How do our bodies remember?

MIT Technology Review Explains: Let our writers untangle the complex, messy world of technology to help you understand what’s coming next. You can read more from the series here.

“Like riding a bike” is shorthand for the remarkable way that our bodies remember how to move. Most of the time when we talk about muscle memory, we’re not talking about the muscles themselves but about the memory of a coordinated movement pattern that lives in the motor neurons, which control our muscles. 

Yet in recent years, scientists have discovered that our muscles themselves have a memory for movement and exercise.

When we move a muscle, the movement may appear to begin and end, but all these little changes are actually continuing to happen inside our muscle cells. And the more we move, as with riding a bike or other kinds of exercise, the more those cells begin to make a memory of that exercise.

When we move a muscle, the movement may appear to begin and end, but all these little changes are actually continuing to happen inside our muscle cells.

We all know from experience that a muscle gets bigger and stronger with repeated work. As the pioneering muscle scientist Adam Sharples—a professor at the Norwegian School of Sport Sciences in Oslo and a former professional rugby player in the UK—explained to me, skeletal muscle cells are unique in the human body: They’re long and skinny, like fibers, and have multiple nuclei. The fibers grow larger not by dividing but by recruiting muscle satellite cells—stem cells specific to muscle that are dormant until activated in response to stress or injury—to contribute their own nuclei and support muscle growth and regeneration. Those nuclei often stick around for a while in the muscle fibers, even after periods of inactivity, and there is evidence that they may help accelerate the return to growth once you start training again. 

Sharples’s research focuses on what’s called epigenetic muscle memory. “Epigenetic” refers to changes in gene expression that are caused by behavior and environment—the genes themselves don’t change, but the way they work does. In general, exercise switches on genes that help make muscles grow more easily. When you lift weights, for example, small molecules called methyl groups detach from the outside of certain genes, making them more likely to turn on and produce proteins that affect muscle growth (also known as hypertrophy). Those changes persist; if you start lifting weights again, you’ll add muscle mass more quickly than before.

In 2018, Sharples’s muscle lab was the first to show that human skeletal muscle has an epigenetic memory of muscle growth after exercise: Muscle cells are primed to respond more rapidly to exercise in the future, even after a monthslong (and maybe even yearslong) pause. In other words: Your muscles remember how to do it.

Subsequent studies from Sharples and others have replicated similar findings in mice and older humans, offering further supporting evidence of epigenetic muscle memory across species and into later life. Even aging muscles have the capacity to remember when you work out.

At the same time, Sharples points to intriguing new evidence that muscles also remember periods of atrophy—and that young and old muscles remember this differently. While young human muscle seems to have what he calls a “positive” memory of wasting—“in that it recovers well after a first period of atrophy and doesn’t experience greater loss in a repeated atrophy period,” he explains—aged muscle in rats seems to have a more pronounced “negative” memory of atrophy, in which it appears “more susceptible to greater loss and a more exaggerated molecular response when muscle wasting is repeated.” Basically, young muscle tends to bounce back from periods of muscle loss—“ignoring” it, in a sense—while older muscle is more sensitive to it and might be more susceptible to further loss in the future. 

Illness can also lead to this kind of “negative” muscle memory; in a study of breast cancer survivors more than a decade after diagnosis and treatment, participants showed an epigenetic muscle profile of people much older than their chronological age. But get this: After five months of aerobic exercise training, participants were able to reset the epigenetic profile of their muscle back toward that of muscle seen in an age-matched control group of healthy women.  

What this shows is that “positive” muscle memories can help counteract “negative” ones. The takeaway? Your muscles have their own kind of intelligence. The more you use them, the more they can harness it to become a lasting beneficial resource for your body in the future. 

Bonnie Tsui is the author of On Muscle: The Stuff That Moves Us and Why It Matters (Algonquin Books, 2025).

Trump is pushing leucovorin as a new treatment for autism. What is it?

MIT Technology Review Explains: Let our writers untangle the complex, messy world of technology to help you understand what’s coming next. You can read more from the series here.

At a press conference on Monday, President Trump announced that his administration was taking action to address “the meteoric rise in autism.” He suggested that childhood vaccines and acetaminophen, the active ingredient in Tylenol, are to blame for the increasing prevalence and advised pregnant women against taking the medicine. “Don’t take Tylenol,” he said. “Fight like hell not to take it.” 

The president’s  assertions left many scientists and health officials perplexed and dismayed. The notion that childhood vaccines cause autism has been thoroughly debunked. 

“There have been many, many studies across many, many children that have led science to rule out vaccines as a significant causal factor in autism,” says James McPartland, a child psychologist and director of the Yale Center for Brain and Mind Health in New Haven, Connecticut.

And although some studies suggest a link between Tylenol and autism, the most rigorous have failed to find a connection. 

The administration also announced that the Food and Drug Administration would work to make a medication called leucovorin available as a treatment for children with autism. Some small studies do suggest the drug has promise, but “those are some of the most preliminary treatment studies that we have,” says Matthew Lerner, a psychologist at Drexel University’s A.J. Drexel Autism Institute in Philadelphia. “This is not one I would say that the research suggests is ready for fast-tracking.” 

