Engineers design soft and flexible 'skeletons' for muscle-powered robots

Our muscles are nature's perfect actuators -- devices that turn energy into motion. For their size, muscle fibers are more powerful and precise than most synthetic actuators. They can even heal from damage and grow stronger with exercise.

For these reasons, engineers are exploring ways to power robots with natural muscles. They've demonstrated a handful of "biohybrid" robots that use muscle-based actuators to power artificial skeletons that walk, swim, pump, and grip. But for every bot, there's a very different build, and no general blueprint for how to get the most out of muscles for any given robot design.

Now, MIT engineers have developed a spring-like device that could be used as a basic skeleton-like module for almost any muscle-bound bot. The new spring, or "flexure," is designed to get the most work out of any attached muscle tissues. Like a leg press that's fit with just the right amount of weight, the device maximizes the amount of movement that a muscle can naturally produce.

The researchers found that when they fit a ring of muscle tissue onto the device, much like a rubber band stretched around two posts, the muscle pulled on the spring, reliably and repeatedly, and stretched it five times more, compared with other previous device designs.

The team sees the flexure design as a new building block that can be combined with other flexures to build any configuration of artificial skeletons. Engineers can then fit the skeletons with muscle tissues to power their movements.

"These flexures are like a skeleton that people can now use to turn muscle actuation into multiple degrees of freedom of motion in a very predictable way," says Ritu Raman, the Brit and Alex d'Arbeloff Career Development Professor in Engineering Design at MIT. "We are giving roboticists a new set of rules to make powerful and precise muscle-powered robots that do interesting things."

Raman and her colleagues report the details of the new flexure design in a paper appearing in the journal Advanced Intelligent Systems. The study's MIT co-authors include Naomi Lynch '12, SM '23; undergraduate Tara Sheehan; graduate students Nicolas Castro, Laura Rosado, and Brandon Rios; and professor of mechanical engineering Martin Culpepper.

Muscle pull

When left alone in a petri dish in favorable conditions, muscle tissue will contract on its own but in directions that are not entirely predictable or of much use.

"If muscle is not attached to anything, it will move a lot, but with huge variability, where it's just flailing around in liquid," Raman says.

To get a muscle to work like a mechanical actuator, engineers typically attach a band of muscle tissue between two small, flexible posts. As the muscle band naturally contracts, it can bend the posts and pull them together, producing some movement that would ideally power part of a robotic skeleton. But in these designs, muscles have produced limited movement, mainly because the tissues are so variable in how they contact the posts. Depending on where the muscles are placed on the posts, and how much of the muscle surface is touching the post, the muscles may succeed in pulling the posts together but at other times may wobble around in uncontrollable ways.

Raman's group looked to design a skeleton that focuses and maximizes a muscle's contractions regardless of exactly where and how it is placed on a skeleton, to generate the most movement in a predictable, reliable way.

"The question is: How do we design a skeleton that most efficiently uses the force the muscle is generating?" Raman says.

The researchers first considered the multiple directions that a muscle can naturally move. They reasoned that if a muscle is to pull two posts together along a specific direction, the posts should be connected to a spring that only allows them to move in that direction when pulled.

"We need a device that is very soft and flexible in one direction, and very stiff in all other directions, so that when a muscle contracts, all that force gets efficiently converted into motion in one direction," Raman says.

Soft flex

As it turns out, Raman found many such devices in Professor Martin Culpepper's lab. Culpepper's group at MIT specializes in the design and fabrication of machine elements such as miniature actuators, bearings, and other mechanisms, that can be built into machines and systems to enable ultraprecise movement, measurement, and control, for a wide variety of applications. Among the group's precision machined elements are flexures -- spring-like devices, often made from parallel beams, that can flex and stretch with nanometer precision.

"Depending on how thin and far apart the beams are, you can change how stiff the spring appears to be," Raman says.

She and Culpepper teamed up to design a flexure specifically tailored with a configuration and stiffness to enable muscle tissue to naturally contract and maximally stretch the spring. The team designed the device's configuration and dimensions based on numerous calculations they carried out to relate a muscle's natural forces with a flexure's stiffness and degree of movement.

The flexure they ultimately designed is 1/100 the stiffness of muscle tissue itself. The device resembles a miniature, accordion-like structure, the corners of which are pinned to an underlying base by a small post, which sits near a neighboring post that is fit directly onto the base. Raman then wrapped a band of muscle around the two corner posts (the team molded the bands from live muscle fibers that they grew from mouse cells), and measured how close the posts were pulled together as the muscle band contracted.

The team found that the flexure's configuration enabled the muscle band to contract mostly along the direction between the two posts. This focused contraction allowed the muscle to pull the posts much closer together -- five times closer -- compared with previous muscle actuator designs.

"The flexure is a skeleton that we designed to be very soft and flexible in one direction, and very stiff in all other directions," Raman says. "When the muscle contracts, all the force is converted into movement in that direction. It's a huge magnification."

The team found they could use the device to precisely measure muscle performance and endurance. When they varied the frequency of muscle contractions (for instance, stimulating the bands to contract once versus four times per second), they observed that the muscles "grew tired" at higher frequencies, and didn't generate as much pull.

"Looking at how quickly our muscles get tired, and how we can exercise them to have high-endurance responses -- this is what we can uncover with this platform," Raman says.

The researchers are now adapting and combining flexures to build precise, articulated, and reliable robots, powered by natural muscles.

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Revolutionary self-sensing electric artificial muscles

Researchers from Queen Mary University of London have made groundbreaking advancements in bionics with the development of a new electric variable-stiffness artificial muscle. Published in Advanced Intelligent Systems, this innovative technology possesses self-sensing capabilities and has the potential to revolutionize soft robotics and medical applications. The artificial muscle seamlessly transitions between soft and hard states, while also sensing forces and deformations. With flexibility and stretchability similar to natural muscle, it can be integrated into intricate soft robotic systems and adapt to various shapes. By adjusting voltages, the muscle rapidly changes its stiffness and can monitor its own deformation through resistance changes. The fabrication process is simple and reliable, making it ideal for a range of applications, including aiding individuals with disabilities or patients in rehabilitation training.

In a study published recently in Advanced Intelligent Systems, researchers from Queen Mary University of London have made significant advancements in the field of bionics with the development of a new type of electric variable-stiffness artificial muscle that possesses self-sensing capabilities. This innovative technology has the potential to revolutionize soft robotics and medical applications.

Muscle contraction hardening is not only essential for enhancing strength but also enables rapid reactions in living organisms. Taking inspiration from nature, the team of researchers at QMUL's School of Engineering and Materials Science has successfully created an artificial muscle that seamlessly transitions between soft and hard states while also possessing the remarkable ability to sense forces and deformations.

Dr. Ketao Zhang, a Lecturer at Queen Mary and the lead researcher, explains the importance of variable stiffness technology in artificial muscle-like actuators. "Empowering robots, especially those made from flexible materials, with self-sensing capabilities is a pivotal step towards true bionic intelligence," says Dr. Zhang.

The cutting-edge artificial muscle developed by the researchers exhibits flexibility and stretchability similar to natural muscle, making it ideal for integration into intricate soft robotic systems and adapting to various geometric shapes. With the ability to withstand over 200% stretch along the length direction, this flexible actuator with a striped structure demonstrates exceptional durability.

