Low muscle strength in adolescence linked to increased risk of early death

Nov. 20, 2012 — Low muscle strength in adolescence is strongly associated with a greater risk of early death from several major causes, suggests a large study published on the British Medical Journal website.

The effect is similar to well established risk factors for early death like being overweight or having high blood pressure, leading the authors to call for young people, particularly those with very low strength, to engage in regular physical activity to boost their muscular fitness.

High body mass index (BMI) and high blood pressure at a young age are known risk factors for premature death, but whether muscular strength in childhood or adolescence can predict mortality is unclear.

So a team of researchers, led by Professor Finn Rasmussen at the Karolinska Institutet in Sweden, tracked more than one million Swedish male adolescents aged 16 to 19 years over a period of 24 years.

Participants underwent three reliable muscular strength tests at the start of the study (knee extension strength, handgrip strength and elbow flexion strength). BMI and blood pressure were also measured. Premature death was defined as death before age 55 years.

During the follow-up period, 26,145 participants (2.3% of the group) died. Suicide was the most common cause of death (22.3%) compared with cardiovascular diseases (7.8%) or cancer (14.9%).

High muscular strength was associated with a 20-35% lower risk of early death from any cause and also from cardiovascular diseases, independently of BMI or blood pressure. No association was seen with cancer deaths.

Stronger adolescents also had a 20-30% lower risk of early death from suicide and were up to 65% less likely to have any psychiatric diagnosis, such as schizophrenia and mood disorders. These results suggest that physically weaker individuals might be more mentally vulnerable, say the authors.

In contrast, male adolescents with the lowest level of muscular strength showed the greatest all-cause mortality and also the greatest mortality in cardiovascular disease and suicide before age 55 years.

Death rates from any cause (per 100,000 person years) ranged between 122.3 and 86.9 for weakest and strongest adolescents respectively. Rates for cardiovascular diseases were 9.5 and 5.6 and for suicide were 24.6 and 16.9.

The authors say that low muscular strength in adolescents "is an emerging risk factor for major causes of death in young adulthood, such as suicide and cardiovascular diseases." The effect sizes of these associations "are similar to classic risk factors such as body mass index and blood pressure," they add.

They suggest that muscular strength tests, in particular handgrip strength, could be assessed with good reliability in almost any place, including clinical settings, schools and workplaces.

They also support the need for regular physical activity in childhood and adolescence, saying: "People at increased risk of long term mortality, because of lower muscular strength, should be encouraged to engage in exercise programmes and other forms of physical activity."

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The above story is reprinted from materials provided by BMJ-British Medical Journal.

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Journal Reference:

F. B. Ortega, K. Silventoinen, P. Tynelius, F. Rasmussen. Muscular strength in male adolescents and premature death: cohort study of one million participants. BMJ, 2012; 345 (nov20 3): e7279 DOI: 10.1136/bmj.e7279

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Muscle-loss study sheds new light on ways to prevent muscle loss, obesity and diabetes

Dec. 19, 2012 — A research study from Nanyang Technological University (NTU) has yielded important breakthroughs on how the body loses muscle, paving the way for new treatments for aging, obesity and diabetes.

The study found that by inhibiting a particular molecule produced naturally in the body, muscle loss due to aging or illnesses can be prevented. Blocking the same molecule will also trigger the body to go into a 'fat-burning mode' which will fight obesity and also treat the common form of diabetes.

The exciting discoveries have led NTU scientists to embark on joint clinical research with local hospitals to further validate their findings which were previously carried out on animals.

Their research on how humans lose muscle during extreme conditions such as chronic diseases or starvation was published last month in Cell Metabolism.

Associate Professor Ravi Kambadur and his team from the NTU School of Biological Sciences found that a protein called Myostatin, which controls muscle cell growth, is responsible for initiating muscle loss.

When excess levels of Myostatin is bound to a muscle cell, it induces heavy loss of mitochondria (the part of the cell responsible for energy production that keeps a cell alive), which in turn causes the muscle cell to waste or lose muscle tissue (atrophy) due to the 'lack of energy'.

Under normal healthy conditions, small loss of Mitochondria is needed for the regeneration of new cells, but when a patient is suffering from chronic diseases or is bedridden (and muscles are not used often), this process is disrupted due to high levels of myostatin which results in increased mitochondrial loss and muscle atrophy.

Prof Kambadur said recent studies have shown that extreme muscle wasting can lead to death.

"For example, about 30 per cent of cancer patients die not because of cancer, but because of muscle loss also known as cachexia," said Prof Kambadur.

"When someone is suffering from a chronic disease and doesn't eat enough, the body starts to generate energy by breaking down muscle proteins and that is the reason we see a lot of muscle wasting under chronic disease conditions."

"Over the years, our research has revealed that this type of muscle wasting is initiated by excess levels of myostatin in the body. If we block myostatin from binding to cells, then muscles won't waste away and we can then mitigate the effects of aging and chronic diseases."

Apart from regulating the growth and loss of muscle, myostatin also regulates whether the body will burn fat or carbohydrates during fasting and meal times.

Blocking myostatin keeps the body in "fat-burning mode" and promotes muscle growth at the same time -- which could potentially make obesity a thing of the past.