The press conference “alarms us researchers who committed our entire careers to better understanding autism,” said the Coalition for Autism Researchers, a group of more than 250 scientists, in a statement.

“The data cited do not support the claim that Tylenol causes autism and leucovorin is a cure, and only stoke fear and falsely suggest hope when there is no simple answer.”

There’s a lot to unpack here. Let’s begin. 

Has there been a “meteoric rise” in autism?

Not in the way the president meant. Sure, the prevalence of autism has grown, from about 1 in 500 children in 1995 to 1 in 31 today. But that’s due, in large part, to diagnostic changes. The latest iteration of the Diagnostic and Statistical Manual of Mental Illnesses, published in 2013, grouped five previously separate diagnoses into a single diagnosis of autism spectrum disorder (ASD).

That meant that more people met the criteria for an autism diagnosis. Lerner points out that there is also far more awareness of the condition today than there was several decades ago. “There’s autism representation in the media,” he says. “There are plenty of famous people in the news and finance and in business and in Hollywood who are publicly, openly autistic.”

Is Tylenol a contributor to autism? 

Some studies have found an association between the use of acetaminophen in pregnancy and autism in children. In these studies, researchers asked women about past acetaminophen use during pregnancy and then assessed whether children of the women who took the medicine were more likely to develop autism than children of women who didn’t take it. 

These kinds of epidemiological studies are tricky to interpret because they’re prone to bias. For example, women who take acetaminophen during pregnancy may do so because they have an infection, a fever, or an autoimmune disease.

“Many of these underlying reasons could themselves be causes of autism,” says Ian Douglas, an epidemiologist at the London School of Hygiene and Tropical Medicine. It’s also possible women with a higher genetic predisposition for autism have other medical conditions that make them more likely to take acetaminophen. 

Two studies attempted to account for these potential biases by looking at siblings whose mothers had used acetaminophen during only one of the pregnancies. The largest is a 2024 study that looked at nearly 2.5 million children born between 1915 and 2019 in Sweden. The researchers initially found a slightly increased risk of autism and ADHD in children of the women who took acetaminophen, but when they conducted a sibling analysis, the association disappeared.  

Rather, scientists have long known that autism is largely genetic. Twin studies suggest that 60% to 90% of autism risk can be attributed to your genes. However, environmental factors appear to play a role too. That “doesn’t necessarily mean toxins in the environment,” Lerner says. In fact, one of the strongest environmental predictors of autism is paternal age. Autism rates seem to be higher when a child’s father is older than 40.

So should someone who is pregnant  avoid Tylenol just to be safe?

No. Acetaminophen is the only over-the-counter pain reliever that is deemed safe to take during pregnancy, and women should take it if they need it. The American College of Obstetricians and Gynecologists (ACOG) supports the use of acetaminophen in pregnancy “when taken as needed, in moderation, and after consultation with a doctor.” 

“There’s no downside in not taking it,” Trump said at the press conference. But high fevers during pregnancy can be dangerous. “The conditions people use acetaminophen to treat during pregnancy are far more dangerous than any theoretical risks and can create severe morbidity and mortality for the pregnant person and the fetus,” ACOG president Steven Fleischman said in a statement.

What about this new treatment for autism? Does it work? 

The medication is called leucovorin. It’s also known as folinic acid; like folic acid, it’s a form of folate, a B vitamin found in leafy greens and legumes. The drug has been used for years to counteract the side effects of some cancer medications and as a treatment for anemia. 

Researchers have known for decades that folate plays a key role in the fetal development of the brain and spine. Women who don’t get enough folate during pregnancy have a greater risk of having babies with neural tube defects like spina bifida. Because of this, many foods are fortified with folic acid, and the CDC recommends that women take folic acid supplements during pregnancy. “If you are pregnant and you’re taking maternal prenatal vitamins, there’s a good chance it has folate already,” Lerner says.

“The idea that a significant proportion of autistic people have autism because of folate-related difficulties is not a well established or widely accepted premise,” says McPartland.

However, in the early 2000s, researchers in Germany identified a small group of children who developed neurodevelopmental symptoms because of a folate deficiency. “These kids are born pretty normal at birth,” says Edward Quadros, a biologist at SUNY Downstate Health Sciences University in Brooklyn, New York. But after a year or two, “they start developing a neurologic presentation very similar to autism,” he says. When the researchers gave these children folinic acid, some of their symptoms improved, especially in children younger than six. 

Because the children had low levels of folate in the fluid that surrounds the spine and brain but normal folate levels in the blood, the researchers posited that the problem was the transport of folate from the blood to that fluid. Research by Quadros and other scientists suggested that the deficiency was the result of an autoimmune response. Children develop antibodies against the receptors that help transport folate, and those antibodies block folate from crossing the blood-brain barrier. High doses of folinic acid, however, activate a second transporter that allows folate in, Quadros says. 

There are also plenty of individual anecdotes suggesting that leucovorin works. But the medicine has only been tested as a treatment for autism in four small trials that used different doses and measured different outcomes. The evidence that it can improve symptoms of autism is “weak,” according to the Coalition of Autism Scientists. “A much higher standard of science would be needed to determine if leucovorin is an effective and safe treatment for autism,” the researchers said in a statement.