the study to get an accurate picture and/or that moderate-intensity activity may be more effective at lowering blood pressure as suggested by some previous research.

Stroke is the third leading cause of death and a leading cause of serious disability in the United States, so it’s important to identify modifiable risk factors for primary prevention, Sattelmair said.

An inverse association between physical activity and stroke risk is consistent across genders. But there tend to be differences between men and women regarding stroke risk and physical activity patterns.

“The exact relation between walking and stroke risk identified in this study is not directly generalizable to men,” Sattelmair said. “In previous studies, the relation between walking and stroke risk among men has been inconsistent.”

The study is limited because it was observational and physical activity was self-reported. But strengths are that it was large and long-term with detailed information on physical activity, he said.

Further study is needed on more hemorrhagic strokes and with more ethnically diverse women, Sattelmair said.

The American Heart Association recommends for substantial health benefits, adults should do at least 150 minutes a week of moderate-intensity or 75 minutes a week of vigorous-intensity aerobic physical activity or a combination.

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Article adapted by MD Sports from original press release.
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Contact: Birdgette McNeill
American Heart Association

Molecular switch found in mice could lead to future obesity treatments, scientists say

A surprise discovery — that calorie-burning brown fat can be produced experimentally from muscle precursor cells in mice — raises the prospect of new ways to fight obesity and overweight, say scientists from Dana-Farber Cancer Institute.

Reporting in the Aug. 21 issue of the journal Nature, the researchers demonstrated that brown fat, which is known as the “good” form of fat — so called because it burns calories and releases energy, unlike “bad” white fat that simply stores extra calories — can be generated from unspecialized precursors that routinely spawn skeletal muscle.

The team led by Dana-Farber’s Bruce Spiegelman, PhD, showed that a previously known molecular switch, PRDM16, regulates the creation of brown fat from immature muscle cells. They also determined that the process is a two-way street: Knocking out PRDM16 in brown fat cells can convert them into muscle cells. However, Spiegelman called the latter an “experimental lab trick” for which he currently envisions no practical applications.

The “huge surprise” of the study results, he said, was that muscle precursor cells known as “satellite cells” are able to give birth to brown fat cells under the control of PRDM16.

Spiegelman said the finding confirms that PRDM16 is the “master regulator” of brown fat development. The confirmation will spur ongoing research in his laboratory, he said, to see if drugs that rev up PRDM16 in mice — and potentially, in people — could convert white fat into brown fat and thereby treat obesity. Another strategy, he said, might be to transplant brown fat cells into an overweight person to turn on the calorie-burning process.

“I think we now have very convincing evidence that PRDM16 can turn cells into brown fat cells, with the possibility of combating obesity,” said Spiegelman, the senior author of the paper. The lead author is Patrick Seale, PhD, a postdoctoral fellow in the Spiegelman lab.

Another paper in the same issue of Nature described a different trigger of brown fat production, a molecule called BMP7. A commentary in the journal by Barbara Cannon, an internationally recognized researcher in the biology of fat cells at the University of Stockholm, said that the two reports “take us a step closer to the ultimate goal of promoting the brown fat lineage as a potential way of counteracting obesity.”

The Spiegelman group has long studied fat cells both as a model for normal and abnormal cell development, which relates to cancer, and also because fat cells play such a key role in the growing epidemics of obesity and diabetes.

There is much interest in brown fat’s role in regulating metabolism. Rodents and human infants have abundant brown fat that dissipates food energy as heat to protect against the cold. Though human adults have little brown fat, it apparently does have a metabolic function, including the potential to be amplified in some way to combat obesity.

In 2007, Spiegelman and colleagues reported they had inserted PRDM16 genes into white fat precursors, which they implanted under the skin of mice. The PRDM16 switch coaxed the white fat precursors to produce brown fat cells instead of white. To Spiegelman, this suggested the possibility of transplanting PRDM16-equipped white fat precursors into people who are at high risk of becoming obese, to shift their metabolism slightly into a calorie-burning mode.

The new research adds another potential source of brown fat — the muscle cell progenitors, or myoblasts, that exist in the body to replace mature muscle cells as needed. The progenitors, which can be thought of as “adult stem cells,” are committed to becoming specialized muscle cells when activated by appropriate signals, or, as the study revealed, brown fat cells when PDRM16 is turned on. The PRDM16 trigger “is very powerful at what it does,” said Spiegelman, who is also a professor of cell biology at Harvard Medical School.

