TENDINOPATHY PATHOPHYSIOLOGY, PAIN & LOAD MANAGEMENT

Tendinopathy is not simply “inflammation”

Persistent tendon pain has traditionally been described as tendinitis, suggesting inflammation, or tendinosis, suggesting degeneration.

Neither term fully captures what is happening clinically.

The preferred term is tendinopathy: persistent tendon pain and loss of function related to mechanical loading, regardless of exactly what the tendon looks like on imaging.

This distinction matters because chronic tendinopathy is not primarily driven by a classic inflammatory process. Instead, it reflects a cell-mediated response to load, with changes in tenocyte behaviour and the extracellular matrix.

That changes the rehabilitation question from:

“How do we stop irritating the damaged tendon?”

to:

“How much load can this tendon currently tolerate, and how can we progressively increase that capacity?”

Complete rest is therefore rarely the long-term solution.

Load is the central variable

Tendons are highly responsive to mechanical load.

Tenocytes continuously sense strain and modify the tendon matrix in response. Problems develop when cumulative loading — including its volume, intensity and frequency — exceeds the tendon’s current capacity and available recovery.

This can happen through obvious overload, such as a sudden increase in running, jumping or sprinting.

But under-loading can also contribute.

A period of inactivity may reduce tendon capacity, meaning that a workload that was previously normal becomes excessive when activity suddenly resumes.

The problem is therefore not simply “too much load.”

It is a mismatch between load and capacity.

The tendon continuum: reactive, disrepair and degenerative

The Cook and Purdam continuum model describes tendinopathy as a spectrum rather than three completely separate conditions.

Reactive tendinopathy

A reactive tendon often follows a sudden spike in tensile or compressive load.

Tenocytes increase the production of proteoglycans and water, causing the tendon to temporarily thicken. This is an attempted adaptation to excessive load rather than a classic inflammatory reaction.

This stage is more reversible and often responds well to reducing the provocative load while maintaining low-strain loading.

Tendon disrepair

With repeated overload, collagen organisation becomes increasingly disrupted and changes in vascular and neural growth begin to appear.

The tendon is attempting to repair itself, but the remodelling process cannot keep pace with the repeated loading stimulus.

Loading becomes progressively more structured, with higher-strain and energy-storage work restricted while capacity is rebuilt.

Degenerative tendinopathy

Later-stage tendinopathy involves areas of significant matrix disorganisation and cellular change.

Importantly, degenerative does not mean hopeless.

Degenerative areas are often focal rather than affecting the entire tendon. Rehabilitation therefore aims to improve the capacity of the surrounding viable tendon rather than attempting to completely reverse every structural abnormality.

Many athletes have significant degenerative changes on imaging while remaining highly functional and completely pain-free.

Pain and tendon structure are not the same thing

One of the most important concepts in tendinopathy is that pain does not provide a direct measurement of structural damage.

A tendon can look significantly abnormal on imaging without causing symptoms.

Conversely, a person can experience substantial tendon pain despite relatively unremarkable imaging.

Several biological mechanisms may contribute to tendon pain, including changes in proteoglycans and water content, altered tenocyte signalling, increased neural and vascular growth, and local metabolic changes.

Together, these processes can make the local nervous system more sensitive to mechanical loading.

This helps explain why relatively small loads can sometimes become painful without representing a new injury.

Allodynia and hyperalgesia

Two pain phenomena are particularly useful in understanding tendon symptoms.

Allodynia occurs when a normally non-painful activity becomes painful.

Walking, stairs or relatively light jumping may therefore become provocative even though these activities would not normally threaten the tendon.

Hyperalgesia occurs when a normally mildly provocative stimulus produces a disproportionately large pain response.

Tenderness during tendon palpation is a common example.

These responses reflect a sensitised pain system rather than automatically indicating that structural damage is progressing.

A painful tendon is not necessarily about to rupture

Patients are often concerned that continuing to load a painful tendon will eventually cause it to tear.

The relationship is not that simple.

Tendon ruptures frequently occur in tendons with previously asymptomatic degenerative changes, while painful tendinopathy does not necessarily represent a pre-rupture state.

This reinforces the importance of separating symptoms from structure.

Telling someone that their tendon is “degenerated” based on an imaging report can unnecessarily create fear if the term is interpreted as meaning the tissue is inevitably failing.

