Muscle Fibrosis and Aging: Why Strength Fades and What Can Be Done
As we age, many people assume that weakness and muscle loss are inevitable. While some decline in strength is expected, much of what we attribute to “aging” is actually due to specific biological processes, particularly muscle fibrosis. Unlike muscle atrophy alone, fibrosis involves a shift in tissue architecture, replacing healthy muscle fibers with stiff, disorganized collagen. This change reduces mobility, strength, and responsiveness to exercise.
Understanding muscle fibrosis is key to reversing age-related declines in performance and function.
What Is Muscle Fibrosis?
Muscle fibrosis is the excessive accumulation of extracellular matrix (ECM), primarily collagen, within skeletal muscle. It is part of the natural response to injury, but with chronic inflammation or disuse, this process can become dysregulated. In aging muscle, fibroblasts become overactive, producing more matrix proteins than necessary.
This stiffens the tissue, restricts elasticity, and interferes with the satellite cells responsible for muscle repair. Over time, fibrosis contributes to:
- Loss of contractile force
- Reduced response to exercise
- Slower healing after injury
- Impaired mobility and joint function
What Causes Fibrosis in Aging Muscle?
Aging muscle is more vulnerable to fibrotic changes due to several overlapping factors:
- Chronic low-grade inflammation (inflammaging)
- Mitochondrial dysfunction and oxidative stress
- Reduced clearance of damaged proteins
- Altered growth factor signaling, especially involving TGF-β and PDGF
- Hormonal changes, including declines in testosterone and growth hormone
Clinical Implications
Fibrosis reduces the quality of aging muscle even in physically active individuals. Patients often present with:
- Persistent stiffness despite stretching or foam rolling
- Plateauing strength despite consistent training
- Limited range of motion after injury
- Poor recovery from surgery or disuse
Standard resistance training may not fully reverse these effects unless fibrosis is addressed directly.
Modern Strategies to Combat Fibrosis
At the Performance Medicine Institute, we implement a multi-pronged approach to slow or reverse muscle fibrosis:
- Progressive resistance training: with a focus on eccentric loading to stimulate remodeling
- Class IV laser and TECAR therapy: to modulate fibroblast activity and improve circulation
- Testosterone therapy or growth hormone secretagogues: to restore anabolic tone
- Anti-fibrotic supplements: such as curcumin, berberine, and omega-3 fatty acids
- Nutritional support: including amino acids and mitchondrial cofactors
- Regenerative therapies: PRP, shockwave, or BMAC when localized fibrosis is prominent
Fibrosis does not improve overnight. However, with consistent intervention, aging muscle can regain flexibility, strength, and resilience.
Our Approach
We start with a detailed functional assessment by testing not just muscle strength, but also passive and active range of motion, fascial compliance, and soft tissue density. When fibrosis is suspected, we tailor the treatment plan using advanced modalities in conjunction with guided exercise and metabolic support.
For patients recovering from injury or surgery, these strategies can significantly improve long-term outcomes and reduce re-injury risk.
Conclusion
Muscle weakness in aging is not just about losing mass. Fibrosis plays a major role in limiting performance and recovery. By targeting the biological pathways that lead to scarring, we can restore more youthful muscle function and help patients maintain an active lifestyle well into later decades. Contact Us today to learn more about our regenerative strategies for aging muscle.
References
Gumucio, J. P., Schonk, M. M., Kharaz, Y. A., Comerford, E., & Mendias, C. L. (2020). Scleraxis is required for the growth of adult tendons in response to mechanical loading. JCI Insight, 5(13), e138295.
Mendias, C. L., Enselman, E. R. S., Olszewski, A. M., Gumucio, J. P., Edon, D. L., Konnaris, M. A., … & Bedi, A. (2020). The use of recombinant human growth hormone to protect against muscle weakness in patients undergoing anterior cruciate ligament reconstruction: A pilot, randomized placebo-controlled trial. American Journal of Sports Medicine, 48(8), 1916–1928.
Gumucio, J. P., Flood, M. D., Bedi, A., Kramer, H. F., Russell, A. J., & Mendias, C. L. (2017). Inhibition of prolyl 4-hydroxylase decreases muscle fibrosis following chronic rotator cuff tear. Bone & Joint Research, 6(1), 57–65.