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Article adapted by MD Sports from original press release.
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Contact: Bill Schaller
Dana-Farber Cancer Institute 

Other authors of the paper include Bryan Bjork, PhD, and David R. Beier, PhD, MD, of Brigham and Women’s Hospital; Michael Rudnicki, PhD, of the Ottawa Health Research Institute; and Hediye Erdjument-Bromage, PhD, and Paul Tempst, PhD, of Memorial Sloan-Kettering Cancer Center.

Dana-Farber Cancer Institute (www.dana-farber.org) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute.

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

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

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

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

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

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

This study provides functional outcomes that build on an earlier mechanistic study co-led by Tarnopolsky and Dr. S. Melov at the Buck Institute of Age Research, published in PLoS One this year, which provided evidence that six months of resistance exercise reversed some of the muscle gene expression abnormalities associated with the aging process.
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Article adapted by MD Sports Weblog from original press release.
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Contact: Veronica McGuire
McMaster University

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

New research on the effects of the female sex hormone estrogen in the brain lend credence to what many women have suspected about the hormonal changes that accompany aging: Menopause can make you fat.Scientists long have sought to understand how changes in hormones during menopause could account for the increase in appetite and accompanying weight gain that often occurs among aging women.

In a series of animal experiments described today at the 234th national meeting of the American Chemical Society, the world’s largest scientific society, researchers showed how estrogen receptors located in the hypothalamus serve as a master switch to control food intake, energy expenditure and body fat distribution. When these receptors are destroyed, the animals immediately begin to eat more food, burn less energy and pack on pounds.

This research seems to support a link between estrogen and regulation of obesity, especially the dangerous accumulation of abdominal fat linked to heart disease, diabetes, and cancer, says Deborah J. Clegg, Ph. D., assistant professor of psychiatry at the University of Cincinnati Academic Health Center, who is directing the studies.

The findings may also help scientists develop more targeted hormone replacement therapies, capable of stimulating estrogen receptors in one part of the brain or body while dampening it in the next, Clegg says.

Estrogen receptors are located on cells throughout a woman’s body. Previous studies have shown that one type of estrogen receptor, known as estrogen receptor alpha or ER-alpha, plays a role in regulating food intake and energy expenditure. But scientists have been unable to pinpoint exactly where these fat-regulating receptors reside or how they work to govern these behaviors.

To determine the effect of dwindling estrogen levels in the brain, Clegg and her colleagues are focusing on two ER-alpha rich regions located in the hypothalamus, an area of the brain that controls body temperature, hunger and thirst. The first region, called the ventromedial nucleus or VMN, is a key center for energy regulation.

Using a relatively new gene-silencing technique called RNA interference, the researchers in earlier research deactivated the alpha-receptors in the VMN. The estrogen receptors in other regions of the brain maintained their normal capacity.

When estrogen levels in the VMN dipped, the animals’ metabolic rate and energy levels also plummeted. The findings show the animals quickly developed an impaired tolerance to glucose and a sizable weight gain, even when their caloric intake remained the same. What’s more, the excess weight went straight to their middle sections, creating an increase in visceral fat.

The findings suggested that the ER-alpha in this region plays an essential role in controlling energy balance, body fat distribution and normal body weight.

Clegg now plans to perform a similar experiment to deactivate ER-alpha in the arcuate nucleus region of the hypothalamus. This region contains two populations of neurons: one puts the brake on food intake and the other stimulates food intake. Clegg anticipates that a loss of estrogen in this region may create an increase in the animals’ appetites as well as their weight.

Clegg says her studies address an area that is sorely needed given the incidence and impact of gender differences in obesity and its complications.

“The accumulation of abdominal fat puts both men and women at a heightened risk of cardiovascular disease, diabetes, and insulin resistance,” she says. “Women are protected from these negative consequences as long as they carry their weight in their hips and saddlebags. But when they go through menopause and the body fat shifts to the abdomen, they have to start battling all of these medical complications.”

By identifying the critical brain regions that determine where body fat is distributed, Clegg says her findings may help scientists design hormone replacement therapies to better manage and manipulate estrogen levels.

“If we could target those critical regions and estrogen receptors associated with weight gain and energy expenditure, we could perhaps design therapies that help women sidestep many of the complications brought on by the onset of menopause,” she says.

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Article adapted by MD Sports Weblog from original press release.
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Contact: Charmayne Marsh
American Chemical Society

 The American Chemical Society — the world’s largest scientific society — is a nonprofit organization chartered by the U.S. Congress and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.

Deborah J. Clegg, Ph.D., is assistant professor of psychiatry at the University of Cincinnati Academic Health Center in Cincinnati, Ohio.

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