The Tendon Pendulum: How Rehab Keeps Swinging Between Certainty and Confusion

updated 7/17/26

From tendinitis and casting to PRP and progressive loading, the history of tendon rehabilitation is really the history of changing our minds.

Early in my career when I looked a patient’s scrip and it said “patellar tendonitis” my stomach would sink. I knew I would spend the next three months scraping, stretching, and coming up with excuses for why they weren’t getting better.

One patient changed that, it was a girl softball player who came to therapy in tears because her “patellar tendonitis” was so painful she had trouble walking, much less play ball. I was determined to not let this girl continue to suffer. After a couple weeks of searching, I found “the knees over toes guy”. I had her follow the program, as much as she could and after around two months she was making good progress! I was blown away, this is the most progress I had made with any patient with anterior knee pain, much less someone as severe as her. Why did this work, what was different, how could I replicate this success?

I spent almost the next three years of my career researching down the tendon rabbit hole trying to find answers. Here is the culmination of my findings.

There are few diagnoses in rehabilitation that have changed as dramatically as tendinopathy.

First it was inflammation.

Then we decided inflammation didn't exist.

Then everyone started talking about degeneration.

Then came eccentric exercise.

Then heavy slow resistance.

Then tendon neurobiology.

Now?

We're finally realizing the story was never that simple.

Unfortunately, plenty of clinicians are still practicing as though it's 1998.

Chapter 1: When Everything Was “Tendinitis"

"The traditional view of tendonitis is a tendon injury resulting from repetitive mechanical load with a subsequent inflammatory response."
— Almekinders & Temple, 1998

For decades, that sentence wasn't controversial.

It was simply accepted.

We diagnosed tendinitis because we believed painful tendons were inflamed.

We prescribed anti-inflammatories because we believed inflammation was the problem.

We immobilized tendons because we believed rest promoted healing.

We weren't being irrational.

We were following the best model we had.

Treatment reflected that idea:

• Ice

• Ultrasound

• Anti-inflammatory medications

• Rest

• Deep transverse friction massage (taught to me by ATCs in my undergraduate studies, but nobody could really explain why we were rubbing inflamed tissue harder.)

• Cortisone injections

• Braces and splints

• Walking boots

• Casting

• Avoid painful movement

The assumption seemed logical.

Pain equals inflammation.

Except researchers kept examining chronic painful tendons and weren't finding the robust inflammatory infiltrates they expected (Khan et al., 2002).

Immobilize It and Wait

If inflammation was believed to be the problem, then the logical solution was simple:

Keep the tendon still.

For decades, painful tendons were commonly treated with braces, casts, walking boots, splints, and prolonged activity restriction. The thinking was straightforward: if movement irritated the tendon, removing movement would allow it to heal (Khan et al., 2002).

In some situations—such as an acute tendon rupture or immediately after surgical repair—temporary immobilization is absolutely necessary to protect healing tissue. But that approach gradually spilled over into the treatment of chronic tendon pain, where the evidence has proven far less supportive (Magnusson, Kjaer, & Langberg, 2010).

The problem is that tendons are living tissues that depend on mechanical loading to maintain their structure and function. Extended immobilization reduces collagen synthesis, decreases tendon stiffness and mechanical properties, and lowers the tissue's ability to tolerate future loading (Kjaer et al., 2009; Magnusson et al., 2010).

Patients often return from weeks in a brace or walking boot with less pain simply because they've stopped stressing the tendon—but they also return with a tendon that is less prepared for the demands of everyday life.

In hindsight, we weren't just treating inflammation.

We were often deconditioning the very tissue we were trying to heal.

That realization helped set the stage for one of the biggest shifts in modern rehabilitation: moving away from prolonged protection and toward progressive, well-managed loading (Cook & Purdam, 2009).

Chapter 2: The Pendulum Swings Too Far

In the late 1990s and early 2000s, work by Jill Cook, Craig Purdam, and others fundamentally changed how we viewed chronic tendon pain.

The word tendinosis became popular.

The tendon wasn't inflamed.

It was degenerating.

Collagen became disorganized.

Ground substance increased.

Cells looked abnormal.

Blood vessels grew into the tissue.

Suddenly clinicians proclaimed:

"There's no inflammation."

That statement became almost as inaccurate as the original one.

Chapter 3: We Accidentally Declared War on Inflammation

The phrase,

"Tendons aren't inflammatory,"

spread rapidly through courses, textbooks, and social media.

Reality?

Acute tendon injuries absolutely involve inflammatory processes.

Even chronic tendinopathy demonstrates immune cell activity and inflammatory signaling. It's simply not the overwhelming inflammatory response we originally imagined.

Modern tendon biology shows inflammation isn't binary.

It's regulated.

Localized.

Dynamic.

