Posts tagged muscles
Articles and news from the latest research reports.
The U.S. Food and Drug Administration (FDA) today allowed marketing of the DEKA Arm System, the first prosthetic arm that can perform multiple, simultaneous powered movements controlled by electrical signals from electromyogram (EMG) electrodes.
EMG electrodes detect electrical activity caused by the contraction of muscles close to where the prosthesis is attached. The electrodes send the electrical signals to a computer processor in the prosthesis that translates them to a specific movement or movements.
The EMG electrodes in the DEKA Arm System convert electrical signals into up to 10 powered movements, and it is the same shape and weight as an adult arm. In addition to the EMG electrodes, the DEKA Arm System contains a combination of mechanisms including switches, movement sensors, and force sensors that cause the prosthesis to move.
“This innovative prosthesis provides a new option for people with certain kinds of arm amputations,” said Christy Foreman, director of the Office of Device Evaluation at the FDA’s Center for Devices and Radiological Health. “The DEKA Arm System may allow some people to perform more complex tasks than they can with current prostheses in a way that more closely resembles the natural motion of the arm.”
The FDA reviewed clinical information relating to the device, including a 4-site Department of Veterans Affairs study in which 36 DEKA Arm System study participants provided data on how the arm performed in common household and self-care tasks. The study found that approximately 90 percent of study participants were able to perform activities with the DEKA Arm System that they were not able to perform with their current prosthesis, such as using keys and locks, preparing food, feeding oneself, using zippers, and brushing and combing hair.
The DEKA Arm System can be configured for people with limb loss occurring at the shoulder joint, mid-upper arm, or mid-lower arm. It cannot be configured for limb loss at the elbow or wrist joint.
Data reviewed by the FDA also included testing of software and electrical and battery systems, mitigations to prevent or stop unintended movements of the arm and hand mechanisms, durability testing (such as ability to withstand exposure to common environmental factors such as dust and light rain), and impact testing.
The FDA reviewed the DEKA Arm System through its de novo classification process, a regulatory pathway for some novel low- to moderate-risk medical devices that are first-of-a-kind.
The DEKA Arm System is manufactured by DEKA Integrated Solutions in Manchester, N.H.
Higher vitamin D levels in pregnancy could help babies become stronger
Children are likely to have stronger muscles if their mothers had a higher level of vitamin D in their body during pregnancy, according to new research from the Medical Research Council Lifecourse Epidemiology Unit (MRC LEU) at the University of Southampton.
Low vitamin D status has been linked to reduced muscle strength in adults and children, but little is known about how variation in a mother’s status during pregnancy affects her child.
Low vitamin D concentrations are common among young women in the UK, and although women are recommended to take an additional 10μg/day of vitamin D in pregnancy, supplementation is often not taken up.
In the research, published in the January edition of the Journal of Clinical Endocrinology and Metabolism, vitamin D levels were measured in 678 mothers in the later stages of pregnancy.
When the children were four years old, grip strength and muscle mass were measured. Results showed that the higher the levels of vitamin D in the mother, the higher the grip strength of the child, with an additional, but less pronounced association between mother’s vitamin D and child’s muscle mass.
Lead researcher Dr Nicholas Harvey, Senior Lecturer at the MRC LEU at the University of Southampton, comments: “These associations between maternal vitamin D and offspring muscle strength may well have consequences for later health; muscle strength peaks in young adulthood before declining in older age and low grip strength in adulthood has been associated with poor health outcomes including diabetes, falls and fractures. It is likely that the greater muscle strength observed at four years of age in children born to mothers with higher vitamin D levels will track into adulthood, and so potentially help to reduce the burden of illness associated with loss of muscle mass in old age.”
The 678 women who took part in the study are part of the Southampton Women’s Survey, one of the largest and best characterised such studies globally.
