Tag: muscle strength

Categories : AgeingTags :

Standing on One Leg is a Good Indicator of Ageing

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Photo by RDNE Stock project

How long a person can stand on one leg is a more tell-tale measure of ageing than changes in strength or gait, according to new Mayo Clinic research published in the journal PLOS ONE.

Good balance, muscle strength and an efficient gait contribute to people’s independence and well-being as they age. How these factors change, and at what rate, can help clinicians develop programs to ensure healthy ageing. Individually, people can train their balance without special equipment and work on maintaining it over time.

In this study, 40 healthy, independent people over 50 underwent walking, balance, grip strength and knee strength tests. Half of the participants were under 65; the other half were 65 and older.

In the balance tests, participants stood on force plates in different situations: on both feet with eyes open, on both feet with eyes closed, on the non-dominant leg with eyes open, and on the dominant leg with eyes open. In the one-legged tests, participants could hold the leg they weren’t standing on where they wanted. The tests were 30 seconds each.

Standing on one leg, specifically the nondominant leg, showed the highest rate of decline with age.

“Balance is an important measure because, in addition to muscle strength, it requires input from vision, the vestibular system and the somatosensory systems,” says Kenton Kaufman, PhD, senior author of the study and director of the Motion Analysis Laboratory at Mayo Clinic. “Changes in balance are noteworthy. If you have poor balance, you’re at risk of falling, whether or not you’re moving. Falls are a severe health risk with serious consequences.”

Unintentional falls are the leading cause of injuries among adults who are 65 and older. Most falls among older adults result from a loss of balance.

In the other tests:

  • Researchers used a custom-made device to measure participants’ grip. For the knee strength test, participants were in a seated position and instructed to extend their knee as forcefully as possible. Both the grip and knee strength tests were on the dominant side. Grip and knee strength showed significant declines by decade but not as much as balance. Grip strength decreased at a faster rate than knee strength, making it better at predicting aging than other strength measures.
  • For the gait test, participants walked back and forth on an 8-metre, level walkway at their own pace and speed. Gait parameters didn’t change with age. This was not a surprising result since participants were walking at their normal pace, not their maximum pace, Dr Kaufman says.
  • There were no age-related declines in the strength tests that were specific to sex. This indicates that participants’ grip and knee strength declined at a similar rate. Researchers did not identify sex differences in the gait and balance tests, which suggests that male and female subjects were equally affected by age.

Dr Kaufman says that people can take steps to train their balance. For example, by standing on one leg, you can train yourself to coordinate your muscle and vestibular responses to maintain correct balance. If you can stand on one leg for 30 seconds, you are doing well, he says.

“If you don’t use it, you lose it. If you use it, you maintain it,” Dr Kaufman says. “It’s easy to do. It doesn’t require special equipment, and you can do it every day.”

Source: Mayo Clinic

Categories : AgeingTags :

New Study Explains Why we Move More Slowly with Age

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It’s one of the inescapable realities of aging: The older we get, the slower we tend to move – whether we’re walking around the block or just reaching for the remote control. A new study led by CU Boulder engineers helps explain why.

The research is one of the first studies to experimentally tease apart the competing reasons why people over age 65 might not be as quick on their feet as they used to be. The group reported that older adults may move slower, at least in part, because it costs them more energy than younger people – perhaps not too shocking for anyone who’s woken up tired the morning after an active day.

The findings could one day give doctors new tools for diagnosing a range of illnesses, including Parkinson’s disease, multiple sclerosis and even depression and schizophrenia, said study co-author Alaa Ahmed. 

“Why we move the way we do, from eye movements to reaching, walking and talking, is a window into aging and Parkinson’s,” said Ahmed, professor in the Paul M. Rady Department of Mechanical Engineering. “We’re trying to understand the neural basis of that.”

She and her colleagues published their findings this month in the journal JNeurosci.

For the study, the group asked subjects age 18 to 35 and 66 to 87 to complete a deceptively simple task: to reach for a target on a screen, akin to playing a video game on a Nintendo Wii. By analysing patterns of these reaches, the researchers discovered that older adults seemed to modify their motions under certain circumstances to conserve their more limited supplies of energy. 

“All of us, whether young or old, are inherently driven to get the most reward out of our environment while minimising the amount of effort to do so,” said Erik Summerside, a co-lead author of the new study who earned his doctorate in integrative physiology from CU Boulder in 2018.