Changing throughout the healing process (Dean et al., 2016).

Chapter 4: Enter the Eccentric Revolution

Then Alfredson published his famous Achilles protocol.

Three sets.

Fifteen repetitions.

Twice daily.

Seven days per week.

Twelve weeks.

As a side note I don’t know any patient who actually completed this extensive and painful protocol, but I suppose if/when they didn’t we can blame the patient on “not doing their homework”.

Suddenly every tendon received eccentric exercises.

Some patients improved dramatically.

Many did well.

Some didn't.

Which raised an uncomfortable question:

Was eccentric loading uniquely beneficial?

The tendon itself isn't contractile. It experiences tensile force regardless of whether that force is produced during a concentric, eccentric, or isometric muscle contraction. What appears to matter most is the magnitude, duration, and progression of the load—not the direction of muscle shortening.

Or was it simply one effective way to progressively load a tendon?

Chapter 5: Heavy Slow Resistance Changes the Conversation

Research comparing heavy slow resistance with eccentric programs found remarkably similar outcomes (Beyer et al., 2015).

It turns out tendons appear to care less/can’t tell the difference whether a contraction is eccentric or concentric...

...and far more about receiving an appropriate mechanical stimulus.

The conversation shifted from:

"Which exercise is best?"

to

"How much load can this tendon tolerate, and how should we progress it?"

Chapter 6: The Isometric Craze

Remember when everyone thought 45-second isometrics were analgesic magic?

Then later studies showed...

Sometimes.

Not always.

Patient dependent.

Classic tendon pendulum.

You could literally write:

One study later...

Every tendon patient in the world was holding wall sits.

Five years later...

We quietly admitted the effect wasn't nearly as universal as we hoped.

Chapter 7: The Continuum Changes Everything

Just when it seemed we'd finally figured tendons out...

...we complicated them again.

In 2009, Jill Cook and Craig Purdam proposed the Continuum Model of Tendinopathy.

Instead of viewing tendons as either healthy or degenerated, they suggested tendon pathology exists along a spectrum.

Reactive tendon.

Tendon dysrepair.

Degenerative tendon.

This explained something clinicians had struggled with for years.

Not every painful tendon looked the same.

Not every tendon needed the same treatment.

Some tendons were temporarily overloaded.

Others had accumulated years of structural change.

Perhaps most importantly...

The model suggested tendons could move both directions along the continuum depending on loading.

That was a huge shift.

Instead of asking,

"What's wrong with the tendon?"

we started asking,

"Where is this tendon today?"

Chapter 8: Pain Doesn't Equal Damage

One of the biggest lessons from tendon research is that pain and tendon structure often disagree.

Some terrible-looking tendons don't hurt.

Some painful tendons show relatively minor structural changes.

Ultrasound and MRI frequently reveal tendon abnormalities in completely asymptomatic athletes (Docking & Cook, 2019).

Some elite volleyball players have ugly patellar tendons for years...

...and never miss a game.

Conversely...

Some patients have exquisite pain with very little structural abnormality.

Sound familiar?

We've seen this same story with lumbar discs, menisci, labral tears, and rotator cuff pathology.

Imaging is one piece of the puzzle—not the entire diagnosis.

Chapter 9: The Mechanotherapy Era — When We Finally Asked Why?

For years, rehabilitation argued about which exercise was best.

Eccentrics.

Heavy slow resistance.

Isometrics.

Plyometrics.

Every few years, another program became the new gold standard.

But eventually researchers began asking a better question.

Why does loading work at all?

The answer wasn't found in the exercise.

It was found in the tendon.

Unlike muscle, tendons don't contract.

Unlike cartilage, they're richly connected to muscle and exposed to enormous mechanical forces every day.

Their job is simple.

Transmit force.

Store energy.

Release energy.

To do that, tendons are constantly adapting to the loads placed upon them.

This gave rise to the concept of mechanotherapy—the idea that appropriately dosed mechanical loading doesn't simply strengthen a tendon.

It acts as medicine.

Mechanical force is converted into a biological signal, a process known as mechanotransduction. When a tendon is loaded, its resident cells—tenocytes—sense the deformation of the surrounding collagen matrix and respond by altering gene expression, collagen synthesis, extracellular matrix turnover, and tissue remodeling (Kjaer et al., 2009; Wang, 2006).

In other words...

The tendon doesn't just experience load.

It listens to it.

Load tells the tendon whether it needs to become stronger, stiffer, or more resilient.

Too little loading, and the tendon begins to lose its mechanical capacity.

Too much loading too quickly, and the tissue becomes overwhelmed before it can adapt.

Somewhere in between lies the "sweet spot" where adaptation exceeds breakdown.

That's why modern rehabilitation focuses less on finding the perfect exercise and more on prescribing the right dose of load.