Professor Cyrus Cooper, Professor of Rheumatology and Director of the MRC LEU at the University of Southampton, who oversaw this work, added: “This study forms part of a larger programme of research at the MRC Lifecourse Epidemiology Unit and University of Southampton in which we are seeking to understand how factors such as diet and lifestyle in the mother during pregnancy influence a child’s body composition and bone development. This work should help us to design interventions aimed at optimising body composition in childhood and later adulthood and thus improve the health of future generations.”
(Source: southampton.ac.uk)
Why your brain tires when exercising
A marathon runner approaches the finishing line, but suddenly the sweaty athlete collapses to the ground. Everyone probably assumes that this is because he has expended all energy in his muscles. What few people know is that it might also be a braking mechanism in the brain which swings into effect and makes us too tired to continue. What may be occurring is what is referred to as ‘central fatigue’.
"Our discovery is helping to shed light on the paradox which has long been the subject of discussion by researchers. We have always known that the neurotransmitter serotonin is released when you exercise, and indeed, it helps us to keep going. However, the answer to what role the substance plays in relation to the fact that we also feel so exhausted we have to stop has been eluding us for years. We can now see it is actually a surplus of serotonin that triggers a braking mechanism in the brain. In other words, serotonin functions as an accelerator but also as a brake when the strain becomes excessive," says Associate Professor Jean-François Perrier from the Department of Neuroscience and Pharmacology, who has spearheaded the new research.
Help in the battle against doping
Jean-François Perrier hopes that mapping the mechanism that prompts central fatigue will be useful in several ways. Central fatigue is a phenomenon which has been known for about 80 years; it is a sort of tiredness which, instead of affecting the muscles, hits the brain and nervous system. By conducting scientific experiments, it is possible to observe and measure that the brain sends insufficient signals to the muscles to keep going, which in turn means that we are unable to keep performing. This makes the mechanism behind central fatigue an interesting area in the battle against doping, and it is for this reason that Anti Doping Danmark has also helped fund the group’s research.
"In combating the use of doping, it is crucial to identify which methods athletes can use to prevent central fatigue and thereby continue to perform beyond what is naturally possible. And the best way of doing so is to understand the underlying mechanism," says Jean-François Perrier.
Developing better drugs
The brain communicates with our muscles using so-called motoneurons. In several diseases, motoneurons are hyperactive. This is true, for example, of people suffering from spasticity and cerebral palsy, who are unable to control their movements. Jean-François Perrier therefore hopes that, in the long term, this new knowledge can also be used to help develop drugs against these symptoms and to find out more about the effects of antidepressants.
"This new discovery brings us a step closer to finding ways of controlling serotonin. In other words, whether it will have an activating effect or trigger central fatigue. It is all about selectively activating the receptors which serotonin attaches to," explains Jean-François Perrier.
"For selective serotonin re-uptake inhibitor (SSRI) drugs which are used as antidepressants, we can possibly help explain why those who take the drugs often feel more tired and also become slightly clumsier than other people. What we now know can help us develop better drugs," concludes Jean-François Perrier.
Theresa Klein talks about Achilles, the first machine to move in a biologically accurate way.
"Our robot, named Achilles, is the first to walk in a biologically accurate way. That means it doesn’t just move like a person, but also sends commands to the legs like the human nervous system does.
Each leg has eight muscles—Kevlar straps attached to a motor on one end and to the plastic skeleton on the other. As the motor turns, it pulls the strap, mimicking the way our muscles contract. Some of Achilles’ muscles extend from the hip or thigh to the lower leg so they can project forces all the way down the limb. This allows us to put most of the motors in the hips and thighs. Placing them up high keeps the lower leg light, so that it can swing quickly like a human’s lower leg.
In people, neurons in the spinal column send out rhythmic signals that control our legs. It’s like a metronome, and sensory feedback from the legs alters the pace. Your brain can step in to make corrections, but it doesn’t explicitly control every muscle, which is essentially why you can walk without thinking about it. For our robot, a computer program running off an external PC controls movement in a similar way. With each step, the computer sends a signal to flex one hip muscle and extend the other. The computer changes the timing of those signals based on feedback from the legs’ load and angle sensors. A similar control system handles the lower muscles.
