South Korean researchers have identified a key protein that explains why exercise is less efficient with age and provides new hope for treating age-related decline in muscle and bone.
As we age, this protein called CLCF1 naturally decreases, but stimulation occurs during exercise in young people.
The study, published in Nature Communications, demonstrates how this single molecule coordinates the beneficial effects of physical activity on muscle strength and bone density. Scientists have found that restoring CLCF1 levels in older mice greatly improves their physical performance and bone health.
Disconnection of age movement
Exercise produces different results among young and older people, but so far, biological reasons are not clear. Dr. Yong Ryoul Yang of the Korean Institute of Biosciences and Biotechnology led a team that spotted spikes in CLCF1 levels immediately after exercise for young people, while older people need 12 weeks of ongoing training to see similar growth.
“This study lays the foundation for why exercise decreases with age,” Yang explained.
The protein acts as a molecular messenger, released by the muscle during physical activity to enhance muscle function and bone formation while inhibiting bone collapse.
Excellent recovery results
When researchers administered CLCF1 to elderly mice, the results were astonishing:
- Grip strength significantly increased within two weeks
- Running endurance increased by 70%
- Enlarge the size of muscle fibers without affecting the number of fibers
- Increased bone density while decreased fractured cells
- Glucose metabolism improves
Various mechanisms of action
Studies have shown that CLCF1 works through multiple pathways at the same time. In muscle, it enhances glucose uptake and powers the cellular energy plant of mitochondria. The protein also activates specific signaling molecules that promote muscle growth and repair.
For bones, CLCF1 exhibits a dual effect – it inhibits osteoclasts, which break down bone tissue while promoting osteoblasts, thus producing new bones. This coordinated approach addresses both sides of age-related bone loss.
Importantly, the team found that during exercise, bacteria produced smaller CLCF1 than the carbonate crystals produced by the chemically synthesized version. These microscopic crystals measure only 30.7 nanometers, while the artificial version of 61.1 nanometers produces denser and stronger bone structures.
Blocking research confirms importance
To confirm the important role of CLCF1, the researchers created a molecular blocker called ECNTFR that prevents proteins from working. When mice receive this blocker during exercise training, they lose all the typical benefits of physical exercise.
Exercise usually upregulates genes involved in energy metabolism and muscle function, but blockers completely eliminate these improvements. This clearly demonstrates that CLCF1 mediates the positive effects of exercise on musculoskeletal health.
Genetically modified mice show long-term benefits
Scientists also created transgenic mice that continuously produce elevated levels of CLCF1. Compared with normal mice, these animals showed excellent muscle function, enhanced grip, improved running ability, and increased bone mass.
Transgenic mice exhibit greater muscle fibers and better glucose tolerance, suggesting that maintaining high CLCF1 levels can provide sustained benefits for aging muscles and bones.
Clinical significance
These findings offer several potential treatments. CLCF1 levels in the blood can serve as a biomarker for monitoring exercise efficiency in older adults. More ambitious, CLCF1 supplements may help older people who are unable to strengthen their exercise due to physical limitations.
The study also shows that resistance training is particularly important for older people, as this type of exercise most effectively stimulates the production of CLCF1, even in aging muscles.
Currently, treatments for age-related muscle loss (sarcopenia) and skeletal weakness (osteoporosis) address these diseases separately. The ability of CLCF1 to simultaneously improve muscle and bone health may represent a significant advance in the treatment of musculoskeletal aging.
The study involved human participants in multiple cohorts and was supported by several Korean research bases, indicating strong institutional support in this study.
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