By applying different voltages, the artificial muscle can rapidly adjust its stiffness, achieving continuous modulation with a stiffness change exceeding 30 times. Its voltage-driven nature provides a significant advantage in terms of response speed over other types of artificial muscles. Additionally, this novel technology can monitor its deformation through resistance changes, eliminating the need for additional sensor arrangements and simplifying control mechanisms while reducing costs.

The fabrication process for this self-sensing artificial muscle is simple and reliable. Carbon nanotubes are mixed with liquid silicone using ultrasonic dispersion technology and coated uniformly using a film applicator to create the thin layered cathode, which also serves as the sensing part of the artificial muscle. The anode is made directly using a soft metal mesh cut, and the actuation layer is sandwiched between the cathode and the anode. After the liquid materials cure, a complete self-sensing variable-stiffness artificial muscle is formed.

The potential applications of this flexible variable stiffness technology are vast, ranging from soft robotics to medical applications. The seamless integration with the human body opens up possibilities for aiding individuals with disabilities or patients in performing essential daily tasks. By integrating the self-sensing artificial muscle, wearable robotic devices can monitor a patient's activities and provide resistance by adjusting stiffness levels, facilitating muscle function restoration during rehabilitation training.

"While there are still challenges to be addressed before these medical robots can be deployed in clinical settings, this research represents a crucial stride towards human-machine integration," highlights Dr. Zhang. "It provides a blueprint for the future development of soft and wearable robots."

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First hominin muscle reconstruction shows 3.2 million-year-old 'Lucy' could stand as erect as we can

A Cambridge University researcher has digitally reconstructed the missing soft tissue of an early human ancestor -- or hominin -- for the first time, revealing a capability to stand as erect as we do today.

Dr Ashleigh Wiseman has 3D-modelled the leg and pelvis muscles of the hominin Australopithecus afarensis using scans of 'Lucy': the famous fossil specimen discovered in Ethiopia in the mid-1970s.

Australopithecus afarensis was an early human species that lived in East Africa over three million years ago. Shorter than us, with an ape-like face and smaller brain, but able to walk on two legs, it adapted to both tree and savannah dwelling -- helping the species survive for almost a million years.

Named for the Beatles classic 'Lucy in the Sky with Diamonds', Lucy is one of the most complete examples to be unearthed of any type of Australopithecus -- with 40% of her skeleton recovered.

Wiseman was able to use recently published open source data on the Lucy fossil to create a digital model of the 3.2 million-year-old hominin's lower body muscle structure. The study is published in the journal Royal Society Open Science.

The research recreated 36 muscles in each leg, most of which were much larger in Lucy and occupied greater space in the legs compared to modern humans.

For example, major muscles in Lucy's calves and thighs were over twice the size of those in modern humans, as we have a much higher fat to muscle ratio. Muscles made up 74% of the total mass in Lucy's thigh, compared to just 50% in humans.

Paleoanthropologists agree that Lucy was bipedal, but disagree on how she walked. Some have argued that she moved in a crouching waddle, similar to chimpanzees -- our common ancestor -- when they walk on two legs. Others believe that her movement was closer to our own upright bipedalism.

Research in the last 20 years have seen a consensus begin to emerge for fully erect walking, and Wiseman's work adds further weight to this. Lucy's knee extensor muscles, and the leverage they would allow, confirm an ability to straighten the knee joints as much as a healthy person can today.

"Lucy's ability to walk upright can only be known by reconstructing the path and space that a muscle occupies within the body," said Wiseman, from Cambridge University's McDonald Institute for Archaeological Research.

"We are now the only animal that can stand upright with straight knees. Lucy's muscles suggest that she was as proficient at bipedalism as we are, while possibly also being at home in the trees. Lucy likely walked and moved in a way that we do not see in any living species today," Wiseman said.

"Australopithecus afarensis would have roamed areas of open wooded grassland as well as more dense forests in East Africa around 3 to 4 million years ago. These reconstructions of Lucy's muscles suggest that she would have been able to exploit both habitats effectively."

Lucy was a young adult, who stood at just over one metre tall and probably weighed around 28kg. Lucy's brain would have been roughly a third of the size of ours.

To recreate the muscles of this hominin, Wiseman started with some living humans. Using MRI and CT scans of the muscle and bone structures of a modern woman and man, she was able to map the "muscle paths" and build a digital musculoskeletal model.

Wiseman then used existing virtual models of Lucy's skeleton to "rearticulate" the joints -- that is, put the skeleton back together. This work defined the axis from which each joint was able to move and rotate, replicating how they moved during life.

Finally, muscles were layered on top, based on pathways from modern human muscle maps, as well as what little "muscle scarring" was discernible (the traces of muscle connection detectable on the fossilised bones). "Without open access science, this research would not have been possible," said Wiseman.

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The surprising science behind long-distance bird migration

A team of scientists led by researchers at the University of Massachusetts Amherst has recently made a surprising discovery, with the help of a wind tunnel and a flock of birds. Songbirds, many of which make twice-yearly, non-stop flights of more than 1,000 miles to get from breeding range to wintering range, fuel themselves by burning lots of fat and a surprising amount of the protein making up lean body mass, including muscle, early in the flight. This flips the conventional wisdom on its head, which had assumed that migrating birds only ramped up protein consumption at the very end of their journeys, because they would need to use every ounce of muscle for wing-flapping, not fuel. The results appeared recently in the Proceedings of the National Academy of Sciences.

"Birds are amazing animals," says Cory Elowe, the paper's lead author and a postdoctoral researcher in biology at UMass Amherst, where he received his Ph.D. "They are extreme endurance athletes; a bird that weighs half an ounce can fly, non-stop, flapping for 100 hours at a time, from Canada to South America. How is this possible? How do they fuel their flight?"

For a very long time, biologists assumed that birds fueled such feats of endurance by burning fat reserves. And indeed, fat is an important part of migratory birds' secret mix. "The birds in our tests burned fat at a consistent rate throughout their flights," says Elowe. "But we also found that they burn protein at an extremely high rate very early in their flights, and that the rate at which they burn protein tapers off as the duration of the flight increases."

"This is a new insight," says Alexander Gerson, associate professor of biology at UMass Amherst and the paper's senior author. "No one has been able to measure protein burn to this extent in birds before."

"We knew that birds burned protein, but not at this rate, and not so early in their flights," continues Gerson. "What's more, these small songbirds can burn 20% of their muscle mass and then build it all back in a matter of days."

To make this breakthrough, Elowe had help from the bird banding operators at Long Point Bird Observatory, in Ontario, along the northern shore of Lake Erie. Every fall, millions of birds gather near the observatory on their journey to their wintering grounds -- including the blackpoll warbler, a small songbird that travels thousands of miles during its migration. After capturing 20 blackpolls and 44 yellow-rumped warblers -- a shorter distance migrant -- using mist nets, Elowe and his colleagues then transported the birds to the Advanced Facility for Avian Research at Western University, which has a specialized wind tunnel built specifically for observing birds in flight.