Because obesity is one of the main causes of the most common form of diabetes, Type 2 diabetes, blocking myostatin could also treat diabetes. In the US, 90 to 95 per cent of diabetes cases are Type 2, as reported by the Centers for Disease Control and Prevention.

According to Singapore's Health Promotion Board, diabetes is among the top ten causes of death locally. In 2010, it was reported by Ministry of Health that 11.3 per cent of the Singaporean adults aged 18 to 69 years are affected by diabetes while 10.8 percent were obese.

"In near future, myostatin blockers could increase fat utilisation in the body and give you the benefits of exercise, without actually doing intense physical activity," Prof Kambadur explained.

"This would be a good alternative treatment for people who are unable to exercise, such as those who are bed-ridden or are in cancer treatment, who are most at risk of massive muscle loss."

Prof Kambadur added that while blocking myostatin sounds like a good idea, there is a need to study the long term effects, as the molecule is needed to regulate cell growth for normal body operation.

Other studies on myostatin conducted by Prof Kambadur's group have also yielded interesting results.

For instance, people who exercise regularly have been found to have lower levels of myostatin as compared to those who do not. Studies have also found that older people have more myostatin and this can explain why when one ages, muscles become weaker.

Prof Kambadur's research projects on myostatin are funded by Ministry of Education, Biomedical Research Council and the National Research Foundation's (NRF) Competitive Research Programme (CRP). The research on myostatin is conducted in collaboration with Associate Professor Mridula Sharma from the National University of Singapore. The husband-and-wife team have collaborated on various research projects in the area of skeletal muscle for many years.

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The above story is reprinted from materials provided by Nanyang Technological University.

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Sudarsanareddy Lokireddy, Isuru W. Wijesoma, Serena Teng, Sabeera Bonala, Peter D. Gluckman, Craig McFarlane, Mridula Sharma, Ravi Kambadur. The Ubiquitin Ligase Mul1 Induces Mitophagy in Skeletal Muscle in Response to Muscle-Wasting Stimuli. Cell Metabolism, 2012; 16 (5): 613 DOI: 10.1016/j.cmet.2012.10.005

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Fat molecule ceramide may factor in muscle loss in older adults

Oct. 31, 2012 — As men and women age, increasing quantities of fat tissue inevitably take up residence in skeletal muscle. A small study of older and younger men conducted at the Jean Mayer USDA Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University suggests that a build-up of a fat molecule known as ceramide might play a leading role in muscle deterioration in older adults.

The results of the study were published online this month by the Journal of Applied Physiology, a publication of the American Physiological Society.

The study enrolled ten 10 men in their mid-seventies to nine men in their early twenties. None of the men carried excess weight or had chronic health problems and none had exercised in six months. Ceramide was measured in a muscle biopsy taken at baseline. The participants performed a single bout of exercise (three sets of ten repetitions of knee extensions and leg presses) followed by two muscle biopsies which the authors used to examine how the exercise impacted muscle growth response.

"There is a known relationship between elevated ceramide levels and unhealthy muscle in obese adults, but to the best of our knowledge, this had not been studied in healthy weight, older adults," said Donato Rivas, Ph.D., the study's first author and a scientist in the Nutrition, Exercise Physiology and Sarcopenia Laboratory at the USDA HNRCA at Tufts University. "Our analysis of the muscle biopsies showed an accumulation of two types of ceramide molecules containing saturated fatty acids that were 156% and 30% higher in the older men. Furthermore, having higher accumulation of one of these saturated fatty acid types was associated with having less leg muscle mass in both younger and older men."

"Although it is well known that fat tissue replaces some of our muscle tissue as we grow older, we are seeking to understand whether some fat molecules are more damaging to muscle than others," said Roger A. Fielding, Ph.D., senior author and director of the Nutrition, Exercise Physiology and Sarcopenia Laboratory. "We suspect that the increased storage of ceramide we saw in the older men, exacerbated by the presence of saturated fat, has a part in weakening the anabolic signaling that responds to resistance exercises and helps with the assembly of new muscle."

Learning more about ceramide activity through larger, long-term interventional trials involving older and younger men and women may identify a role in dietary or therapeutic drug interventions for sarcopenia, an age-related condition of muscle loss and function.

"The deterioration of muscle is compounded by a loss of muscle strength, which really begins to decline around age 50 and appears to be a factor in the visible decrease in mobility people exhibit around age 80," added Fielding, who is also a professor at the Friedman School of Nutrition Science and Policy at Tufts University and at Tufts University School of Medicine. "Previous research done at Tufts and other institutions suggests that even with limited exercise older adults can maintain and build some new muscle. Until there is enough research to develop specific exercise and dietary interventions, staying as physically active as deemed safe by your health care provider can only benefit aging muscle."

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The above story is reprinted from materials provided by Tufts University, Health Sciences Campus.

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D. A. Rivas, E. P. Morris, P. H. Haran, E. P. Pasha, M. d. S. Morais, G. G. Dolnikowski, E. M. Phillips, R. A. Fielding. Increased ceramide content and NF B signaling may contribute to the attenuation of anabolic signaling after resistance exercise in aged males.. Journal of Applied Physiology, 2012; DOI: 10.1152/japplphysiol.00412.2012

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