Irregular sleep patterns linked to early muscle aging and reduced strength over time

Inside every muscle cell, there’s a clock. Not the kind that ticks on your wall or buzzes on your wrist, but a natural timekeeping system that helps your body stay in rhythm. This clock controls when muscle cells repair themselves, when they grow, and when they clear out broken proteins.

According to a new study from King’s College London, messing with this clock — as shift workers often do — might speed up muscle aging and reduce your strength over time.

Published in Proceedings of the National Academy of Sciences (PNAS), the research reveals that your muscle clock helps protect against a condition called sarcopenia. That’s the gradual loss of muscle strength and size that comes with aging. And the key takeaway? Staying up at night or frequently switching your sleep schedule could make that happen faster.

“We impaired the muscle clock function in zebrafish by overexpressing a malfunctioning clock protein,” explained lead author Jeffrey Kelu, a research associate at King’s College London. “We then monitored the fish for two years, comparing them to healthy controls.”

Zebrafish, often used in studies like these, share about 70% of their genes with humans. Their transparent bodies also make it easier to watch muscle changes under a microscope. And what scientists saw in those fish may reflect what happens in people who regularly disrupt their sleep-wake cycles.

Muscles work hard all day. When you walk, lift, or even just stretch, tiny tears and defects form in muscle fibers. At night, your muscle clock turns on a special process that helps clear out these damaged parts. This process, called protein turnover, uses systems like autophagy and the ubiquitin–proteasome system (UPS) to break down old proteins and make room for fresh ones.

But when this clock is broken or disturbed, that nightly cleanup doesn’t happen correctly.

The study showed that zebrafish with a disrupted muscle clock experienced poor protein turnover. At first, this didn’t seem to matter much. At six months and one year, their muscles looked normal compared to fish with working clocks. But by age two — a senior age for a fish — the differences were striking. The fish were shorter, weighed less, and swam slowly or not at all.

“These are hallmarks of sarcopenia and overall decline in mobility, which has been reported in shift workers,” Kelu said.

Even when these altered fish were raised in controlled environments with light and feeding cues (called "zeitgebers"), they still suffered long-term effects. Their muscles didn’t thrive with age, and their overall health declined more rapidly than the control group.

Circadian rhythm isn't just about sleep. It’s a 24-hour biological cycle that affects almost every part of the body, including the heart, metabolism, brain, and muscles.

In skeletal muscles, this rhythm controls a delicate balance between building new proteins (anabolism) and breaking down old ones (catabolism). When the rhythm is working, protein breakdown increases at night, which actually helps muscle growth.

However, in the study, disrupting this rhythm by blocking muscle clock genes caused the opposite effect. Growth happened during the night when it wasn’t supposed to, and nighttime muscle function was impaired. The root cause? A breakdown in the balance between two key clock proteins: Ror and Rev-erb. These proteins help regulate UPS and autophagy pathways.

Normally, Rev-erb and Ror work together to keep the process stable. But when the muscle clock fails, that balance is lost. This leads to reduced protein degradation at night, which causes damaged proteins to pile up in muscle cells.

Over time, this buildup reduces muscle performance and triggers sarcopenia-like changes, even in the absence of physical inactivity or poor diet.

“We recently showed that zebrafish display circadian variation in muscle growth rate, even in the absence of physical activity and feeding,” the paper noted. “A striking observation was that proteasome inhibition could enhance muscle growth specifically at night, but only if the circadian clock was unperturbed.”

The research carries major implications for real-world jobs. Around four million people in the UK work shifts, from doctors and nurses to factory workers and delivery drivers. Many have irregular schedules that keep them awake at night and asleep during the day — the opposite of what the body's natural clock expects.

“In the UK, approximately four million shift workers play a vital role in keeping businesses and emergency services operational around the clock,” Kelu said. “Our study provides further evidence that the disruption of circadian rhythms in shift workers compromises multiple aspects of health.”

In these workers, muscle clocks are repeatedly thrown off, causing long-term damage to how muscles repair and maintain themselves. Not only does this raise the risk for sarcopenia, but it may also contribute to broader aging issues like reduced mobility and higher injury risk.

Older adults already have weaker circadian rhythms, and this research suggests that further disruption — from poor sleep or late-night eating — could worsen their physical decline. Even dementia and other cognitive disorders have been linked to broken biological clocks, making circadian health a growing focus in aging research.

In fact, previous work in mice showed that deleting key circadian genes could mimic aging effects. In contrast, time-restricted feeding — limiting food to certain hours — extended lifespan in mice with intact clocks, but not in those with broken ones.

The findings from this study don’t just explain why disrupted rhythms harm muscle health. They also open the door to new kinds of treatments.

“Our findings highlight the possibility of using circadian biology to develop treatments aimed at preventing muscle decline in shift workers,” Kelu said. “Preclinical studies using drugs to modulate specific clock proteins are currently underway. This paves the way for future therapies that could improve ageing in shift workers.”

By targeting proteins like Ror and Rev-erb, scientists may one day restore balance to the muscle clock. In the lab, blocking the effects of Rev-erb returned muscle growth in zebrafish to normal, showing that this pathway is drug-sensitive. If these results hold true in humans, medications might help protect shift workers from the effects of long-term schedule changes.

Professor Simon Hughes, a co-author of the study, added: “This work shows how studying something as complicated as muscle growth in a simple system, like little fish larva, can really teach us something. Of course, someone then has to check if it’s also true in people — but at least the fish show us where to look.”

That next step, testing these findings in humans, is already in motion. Researchers believe that by understanding how the body’s internal clocks influence muscle function, they can design better strategies for healthy aging.

As research moves forward, the message becomes clearer: your body isn’t just paying attention to what you eat and how much you exercise. It also matters when you do it. Staying in sync with your internal clock could be just as important for your muscles as lifting weights or eating protein.

Note: The article above provided above by The Brighter Side of News.

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