Elowe measured the birds' fat and lean body mass pre-flight, then, when the sun set, let the birds free in the wind tunnel. Because the birds naturally migrate at night, Elowe and his colleagues would then stay awake -- at one point, for 28 hours -- watching for when a bird would decide to rest. At that point, the researchers would collect the bird and again measure its fat and lean body mass content, comparing them with the pre-flight measurements.

"One of the biggest surprises was that every bird still had plenty of fat left when it chose to end its flight," says Elowe. "But their muscles were emaciated. Protein, not fat, seems to be a limiting factor in determining how far birds can fly."

The researchers still don't quite know why the birds are burning such vast stores of protein so early in their journeys, but the possible answers open up a wide range of future research avenues.

"How exactly is it possible to burn up your muscles and internal organs, and then rebuild them as quickly as these birds do," wonders Gerson. "What insights into the evolution of metabolism might these birds yield?"

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Glassfrogs achieve transparency by packing red blood cells into mirror-coated liver

New research shows that glassfrogs -- known for their highly transparent undersides and muscles -- perform their "disappearing acts" by stowing away nearly all of their red blood cells into their uniquely reflective livers. The study, led by scientists at the American Museum of Natural History and Duke University, is being published Friday in the journal Science. The work could lead to new avenues of research tied to blood clots, which the frogs somehow avoid while packing and unpacking about 90 percent of their red blood cells into their livers on a daily basis.

"There are more than 150 species of known glassfrogs in the world, and yet we're really just starting to learn about some of the really incredible ways they interact with their environment," said co-lead author Jesse Delia, a Gerstner postdoctoral fellow in the Museum's Department of Herpetology.

Glassfrogs, which live in the American tropics, are nocturnal amphibians that spend their days sleeping upside down on translucent leaves that match the color of their backs -- a common camouflage tactic. Their tummies, however, show something surprising: translucent skin and muscle that allows their bones and organs to be visible, giving the glassfrog its common name. Recent research has proposed that this adaptation masks the frogs' outlines on their leafy perches, making them harder for predators to spot.

Transparency is a common form of camouflage among animals that live in water, but it's rare on land. In vertebrates, attaining transparency is difficult because their circulatory system is full of red blood cells that interact with light. Studies have shown that ice fish and larval eels achieve transparency by not producing hemoglobin and red blood cells. But glassfrogs use an alternative strategy, according to the findings of the new study.

"Glassfrogs overcome this challenge by essentially hiding red blood cells from view," said Carlos Taboada, the study's co-lead author from Duke University. "They almost pause their respiratory system during the day, even at high temperatures."

At Duke, the researchers used a technique called photoacoustic imaging, which uses light to induce sound-wave propagation from red blood cells. This allows researchers to map the location of the cells within sleeping frogs without restraint, contrast agents, sacrifice, or surgical manipulation -- particularly important to this study because glassfrog transparency is disrupted by activity, stress, anesthesia, and death.

The researchers focused on one particular species of glassfrog, Hyalinobatrachium fleischmanni. They found that resting glassfrogs increase transparency two- to threefold by removing nearly 90 percent of their red blood cells from circulation and packing them within their liver, which contains reflective guanine crystals. Whenever the frogs need to become active again, they bring the red blood cells back into the blood, which gives the frogs the ability to move around -- at which point, light absorption from these cells breaks transparency.

In most vertebrates, aggregating red blood cells can lead to potentially dangerous blood clots in veins and arteries. But glassfrogs don't experience clotting, which raises a set of significant questions for biological and medical researchers.

"This is the first of a series of studies documenting the physiology of vertebrate transparency, and it will hopefully stimulate biomedical work to translate these frogs' extreme physiology into novel targets for human health and medicine," Delia said.

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Trunk dexterity explained: Scientists decipher facial motor control in elephants

Elephants have an amazing arsenal of face, ear and trunk movements. The trunk consists of far more muscles than the entire human body and can perform both powerful and very delicate movements. A team of scientists from the Humboldt University of Berlin and the Leibniz Institute for Zoo and Wildlife Research (Leibniz-IZW) now examined the facial motor nucleus of African and Asian elephants, the brain structure that controls the facial muscles of these animals. This nucleus contains more facial motor neurons than in any other terrestrial mammal, the scientists show in a paper published in the journal Science Advances. African elephants in particular have particularly prominent neuron clusters for the control of the trunk "fingers."

One of the most remarkable body parts in the animal kingdom is the elephant trunk. It is extremely muscular and strong, containing far more muscles than the entire human body, and yet it is very sensitive and capable of carefully performed, finely tuned motor actions. The way elephants use the tip of their trunk strongly resembles a human hand, and they actually have so-called fingers at the tip. Lena Kaufmann and colleagues in Michael Brecht's laboratory at HU Berlin and Thomas Hildebrandt's Department of Reproduction Management at the Leibniz-IZW for the first time have now studied and described in detail the so-called elephant facial nucleus -- the brain structure responsible for controlling the elephants' facial muscles, from the ears to the tip of the trunk.

"The elephant's facial motor nucleus is unique in several ways. For example, it contains more facial motor neurons than all other terrestrial mammals," says first author Lena Kaufmann (HU Berlin). The scientists counted about 54,000 neurons in the facial nucleus of Asian elephants (Elephas maximus), whereas the African savanna elephant (Loxodonta africana) even has about 63,000. The team attributed the higher number of facial nucleus neurons in African savanna elephants to their larger ears and more elaborate trunk tip. "African savanna elephants have two so-called fingers at the trunk tip with which they grip objects," says Thomas Hildebrandt (Leibniz-IZW). "This kind of pincer grip requires much dexterity with the trunk tip. Not surprisingly, we see in the brains of African elephants prominent neuron clusters for the control of the fingertips." Asian elephants have only one finger and tend to wrap their trunk around objects; hence their finger-tip is less prominently represented in their brain.

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Skin: An additional tool for the versatile elephant trunk

A new study from Georgia Institute of Technology suggests that an elephant's muscles aren't the only way it stretches its trunk -- its folded skin also plays an important role. The combination of muscle and skin gives the animal the versatility to grab fragile vegetation and rip apart tree trunks.

The research, in collaboration with Zoo Atlanta, finds that an elephant's skin doesn't uniformly stretch. The top of the trunk is more flexible than the bottom, and the two sections begin to diverge when an elephant reaches more than 10%. When stretching for food or objects, the dorsal section of the trunk slides further forward.

The findings could improve robotics, which today are typically built for either great strength or flexibility. Unlike an elephant's trunk, the machines can't do both.

As an example, the study's authors point to soft robotics. Their fluid-filled cavities allow flexible movements but can easily break when forces are applied. The researchers say the elephant findings suggest that wrapping soft robotics with a skin-like structure could give the machines protection and strength while continuing to allow flexibility.

The paper is published in the Proceedings of the National Academy of Sciences (PNAS) by the same Georgia Tech team that authored a study last summer about how elephants use their trunk muscles to inhale food and water.

"When people extend their tongue -- a muscle-filled, boneless tissue similar in composition to an elephant's trunk -- it stretches uniformly. We expected the same when we challenged an elephant to reach for food," said Andrew Schulz, the study's lead author and a Ph.D. student in Georgia Tech's George W. Woodruff School of Mechanical Engineering. He and the team filmed two African savanna elephants reaching for bran cubes and apples at Zoo Atlanta.

