Insights into how muscle adapts to endurance

Duke University Medical Center researchers have identified the skeletal muscle changes that occur in response to endurance exercise and have better defined the role of vascular endothelial growth factor (VEGF) in creating new blood vessels, known as angiogenesis, in the process.

VEGF is a protein known to trigger blood vessel growth by activating numerous genes involved in angiogenesis.

The researchers’ new insights could provide a roadmap for medical investigators as they seek to use VEGF in treating human conditions characterized by lack of adequate blood flow, such as coronary artery disease or peripheral arterial disease.

Using mice as animal models, the researchers found that exercise initially stimulates the production of VEGF, which then leads to an increase in the number of capillaries within a specific muscle fiber type, ultimately leading to an anaerobic to aerobic change in the muscle fibers supplied by those vessels. The VEGF gene produces a protein that is known to trigger blood vessel growth.

The results of the Duke experiments were presented by cardiologist Richard Waters, M.D., Nov. 8, 2004, at the American Heart Association’s annual scientific sessions in New Orleans.

“It is known that exercise can improve the symptoms of peripheral arterial disease in humans and it has been assumed that angiogenesis played a role in this improvement,” Waters said. “However, the clinical angiogenesis trials to date utilizing VEGF have been marginally successful and largely disappointing, so we felt it would be better at this point to return to animal studies in an attempt to better understand the angiogenic process.”

The Duke team performed their experiments using a mouse model of voluntary exercise. This experimental approach is important, they explained, because most skeletal muscle adaptation studies utilize electrical stimulation of the muscle, which is much less physiologic and does not as closely mimic what would be expected in human exercise.

When placed in the dark with a running wheel, mice will instinctively run, the researchers said. In the Duke experiments, 41 out of 42 mice “ran” up to seven miles each night. At regular intervals over a 28-day period, the researchers then performed detailed analysis of capillary growth and the subsequent changes in muscle fiber type and compared these findings to sedentary mice.

Mammalian muscle is generally made up of two different fiber types – slow-twitch fibers requiring oxygen to function, and the fast-twitch fibers, which function in the absence of oxygen by breaking down glucose. Because of their need for oxygen, slow-twitch fibers tend to have a higher density of capillaries.

“Exercise training is probably the most widely utilized physiological stimulus for skeletal muscle, but the mechanisms underlying the adaptations muscle fibers make in response to exercise is not well understood,” Waters said. “What we have shown in our model is that increases in the capillary density occur before a significant change from fast-twitch to slow-twitch fiber type, and furthermore, that changes in levels of the VEGF protein occur before the increased capillary density.”

“Interestingly, capillary growth appears to occur preferentially among fast-twitch fibers, and it is these very fibers that likely change to slow-twitch fibers,” Waters said. “Since exercise has the potential to impact an enormous number of clinical conditions, therapeutic manipulations intended to alter the response to exercise would benefit from a more detailed understanding of what actually happens to muscle as a result of exercise.”

The exact relationship between VEGF, exercise induced angiogenesis, and muscle fiber type adaptation is still not clear and will become the focus of the group’s continuing research. The findings from the current study, however, are providing important temporal and spatial clues to the adaptability process.

“Our data suggests that angiogenesis is one of the key early steps in skeletal muscle adaptation and may be an essential step in the adaptability process,” Waters continued. “This understanding could be crucial for designing new studies that can be performed to inhibit the angiogenic response to exercise in order to directly test the links between angiogenesis and skeletal muscle plasticity.”

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The research team was supported by grants from the American Heart Association and the U.S. Department of Veterans Affairs.

Other members of the Duke team were Ping Li, Brian Annex, M.D., and Zhen Yan, Ph.D. Svein Rotevatn, Haukeland University Hospital, Bergen, Norway, was also a member of the team.

Duke University Medical Center researchers have identified the skeletal muscle changes that occur in response to endurance exercise and have better defined the role of vascular endothelial growth factor (VEGF) in creating new blood vessels, known as angiogenesis, in the process.

VEGF is a protein known to trigger blood vessel growth by activating numerous genes involved in angiogenesis.

The researchers’ new insights could provide a roadmap for medical investigators as they seek to use VEGF in treating human conditions characterized by lack of adequate blood flow, such as coronary artery disease or peripheral arterial disease.

Using mice as animal models, the researchers found that exercise initially stimulates the production of VEGF, which then leads to an increase in the number of capillaries within a specific muscle fiber type, ultimately leading to an anaerobic to aerobic change in the muscle fibers supplied by those vessels. The VEGF gene produces a protein that is known to trigger blood vessel growth.

The results of the Duke experiments were presented by cardiologist Richard Waters, M.D., Nov. 8, 2004, at the American Heart Association’s annual scientific sessions in New Orleans.