Modeling human movement has applications outside of robotics. It could also help us understand how people recover after spinal-cord injuries, for example. But our robot is still a very simplified model—it has no torso and can’t handle complex terrain. Initially, we also had a problem with its feet slipping. We thought about different types of rubber to give its feet more grip but eventually realized a solution already exists. Now, the robot wears a pair of Keds.”
Implications for treating muscular dystrophy and other muscle wasting diseases
Working with mice, Johns Hopkins researchers have solved a key part of a muscle regeneration mystery plaguing scientists for years, adding strong support to the theory that muscle mass can be built without a complete, fully functional supply of muscle stem cells.
"This is good news for those with muscular dystrophy and other muscle wasting disorders that involve diminished stem cell function," says Se-Jin Lee, M.D., Ph.D., lead author of a report on the research in the August issue of the Proceedings of the National Academy of Sciences and professor of molecular biology and genetics at the Johns Hopkins University School of Medicine.
Muscles that do nothing can keep you warm and thin
Muscles that burn energy without contracting have yielded new clues about how the body retains a constant temperature – and they may provide new targets for combating obesity.
Traditionally, the body’s main thermostat was thought to be brown fat. It raids the body’s white fat stores in cold conditions to burn energy and keep the body warm.
Muscles also play a role in keeping the body warm by contracting and triggering the shiver response – but this is only a short-term fix because prolonged shivering damages muscles. Now it seems that muscles have another way to turn up the heat.
"Our findings demonstrate for the first time that muscle, which accounts for 40 per cent of body weight in humans, can generate heat independent of shivering," says Muthu Periasamy of Ohio State University in Columbus.
Sarcolipin: idle body’s thermostat (Image: David Trood/Stone/Getty)
Surviving the chill
Through experiments on mice that had their usual thermostat – brown fat – surgically removed, Periasamy and his colleagues proved that a protein called sarcolipin helps muscle cells keep the body warm by burning energy, almost like an idling motor car, even if the muscles do not contract.
All of the mice had their brown fat removed, but some of them had been genetically engineered to lack sarcolipin too. These rodents could not survive when held at 4 °C, and died of hypothermia within 10 hours. By contrast, mice that could make sarcolipin were able to survive the chilly temperatures and maintained their core body temperature – despite having no brown fat.
Periasamy also showed that an inability to make sarcolipin made mice 33 per cent heavier than normal when fed a high-fat diet. This suggests that idling muscles might also help combat obesity by burning off excess energy. The search is now on for drugs that perform the same role, triggering idling muscles to burn off excess fat.
"The most interesting finding is that mice unable to make sarcolipin are more susceptible to obesity," says Andy Whittle of the University of Cambridge, who is testing spicy dietary treatments to ramp up the fat-burning activity of brown fat. "The research demonstrates that muscle is an important component even in mice, which have comparatively more brown fat than humans. In humans, burning fat in muscle is likely to be even more important for proper energy balance."
(Source: newscientist.com)
Scientists have found a way of growing new blood vessels inside the body. They used cells derived from skin, that when injected into a damaged leg in massive numbers, moulded into the shape of a small blood vessel. This improved blood supply to withered muscles, giving them a new lease of life.
The technique, developed at King’s College London, could also be used to repair the damage done by heart attacks. Professor Qingbo Xu, who is funded by the British Heart Foundation, started by taking human skin cells. Using a cocktail of genes and chemicals, he turned them into early-stage blood vessel cells, programmed to form blood vessels.
He then injected half a million of these cells into the hind leg of a mouse whose foot muscles had been damaged due to poor circulation. These formed a small blood vessel that ferried blood to the damaged muscle, allowing it to repair itself, enabling the creature to put some weight on its foot, the journal Proceedings of the National Academy of Sciences reports.
The professor hopes that injected into the heart, the same cells could be used to heal damage done by heart attacks.