Can Muscle Fibrosis Persist After a Strain?

Yes. After a significant or repeated muscle injury, excess extracellular matrix and collagen can persist instead of remodeling back toward normal muscle architecture. But fibrotic scar tissue is not necessarily biologically inert. Experimental studies show that mechanical interventions can reduce collagen deposition, suppress profibrotic signaling and increase matrix remodeling. Shockwave and manual mechanical therapies have both produced antifibrotic effects in experimental models. The strongest evidence is currently mechanistic and preclinical, but it establishes an important principle: abnormal connective tissue can change.

That matters clinically because a healed muscle injury may leave behind excess extracellular matrix that changes tissue mechanics and load tolerance. Treatment should therefore focus on restoring motion, tissue quality and load capacity rather than assuming an old scar is permanent.

A note on terms. In this article, "fibrosis" refers to excessive extracellular-matrix and collagen deposition documented in the scientific literature. Clinicians often use the term "adhesion" to describe the mechanically restricted tissue that can result from abnormal connective-tissue remodeling. The two terms overlap, but not every clinically restricted area has been confirmed as fibrosis on a biopsy.

What Happens After a Muscle Strain?

Muscle healing is not simply scar formation. Regenerating muscle fibers and extracellular matrix remodel together, and appropriately timed mechanical loading helps restore tissue architecture.

Skeletal muscle has a strong capacity to regenerate. A review of the basic mechanisms describes three overlapping phases: an inflammatory phase in which macrophages clear necrotic debris and help promote repair, activation and differentiation of satellite cells (the muscle's resident stem cells), and growth and remodeling of the regenerated tissue (Ciciliot, 2010). New fibers initially carry their nuclei in a central position, and a 2023 review pointed out how little is still known about how these regenerating fibers mature back into normal-sized fibers (Pizza, 2023).

In practical terms, healing normally includes:

• inflammation and clearance of damaged tissue
• satellite-cell activation
• formation and maturation of new muscle fibers
• remodeling of the extracellular matrix that surrounds and connects them

Some collagen deposition is a normal part of this process. Not all post-injury scar is pathologic fibrosis.

What Is Muscle Fibrosis?

Fibrosis is excessive extracellular-matrix deposition that persists instead of remodeling normally. In severe or repeatedly injured muscle, fibrotic tissue can interfere with normal regeneration and function.

Reviews consistently define skeletal-muscle fibrosis as excessive deposition of extracellular matrix (Dewi, 2025; Gong, 2026). A review focused on acute muscle injury explained that minor injuries can regenerate completely, but in severe injuries fibrous scar can prevent the muscle from recovering its full functional capacity, alter normal tissue biomechanics and create an environment associated with pain (Gardner, 2020). Another review noted that scarred fibrotic tissue impedes local function and may be associated with abnormal pain conduction or reinjury (Sheets, 2022).

Potential consequences include:

• impaired regeneration
• altered mechanical properties of the muscle
• reduced extensibility
• impaired contractile function
• possible susceptibility to reinjury

These reviews also acknowledge a gap: treatments for existing fibrous scar are still not well established, and translating laboratory findings into consistent clinical results remains challenging (Sheets, 2022; Dewi, 2025). That is the honest context for the evidence below.

What Drives Fibrosis?

At the molecular level, TGF-β/Smad signaling is one of the major pathways driving excessive extracellular-matrix deposition after muscle injury. A review of strategies for preventing fibrosis after injury described TGF-β1 as the primary pro-fibrogenic growth factor in this setting (Garg, 2015). A 2026 review described the TGF-β/Smad pathway as a central driver of fibrosis that promotes differentiation of fibro/adipogenic progenitors (FAPs) into collagen-producing myofibroblasts, with mechanical signaling through YAP/TAZ amplifying the response (Gong, 2026).

Fibro/adipogenic progenitor cells help coordinate normal repair, but persistent activation can contribute to excessive matrix deposition and fibrosis. Inflammation, oxidative stress and other regulatory pathways also contribute.

This biology is useful for understanding why some injuries heal well and others do not. It is not something measured in a clinic visit. Novo does not test TGF-β levels, and the exam focuses on how the tissue moves and tolerates load.

Is Fibrosis Permanent?

Fibrosis is not necessarily a permanent inert scar. Extracellular matrix remains biologically active and can remodel in response to mechanical and biochemical signaling. Both shockwave and manual mechanical therapies have demonstrated antifibrotic effects in experimental models, including reductions in collagen deposition and TGF-β-related signaling.

It is important to separate two kinds of evidence. Biological and histologic evidence shows what happens to collagen, signaling molecules and cells in animal models or cell cultures. Human clinical outcome evidence shows whether people have less pain and better function. The first is currently stronger for fibrosis itself. The second is growing but rarely includes biopsies.

Manual Therapy and Fibrosis: What the Studies Show

Mechanical manual therapy can influence connective-tissue biology. The most direct evidence comes from a rat model of repetitive overuse injury developed to study work-related musculoskeletal disorders.

