Backpack massages muscles when it detects they’re fatigued

Someone wearing the backpack while lifting dumbbells and recovering
People wore the backpack while lifting dumbbells and then enjoyed a nice massage
Huang et al., 2026, Cell Reports Physical Science

A backpack can detect when muscles become fatigued and automatically massage the affected areas. This seems to help muscles recover better than heat therapy or pre-programmed massages, like those delivered by chairs and cushions.

About 1 in 6 adults in the UK have some form of back pain. This can occur when back muscles become fatigued through exertion or prolonged or repetitive activity. Persistent fatigue can impair local blood flow and tissue recovery, potentially contributing to chronic pain.


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Tired back muscles can be relieved through heat therapy and automated massage, which often involves rollers moving across the back in pre-programmed patterns. But these tend to be standardised treatments that don’t take into account people’s individual muscular issues, says Chengsong Yu at the Wuhan Institute of Technology in China.

Looking for a more bespoke approach, Yu and his colleagues have developed a wearable system, like a backpack, that uses electrodes on the skin to monitor electrical activity in four groups of back muscles. The system then determines which muscles are fatigued, and how much. Cables move a soft massage head to the affected areas, where sensor feedback allows the system to continually adjust the force according to the fatigue levels, says Yu.

To test their device, the researchers asked 11 men and four women, aged 20 to 26, with no known health issues, to spend 2 minutes resting, followed by 2 minutes repeatedly lifting dumbbells while seated. This induces fatigue in the rhomboids, the muscles between the shoulder blades.

All the participants wore the backpack during the dumbbell exercise so it could record their muscles’ electrical activity, but only some then received the backpack’s massage. The remaining participants divided into groups that received another type of pre-programmed massage, had heat therapy or rested.

During the exercise, the electrical activity in the participants’ rhomboids fell as the muscles became fatigued, indicating weaker muscle activation. But after the backpack treatment, this activity was about 2.6 times higher compared with after the pre-programmed massage, indicating greater recovery. It was also about 1.9 times higher than after heat treatment, and four times higher than after resting.

“We were encouraged by how clearly the adaptive system improved muscle recovery compared with preprogrammed mechanostimulation and thermal stimulation,” says Yu.

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Conor Walsh at Harvard University says the device is a move in a “creative direction” for combining soft robotics with mechanical therapy to address back pain and muscle fatigue. But it needs to be lighter and less bulky before it can become a practical solution, he says.

“There are definitely some very interesting engineering features in the system, and I see a lot of value in this as a proof of concept for this technology,” says Olivier Lambercy at ETH Zurich in Switzerland. “But if you want to use it in the context of people working on the assembly line as they claim, I think this is a bit far into the future.”  

The team hopes to make the design smaller and more compact, and to test it in a larger group of people working in real-world conditions that may cause back pain, says Yu.

Journal Reference:

Cell Reports Physical Science
DOI: 10.1016/j.xcrp.2026.103505

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Severe meningitis outbreak caused by bacteria that took genes from microbiome

A student being vaccinated against meningitis at the University of Kent on 18 March 2026
A student being vaccinated against meningitis at the University of Kent on 18 March 2026
Victoria Jones/Shutterstock

A severe outbreak of invasive meningococcal disease, which can cause meningitis and sepsis, in Kent earlier this year was driven by a strain of bacteria that took genes from harmless microbes. This helped the bacteria evade the immune system and obtain iron from blood, boosting their growth.

“What was really unusual about the outbreak is quite how explosive it was,” says Emma Wall at Queen Mary University of London, who wasn’t involved in the discovery. “[The bacterium] clearly gained a set of genetic changes that made it better at hiding from the immune system and better at harvesting nutrients. That made it a really super powerful bug.”


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In March, 21 people – mostly university or high school students – are known to have become infected with a strain of the bacteria Neisseria meningitidis group B at a nightclub in Canterbury, Kent in the UK. N. meningitidis usually spreads via close and prolonged contact with saliva from an infected person via things like kissing and sharing drinks or vapes.

