Ageing Muscles May Sacrifice Strength To Prevent Cell Damage, Study Reveals

Scientists uncover how cardiolipin affects muscle ageing and discover a protective mechanism that could open new avenues for treating age-related muscle loss.

Scientists have identified a protective mechanism involving cardiolipin that may explain why muscles change as they age

Source : ABPLIVE AI

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Key points generated by AI, verified by newsroom

• Scientists linked cardiolipin molecule to age-related muscle decline.
• Lowered cardiolipin triggers a protective muscle fiber switch.
• Restoring cardiolipin levels reversed muscle wasting in mice.
• Research suggests new treatments for age-related muscle loss.

Muscles naturally lose strength as people age, but scientists have discovered that this decline may involve an unexpected protective response. A new study by the University of Copenhagen has identified a key molecule linked to muscle ageing and found that restoring some of its levels reversed signs of muscle wasting in mice. The findings could help researchers develop future treatments for age-related muscle decline, although further studies are needed to establish whether the approach works in humans.

Why Ageing Muscles Change Their Fibre Type

Muscles contain different types of fibres that serve distinct purposes. Fast-twitch fibres generate powerful, rapid movements but tire quickly, while slow-twitch fibres support sustained activity and rely heavily on mitochondria, the structures responsible for producing energy within cells.

As people age, mitochondrial function becomes less efficient and muscle strength declines. Yet ageing muscles tend to develop a higher proportion of slow-twitch fibres. Researchers have also observed similar changes in conditions associated with muscle wasting.

To understand this apparent contradiction, the scientists examined cardiolipin, a specialised fat molecule found mainly in the inner membrane of mitochondria. It helps maintain their structure and supports the processes needed for normal cellular function.

The study found that cardiolipin levels declined in the muscle mitochondria of ageing or diseased mice and humans. To investigate its role, researchers reduced the molecule's levels in young mice. Their muscles subsequently showed a shift from fast-twitch to slow-twitch fibres, resembling changes seen during ageing.

Restoring cardiolipin to around two-thirds of its normal concentration began reversing muscle wasting and prevented premature deaths in the affected mice.

How Muscles Trade Strength For Protection

Further experiments suggested that the shift towards slow-twitch fibres serves a protective purpose rather than simply reflecting declining muscle function.

When cardiolipin levels fall, damaged mitochondria produce increased amounts of reactive oxygen species (ROS). Although these molecules can damage cellular structures, they also act as signals that alert cells to stress.

Researchers found that ROS helped trigger the change in muscle fibre type. Reducing ROS with antioxidants made the transition less pronounced in muscle cells lacking cardiolipin. The team also identified ERRγ, a protein that helps coordinate mitochondrial changes and muscle fibre adaptation. Inhibiting this protein in laboratory-grown muscle cells stopped the transition.

The researchers then investigated how these changes helped muscles cope with stress. Mice with insufficient cardiolipin absorbed more glucose from their bloodstream, but the additional sugar was not used primarily to generate energy. Instead, experiments using specially labelled glucose showed that muscle cells redirected it towards producing their own antioxidants, helping protect against excess ROS.

"The fiber switch is not the muscle failing, but the muscle trading power for protection. That's also why interfering with it can backfire: when we gave the mice antioxidants to mop up the ROS, their muscles fared worse, not better," says Assistant Professor Fabian Finger, first and co-corresponding author, from the University of Copenhagen.

Could The Discovery Lead To New Treatments?

The findings could point towards new approaches to age-related muscle wasting, but the researchers have yet to establish whether the same interventions can reverse muscle loss in humans. The experiments examining the protective mechanism and restoring muscle function were conducted in mice, while human samples were used to confirm the decline in cardiolipin levels with age.

Researchers already have ways to influence this molecule. The US Food and Drug Administration recently granted accelerated approval to elamipretide, a medication designed to help stabilise cardiolipin, for Barth syndrome, a rare inherited disorder. However, its effectiveness against ordinary age-related muscle loss remains unknown.

ERRγ could offer another avenue for investigation. The protein belongs to the nuclear receptor family, whose members are established targets for many medicines. Drugs that activate ERRγ are also being studied in preclinical research for other medical applications.

Future treatments could therefore focus on restoring cardiolipin or influencing the muscle's protective response through ERRγ.

"What encourages me most is that even a partial recovery of cardiolipin was enough to bring the muscle back. The question now is whether we can increase cardiolipin in aging muscle or target ERRγ to promote healthy adaptations. This is where the therapeutic potential lies," says senior author Zachary Gerhart-Hines, Associate Professor at the NNF Centre for Basic Metabolic Research, University of Copenhagen.

For now, the research offers a new perspective on muscle ageing: some changes that reduce strength may also help protect cells from further damage. Whether scientists can use this mechanism to preserve muscle strength in older people remains an important question for future research.

[Disclaimer: The information provided in the article is intended for general informational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified healthcare provider with any questions you may have regarding a medical condition.]

(With inputs from ANI)

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