Archive for the ‘Increase muscle’ Category

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

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

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

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

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

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

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

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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.
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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

 

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/ 

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/ 

University of Pittsburgh School of Medicine researchers have successfully used gene therapy to accelerate muscle regeneration in experimental animals with muscle damage, suggesting this technique may be a novel and effective approach for improving skeletal muscle healing, particularly for serious sports-related injuries. These findings are being presented at the American Society of Gene Therapy annual meeting in Baltimore, May 31 to June 4.

Skeletal muscle injuries are the most common injuries encountered in sports medicine. Although such injuries can heal spontaneously, scar tissue formation, or fibrosis, can significantly impede this process, resulting in incomplete functional recovery. Of particular concern are top athletes, who, when injured, need to recover fully as quickly as possible.
In this study, the Pitt researchers injected mice with a gene therapy vector containing myostatin propeptide–a protein that blocks the activity of the muscle-growth inhibitor myostatin–three weeks prior to experimentally damaging the mice’s skeletal muscles. Four weeks after skeletal muscle injury, the investigators observed an enhancement of muscle regeneration in the gene-therapy treated mice compared to the non-gene-therapy treated control mice. There also was significantly less fibrous scar tissue in the skeletal muscle of the gene-therapy treated mice compared to the control mice.
According to corresponding author Johnny Huard, Ph.D., the Henry J. Mankin Endowed Chair and Professor in Orthopaedic Surgery, University of Pittsburgh School of Medicine, and Director of the Stem Cell Research Center of Children’s Hospital of Pittsburgh, this approach offers a significant, long-lasting method for treating serious, sports-related muscle injuries.
“Based on our previous studies, we expect that gene-therapy treated cells will continue to overproduce myostatin propeptide for at least two years. Since the remodeling phase of skeletal muscle healing is a long-term process, we believe that prolonged expression of myostatin propeptide will continue to contribute to recovery of injured skeletal muscle by inducing an increase in muscle mass and minimizing fibrosis. This could significantly reduce the amount of time an athlete needs to recover and result in a more complete recovery,” he explained.
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Others involved in this study include, Jinhong Zhu, M.D., Yong Li, M.D., Ph.D., of the Growth and Development Laboratory, Children’s Hospital of Pittsburgh; and Chunping Qiao, M.D., and Xiao Xiao, M.D., Ph.D., of the Molecular Therapies Laboratory, department of orthopaedic surgery, University of Pittsburgh School of Medicine.
University of Pittsburgh School of Medicine researchers have successfully used gene therapy to accelerate muscle regeneration in experimental animals with muscle damage, suggesting this technique may be a novel and effective approach for improving skeletal muscle healing, particularly for serious sports-related injuries.
Skeletal muscle injuries are the most common injuries encountered in sports medicine. Although such injuries can heal spontaneously, scar tissue formation, or fibrosis, can significantly impede this process, resulting in incomplete functional recovery. Of particular concern are top athletes, who, when injured, need to recover fully as quickly as possible.
In this study, the Pitt researchers injected mice with a gene therapy vector containing myostatin propeptide–a protein that blocks the activity of the muscle-growth inhibitor myostatin–three weeks prior to experimentally damaging the mice’s skeletal muscles. Four weeks after skeletal muscle injury, the investigators observed an enhancement of muscle regeneration in the gene-therapy treated mice compared to the non-gene-therapy treated control mice. There also was significantly less fibrous scar tissue in the skeletal muscle of the gene-therapy treated mice compared to the control mice.
According to corresponding author Johnny Huard, Ph.D., the Henry J. Mankin Endowed Chair and Professor in Orthopaedic Surgery, University of Pittsburgh School of Medicine, and Director of the Stem Cell Research Center of Children’s Hospital of Pittsburgh, this approach offers a significant, long-lasting method for treating serious, sports-related muscle injuries.
“Based on our previous studies, we expect that gene-therapy treated cells will continue to overproduce myostatin propeptide for at least two years. Since the remodeling phase of skeletal muscle healing is a long-term process, we believe that prolonged expression of myostatin propeptide will continue to contribute to recovery of injured skeletal muscle by inducing an increase in muscle mass and minimizing fibrosis. This could significantly reduce the amount of time an athlete needs to recover and result in a more complete recovery,” he explained.
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Article adapted by MD Sports from original press release.
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Contact: Jim Swyers

Others involved in this study include, Jinhong Zhu, M.D., Yong Li, M.D., Ph.D., of the Growth and Development Laboratory, Children’s Hospital of Pittsburgh; and Chunping Qiao, M.D., and Xiao Xiao, M.D., Ph.D., of the Molecular Therapies Laboratory, department of orthopaedic surgery, University of Pittsburgh School of Medicine.

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

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.

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.