A more useful message is that the tendon can still become stronger and more functional even when imaging abnormalities remain.

Isometric exercise can help — but not everyone responds

Heavy isometric contractions became widely used in tendon rehabilitation because they can produce short-term pain relief in some patients.

A commonly used example is:

5 sets of 30–45 second holds at a challenging but tolerable effort, with approximately two minutes of recovery between sets.

However, the analgesic effect should not be presented as universal.

Some patients experience significant immediate pain reduction, while others experience little change.

Isometrics are therefore a useful loading and symptom-modulation option, particularly in reactive presentations, rather than a mandatory first step for every tendon.

The broader evidence supports something more important: consistent, progressive loading.

Use pain to regulate load, not automatically stop it

The pain-monitoring model provides a practical way to regulate tendon rehabilitation.

Using a 0–10 pain scale:

0–2/10: generally acceptable. Current loading can be maintained and may sometimes be progressed.

3–5/10: can still be acceptable if symptoms settle quickly and there is no worsening of next-day pain or morning stiffness. Maintain the current dose rather than progressing.

5/10 or greater, worsening symptoms across sessions, or increased next-day morning stiffness suggest that the load has exceeded current capacity.

The important point is that some pain does not automatically mean exercise must stop.

Instead, pain becomes feedback for adjusting the dose.

Match the loading strategy to the tendon

The rehabilitation strategy should also reflect the likely stage of the tendon.

For a reactive tendon, the priority is to reduce high-strain or compressive loading while maintaining tolerable low-strain loading, often including isometrics.

During disrepair, progressive isotonic strengthening becomes more important while high-strain plyometric activity remains restricted.

With degenerative tendinopathy, rehabilitation focuses on increasing the capacity of the viable tendon, strengthening the surrounding kinetic chain and managing the specific load patterns that repeatedly provoke symptoms.

The exact contraction type — isometric, concentric, eccentric or isotonic — may be less important than previously believed.

What matters most is that loading is progressive, sufficiently demanding, consistently performed and appropriately monitored.

Do not rehabilitate the tendon in isolation

Persistent tendon pain can reduce voluntary activation of the associated muscles, a phenomenon known as arthrogenic muscle inhibition.

The athlete may also unconsciously change movement patterns to unload the painful structure.

For example, an athlete with patellar tendinopathy may alter knee and hip mechanics during landing.

Rehabilitation should therefore restore:

• muscle strength

• voluntary activation

• tendon capacity

• movement and landing mechanics

• wider kinetic-chain capacity

Treating only the painful tendon may leave the system that loads it unchanged.

In-season rehabilitation does not always require stopping sport

One of the biggest challenges in tendinopathy is managing an athlete who needs to continue training or competing.

Rather than automatically prescribing “rest until pain-free,” rehabilitation can be reverse-engineered from the demands of the sport.

First determine what full sport participation actually requires.

For a jumping athlete, this might include:

• total jumps

• landing frequency

• average jump intensity

• maximal jump exposure

• sport-specific cutting or deceleration

Rehabilitation can then build progressively toward those demands.

A simplified progression may look like:

No high-strain exposure → low-volume controlled loading → moderate sport-specific volume → near-full volume → maximal-intensity exposure → full participation.

Maximum-intensity efforts are generally reintroduced later than lower-intensity volume.

Every stage remains regulated by the athlete’s symptom response rather than by the calendar alone.

Return to sport is not the end of rehabilitation

An athlete can become pain-free before full tendon function has returned.

Strength, tendon stiffness, movement mechanics or tolerance to repeated loading may still remain below the athlete’s previous level even when symptoms have resolved.

Monitoring should therefore continue after return to sport.

Tendon-specific tools such as the VISA-A for Achilles tendinopathy and VISA-P for patellar tendinopathy can track pain, function and participation.

However, questionnaires should not be used alone.

A more complete picture includes:

• pain

• functional capacity

• strength

• confidence and fear

• sport-specific performance

• tolerance to repeated loading

The central principle of tendinopathy rehabilitation is therefore simple:

The tendon needs load.

The challenge is not eliminating mechanical stress but determining the right dose for the tendon’s current capacity, progressing it systematically, and using symptoms and function to guide each step.