“It is known that exercise can improve the symptoms of peripheral arterial disease in humans and it has been assumed that angiogenesis played a role in this improvement,” Waters said. “However, the clinical angiogenesis trials to date utilizing VEGF have been marginally successful and largely disappointing, so we felt it would be better at this point to return to animal studies in an attempt to better understand the angiogenic process.”

The Duke team performed their experiments using a mouse model of voluntary exercise. This experimental approach is important, they explained, because most skeletal muscle adaptation studies utilize electrical stimulation of the muscle, which is much less physiologic and does not as closely mimic what would be expected in human exercise.

When placed in the dark with a running wheel, mice will instinctively run, the researchers said. In the Duke experiments, 41 out of 42 mice “ran” up to seven miles each night. At regular intervals over a 28-day period, the researchers then performed detailed analysis of capillary growth and the subsequent changes in muscle fiber type and compared these findings to sedentary mice.

Mammalian muscle is generally made up of two different fiber types – slow-twitch fibers requiring oxygen to function, and the fast-twitch fibers, which function in the absence of oxygen by breaking down glucose. Because of their need for oxygen, slow-twitch fibers tend to have a higher density of capillaries.

“Exercise training is probably the most widely utilized physiological stimulus for skeletal muscle, but the mechanisms underlying the adaptations muscle fibers make in response to exercise is not well understood,” Waters said. “What we have shown in our model is that increases in the capillary density occur before a significant change from fast-twitch to slow-twitch fiber type, and furthermore, that changes in levels of the VEGF protein occur before the increased capillary density.”

“Interestingly, capillary growth appears to occur preferentially among fast-twitch fibers, and it is these very fibers that likely change to slow-twitch fibers,” Waters said. “Since exercise has the potential to impact an enormous number of clinical conditions, therapeutic manipulations intended to alter the response to exercise would benefit from a more detailed understanding of what actually happens to muscle as a result of exercise.”

The exact relationship between VEGF, exercise induced angiogenesis, and muscle fiber type adaptation is still not clear and will become the focus of the group’s continuing research. The findings from the current study, however, are providing important temporal and spatial clues to the adaptability process.

“Our data suggests that angiogenesis is one of the key early steps in skeletal muscle adaptation and may be an essential step in the adaptability process,” Waters continued. “This understanding could be crucial for designing new studies that can be performed to inhibit the angiogenic response to exercise in order to directly test the links between angiogenesis and skeletal muscle plasticity.”

 

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Article adapted by MD Sports from original press release.
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Contact: Richard Merritt
Duke University Medical Center 

The research team was supported by grants from the American Heart Association and the U.S. Department of Veterans Affairs

Cereal and Milk Good for Exercise Muscle Recovery

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

Making Muscle From ‘Good’ Fat

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.

Super protein creates fat burning Metabolic ‘shield” against weight gain…

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

Moderate exercise prevents extreme weight gain with age

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.

Low-Fat Diet Hurts Runners Perfomance, Suppresses Immune Function, and Increases Infection Risk

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

Pycnogenol® Improves Blood Flow, Relieves Muscle Cramp And Pain In Athletes

A study published in Angiology shows that supplementation with the pine bark extract Pycnogenol® (pic-noj-en-all) improves blood flow to the muscles which speeds recovery after physical exercise. The study of 113 participants demonstrated that Pycnogenol significantly reduces muscular pain and cramps in athletes and healthy, normal individuals.

“With the millions of athletes worldwide, this truly is a profound breakthrough and extremely significant for all individuals interested in muscle cramp and pain relief with a natural approach. These findings indicate that Pycnogenol can play an important role in sports by improving blood flow to the muscles and hastening post-exercise recovery, said Dr. Peter Rohdewald, a lead researcher of the study.

Researchers at L’Aquila University in Italy and at the University of Würzburg in Germany studied the effects of Pycnogenol® on venous disorders and cramping in two separate studies.

The first study consisted of 66 participants who had experienced normal cramping at some point, had venous insufficiency, or were athletes who suffer from exercise-induced cramping. The first two weeks of the study was an observation period and participants did not supplement with Pycnogenol®. Symptoms related to venous disorders, and the number of cramping episodes each participant experienced over the two observation weeks was recorded.

Next, all the participants were given 200 mg of Pycnogenol once a day for four weeks. After the treatment phase, participants’ symptoms and cramping episodes were recorded for one week without any Pycnogenol supplementation.

The researchers found a significant decrease in the number of cramps the participants experienced while supplementing with Pycnogenol.® Participants who had experienced normal cramping had a 25 percent reduction in the number of cramps experienced while taking Pycnogenol.

Participants with venous insufficiency experienced a 40 percent reduction in the number of cramps, and athletes with frequent cramping experienced a 13 percent reduction in the number of cramps while on Pycnogenol.®

The second study involved 47 participants with diabetic microangiopathy (a disorder of the smallest veins commonly associated with diabetes), or intermittent claudication (a blood vessel disease that causes the legs to easily cramp).This study also used a two-week pre-trial observation period followed by a week of supplementing with Pycnogenol (200 mg per day for one week), followed by a week of observation without Pycnogenol® supplementation.