• Fibrosis reduction. Rats performed a high-repetition, high-force task for 12 weeks, and one group received modeled manual therapy five days a week during that period. In a repetitive-overuse model, modeled manual therapy significantly reduced collagen and TGF-β1 deposition in fibrotic connective tissues while improving strength and function. Treated animals also showed fewer discomfort-related behaviors and better task performance (Bove, 2016).
• Prevention across tissues. Related work found that manual therapy prevented the accumulation of procollagen I and other fibrogenic changes in muscle, tendon and nerve during repetitive overuse. In that study, skin rolling, muscle mobilization and traction three times a week also prevented increases in inflammatory and fibrogenic macrophages, extraneural fibrosis and sensorimotor decline (Barbe, 2021a).
• Blunt muscle trauma. In a blunt-trauma skeletal-muscle fibrosis model, massage-based mechanical treatment reduced collagen accumulation, while combination therapy further suppressed TGF-β1/CTGF signaling and normalized matrix-remodeling pathways. The study compared massage, electroacupuncture and the two combined. Massage alone lowered collagen-fiber content, and the combination produced the largest effect, so the molecular findings should not be attributed to massage alone (Zhao, 2021).
• Human muscle biopsies. Human biopsy research confirms that massage is not biologically inert. Mechanical treatment activates mechanotransduction pathways and alters inflammatory and regenerative signaling inside skeletal muscle. In 11 young men, 10 minutes of massage applied to one exercise-damaged quadriceps activated the mechanosensitive signaling proteins FAK and ERK1/2, potentiated PGC-1α signaling linked to mitochondrial biogenesis, limited the rise in NF-κB activity and reduced the inflammatory cytokines TNF-α and IL-6 (Crane, 2012). That study did not measure fibrosis.

The direct human evidence for histologic reversal of chronic musculoskeletal fibrosis remains less developed than the experimental evidence, but the concept that mechanical treatment can alter connective tissue is biologically well supported. More on how much force hands can apply to different tissues is in can manual therapy change an adhesion?

Developing vs. Established Fibrosis

Mechanical treatment appears more effective when introduced before fibrotic remodeling becomes deeply established, although experimental evidence also suggests that established fibrosis remains biologically modifiable.

The clearest example comes from the same research group. When rats had already developed inflammation and fibrosis after 14 weeks of the overuse task, seven weeks of manual therapy combined with rest improved most measures compared with untreated animals and enhanced the anti-inflammatory cytokine IL-10. However, rest alone also lowered some markers, including collagen I, and the authors concluded that manual therapy during rest had modest effects compared with rest alone, in contrast with its robust preventive effects (Barbe, 2021b). Separately, a non-muscle model found that repeated shockwave sessions thinned an established fibrous capsule over time (Fischer, 2015).

Old fibrosis should not be described as irreversible. It does appear to be a harder target, which is one reason recurrent and long-standing injuries are treated as a combined loading and tissue problem rather than with one technique.

Shockwave and Fibrotic Tissue

Shockwave research points in the same direction. In an experimental skeletal-muscle fibrosis model in which the knee was immobilized for four weeks, radial shockwave combined with ultrashort-wave diathermy reduced fibrosis and contracture and lowered the overexpression of TGF-β1 and HIF-1α. The combined treatment outperformed either therapy alone (Huang, 2021). Human scar-derived fibroblasts exposed to ESWT showed reduced expression of TGF-β1, alpha-smooth-muscle actin, collagen I and fibronectin—key markers associated with fibrotic tissue formation (Cui, 2018). That is human cell evidence, not a clinical trial.

The evidence does not support a simplistic model in which a shockwave physically shatters collagen. A more biologically plausible model is mechanotransduction, in which mechanical energy changes cell behavior, signaling and matrix turnover. The full picture, including the human clinical muscle-injury research, is in shockwave therapy for chronic muscle injury and fibrosis.

What "Breaking Up" Scar Tissue Should Mean

"Breaking up scar tissue" is a common phrase, but it suggests uncontrolled tearing, which is not what the research describes. A more accurate description of what treatment aims to do is to help remodel fibrotic scar tissue: reduce fibrotic collagen and profibrotic signaling, increase extracellular-matrix turnover, alter myofibroblast activity and restore more normal tissue architecture and movement. That is also how Novo describes the goal of Manual Adhesion Release.

What This Means for a Recurrent Strain

A muscle that has been strained more than once may have more than one problem: reduced strength and endurance, an early return to sport, altered myoconnective healing and, in some cases, fibrotic remodeling that changes how the tissue stretches and absorbs load. Skilled clinical examination identifies mechanically abnormal or restricted tissue behavior, and that finding, together with strength and load testing, helps decide whether tissue treatment is justified alongside loading.

Fibrosis is one possible contributor. It is not assumed in every case, and progressive loading remains the foundation for restoring muscle capacity. For calf injuries specifically, the first step is making sure the problem is a muscle injury at all. See soleus vs. gastrocnemius injury. In the thigh, chronic rectus femoris injuries around the central tendon are another example, discussed in rectus femoris central tendon injuries. In the chest, a lingering pectoralis major strain is a further example, once a tendon tear has been excluded; see pectoralis major strain vs. tear.

How Novo Uses This Evidence

We start by identifying the structure involved and ruling out tendon, nerve and medical causes. When the exam finds restricted, poorly tolerant tissue after a previous injury, treatment may combine progressive loading with manual treatment or shockwave aimed at remodeling that tissue, with function re-measured as care progresses. See how this applies to chronic calf pain and muscle injury, and how we think about fibrous muscle adhesion more broadly.

References

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