"But when we looked at our high-speed camera footage and plotted the trunk's movements, we were surprised. The top and bottom weren't the same at all," Schulz said.

After seeing the video, Schulz stretched the tissue of a dissected elephant to better understand the skin's elasticity. That's when he found that the top of the skin, which is folded, is 15% more flexible than the wrinkled bottom side. It's also when the team realized they weren't just seeing muscle movement on the video. They were also tracking a thick sheet of skin.

"Flexible skin folds are the elephant's innovation," said David Hu, Schulz's advisor and a professor in the Woodruff School and the School of Biological Sciences. "They protect the dorsal section and make it easier for the elephant to reach downward, the most common gripping style when picking up items."

The Georgia Tech study also found that an elephant trunk differs in another way from other boneless, muscle-filled appendages found in nature, such as squid and octopus tentacles. Instead of extending evenly, an elephant telescopically stretches its trunk like an umbrella, gradually lengthening in waves.

An elephant first extends the section that includes the tip of its trunk, then the adjacent section and so on, gradually working its way back toward its body. Schulz says the progressive movement towards the base is intentional.

"Elephants are like people: they're lazy," he said. "The section at the end of the trunk is 1 liter of muscle. The section closest to its mouth is 11-15 liters of muscle. An elephant will first stretch the end of its trunk, then the adjacent section, because they're easier to move. If an elephant doesn't have to work very hard to reach something, it won't."

Schulz said he had to rely on a drawing from 1908 when learning about trunk anatomy because scientists and engineers haven't done much research on the biomechanics of elephants during the last century. Part of his curiosity of elephants is based on helping them; he thinks a better understanding of the animals will lead to better conservation efforts. As a mechanical engineer, Schulz also sees the applications of robotics.

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The secret to staying young: New research highlights power of life long exercise to keep muscles healthy

Lifelong physical activity could protect against age-related loss of muscle mass and function, according to research published in The Journal of Physiology. Individuals aged 68 and above who were physically active throughout their life have healthier ageing muscle that has superior function and is more resistant to fatigue compared to inactive individuals, both young and old.

This is the first study to investigate muscle, stem cell and nerve activity in humans. The researchers from University of Copenhagen, Denmark, found that elderly individuals who keep physically active throughout their adult life, whether by taking part in resistance exercise, ball games, racket sports, swimming, cycling, running and/or rowing had a greater number of muscle stem cells, otherwise known as satellite cells in their muscle. These cells are important for muscle regeneration and long-term growth and protect against nerve decay.

46 male participants took part in the study. They were divided into three groups: young sedentary (15), elderly lifelong exercise (16) and elderly sedentary (15). They performed a heavy resistance exercise, sitting in a mechanical chair performing a knee extension movement to evaluate muscle function. The amount of force produced was measured. Blood samples were taken, and muscle biopsies were analysed from both legs. The researchers found elderly lifelong exercisers outperformed both the elderly and young sedentary adults.

Lead author, Casper Soendenbroe, University of Copenhagen, Denmark said:

"This is the first study in humans to find that lifelong exercise at a recreational level could delay some detrimental effects of ageing. Using muscle tissue biopsies, we've found positive effects of exercise on the general ageing population. This has been missing from the literature as previous studies have mostly focused on master athletes, which is a minority group. Our study is more representative of the general population aged 60 and above, as the average person is more likely to take part in a mixture of activities at a moderate level. That's why we wanted to explore the relation between satellite cell content and muscle health in recreationally active individuals. We can now use this as a biomarker to further investigate the link between exercise, ageing and muscle health."

"The single most important message from this study, is that even a little exercise seems to go a long way, when it comes to protecting against the age-related decline in muscle function. This is an encouraging finding which can hopefully spur more people to engage in an activity that they enjoy. We still have much to learn about the mechanisms and interactions between nerves and muscles and how these change as we age. Our research takes us one step closer."

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Artificial muscles made of proteins

Dr. Stefan Schiller and Dr. Matthias Huber from the University of Freiburg's livMatS Cluster of Excellence have succeeded in developing a muscle solely on the basis of natural proteins. The autonomous contractions of the material, which the researchers presented in the journal Advanced Intelligent Systems, can be controlled with the help of pH and temperature changes. The movements are driven by a chemical reaction that consumes molecular energy for this purpose. "Our artificial muscle is still a prototype," says Schiller. "However, the high biocompatibility of the material and the possibility of adjusting its composition to match particular tissue could pave the way for future applications in reconstructive medicine, prosthetics, pharmaceutics, or soft robotics."

In the past, scientists have already taken natural proteins as a basis for developing artificial muscle systems and built them into miniscule molecular machines or into polymers. However, it has not yet been possible to develop synthetic muscle materials that are entirely bio-based and move autonomously with the help of chemical energy.

Material based on the natural protein elastin

The material used by the Freiburg team is based on elastin, a natural fibrous protein that also occurs in humans, for instance giving elasticity to the skin and blood vessels. Following the model of this protein, the researchers developed two elastin-like proteins, one of which responds, for example, to fluctuations in pH, the other to changes in temperature. The scientists combined the two proteins by means of photochemical cross-linking to form a bilayered material. It is possible in this process to flexibly shape the material and set the direction of its movement.

Contractions can be switched on and off with the help of temperature changes

The researchers succeeded in inducing the rhythmic contractions by using a chemical energy source as fuel, in this case sodium sulfite. In an oscillating chemical reaction in which the pH changes in cycles due to a special linkage of several reactions, the added energy was converted into mechanical energy via non-equilibrium states of the material. In this way, the researchers induced the material to contract autonomously in a cyclical manner. They were also able to switch the contractions on and off with the help of temperature changes: The oscillating chemical reaction started at a temperature of around 20 degrees Celsius, and the material began to make rhythmic movements. In the process, it was possible to program certain states for the material to assume and to reset them again with another stimulus. The scientists thus achieved a simple system for implementing learning and forgetting at the material level.

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Muscular study provides new information about how the largest dinosaurs moved and evolved

New research led by the University of Bristol has revealed how giant 50-tonne sauropod dinosaurs, like Diplodocus, evolved from much smaller ancestors, like the wolf-sized Thecodontosaurus.

In a new study published today in the journal Royal Society Open Science, researchers present a reconstruction of the limb muscles of Thecodontosaurus, detailing the anatomy of the most important muscles involved in movement.

Thecodontosaurus was a small to medium sized two-legged dinosaur that roamed around what today is the United Kingdom during the Triassic period (around 205 million years ago).

This dinosaur was one of the first ever to be discovered and named by scientists, in 1836, but it still surprises scientists with new information about how the earliest dinosaurs lived and evolved.

Antonio Ballell, PhD student in Bristol's School of Earth Sciences and lead author of the study, said: "The University of Bristol houses a huge collection of beautifully preserved Thecodontosaurus fossils that were discovered around Bristol. The amazing thing about these fossilised bones is that many preserve the scars and rugosities that the limb musculature left on them with its attachment."

These features are extremely valuable in scientific terms to infer the shape and direction of the limb muscles. Reconstructing muscles in extinct species requires this kind of exceptional preservation of fossils, but also a good understanding of the muscle anatomy of living, closely related species.