N. meningitidis lives harmlessly in the nose and throat of between 5 and 10 per cent of people without health problems, but genetic changes can cause it to become more invasive and enter the bloodstream, leading to invasive meningococcal disease (IMD). This can cause sepsis, a life-threatening immune reaction to the bacteria, or meningitis, where bacteria infect the thin lining surrounding the brain and spinal cord, causing inflammation.

All the IMD cases in Kent occurred within about a week. They were treated in hospital, with nine requiring intensive care. “The incredibly rapid nature of the outbreak was unprecedented [for the UK],” says Wall. “Usually these [outbreaks] roll over two or three weeks and there’s one or two cases that end up in hospital.”

To understand this, Martin Maiden at the University of Oxford and his colleagues sequenced the entire genome of live N. meningitidis in blood samples taken from six of the cases, including the two people who died.

The bacterial genomes from the six cases were almost identical, suggesting the outbreak started from one person. Next, the team compared one of these genomes with 48,000 others from Neisseria strains collected during prior outbreaks or from people without known health problems.

This revealed that the Kent strain had acquired several genes from a harmless strain of Neisseria meningitidis and another bacterium that lives harmlessly in up to 28 per cent of adults, called Neisseria cinerea. Bacteria constantly carry out such genetic exchanges via a process called horizontal transfer, which can involve them forming tiny tunnels between each other, through which they transfer copies of genes.

Some of the genes acquired by the Kent strain enhanced its uptake of iron from blood, which it needs to survive and replicate. Others reduced the amount of sugar that was coating a tail-like structure, called the pilus, on the bacteria. This enabled them to clump together and evade destruction by immune cells, such as neutrophils. “Neutrophils will try and come and eat an individual bacteria, but they can’t eat a clump; it’s too big,” says Wall.

“There was this catalogue of changes that made this organism really transmissible, but also really invasive,” says Maiden. This meant that several people became very ill and were then less able to transmit the infection to the public. “If you’re ill, you’re not going to be going around transmitting organisms, so the outbreak ended very quickly,” says Maiden.

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It’s unclear when exactly these genetic changes occurred in the person who is thought to have initiated the outbreak, but they probably happened gradually, until there was the right combination of genetics and social mixing, says Maiden.

Such insights could support the development of better vaccines against N. meningitidis if we can target the features that make the bacteria particularly invasive, says Wall. But they won’t help us predict the next highly invasive strain. “[These bacteria are] inherently highly unpredictable,” says Maiden.

Following the Kent outbreak, the UK government launched a menB vaccination programme for young people starting university or further education in September or October this year. Symptoms of IMD include fever, headache, a stiff neck, joint and muscle pain, and a rash that doesn’t fade when pressed with glass.

Reference:

bioRxiv
DOI: 10.64898/2026.09.17.752363

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Why it is time to restate the case for the importance of research on animals

Pete Ryan

All of a sudden, governments have begun to talk about something that once seemed impossible: the end of animal testing. Last year, the US and the UK both unveiled road maps intended to help move us towards this goal. A few months ago, the European Commission did likewise. The coming of age of technological alternatives to some kinds of animal research is to be celebrated. A few of these alternatives are actually more revealing than the animal experiments they replace. But if nations overstate what is possible, they risk reigniting a heated and painful row.

We see this overstatement not only in news headlines, but even in the titles of policy documents themselves. Some of these talk of “phasing out” animal testing, when the truth is that animal testing cannot and will not be ended entirely.

Some scientists had their property set on fire. Molotov cocktails were used

There will always be a need for certain kinds of animal research to ask fundamental biological questions and ensure drug safety. This means that, while pursuing the reduction in animal tests as far as possible, we simultaneously need to be restating the case for why animal testing is so important.

To see what happens if we don’t, look back to the late 20th and early 21st centuries, when extreme animal rights activists violently harassed and intimated scientists. Some researchers had their property set on fire. Molotov cocktails were used. National newspapers reported on calls to murder those carrying out animal experiments.

If we send out the message that animal testing can be phased out, we risk painting the scientists who continue it as wilfully causing harm to animals. Such a misunderstanding could take us back to those dark and violent times, while prematurely abandoning the kinds of animal tests for which there are no reliable alternatives would risk our health and safety.

So let’s be clear-eyed. The push to reduce animal testing where safe and possible is truly welcome. But the end of animal testing as a whole remains impossible.

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