Using engineering to understand the brain

Ahmed added that researchers have long known that older adults tend to be slower because their movements are less stable and accurate. But other factors could also play a role in this fundamental part of growing up.

According to one hypothesis, the muscles in older adults may work less efficiently, meaning that they burn more calories while completing the same tasks as younger adults – like running a marathon or getting up to grab a soda from the refrigerator.

Alternatively, aging might also alter the reward circuitry in the human brain. Ahmed explained that as people age, their bodies produce less dopamine, a brain chemical responsible for giving you a sense of satisfaction after a job well done. If you don’t feel that reward as strongly, the thinking goes, you may be less likely to move to get it. People with Parkinson’s disease experience an even sharper decline in dopamine production.

In the study, the researchers asked more than 80 people to sit down and grab the handle of a robotic arm, which, in turn, operated the cursor on a computer screen. The subjects reached forward, moving the cursor toward a target. If they succeeded, they received a reward – not a big one, but still enough to make their brains happy.

“Sometimes, the targets exploded, and they would get point rewards,” Ahmed said. “It would also make a ‘bing bing’ sound.”

Moving slower but smarter

That’s when a contrast between the two groups of people began to emerge.

Both the 18 to 35-year-olds and 66 to 87-year-olds arrived at their targets sooner when they knew they would hear that ‘bing bing’ – roughly 4% to 5% sooner over trials without the reward. But they also achieved that goal in different ways.

The younger adults, by and large, moved their arms faster toward the reward. The older adults, in contrast, mainly improved their reaction times, beginning their reaches about 17 milliseconds sooner on average.

When the team added an 8-pound (3.6kg) weight to the robotic arm for the younger subjects, those differences vanished.

“The brain seems to be able to detect very small changes in how much energy the body is using and adjusts our movements accordingly,” said Robert Courter, a co-lead author of the study who earned his doctorate in integrative physiology from CU Boulder in 2023. “Even when moving with just a few extra pounds, reacting quicker became the energetically cheaper option to get to the reward, so the young adults imitated the older adults and did just that.”

The research seems to paint a clear picture, Ahmed said. Both the younger and older adults didn’t seem to have trouble perceiving rewards, even small ones. But their brains slowed down their movements under tiring circumstances.

“Putting it all together, our results suggest that the effort costs of reaching seem to be determining what’s slowing the movement of older adults,” Ahmed said.

The experiment can’t completely rule out the brain’s reward centres as a culprit behind why we slow down when we age. But, Ahmed noted, if scientists can tease out where and how these changes emerge from the body, they may be able to develop treatments to reduce the toll of aging and disease.

Source: University of Colorado Boulder

Categories : AgeingTags :

Genetic Predisposition for Muscle Strength may Predict Longer Lifespan

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A study conducted at the University of Jyväskylä showed that a genetic predisposition for higher muscle strength predicts a longer lifespan and a lower risk for developing common diseases. This study, published in The Journals of Gerontology: Series A, is the most comprehensive international study to date on hereditary muscle strength and its relationship to morbidity. The genome and health data of more than 340 000 Finns was used in the research.

Muscle strength, especially hand grip strength, can indicate an individual’s physiological resources to protect against age-related diseases and disabilities, as well as their ability to cope with them. Age-related loss of muscle strength is individual and influenced not only by lifestyle but also by genetics.

The study revealed that individuals with a genetic predisposition for higher muscle strength have a slightly lower risk for common noncommunicable diseases and premature mortality. It did not however predict better survival after acute adverse health events compared to the time before illness onset.  

“It seems that a genetic predisposition for higher muscle strength reflects more on an individual’s intrinsic ability to resist and protect oneself against pathological changes that occur during aging than the ability to recover or completely bounce back after severe adversity,” says doctoral researcher Päivi Herranen from the Faculty of Sport and Health Sciences. 

A unique study population  

Muscle strength is a multifactorial trait influenced by lifestyle and environmental factors but also by numerous genetic variants, each with a very small effect on muscle strength. In this study, the genetic predisposition for muscle strength was defined by constructing a polygenic score for muscle strength, which summarises the effects of hundreds of thousands of genetic variants into a single score. The polygenic score makes it possible to compare participants with an exceptionally high or low genetic predisposition for muscle strength, and to investigate associations with inherited muscle strength and other phenotypes, in this case, common diseases.  