Antonio Ballell added: "In the case of dinosaurs, we have to look at modern crocodilians and birds, that form a group that we call archosaurs, meaning 'ruling reptiles'. Dinosaurs are extinct members of this lineage, and due to evolutionary resemblance, we can compare the muscle anatomy in crocodiles and birds and study the scars that they leave on bones to identify and reconstruct the position of those muscles in dinosaurs."

Professor Emily Rayfield, co-author of the study, said: "These kinds of muscular reconstructions are fundamental to understand functional aspects of the life of extinct organisms. We can use this information to simulate how these animals walked and ran with computational tools."

From the size and orientation of its limb muscles, the authors argue that Thecodontosaurus was quite agile and probably used its forelimbs to grasp objects instead of walking.

This contrasts with its later relatives, the giant sauropods, which partly achieved these huge body sizes by shifting to a quadrupedal posture. The muscular anatomy of Thecodontosaurus seems to indicate that key features of later sauropod-line dinosaurs had already evolved in this early species.

Professor Mike Benton, another co-author, said: "From an evolutionary perspective, our study adds more pieces to the puzzle of how the locomotion and posture changed during the evolution of dinosaurs and in the line to the giant sauropods.

"How were limb muscles modified in the evolution of multi-ton quadrupeds from tiny bipeds? Reconstructing the limb muscles of Thecodontosaurus gives us new information of the early stages of that important evolutionary transition."

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Innovative approach brings cell-reprograming therapy for heart failure closer to reality

Not too long ago the idea of taking, for instance a skin cell and transforming it into a muscle cell was unthinkable. About 10 years ago, however, revolutionary research showed that it is indeed possible to reprogram differentiated adult cells into other types fully capable of conducting new functions.

Cell reprogramming is a main interest of the lab of Dr. Todd Rosengart, chair and professor of the Michael E. DeBakey Department of Surgery at Baylor College of Medicine, whose research focuses on finding innovative therapeutic approaches for heart failure.

"Heart failure remains the leading cause of death from heart disease," said Rosengart, DeBakey-Bard Chair in Surgery and professor of molecular and cellular biology at Baylor. "Nearly 5 million Americans can be expected to develop advanced congestive heart failure, and heart transplant or mechanical circulatory support implantation currently are the only options for patients with end-stage heart disease. However, these options are limited. We need to improve how to treat this devastating condition."

After a heart attack, the parts of the heart muscle that die do not regenerate into new heart tissue; instead, they are replaced by a scar that does not help the heart to beat. "The idea behind cell reprograming is to coach the heart to heal itself by inducing the scar tissue, which is made mostly of fibroblasts, to change into functional heart muscle," said Rosengart, professor of heart and vascular disease at the Texas Heart Institute.

Researchers have succeeded at reprograming fibroblasts from small animals to become heart muscle, with dramatic improvements in heart function. The challenge has been to apply this technology to human cells -- human fibroblasts are more resistant to reprograming. In this study, Rosengart and his colleagues explored a novel strategy to enhance the reprogramming efficiency of human fibroblasts.

"While human fibroblasts resist being reprogramed, endothelial cells, those that line the blood vessels, are known to be more flexible -- they have the capacity to naturally transdifferentiate or change into other cells," said co-first author Dr. Megumi Mathison, associate professor of surgery at Baylor. "This gave us the idea of using this endothelial cell plasticity to improve the reprograming efficiency."

The researchers' idea was to first induce fibroblasts to transition into an endothelial cell-like state and then treat these cells with their reprograming cocktail that directs them to change into cardiomyocytes. The expectation was that transitioning into endothelial cell-like cells, a cell type more open to reprogramming than fibroblasts, would facilitate the desired change into heart muscle.

"We were delighted to see that our approach significantly enhanced reprogramming efficiency both in human and rat fibroblasts," Mathison said. "Previously, inducing cardiomyocytes from fibroblasts directly was only 3% efficient. With our new approach, the efficiency increased 5 times. It took about two to three weeks for the fibroblasts to transition into cardiomyocytes in the lab. It was exciting to see the reprogrammed cells contracting in synchrony with surrounding cardiomyocytes."

The researchers' experimental results with the rat model show that their new strategy can revert large scar tissue into working muscle, supporting continuing their investigations to bring this procedure to the clinic.

"Although more research is needed, we anticipate that this novel approach can become part of the next generation of biological therapies," Rosengart said. "In a future scenario, patients with congestive heart failure would come to the catheterization laboratory, commonly referred to as the cath lab, in a hospital. The cath lab has diagnostic imaging equipment that helps surgeons visualize the chambers of the heart and surrounding blood vessels as they conduct procedures. Assisted by this equipment, the surgeon would inject the factors that promote the transition from fibroblasts to endothelial cells and then to cardiomyocytes directly into the heart. Follow ups would monitor the progress of the procedure."

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New muscle layer discovered on the jaw

Human anatomy still has a few surprises in store for us: researchers at the University of Basel have discovered a previously overlooked section of our jaw muscles and described this layer in detail for the first time.

The masseter muscle is the most prominent of the jaw muscles. If you place your fingers on the back of your cheeks and press your teeth together, you'll feel the muscle tighten. Anatomy textbooks generally describe the masseter as consisting of one superficial and one deep part.

Now, researchers led by Dr. Szilvia Mezey from the Department of Biomedicine at the University of Basel and Professor Jens Christoph Türp from the University Center for Dental Medicine Basel (UZB) have described the structure of the masseter muscle as consisting of an additional third, even deeper layer. In the scientific journal Annals of Anatomy, they propose that this layer be given the name Musculus masseter pars coronidea -- in other words, the coronoid section of the masseter -- because the newly described layer of muscle is attached to the muscular (or "coronoid") process of the lower jaw.

The anatomical study was based on detailed examination of formalin-fixed jaw musculature, computer tomographic scans and the analysis of stained tissue sections from deceased individuals who had donated their bodies to science. This was in addition to MRI data from a living person.

As if a new animal species had been discovered

"This deep section of the masseter muscle is clearly distinguishable from the two other layers in terms of its course and function," explains Mezey. The arrangement of the muscle fibers, she says, suggests that this layer is involved in the stabilization of the lower jaw. It also appears to be the only part of the masseter that can pull the lower jaw backwards -- that is, toward the ear.

A look at historical anatomy studies and textbooks reveals that the structure of the masseter muscle has already raised questions in the past. In a previous edition of Gray's Anatomy, from the year 1995, the editors also describe the masseter muscle as having three layers, although the cited studies were based on the jaw musculature of other species and partly contradicted one another.

Other individual studies from the early 2000s also reported three layers, but they divided the superficial section of the masseter into two layers and agreed with standard works in their description of the deeper section.

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Scientists can control brain circuits, behavior, and emotion using light

Controlling signal transmission and reception within the brain circuits is necessary for neuroscientists to achieve a better understanding of the brain's functions. Communication among neuron and glial cells is mediated by various neurotransmitters being released from the vesicles through exocytosis. Thus, regulating vesicular exocytosis can be a possible strategy to control and understand brain circuits.

