Musculoskeletal fibroaging is the term Dr. Scott King uses for a pattern he sees in practice: muscle and fascia become stiffer and less mobile as connective-tissue changes accumulate over time. It is a clinical framework, not a formal medical diagnosis. The question it asks is whether part of what we call "getting older" is a measurable loss of tissue motion that can sometimes be changed.
The pattern Dr. King describes
Healthy fascia and muscle glide against each other in organized, parallel fiber patterns. When an area is injured, overused, or under-moved for long enough, the body can lay down repair tissue in a disorganized crosshatch instead. In Dr. King's framework, each later cycle of minor strain and incomplete repair adds another layer. Over years, that can build into dense, restricted tissue: a slow accumulation, not a single event. Patients and providers often write it off as an inevitable part of aging. Dr. King examines for it as adhesion, something that can be found by hand and often treated.
What the research establishes
The term comes from research on aging and fibrosis. A 2021 review in Ageing Research Reviews named "fibroageing" as the general tendency toward fibrosis that comes with an aging extracellular matrix. The same mechanism is implicated in age-related fibrosis of the lungs, liver, kidneys, and heart. Harvard Stem Cell Institute runs a dedicated Aging & Fibrosis research initiative, the Harvard Fibrosis Network, which brings investigators together across organs to find what fibrotic disease has in common as the body ages. This is an active, cross-disciplinary research area, not a fringe idea.
The 2021 review describes how extracellular matrix molecules stiffen with age through glycation and crosslinking. That stiffness then activates further fibrotic signaling. The result is a self-reinforcing loop tied to cellular senescence, the senescence-associated secretory phenotype (SASP), and YAP/TAZ mechanotransduction. The authors note this loop helps explain why fibrosis becomes far more common with age across organs. Idiopathic pulmonary fibrosis, for example, is uncommon before 50 and rises sharply after 60.
Muscle has its own version of this mechanism. A January 2026 review in Frontiers in Immunology describes how reactive oxygen species upregulate TGF-β1 signaling. That drives fibro-adipogenic progenitor cells (FAPs) to become myofibroblasts, the cells responsible for excess collagen deposition in muscle. As the matrix stiffens from that collagen, the stiffness triggers further fibrotic signaling.
Senescent cells add to it. A March 2026 paper in Endocrinology and Metabolism found that senescent fibro-adipogenic progenitors secrete TGF-β as part of their SASP. That stimulates both the cells themselves and neighboring fibroblasts to overproduce collagen, which aggravates fibrosis. We cover this in more detail in our post on shockwave therapy and cellular aging.
Where the framework and the research meet
The research above describes fibrosis in organs and in muscle. "Musculoskeletal fibroaging" applies it to muscle and fascia. Dr. King's hypothesis is that the same stiffening loop contributes to the adhesion he finds on exam. Muscle and fascia are loaded every day and are rarely examined closely enough to catch these changes early. Unlike organ fibrosis, they can be reached directly with hands-on and device-assisted treatment. That link is a reasonable inference from the research. It has not been directly tested.
How common is age-related stiffness?
Stiffness affects most adults at every age and gets worse after 60. A 2021 study in Musculoskeletal Care measured stiffness in 282 healthy adults with no rheumatological diagnosis. Over half reported at least some stiffness in every age group. Adults 60 and older scored nearly double the overall median and were the only group to report meaningful physical or functional impact.
Dr. King reads that gap as consistent with his framework: stiffness that starts as an occasional nuisance becomes a functional problem once tissue changes have had years to build. The study measured stiffness, not adhesion, so it cannot show what causes it.
Is fibroaging the same as normal aging?
In Dr. King's framework, no. He treats fibroaging as a process that correlates with age, not an unavoidable consequence of it. That changes what a patient does about it. "Normal aging" is something to accept or work around. Adhesion can be found by hand and treated with the same soft-tissue and shockwave-based therapies used at any age. Two people the same age can have very different tissue depending on injury history, activity, and how much adhesion was treated or left to accumulate.
What are the signs?
The clearest signs are stiffness that is worse first thing in the morning or after sitting, and a gradual loss of range of motion in the same one or two areas over months or years. The tissue feels dense, ropey, or "stuck" when pressed, not just sore. Patients often describe an area that "never quite loosens up anymore" after a warmup, or pain during activities that used to feel fine. Because it builds slowly, it is easy to blame on age instead of the palpable adhesion that may be involved. A hands-on exam tells you more than an assumption about getting older.
Can fibroaging be treated?
In Dr. King's experience, often yes. The tissue does not become untreatable with time. It means addressing years of accumulated adhesion instead of one recent strain. Dr. King combines manual soft-tissue work with device-assisted therapy, including EMTT for deeper, harder-to-reach adhesion, and shockwave therapy. Recent laboratory research suggests shockwave can reduce cellular senescence markers. Whether it does so in human muscle and fascia has not been shown. The Musculoskeletal Fibroaging section of our adhesion page explains how this fits into Dr. King's broader framework.
Getting evaluated in Centennial
If stiffness in the same area has been building for years, it is worth a hands-on exam before you put it down to age. Dr. King's Centennial clinic, serving the Denver Tech Center, examines which tissue is restricted and which is simply older, and treats the adhesion that is present. Book a New Patient Exam.
Sources
- 2021 review in Ageing Research Reviews naming "fibroageing." (link)
- Harvard Stem Cell Institute's Aging & Fibrosis research initiative. (link)
- 2021 study in Musculoskeletal Care measuring stiffness in 282 healthy adults. (link)
- Review in Frontiers in Immunology (January 2026). (link)
- Paper in Endocrinology and Metabolism (March 2026) on senescent fibro-adipogenic progenitors. (link)
