Watercress May Boost Exercise Recovery

UK researchers believe that eating watercress may alleviate the oxidative stress that comes with heavy bouts of exercise.   Watercress contains an array of nutritional compounds such as β-carotene and α-tocopherol which may increase protection against exercise-induced oxidative stress. The leafy green vegetable was the focus of a recent study published in the British Journal of Nutrition.

Ten healthy males were assigned to eight weeks of watercress consumption followed by eight weeks of control (no watercress). Blood samples were analyzed for DNA damage and lipid peroxidation at baseline (before supplementation), at rest (before exercise), and following exercise.

Exercise resulted in an increase in DNA damage and lipid peroxidation when subjects took part in the control phase of the study, but when watercress was added to the diet, markers of DNA damage and lipid peroxidation were significantly reduced. Even acute supplementation improved DNA and lipid protection, suggesting that only small amounts of the leafy green were needed to reduce oxidative stress in the body.

Blood analysis revealed notable increases of xanthophylls, alpha-tocopherol, and gamma-tocopherol with watercress consumption. The researchers proposed that these compounds might have a role in increased protection against oxidative stress.

The main findings show an exercise-induced increase in DNA damage and lipid peroxidation over both acute and chronic control supplementation phases (< 0·05 v. supplementation), while acute and chronic watercress attenuated DNA damage and lipid peroxidation and decreased H2O2 accumulation following exhaustive exercise (P < 0·05 v. supplementation), while acute and chronic watercress attenuated DNA damage and lipid peroxidation and decreased H2O2 accumulation following exhaustive exercise (P < 0·05 v. control). A marked increase in the main lipid-soluble antioxidants (α-tocopherol, γ-tocopherol and xanthophyll) was observed following watercress supplementation (P < 0·05 v. control) in both experimental phases. These findings suggest that short- and long-term watercress ingestion has potential antioxidant effects against exercise-induced DNA damage and lipid peroxidation.

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.”

###

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.
———————————–

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

Body chemical ‘switch’ turns muscle atrophy on

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

###

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

Writer: Maggie Morris, (765) 494-2432, maggiemorris@purdue.edu

Sources: Amber Pond, (765) 494-6185, pond@purdue.edu 

Kevin Hannon, (765) 494-5949, hannonk@purdue.edu

Related Web sites: 

Purdue School of Veterinary Medicine: http://www.vet.purdue.edu/ 

FASEB Journal: http://www.fasebj.org/ 

STORY AND PHOTO CAN BE FOUND AT: http://news.uns.purdue.edu/UNS/html4ever/2006/060524.Pond.atrophy.html

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Contact: Maggie Morris
Purdue University 

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

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

Exercise Is The Best Medicine

Governor Sonny Perdue signed a proclamation recognizing May as Exercise is Medicine Month in Georgia. Exercise is Medicine is a national program, founded by the American College of Sports Medicine (ACSM) with The Coca-Cola Company, which encourages consumers to speak with their doctors about an appropriate level of exercise, plan their exercise regimen, track it and stick to it.

Health Benifits Of Weight Lifting For Elderly

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

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

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

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

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

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

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

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

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

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

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

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

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

Testosterone Supplements For Elderly Could Improve Strength

The University of Manchester is investigating whether increasing the testosterone levels of frail elderly men could improve their strength, energy and mobility.

This is the first study in the world to examine how testosterone treatment may impact this age-group, led by Professor Fred Wu of the Department of Endocrinology at Manchester Royal Infirmary.

Professor Wu said: “Levels of the male hormone testosterone fall by about 1% a year in men over 40, leading to decreases in muscle size and strength, increased body fat and thinner bones. The changes are also associated with decreased sexual interest, fatigue, mobility problems, depression, increased risk of falling and a general sense of weakness.

“Tests on younger and healthy older men suggest that testosterone replacement could help reverse these symptoms in the frail and elderly.”

Professor Wu’s team is expecting to publish the results in two years’ time, and hopes that if the treatment is proven to be effective it may be adopted as standard practice by the NHS.

As well as increasing strength, mobility and quality of life for elderly men, the move could significantly reduce the accident-rate and care requirements of this group and ultimately reduce demands on the NHS and social services.

Men aged 65+ who have lost weight, are easily tired, slow in walking and feel generally weak for no specific reason are being recruited for the study. Only those volunteers found to have low testosterone levels can be included in the trial.