However, it has been difficult to freely control the activity of brain cells in a spatiotemporal manner using pre-existing techniques. One is an indirect approach that involves artificially controlling the membrane potential of cells, but it comes with problems of changing the acidity of the surrounding environment or causing unwanted misfiring of neurons. Moreover, it is not applicable for use in cells that do not respond to the membrane potential changes, such as glial cells.

To address this problem, South Korean researchers led by Director C. Justin LEE at the Center for Cognition and Sociality within the Institute for Basic Science (IBS) and professor HEO Won Do at Korea Advanced Institute of Science and Technology (KAIST) developed Opto-vTrap, a light-inducible and reversible inhibition system that can temporarily trap vesicles from being released from brain cells. Opto-vTrap directly targets transmitters containing vesicles, and it can be used in various types of brain cells, even the ones that do not respond to membrane potential changes.

In order to directly control the exocytotic vesicles, the research team applied a technology they previously developed in 2014, called light-activated reversible inhibition by assembled trap (LARIAT). This platform can inactivate various types of proteins when illuminated under blue light by instantly trapping the target proteins, like a lariat. Opto-vTrap was developed by applying this LARIAT platform to vesicle exocytosis. When the Opto-vTrap expressing cells or tissues are shined under blue light, the vesicles form clusters and become trapped within the cells, inhibiting the release of transmitters.

Most importantly, the inhibition triggered using this new technique is temporary, which is very important for neuroscience research. Other previous techniques that target vesicle fusion proteins damage them permanently and disable the target neuron for up to 24 hours, which is not appropriate for many behavioral experiments with short time constraints. By comparison, vesicles that were inactivated using Opto-vTrap decluster in about 15 minutes, and the neurons regain their full functions within an hour.

Opto-vTrap directly controls the signal transmitters' release, enabling the researchers to freely control brain activity. The research team verified the usability of Opto-vTrap in cultured cells and brain tissue slices. Furthermore, they tested the technique in live mice, which enabled them to temporarily remove fear memory from fear-conditioned animals.

In the future, Opto-vTrap will be used to uncover complex interactions between multiple parts of the brain. It will be a highly useful tool for studying how certain brain cell types affect brain function in different circumstances.

Professor Heo stated, "Since Opto-vTrap can be used in various cell types, it is expected to be helpful in various fields of brain science research," He explained, "We plan to conduct a study to figure out the spatiotemporal brain functions in various brain cell types in a specific environment using Opto-vTrap technology."

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Exercise improves health through changes on DNA

While it is widely known that regular physical exercise decreases the risk of virtually all chronic illnesses, the mechanisms at play are not fully known. Now scientists at the University of Copenhagen have discovered that the beneficial effects of physical exercise may in part result from changes to the structure of our DNA. These changes are referred as 'epigenetic'.

DNA is the molecular instruction manual found in all our cells. Some sections of our DNA are genes, which are instructions for building proteins -- the body's building blocks -- while other sections are called enhancers that regulate which genes are switched on or off, when, and in which tissue. The scientists found, for the first time, that exercise rewires the enhancers in regions of our DNA that are known to be associated with the risk to develop disease.

"Our findings provide a mechanism for the known beneficial effects of exercise. By connecting each enhancer with a gene, we further provide a list of direct targets that could mediate this effect," says Professor Romain Barrès from the Novo Nordisk Foundation Center for Basic Metabolic Research, the senior author of the research, which was published in Molecular Metabolism.

Exercise improves health of organs including the brain

The team of scientists hypothesized that endurance exercise training remodels the activity of gene enhancers in skeletal muscle. They recruited healthy young men and put them through a six-week endurance exercise program. The scientists collected a biopsy of their thigh muscle before and after the exercise intervention and examined if changes in the epigenetic signature of their DNA occurred after training.

The scientists discovered that after completing the endurance training program, the structure of many enhancers in the skeletal muscle of the young men had been altered. By connecting the enhancers to genetic databases, they discovered that many of the regulated enhancers have already been identified as hotspots of genetic variation between individuals -- hotspots that have been associated with human disease.

The scientists speculate that the beneficial effects of exercise on organs distant from muscle, like the brain, may largely be mediated by regulating the secretion of muscle factors. In particular, they found that exercise remodels enhancer activity in skeletal muscle that are linked to cognitive abilities, which opens for the identification of exercise training-induced secreted muscle factors targeting the brain.

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Championing chrononutrition with protein, the morning elixir for muscle growth

Proteins constitute an essential dietary component that help in the growth and repair of the body. Composed of long chains of amino acids, proteins promote the growth of skeletal muscles, the group of muscles that help us move. Humans have been aware of the benefits of proteins for long. However, recent studies have shown that having the right amount of protein at the right time of the day is essential for proper growth. This is called 'Chrononutrition,' in which when you eat is as important as what and how you eat.

The reason behind this is the body's internal biological clock, called the 'circadian rhythm.' This rhythm is followed by all cells and controls life functions like metabolism and growth. Interestingly, protein digestion and absorption have been found to fluctuate across day and night according to this clock. Moreover, earlier studies have reported that intake of protein at breakfast and lunch promotes skeletal muscle growth in adults. However, details on the effect of the time of protein intake on muscle growth and function have remained elusive till date.

Fortunately, researchers from Waseda University, led by Professor Shigenobu Shibata, recently endeavored to understand the effect of the distribution of protein intake through the day on muscles. They fed laboratory mice two meals per day containing either high (11.5% by proportion) or low (8.5% by proportion) protein concentrations. The researchers noted that protein intake at breakfast induced an increase in muscle growth, determined by assessing induced hypertrophy of the plantaris muscle in the leg, when compared with the effects of protein intake at dinner. Specifically, the ratio of muscle hypertrophy determined against the growth of the control muscle was 17% higher in mice fed 8.5% protein at breakfast, than that in mice fed 11.5% protein at dinner, despite the former group consuming a low proportion of protein overall. They also found that intake of a type of protein called the BCCA, short for branched-chain amino acids, early in the day increased the size of skeletal muscles specifically.

To confirm the association of these effects with the workings of the circadian rhythm, the researchers next engineered whole-body mutant Clock?19 or muscle-specific Bmal1 knockout mice lacking the genes that control the biological clock. They repeated diet distribution experiments on these mice but did not observe similar muscle change, which confirmed the involvement of the circadian rhythm in muscle growth in the context of protein intake.

Excited about the findings of their study published in a recent issue of the Cell Reports, Prof. Shibata emphasizes, "Protein-rich diet at an early phase of the daily active period, that is at breakfast, is important to maintain skeletal muscle health and enhance muscle volume and grip strength."

To check if their findings were applicable to humans, the team recruited women in their study and tested if their muscle function, determined by measuring skeletal muscle index (SMI) and grip strength, varied with the timing of the protein-rich diet consumed. Sixty women aged 65 years and above who took protein at breakfast rather than at dinner showed better muscle functions, suggesting the possibility of the findings to be true across species. Additionally, the researchers also found a strong association between SMI and the proportion of protein intake at breakfast relative to total protein intake through the day.

Prof. Shibata is hopeful that the findings of their study will lead to a widespread modification in the current diet regime of most people across the Western and Asian countries, who traditionally consume low amounts of protein at breakfast. He therefore stresses, "For humans, in general, the protein intake at breakfast averages about 15 grams, which is less than what we consume at dinner, which is roughly 28 grams. Our findings strongly support changing this norm and consuming more protein at breakfast or morning snacking time."