Patients with diabetic microangiopathy had a 20.8 percent reduction in pain, while participants with claudication experienced a 21 percent decrease in the amount of pain experienced while supplementing with Pycnogenol.® Results indicated participants who took placebo experienced no decrease in pain.

Cramps are a common problem for people of all ages, ranging to the extreme fit and healthy to people who suffer from health problems. Previously, magnesium was hailed as the natural approach for relieving muscle cramps, however studies continue to show magnesium to be inefficient for reducing muscle cramps.

“Pycnogenol® improves the blood supply to muscle tissue creating a relief effect on muscle cramping and pain. Poor circulation in the muscle is known to cause cramps and Pycnogenol® improved the cramping in patients due to a stimulation of blood flow to their muscle tissue. Nitric oxide (NO) a blood gas, is well known to enhance blood flow and Pycnogenol® may be influencing the activity of NO,” said Rohdewald. “The insufficient production of NO is the common denominator responsible for impaired blood flow in vascular disease.”

Strenuous exercise is known to involve muscle damage which may be followed by symptoms of inflammation. In separate studies published this year and in 2004 and 2005, Pycnogenol® demonstrated its anti-inflammatory effects in clinical trials for asthma, dysmenorrhea and osteoarthritis.

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Article adapted by MD Only Weblog from original press release.
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Contact: Pycnogenol®

About Pycnogenol®
Pycnogenol® is a natural plant extract originating from the bark of the maritime pine that grows along the coast of southwest France and is found to contain a unique combination of procyanidins, bioflavonoids and organic acids, which offer extensive natural health benefits. The extract has been widely studied for the past 35 years and has more than 220 published studies and review articles ensuring safety and efficacy as an ingredient. Today, Pycnogenol® is available in more than 600 dietary supplements, multi-vitamins and health products worldwide.

Researchers discovery gene that enhances muscle performance

A team of researchers, led by scientists at Dartmouth Medical School and Dartmouth College, have identified and tested a gene that dramatically alters both muscle metabolism and performance. The researchers say that this finding could someday lead to treatment for muscle diseases, including helping the elderly who suffer from muscle deterioration and improving muscle performance in endurance athletes.

The researchers report that the enzyme called AMP-activated protein kinase (or AMPK) is directly involved in optimizing muscle activity. The team bred a mouse that genetically expressed AMPK in an activated state. Like a trained athlete, this mouse enjoyed increased capacity to exercise, manifested by its ability to run three times longer than a normal mouse before exhaustion.

One particularly striking feature of the finding was the accumulation of muscle glycogen, the stored form of carbohydrates, a condition that many athletes seek by “carbo-loading” before an event or game. The study appears in the Nov. 14 online issue of the American Journal of Physiology: Endocrinology and Metabolism.

“Our genetically altered mouse appears to have already been an exercise program,” says Lee Witters, the Eugene W. Leonard 1921 Professor of Medicine and Biochemistry at Dartmouth Medical School and professor of biological sciences at Dartmouth College. “In other words, without a prior exercise regimen, the mouse developed many of the muscle features that would only be observed after a period of exercise training.”

Witters, whose lab led the study, explains that this finding has implication for anyone with a muscle disease and especially for the growing proportion of the population that is aging. Deteriorating muscles often make the elderly much more prone to fall, leading to hip and other fractures. According to Witters, there is tremendous interest in the geriatric field to find ways to improve muscle performance.

“We now wonder if it’s possible to achieve elements of muscular fitness without having to exercise, which in turn, raises many questions about possible modes of exercise performance enhancement, including the development of drugs that could do the same thing as we have done genetically,” he says. “This also might raise to some the specter of ‘gene doping,’ something seriously being talked about in the future of high-performance athletes.”

Witters says that the carbohydrate, glucose, is a major fuel that powers muscles, and this contributes directly to a muscle’s ability to repetitively contract during exercise. The activated AMPK in the Dartmouth mouse appears to have increased glycogen content by actually switching on a gene that normally synthesizes liver glycogen.

“The switching on of this liver gene in muscles,” he says, “is a shift in the conception of the biochemistry of muscle metabolism, since many enzyme genes are thought to only be active in just one tissue.”

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Article adapted by MD Sports Weblog from original press release.
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Contact: Sue Knapp
Dartmouth College

Other authors on the paper include Laura Barré, Christine Richardson, and Steven Fiering, all at Dartmouth; Michael Hirshman and Laurie Goodyear of Joslin Diabetes Center in Boston; Joseph Brozinick with Eli Lilly and Company; and Bruce Kemp of the St. Vincent’s Institute in Australia.

This research is funded by the National Institutes of Health.