“In this study, we were able to utilise both genetic information and health outcomes from over 340 000 Finnish men and women,” Herranen explains. “To our knowledge, this is the first study to investigate the association between a genetic predisposition for muscle strength and various diseases on this scale.” 

Further research on the effects of lifestyles is still needed 

Information about the genetic predisposition for muscle strength could be used alongside traditional risk assessment in identifying individuals who are at particularly high risk of common diseases and health adversities. However, further research on the topic is still needed. 

“Based on these results, we cannot say how lifestyle factors, such as physical activity, modify an individual’s intrinsic ability to resist diseases and whether their impact on health differs among individuals due to genetics,” Herranen notes. 

The study utilised the internationally unique FinnGen dataset, compiled through the collaboration of Finnish biobanks. The dataset consisted of 342 443 Finns who had given their consent and provided a biobank sample. The participants were aged 40 to 108 years, and 53% of them were women. The diagnoses selected for the study were based on the leading causes of death and the most significant noncommunicable diseases in Finland. Selected diagnoses included the most common cardiometabolic and pulmonary diseases, musculoskeletal and connective tissue diseases, falls and fractures, mental health and cognitive disorders, cancers, as well as overall mortality and mortality from cardiovascular diseases. 

Source: University of Jyväskylä

Categories : Ageing Regenerative MedicineTags :

Restoring Muscle Strength Lost to Aging or Injury

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A small molecule previously shown to enhance strength in injured or old laboratory mice does so by restoring lost connections between nerves and muscle fibres, Stanford Medicine researchers have found.

The molecule blocks the activity of an aging-associated enzyme, or gerozyme, called 15-PGDH that naturally increases in muscles as they age. The study, which was published in Science Translational Medicine, showed that levels of the gerozyme increase in muscles after nerve damage and that it is prevalent in muscle fibres of people with neuromuscular diseases.

The research is the first to show that damaged motor neurons can be induced to regenerate in response to a drug treatment and that lost strength and muscle mass can be at least partially regained. It suggests that, if similar results are seen in humans, the drug may one day be used to prevent muscle loss of muscle strength due to aging or disease or to hasten recovery from injury.

It’s estimated that sarcopenia, or debilitating muscle frailty, affects about 30% of people over 80 and costs the United States around $380 billion each year.

“There is an urgent, unmet need for drug treatments that can increase muscle strength due to aging, injury or disease,” said Helen Blau, PhD, professor of microbiology and immunology. “This is the first time a drug treatment has been shown to affect both muscle fibres and the motor neurons that stimulate them to contract in order to speed healing and restore strength and muscle mass. It’s unique.”

Blau, the Donald E. and Delia B. Baxter Foundation Professor and director of the Baxter Laboratory for Stem Cell Biology, is the senior author of the study. Postdoctoral scholar Mohsen Bakooshli, PhD, and former postdoctoral scholar Yu Xin Wang, PhD, are the lead authors of the study. Wang is now an assistant professor at the Sanford Burnham Prebys Medical Discovery Institute in San Diego.

Addressing loss of strength

The finding is the latest from the Blau laboratory focused on understanding how muscles weaken from aging or disease, and whether it’s possible to combat this decline. In 2021, the group showed that blocking the activity of 15-PGDH in 24-month-old laboratory mice significantly enhances the animals’ leg strength and endurance when running on a treadmill. (Laboratory mice typically live about 26 to 30 months.) But it wasn’t clear exactly how.

The new research shows that the effect is due to the restoration of lost connections between the nerves and the muscle. These connections, called neuromuscular junctions, are how the brain signals muscles to contract. In aging, some of these connections are lost, causing muscle contractions to become less powerful and muscles to atrophy. People typically lose muscle mass and strength, up to 10% per decade, after the age of 50.

Conditions other than aging can also destabilise these connections, including the disuse of muscles due to bedrest after illness or injury, or muscle-wasting diseases like spinal muscular atrophy or amyotrophic lateral sclerosis (also known as ALS).

Blau’s previous research showed that a molecule called PGE2 is critical to the function of stem cells in muscle fibres that repair damage – including the microtears from exercise that lead to an increase in muscle mass and strength. They subsequently showed that levels of 15-PGDH, which breaks down PGE2, increase in the muscles with age and that the loss of strength with aging could be overcome by inhibiting the activity of this PGE2-degrading enzyme.