The protocol for participants requires five visits to the Wellcome Trust Clinical Research Facility on Grafton Street at Manchester Royal Infirmary over the 12 month period. They will receive either testosterone or a dummy placebo in the form of a gel self-applied daily to the skin, for the first six months of the trial. Their muscle strength, mobility, bone-strength, muscle and fat content and general quality of life will then be assessed by the research team after both six and 12 months.

The research is being undertaken in partnership with Central Manchester and Manchester Children’s University Hospitals NHS Trust. Participants are free to withdraw from the study at any time, and all information will be collected in the strictest confidence.

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Article adapted by MD Sports from original press release.
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Contact: Jo Nightingale or Rachael McGraw
University of Manchester

NOTES FOR EDITORS

The University of Manchester (www.manchester.ac.uk) was formed by the merger of The Victoria University of Manchester and UMIST in October 2004, and with 36,000 students is the largest higher education institution in the country. Its Faculty of Medical & Human Sciences (www.mhs.manchester.ac.uk) is one of the largest faculties of clinical and health sciences in Europe, with a research income of over £37 million.

The School of Medicine (www.medicine.manchester.ac.uk) is the largest of the Faculty’s five Schools, with 1300 staff, almost 2000 undergraduates and a £32M research income. The School encompasses five teaching hospitals, and is closely linked to a range of general hospitals and community practices across the North West of England.

Negative Energy Balance Causes Female Menstrual Disturbance

University Park, Pa. – 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 from original press release.
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Contact: A’ndrea Elyse Messer
Penn State

Androgens Increase Strength Not Muscle Size

USC study finds combining resistance training and androgens gives more muscular bang for the buck

PHILADELPHIA (June 19, 2003)-Men who take supplemental androgens-the male hormone testosterone or similar medications-increase their strength by adding muscle mass, but androgens alone do not pack more might into the muscles, according to studies presented today by University of Southern California researchers.

Treatment with androgens increases lean body mass-which encompasses everything in the body but bone and fat-and strength increases proportionately with the amount of muscle added, says E. Todd Schroeder, Ph.D., postdoctoral fellow in the Department of Medicine at the Keck School of Medicine of USC and adjunct assistant professor in the USC Department of Biokinesiology and Physical Therapy. Schroeder presented his findings at the Endocrine Society’s 85th Annual Meeting.

However, when men use androgen therapy combined with resistance training, such as weightlifting, their gains in strength may far outpace the amount of muscle that can be added with androgens alone. Each muscle cell packs a bigger punch, a concept known as improved muscle quality.

“The results of androgen therapy alone on muscle and strength are not necessarily bad, but they are not optimal,” Schroeder says. “The men did improve their strength, but it was proportional to the muscle mass they added.”

The findings wield health implications beyond the stereotypes of muscle-bound bodybuilders. Schroeder and his colleagues are studying the usefulness of androgens and exercise in helping maintain muscle strength, muscle power and physical function among seniors, for example. They also have studied androgen therapy’s effectiveness in battling wasting among HIV-positive patients.

In their recent study, Schroeder and USC colleagues Michael Terk, M.D., and Fred R. Sattler, M.D., looked at both young men and seniors. They followed two groups: 33 seniors ranging from their mid-60s to late 70s, and 23 HIV-positive men ranging from their early 30s to late 40s.

The younger men were randomly assigned to get 600 milligrams (mg) each week of nandrolone alone or in combination with resistance training. The older men were randomly assigned to receive 20 mg a day of oxandrolone or a placebo. These pharmacologic androgen doses were given over 12 weeks.

Researchers determined maximal strength-the most weight a participant could safely lift or push-using leg press, leg extension and leg flexion machines.

The researchers also measured the cross-sectional area of participants’ thighs and the lean body mass of their lower extremities by magnetic resonance imaging, or MRI. They then determined the strength that participants exerted for each unit of muscle (muscle quality) and how muscle quality changed over time.

Androgens alone increased lean body mass and maximum strength in both groups of men, but “gains were modest,” Schroeder says, and muscle quality did not change, since the muscle size and strength both increased proportionately. However, among those using nandrolone and undergoing resistance training, muscle quality improved significantly: Gains in strength were much greater than the gains that could occur from muscle-mass increase alone.

“It is clear from our studies and others that resistance training is critical for increasing muscle quality, but the effects can probably be augmented with androgens,” Schroeder says. “In addition, not everyone can do resistance training, and a short course of androgens can help get people stronger and more functional.”