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Muscles retain positional memory from fetal life

A research collaboration based in Kumamoto University, Japan has discovered that muscles and the resident stem cells (satellite cells) responsible for muscle regeneration retain memory of their location in the body. This positional memory was found to be based on the expression pattern of the homeobox (Hox) gene cluster, which is responsible for shaping the body during fetal life. These findings are expected to provide clues to elucidate the pathogenesis of muscle diseases such as muscular dystrophy, in which the position of muscle vulnerability varies depending on the type of muscle, and to help develop regenerative medicine based on positional memory.

There are various types of the intractable muscle disease muscular dystrophy and each type has a different symptom location. Similarly, age-related muscle fragility (sarcopenia) does not occur evenly throughout the body. The physical location of the symptoms of these diseases cannot be explained by differences in muscle fiber types or physical activity patterns alone, and requires a new perspective to elucidate their respective pathogeneses.

The developmental origin of cells that form muscles differ in the fetal stage. For example, most of the craniofacial muscles originate from the cranial mesoderm, while the limb muscles originate from the body segments. Development of limb and craniofacial muscles in the fetal period involves specific molecular mechanisms that depends on their origin. However, differences in the properties of mature skeletal muscle depending on body position after birth have not been fully discussed. Thus, a research collaboration worked to visualize the body's positional information by studying the epigenomic state and gene expression patterns of skeletal muscle and the muscle stem cells responsible for regeneration.

Using skeletal muscle and associated muscle stem cells isolated from the heads and hind limbs of adult mice, researchers investigated positional specificity at the epigenomic level using DNA methylome analysis. They found characteristic differences in the DNA methylation status at the homeobox (Hox) loci. Among four regions, A to D, the Hox-A locus in particular had an overall DNA hypermethylation state in hindlimb skeletal muscle and muscle stem cells compared to the head. Additionally, both skeletal muscle and muscle stem cells in the hind limbs showed high expression of the Hox-A gene. Many of these Hox-A genes reflected expression patterns in the fetal period. These findings suggest that skeletal muscle and muscle stem cells remember positional information during fetal life, and that epigenomic regulation by DNA methylation may be involved in positional memory.

The researchers then focused on the Hoxa10 gene, which was highly expressed only in the limb muscles. When hindlimb-derived muscle stem cells expressing Hoxa10 were isolated and transplanted into craniofacial muscles that do not express Hoxa10, Hoxa10 gene expression became detectable in the craniofacial muscles. In other words, hindlimb-derived muscle stem cells were able to innervate the craniofacial muscle with strong retention of positional memory even after ectopic transplantation.

They then created mice lacking the Hoxa10 gene in muscle stem cells to analyze its function. A Hoxa10 deficiency severely impaired the regeneration of hindlimb muscles but had no effect on craniofacial muscle regeneration. A detailed investigation of the mechanism behind the hindlimb muscle regeneration disorder revealed that it is caused by genomic instability due to abnormal chromosome distribution during muscle stem cell division. Furthermore, analysis of human head and leg muscle stem cells also showed that only leg muscle cells expressed the HOX-A gene and that its inhibition resulted in abnormal cell division, confirming that muscle cell positional memory is retained in humans and mice.

This research suggest that the positional memory of muscle stem cells based on the position-specific distribution of Hox gene expression may determine the position-specific properties of skeletal muscle, rather than merely persisting from fetal life.

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Mechanical engineers develop new high-performance artificial muscle technology

In the field of robotics, researchers are continually looking for the fastest, strongest, most efficient and lowest-cost ways to actuate, or enable, robots to make the movements needed to carry out their intended functions.

The quest for new and better actuation technologies and 'soft' robotics is often based on principles of biomimetics, in which machine components are designed to mimic the movement of human muscles -- and ideally, to outperform them. Despite the performance of actuators like electric motors and hydraulic pistons, their rigid form limits how they can be deployed. As robots transition to more biological forms and as people ask for more biomimetic prostheses, actuators need to evolve.

Associate professor (and alum) Michael Shafer and professor Heidi Feigenbaum of Northern Arizona University's Department of Mechanical Engineering, along with graduate student researcher Diego Higueras-Ruiz, published a paper in Science Robotics presenting a new, high-performance artificial muscle technology they developed in NAU's Dynamic Active Systems Laboratory. The paper, titled "Cavatappi artificial muscles from drawing, twisting, and coiling polymer tubes," details how the new technology enables more human-like motion due to its flexibility and adaptability, but outperforms human skeletal muscle in several metrics.

"We call these new linear actuators cavatappi artificial muscles based on their resemblance to the Italian pasta," Shafer said.

Because of their coiled, or helical, structure, the actuators can generate more power, making them an ideal technology for bioengineering and robotics applications. In the team's initial work, they demonstrated that cavatappi artificial muscles exhibit specific work and power metrics ten and five times higher than human skeletal muscles, respectively, and as they continue development, they expect to produce even higher levels of performance.

"The cavatappi artificial muscles are based on twisted polymer actuators (TPAs), which were pretty revolutionary when they first came out because they were powerful, lightweight and cheap. But they were very inefficient and slow to actuate because you had to heat and cool them. Additionally, their efficiency is only about two percent," Shafer said. "For the cavatappi, we get around this by using pressurized fluid to actuate, so we think these devices are far more likely to be adopted. These devices respond about as fast as we can pump the fluid. The big advantage is their efficiency. We have demonstrated contractile efficiency of up to about 45 percent, which is a very high number in the field of soft actuation."

The engineers think this technology could be used in soft robotics applications, conventional robotic actuators (for example, for walking robots), or even potentially in assistive technologies like exoskeletons or prostheses.

"We expect that future work will include the use of cavatappi artificial muscles in many applications due to their simplicity, low-cost, lightweight, flexibility, efficiency and strain energy recovery properties, among other benefits," Shafer said.

Technology is available for licensing, partnering opportunities.

Working with the NAU Innovations team, the inventors have taken steps to protect their intellectual property. The technology has entered the protection and early commercialization stage and is available for licensing and partnering opportunities. For more information, please contact NAU Innovations.

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Study reveals roadmap of muscle decline with age

 Scientists have produced a comprehensive roadmap of muscle aging in mice that could be used to find treatments that prevent decline in muscle mobility and function, according to a report published today in eLife.

The study reveals which molecules in the muscle are most significantly altered at different life stages, and shows that a molecule called Klotho, when administered to mice in old, but not very old, age, was able to improve muscle strength.

Age-related loss of skeletal muscle mass and function -- called sarcopenia -- is associated with loss of mobility and increased risk of falls. Yet, although scientists know how sarcopenia affects the appearance and behaviour of muscle tissues, the underlying molecular mechanisms for sarcopenia remain poorly understood. Current treatments for sarcopenia largely involve prescribing physical activity or dietary modifications, and these have shown moderate success.