“PGE2 is part of the body’s natural healing mechanism, and its levels increase in muscle after injury,” Blau said. “We wanted to learn how age triggers an increase in 15-PGDH, and therefore the degradation and loss of PGE2.”

A lack of nerves

The researchers knew that muscles become less innervated, or infiltrated with nerves, as people and animals age. They wondered if that loss could be what triggers the rising levels of 15-PGDH.

“We found that when you cut the nerve that innervates the leg muscles of mice, the amount of 15-PGDH in the muscle increases rapidly and dramatically,” Blau said. “This was an exciting new insight. But what surprised us most was that when these mice are treated with a drug that inhibits 15-PGDH activity, the nerve grows back and makes contact with the muscle more quickly than in control animals, and that this leads to a faster recovery of strength and function.”

Additional experiments showed that treatment with the drug restored neuromuscular junctions lost during aging and increased muscle strength and function in old laboratory mice. The researchers also identified discrete clumps of 15-PGDH in the muscle fibres of people with several types of neuromuscular disorders suggesting that the gerozyme may have a role in causing these human disorders.

Blau and her colleagues plan to investigate at a molecular level how neural growth is stimulated by blocking 15-PGDH activity. Blau has also co-founded a company, Epirium Bio, to develop similar drugs for use in humans. Although her lab is still conducting animal studies, the company hopes to launch a clinical trial within the next year or so.

“Our next steps will be to examine whether blocking 15-PGDH function in people with spinal muscular atrophy can increase lost muscle strength in combination with gene therapy or other treatments,” Blau said. “We are also looking at ALS to see if something like this might help these patients. It’s really exciting that we are able to affect both muscle function and motor neuron growth.”

Source: Stanford Medicine

Categories : Exercise Neurodegenerative DiseasesTags :

Could an Alzheimer’s Treatment be Lurking in a Bodybuilder’s Supplement?

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A safe treatment against Alzheimer’s progression may be hidden in a common bodybuilding supplement. Researchers recently discovered that a muscle-building supplement called beta-hydroxy beta-methylbutyrate (HMB), may help protect memory, reduce plaques and ultimately help prevent the progression of Alzheimer’s disease. The researchers published their results in the journal Cell Reports.

HMB is a safe over-the-counter supplement, which bodybuilders regularly use to enhance exercise-related muscle strength and growth.

“This may be one of the safest and the easiest approaches to halt disease progression and protect memory in Alzheimer’s disease patients,” said Kalipada Pahan, PhD, at RUSH Medical College.

Studies in mouse models of Alzheimer’s have shown that HMB successfully reduces plaques and increases factors for neuronal growth to protect learning and memory, according to neurological researchers at RUSH.

“Understanding how the disease works is important to developing effective drugs to protect the brain and stop the progression of Alzheimer’s disease,” Pahan said.

Previous studies indicate that a family of proteins known as neurotrophic factors are drastically decreased in the brains of people with Alzheimer’s disease and have been found to help in survival and function of neurons, which are cells that receive and send messages from the body to the brain and vice versa.

“Our study found that after oral consumption, HMB enters into the brain to increase these beneficial proteins, restore neuronal connections and improve memory and learning in mice with Alzheimer’s-like pathology, such as plaques and tangles,” Pahan said.

The study findings indicate that HMB stimulates the nuclear hormone receptor PPARα within the brain that regulates the transport of fatty acids, which is key to the success of HMB as a neuroprotective supplement.

“If mouse results with HMB are replicated in Alzheimer’s disease patients, it would open up a promising avenue of treatment of this devastating neurodegenerative disease,” Pahan said.

Source: Rush University Medical Center

Categories : ExerciseTags :

Compression Garments Offer No Exercise Recovery Benefit

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Man and woman about to sprint
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A meta-analysis of studies on the ability of compression garments, elastic clothing on the limbs or hips, to enhance muscle recovery after exercise found that they provide no recovery benefit. Rather, they should be used to help reduce injury, the reviewers suggest.

Use of compression garments has gained popularity over the last few decades because they are thought to enhance muscle recovery following exercise.

An international research team, led by assistant professor János Négyesi, conducted a review using a generic inverse variance model, which adjusts the weight of individual studies according to sample size, to more accurately assess the effects of compression garments than previous meta-analyses.

