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Exercise in a Pill
Science Behind Muscle Recovery Could Lead to Drugs to Mimic Exercise
By Liza Jane Maltin
March 11, 2002 -- Tired of doing aerobics? Running (or jogging) on empty? How about taking an "exercise pill" instead? With what researchers are discovering about the biochemistry of muscles, the notion might not be as far-fetched as it sounds. The information could one day help chronically ill, immobile people reap all the health benefits of aerobic exercise.
"We think this discovery could lead to the synthesis of new drugs that will allow individuals to acquire the health benefits of regular exercise, even if they cannot exercise," says lead author R. Sanders Williams, MD, dean of the Duke University School of Medicine, in a news release. "It has the potential to improve the lives of patients with heart failure, pulmonary disease, renal failure, diabetes, and other chronic diseases."
Williams' team has been studying the biochemistry of muscles for 20 years. In 1998, they learned that activating a particular pathway in the body could mimic the effects of endurance exercise. From there, they went on to investigate why, and how, muscles react to and change from exercise.
For example, certain types of exercise -- such as weightlifting -- builds muscles, making them bigger. Other types -- such as long-distance running -- causes muscles to change in a way that makes them resistant to fatigue and lowers the exerciser's risk for heart disease and diabetes.
They wanted to know how muscle cells "know" that (and how) they are being exercised, and then translate that information into the genetic expressions that produce various changes in the body.
In the end, they identified an enzyme, or type of protein, that controls production of muscle tissue mitochondria -- the tiny powerhouses within each cell that convert oxygen and other molecules into usable energy. The more people exercise, the more mitochondria their cells produce. This is makes them fitter, because their bodies have more energy available.
Williams' team created mice in which this newly identified enzyme was always active, always "on." Even when these animals just sat around, their muscle cells produced mitochondria as if they were exercising, taking on the attributes of fit, active mice. And these muscular changes are the sort that reduce a person's risk for diabetes, heart disease, and other chronic illnesses.
The findings appear in the April 12 issue of Science.
"An inability to exercise complicates many chronic medical conditions and makes those conditions worse. For example, we know that heart failure patients who exercise regularly feel better, and over time acquire a greater capacity to exercise, but many are unable to perform the amount of exercise necessary to produce the favorable effects," says Williams.
"One application of this discovery, if it leads to the development of drugs to activate this pathway, would be to help improve the quality of life of people who have such chronic disease," he says.
Science Behind Muscle Recovery Could Lead to Drugs to Mimic Exercise
By Liza Jane Maltin
March 11, 2002 -- Tired of doing aerobics? Running (or jogging) on empty? How about taking an "exercise pill" instead? With what researchers are discovering about the biochemistry of muscles, the notion might not be as far-fetched as it sounds. The information could one day help chronically ill, immobile people reap all the health benefits of aerobic exercise.
"We think this discovery could lead to the synthesis of new drugs that will allow individuals to acquire the health benefits of regular exercise, even if they cannot exercise," says lead author R. Sanders Williams, MD, dean of the Duke University School of Medicine, in a news release. "It has the potential to improve the lives of patients with heart failure, pulmonary disease, renal failure, diabetes, and other chronic diseases."
Williams' team has been studying the biochemistry of muscles for 20 years. In 1998, they learned that activating a particular pathway in the body could mimic the effects of endurance exercise. From there, they went on to investigate why, and how, muscles react to and change from exercise.
For example, certain types of exercise -- such as weightlifting -- builds muscles, making them bigger. Other types -- such as long-distance running -- causes muscles to change in a way that makes them resistant to fatigue and lowers the exerciser's risk for heart disease and diabetes.
They wanted to know how muscle cells "know" that (and how) they are being exercised, and then translate that information into the genetic expressions that produce various changes in the body.
In the end, they identified an enzyme, or type of protein, that controls production of muscle tissue mitochondria -- the tiny powerhouses within each cell that convert oxygen and other molecules into usable energy. The more people exercise, the more mitochondria their cells produce. This is makes them fitter, because their bodies have more energy available.
Williams' team created mice in which this newly identified enzyme was always active, always "on." Even when these animals just sat around, their muscle cells produced mitochondria as if they were exercising, taking on the attributes of fit, active mice. And these muscular changes are the sort that reduce a person's risk for diabetes, heart disease, and other chronic illnesses.
The findings appear in the April 12 issue of Science.
"An inability to exercise complicates many chronic medical conditions and makes those conditions worse. For example, we know that heart failure patients who exercise regularly feel better, and over time acquire a greater capacity to exercise, but many are unable to perform the amount of exercise necessary to produce the favorable effects," says Williams.
"One application of this discovery, if it leads to the development of drugs to activate this pathway, would be to help improve the quality of life of people who have such chronic disease," he says.