"Although there are no proven treatments for sarcopenia yet, there are some pharmaceutical treatments entering clinical trials. Interestingly, many of these act on mechanisms that also involve a protein called Klotho," says co-first author Zachary Clemens, Doctoral Student at the Department of Environmental and Occupational Health, University of Pittsburgh, Pennsylvania, US. "Evidence suggests that Klotho levels gradually decline with age, and so we wanted to test whether supplementation with Klotho may attenuate the development of sarcopenia."

The team first characterised and compared changes in the structure, function and gene activity in skeletal muscle across the lifespan in mice. They grouped mice into four age categories -- young, middle-aged, old and oldest-old -- and looked at muscle weight, type of muscle fibers, whether the muscles had accumulated fat, and skeletal muscle function. Although old mice displayed mild sarcopenia, the common clinical features of sarcopenia were only present in the oldest-old mice.

Next, they looked at changes in muscle gene activity and found a progressive disruption in genes known to be associated with the hallmarks of aging from the young to the oldest-old mice.

"To date, most studies in skeletal muscle have focused on the identification of specific pathways that are associated with sarcopenia to identify a molecular mechanism linked to the condition," explains co-first author Sruthi Sivakumar, Doctoral Student at the Department of Bioengineering, University of Pittsburgh. "We employed an integrative approach, where we created a network by converting gene expression levels to protein-protein interactions, and then we studied how this interaction network changed over time."

From this network, the team determined the 'network entropy' of the muscle cells as a means to estimate the loss of molecular order within the system over time. They found the greatest difference in order between the young and old age groups (at which point it reached maximal entropy), with little difference between the old and oldest-old mice. Additionally, when they looked at human muscle gene data from different age groups, they saw that entropy reached its lowest level in the fourth decade of life, after which time entropy escalated. This was of interest to the team as the fourth decade of life is the time point when sarcopenia often starts to develop.

Next, they looked at whether administering Klotho to mice would have beneficial effects on the muscle healing after injury. They found that applying Klotho after muscle injury reduced scarring and increased structures associated with force production in the animals. Injured mice that received Klotho also had better muscle function -- such as muscle twitch and force production -- and their whole-body endurance improved two-fold.

Finally, the team looked at whether giving the mice Klotho could reverse age-related declines in muscle quality and function. They found that Klotho administration led to some improvements in the old mice: force production was improved by 17% and endurance when supporting whole body weight was 60% greater compared to mice without treatment. But this was only seen in the old mice, and not in the oldest-old animals. Further investigation showed that Klotho affected genes associated with the hallmarks of aging in all age groups, but that the oldest-old mice showed a dysregulated gene response.

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Muscle cramp? Drink electrolytes, not water

 If you reach for water when a muscle cramp strikes, you might want to think again. New research from Edith Cowan University (ECU) has revealed drinking electrolytes instead of pure water can help prevent muscle cramps.

The study, published in the Journal of the International Society of Sports Nutrition, found that people who drank electrolyte enhanced water during and after exercise were less susceptible to muscle cramps than those who drank pure water.

Muscle cramps are a common painful condition affecting many people, including around 39 per cent of marathon runners, 52 per cent of rugby players and 60 per cent of cyclists.

Dilution solution

Lead researcher Professor Ken Nosaka, from ECU's School of Medical and Health Sciences, said the study builds on the evidence that a lack of electrolytes contributes to muscle cramps, not dehydration.

"Many people think dehydration causes muscle cramps and will drink pure water while exercising to prevent cramping," he said.

"We found that people who solely drink plain water before and after exercise could in fact be making them more prone to cramps.

"This is likely because pure water dilutes the electrolyte concentration in our bodies and doesn't replace what is lost during sweating."

When cramp strikes

Professor Nosaka began researching the causes of muscle cramps after regularly suffering from them while playing tennis.

The study involved 10 men who ran on a downhill treadmill in a hot (35ºC) room for 40 to 60 minutes to lose 1.5 to 2 per cent of their body weight through sweat in two conditions.

They drank plain water during and after exercise for one condition and took a water solution containing electrolytes in the other condition.

The participants were given an electrical stimulation on their calves to induce muscle cramp. The lower the frequency of the electrical stimulation required, the more the participant is prone to muscle cramp.

"We found that the electrical frequency required to induce cramp increased when people drank the electrolyte water, but decreased when they consumed plain water," said Professor Nosaka.

"This indicates that muscles become more prone to cramp by drinking plain water, but more immune to muscle cramp by drinking the electrolyte water."

Not all water is equal

Electrolytes are minerals including sodium, potassium, magnesium and chloride. They are essential for muscle health and help the body to absorb water.

Oral rehydration solutions contain electrolytes in specific proportions and can be made with water, salt and sugar. They are commonly found in supermarkets and pharmacies.

Professor Nosaka said electrolytes have many benefits for both athletes and the general population.

"Electrolytes are vital to good health -- they help the body to absorb water more effectively than plain water and replace essential minerals lost through sweat or illness," he said.

"People should consider drinking oral rehydration fluids instead of plain water during moderate to intense exercise, when it's very hot or when you are sick from diarrhoea or vomiting."

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One in five has a mutation that provides superior resilience to cold

 Almost one in five people lacks the protein α-actinin-3 in their muscle fibre. Researchers at Karolinska Institutet in Sweden now show that more of the skeletal muscle of these individuals comprises slow-twitch muscle fibres, which are more durable and energy-efficient and provide better tolerance to low temperatures than fast-twitch muscle fibres. The results are published in the scientific journal The American Journal of Human Genetics.

Skeletal muscle comprises fast-twitch (white) fibres that fatigue quickly and slow-twitch (red) fibres that are more resistant to fatigue. The protein α-actinin-3, which is found only in fast-twitch fibres, is absent in almost 20 per cent of people -- almost 1.5 billion individuals -- due to a mutation in the gene that codes for it. In evolutionary terms, the presence of the mutated gene increased when humans migrated from Africa to the colder climates of central and northern Europe.

"This suggests that people lacking α-actinin-3 are better at keeping warm and, energy-wise, at enduring a tougher climate, but there hasn't been any direct experimental evidence for this before," says Håkan Westerblad, professor of cellular muscle physiology at the Department of Physiology and Pharmacology, Karolinska Institutet. "We can now show that the loss of this protein gives a greater resilience to cold and we've also found a possible mechanism for this."

For the study, 42 healthy men between the ages of 18 and 40 were asked to sit in cold water (14 °C) until their body temperature had dropped to 35.5 °C. During cold water immersion, researchers measured muscle electrical activity with electromyography (EMG) and took muscle biopsies to study the protein content and fibre-type composition.

The results showed that the skeletal muscle of people lacking α-actinin-3 contains a larger proportion of slow-twitch fibres. On cooling, these individuals were able to maintain their body temperature in a more energy-efficient way. Rather than activating fast-twitch fibres, which results in overt shivering, they increased the activation of slow-twitch fibers that produce heat by increasing baseline contraction (tonus).

"The mutation probably gave an evolutionary advantage during the migration to a colder climate, but in today's modern society this energy-saving ability might instead increase the risk of diseases of affluence, which is something we now want to turn our attention to," says Professor Westerblad.

Another interesting question is how the lack of α-actinin-3 affects the body's response to physical exercise.

"People who lack α-actinin-3 rarely succeed in sports requiring strength and explosiveness, while a tendency towards greater capacity has been observed in these people in endurance sports," he explains.

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