Contrary to results found in individual research, the meta-analytical evidence suggests that wearing a compression garment during or after training does not facilitate muscle recovery.

“Even data from our previous study supported the idea that such garments have the potential to reduce strength loss after a strenuous workout,” said Dr Négyesi. “However, when we synthesized the data of all relevant studies, we found no effect of compression garments on strength recovery – even when factoring in exercise type and when and where the compression garment is applied.”

The authors think this is a perfect example of contradictory outcomes from individual studies and meta-analytical evidence. Therefore, scientists should be careful when drawing direct conclusions from the results of their studies. Rather, meta-analyses using the most appropriate models can provide more precise and reliable results.

Overall, practitioners, athletes, coaches, and therapists should reconsider compression garments as a means of reducing the harmful effects of physical exercise on muscle strength and seek alternative methods.

The review appears in Sports Medicine.

Source: Tohoku University

Categories : AgeingTags :

Timely Interventions Could Counteract Sarcopenia

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A new study from Karolinska Institutet in Sweden suggests that the early stages of sarcopenia, where muscles weaken with age faster than expected, could be counteracted with timely interventions designed to preserve physical and cognitive function and manage chronic conditions. The study’s findings are published in the Journal of Cachexia, Sarcopenia and Muscle.

Muscle mass and function is lost with ageing. When this decline is more extensive or rapid than expected, it is categorised as sarcopenia, a common condition in the elderly that often lowers quality of life and increases fall and fracture risks.

Researchers examined how different factors such as sex, age, educational level, living arrangement, lifestyle and chronic conditions affected the development of sarcopenia in people aged 60 and above across a 12-year period.

When the study began, almost 10% of the nearly 3200 participants had sarcopenia, 27% had probable sarcopenia and just over 63% no sarcopenia. Measurements such as grip strength, walking speed, speed of rising from a chair five times and calf circumference were used to assess muscle strength and mass and physical performance.

“Perhaps the most interesting result was that after five years, a roughly equal proportion (just over 10 percent) of the individuals with probable sarcopenia had either improved or deteriorated. This suggests that sarcopenia is a dynamic condition that is modifiable especially in the initial stages, which is a hopeful message,” said corresponding author Caterina Trevisan, affiliated researcher at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet.

Physical activity and higher results on cognitive tests improved odds of improvement and lowered mortality risk, while a higher number of chronic conditions, male sex and older age had the opposite correlation. For individuals initially diagnosed with severe sarcopenia, there was little chance of improvement, and many of them (almost 71%) died during the follow-up period.

“Our results support the need of early interventions to preserve physical and cognitive functions and manage chronic conditions in older individuals,” says the study’s last author Anna-Karin Welmer, senior lecturer at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet. “With these tools, we could probably counteract muscle deterioration and the impairment in quality of life this entails. We now need intervention studies to find ways to use these tools to counteract sarcopenia.”

Source: Karolinska Institutet

Categories : Diet and NutritionTags :

Extra Vitamin D Does not Boost Muscles

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Vitamin D supplementation does not have beneficial effects on muscle function, strength, or mass, according to a new meta-analysis, and may even have detrimental effects on muscle strength in people with normal levels of the vitamin.

Vitamin D deficiency, causes a generalised decrease in bone mineral density, resulting in osteopenia and osteoporosis. In young children who have little mineral in their skeleton, this defect results in a variety of skeletal deformities classically known as rickets. It is also believed to cause muscle weakness; affected children have difficulty in standing and walking, whereas the elderly have increasing sway and more frequent falls,thereby increasing their risk of fracture.

The analysis, which is published in the Journal of Bone and Mineral Research, included 54 trials involving 8747 individuals. Overall, no benefits of vitamin D over placebo were observed for improving muscle health. On the contrary, vitamin D appeared to have detrimental effects in terms of increased time spent performing what’s called the Timed Up and Go test, a decrease in maximum strength at knee flexion, and a tendency towards a reduced score of the Short Physical Performance Battery.

“Care should be taken recommending vitamin D supplementation to improve muscle strength and function in people with normal or only slightly impaired vitamin D status,” said lead author Lise Sofie Bislev, MD, PhD, of Aarhus University Hospital, in Denmark. “We need to study further whether it may benefit muscles in those with severe vitamin D deficiency, however.”

Source: Wiley