Finally, results provide researchers insight into how to better design future studies to test strategies to best preserve and even improve muscle strength and physical function among seniors. Similar studies will be important for other types of patients who experience muscle loss and frailty, such as those with cancer, chronic lung disease, chronic renal failure and other conditions.

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Article adapted by MD Sports from original press release.
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Contact: Jon Weiner
University of Southern California

Grants by the National Institute of Diabetes & Digestive & Kidney Diseases and the National Center for Research Resources (General Clinical Research Center) supported the research. Bio Technology General Corp., which makes Oxandrin (oxandrolone), also supported part of the research.

Edward T. Schroeder, Michael Terk and Fred R. Sattler, “Pharmacological Doses of Androgen Do Not Improve Muscle Quality in Young or Older Men: Results from Two Studies,” Endocrine Society’s 85th Annual Meeting, poster P3-212, presentation 11 a.m., June 21. Findings released at news conference 1:30 p.m., June 19.

Slow Exercise Delivers Best Anti-aging Benefits

It’s an inevitable truth: as we get older, our muscles deteriorate and we become weaker. Not only can this be an immensely frustrating change, but it can also have many other, more serious implications. We become clumsier and begin to have more falls, often resulting in broken bones or even more severe injuries. There is wide interest in this phenomenon, but to date, the majority of research has focussed on therapies for older patients with advanced symptoms. Now one study, led by Dr Alexandra Sänger from the University of Salzburg, is taking a new approach: scientists are examining the effects of different exercise regimes in menopausal women, with the aim of developing new strategies for delaying and reducing the initial onset of age related muscle deterioration. Results will be presented on Monday 7th July at the Society for Experimental Biology’s Annual Meeting in Marseille [Poster Session A5].

Dr Sänger’s research group has investigated two particular methods of physical training. Hypertrophy resistance training is a traditional approach designed to induce muscle growth whereas ‘SuperSlow®’ is a more recently devised system which involves much slower movement and fewer repetitions of exercises, and was originally introduced especially for beginners and for rehabilitation. “Our results indicate that both methods increase muscle mass at the expense of connective and fatty tissue, but contrary to expectations, the SuperSlow® method appears to have the greatest effect,” reveals Dr Sänger. “These findings will be used to design specific exercise programmes for everyday use to reduce the risk of injury and thus significantly contribute to a better quality of life in old age.”

The study focussed on groups of menopausal women aged 45-55 years, the age group in which muscle deterioration first starts to become apparent. Groups undertook supervised regimes over 12 weeks, based on each of the training methods. To see what effect the exercise had, thigh muscle biopsies were taken at the beginning and end of the regimes, and microscopically analysed to look for changes in the ratio of muscle to fatty and connective tissue, the blood supply to the muscle, and particularly for differences in the muscle cells themselves. “The results of our experiments have significantly improved our understanding of how muscles respond to different forms of exercise,” asserts Dr Sänger. “We believe that the changes that this new insight can bring to current training systems will have a considerable effect on the lives of both menopausal and older

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Article adapted by MD Sports from original press release.
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Notes to editors

• Hypertrophy resistance training is a method of strength training that is designed to induce muscle growth, also known as hypertrophy.
• SuperSlow® resistance training was developed by Ken Hutchins and is based on the same principle as hypertrophy resistance training, but involves slower movement and fewer repetitions of exercises, which is thought to improve the quality of muscle contraction and thereby strength.

Contact: Holly Astley
Society for Experimental Biology

Caffeine taken with carbohydrates increase muscle energy 66%

Recipe to recover more quickly from exercise: Finish workout, eat pasta, and wash down with five or six cups of strong coffee.

Glycogen, the muscle’s primary fuel source during exercise, is replenished more rapidly when athletes ingest both carbohydrate and caffeine following exhaustive exercise, new research from the online edition of the Journal of Applied Physiology shows. Athletes who ingested caffeine with carbohydrate had 66% more glycogen in their muscles four hours after finishing intense, glycogen-depleting exercise, compared to when they consumed carbohydrate alone, according to the study, published by The American Physiological Society.

The study, “High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is co-ingested with caffeine,” is by David J. Pedersen, Sarah J. Lessard, Vernon G. Coffey, Emmanuel G. Churchley, Andrew M. Wootton, They Ng, Matthew J. Watt and John A. Hawley. Dr. Pedersen is with the Garvan Institute of Medical Research in Sydney, Australia, Dr. Watt is from St. Vincent’s Institute of Medical Research, Fitzroy, Victoria, Australia. All others are with the Royal Melbourne Institute of Technology University (RMIT) in Bundoora, Victoria, Australia.

A fuller audio interview with Dr. Hawley is available in Episode 11 of the APS podcast, Life Lines, at www.lifelines.tv. The show also includes an interview with Dr. Stanley Schultz, whose physiological discovery of how sugar is transported in the gut led to the development of oral rehydration therapy and sports drinks such as Gatorade and Hi-5.

Caffeine aids carbohydrate uptake  

It is already established that consuming carbohydrate and caffeine prior to and during exercise improves a variety of athletic performances. This is the first study to show that caffeine combined with carbohydrates following exercise can help refuel the muscle faster.

“If you have 66% more fuel for the next day’s training or competition, there is absolutely no question you will go farther or faster,” said Dr. Hawley, the study’s senior author. Caffeine is present in common foods and beverages, including coffee, tea, chocolate and cola drinks.

The study was conducted on seven well-trained endurance cyclists who participated in four sessions. The participants first rode a cycle ergometer until exhaustion, and then consumed a low-carbohydrate dinner before going home. This exercise bout was designed to reduce the athletes’ muscle glycogen stores prior to the experimental trial the next day.

The athletes did not eat again until they returned to the lab the next day for the second session when they again cycled until exhaustion. They then ingested a drink that contained carbohydrate alone or carbohydrate plus caffeine and rested in the laboratory for four hours. During this post-exercise rest time, the researchers took several muscle biopsies and multiple blood samples to measure the amount of glycogen being replenished in the muscle, along with the concentrations of glucose-regulating metabolites and hormones in the blood, including glucose and insulin.

The entire two-session process was repeated 7-10 days later. The only difference was that this time, the athletes drank the beverage that they had not consumed in the previous trial. (That is, if they drank the carbohydrate alone in the first trial, they drank the carbohydrate plus caffeine in the second trial, and vice versa.)

The drinks looked, smelled and tasted the same and both contained the same amount of carbohydrate. Neither the researchers nor the cyclists knew which regimen they were receiving, making it a double-blind, placebo-controlled experiment.

Glucose and insulin levels higher with caffeine ingestion

The researchers found the following:  

• one hour after exercise, muscle glycogen levels had replenished to the same extent whether or not the athlete had the drink containing carbohydrate and caffeine or carbohydrate only
• four hours after exercise, the drink containing caffeine resulted in 66% higher glycogen levels compared to the carbohydrate-only drink
• throughout the four-hour recovery period, the caffeinated drink resulted in higher levels of blood glucose and plasma insulin
• several signaling proteins believed to play a role in glucose transport into the muscle were elevated to a greater extent after the athletes ingested the carbohydrate-plus-caffeine drink, compared to the carbohydrate-only drink

 Dr. Hawley said it is not yet clear how caffeine aids in facilitating glucose uptake from the blood into the muscles. However, the higher circulating blood glucose and plasma insulin levels were likely to be a factor. In addition, caffeine may increase the activity of several signaling enzymes, including the calcium-dependent protein kinase and protein kinase B (also called Akt), which have roles in muscle glucose uptake during and after exercise.

Lower dose is next step  

In this study, the researchers used a high dose of caffeine to establish that it could help the muscles convert ingested carbohydrates to glycogen more rapidly. However, because caffeine can have potentially negative effects, such as disturbing sleep or causing jitteriness, the next step is to determine whether smaller doses could accomplish the same goal.

Hawley pointed out that the responses to caffeine ingestion vary widely between individuals. Indeed, while several of the athletes in the study said they had a difficult time sleeping the night after the trial in which they ingested caffeine (8 mg per kilogram of body weight, the equivalent of drinking 5-6 cups of strong coffee), several others fell asleep during the recovery period and reported no adverse effects.

Athletes who want to incorporate caffeine into their workouts should experiment during training sessions well in advance of an important competition to find out what works for them.

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Article adapted by MD Sports from original press release.
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Contact: Christine Guilfoy
American Physiological Society

Physiology is the study of how molecules, cells, tissues and organs function to create health or disease. The American Physiological Society (APS) has been an integral part of this scientific discovery process since it was established in 1887.