The exact exercise matters far less than whether it delivers an appropriate mechanical stimulus.

This also explains why so many different rehabilitation programs appear to work.

Eccentrics.

Heavy slow resistance.

Progressive isotonic exercise.

Even many isometric programs.

They may differ in appearance.

But they're all exposing the tendon to mechanical loading.

Mechanotherapy also helps explain why passive treatments have consistently struggled to outperform exercise.

Ultrasound cannot teach a tendon how to tolerate force.

Massage cannot restore its energy-storage capacity.

PRP may alter the biological environment in some patients, but it cannot replace the repeated mechanical signals required for long-term adaptation.

The tendon ultimately adapts to what you ask it to do.

And that's perhaps the biggest lesson we've learned over the last forty years.

The exercise itself isn't the treatment.

The load is.

Chapter 10: Tendons Are Surprisingly Adaptable

Healthy tendons remodel.

They become stiffer.

Sometimes thicker.

They improve their ability to store and release energy.

Loading stimulates collagen turnover and improves mechanical properties, but adaptation occurs over months—not days (Kjaer et al., 2009).

This helps explain why patients often feel better long before imaging appears "normal."

Function usually returns before structure.

I think this actually strengthens the narrative because it shows that the field didn't just change its exercise philosophy—it also cycled through a series of increasingly sophisticated biological interventions. It fits well between the loading chapters and the modern rehabilitation section.

Chapter 11: The Injection Era — Looking for a Shortcut

If the "tendinitis" era was dominated by rest...

and the "tendinosis" era was dominated by loading...

the next chapter was dominated by injections.

The logic was always appealing.

If exercise wasn't enough, perhaps we could inject something that would accelerate healing.

For decades, corticosteroid injections were among the most common treatments for tendon pain. In the short term, they often worked remarkably well. Pain improved quickly, patients were happy, and everyone felt successful.

The problem?

The long-term results were much less impressive.

Systematic reviews consistently found that while corticosteroid injections often provide excellent short-term pain relief, they offer little long-term advantage over exercise and may even increase recurrence rates in some tendinopathies (Coombes et al., 2010).

As enthusiasm for corticosteroids faded, a new wave of biologic treatments emerged.

Platelet-rich plasma (PRP).

Prolotherapy.

Autologous blood injections.

Stem cells.

Tenocyte injections.

High-volume injections.

Each arrived with considerable excitement and the promise of stimulating tendon healing.

Some patients certainly improved.

But when higher-quality clinical trials accumulated, the results became far less convincing.

For most common tendinopathies, PRP has shown inconsistent or only modest benefits compared with structured exercise programs, and evidence for stem cell therapies remains preliminary (Fitzpatrick et al., 2017; Andriolo et al., 2019).

Shockwave therapy followed a similar trajectory.

Initially promoted as a way to "break up scar tissue" or stimulate healing, it has demonstrated benefits for some conditions—particularly calcific rotator cuff tendinopathy and selected cases of Achilles or plantar heel pain—but it is far from the universal solution it was once advertised to be.

The lesson isn't that injections or adjunctive therapies never work.

They probably do—for some patients, in some situations.

The lesson is that none of them consistently outperform a well-designed loading program.

Exercise keeps surviving every new treatment fad because tendons are mechanical tissues.

They adapt to mechanical stress.

No injection has figured out how to replace that.

Chapter 12: The Tendon Isn't Working Alone

One mistake rehabilitation still makes is treating the tendon like an isolated tissue.

An Achilles tendon doesn't function without:

• Calf strength

• Foot stiffness

• Hip strength

• Running mechanics

• Training load

• Sleep

• Recovery

• Overall metabolic health

Likewise, patellar tendon pain often reflects deficits well beyond the tendon itself.

The tissue matters.

The system matters more.

Chapter 13: Modern Tendon Rehabilitation

Today's evidence suggests tendon rehabilitation should be based on restoring function—not simply progressing through a list of exercises.

Phase 1: Calm the Tendon

Reduce irritability while maintaining as much capacity as possible.

• Relative load modification

• Education

• Isometrics (when appropriate)

• Maintain cardiovascular fitness

• Continue tolerable movement

Phase 2: Restore Movement

Normalize movement quality and reduce unnecessary compensations.

• Restore mobility where appropriate

• Improve strength of adjacent joints

• Address movement strategies

Phase 3: Build Capacity

Progressively increase the tendon's tolerance to force.

• Progressive isotonic loading

• Heavy slow resistance

• Unilateral strengthening

Phase 4: Build Rate of Force Development

Prepare the tendon for faster loading.

• Faster concentric movements

• Medicine ball drills

• Explosive strengthening

Phase 5: Restore Energy Storage

Reintroduce the spring-like function of tendon.

• Hopping

• Skipping

• Bounding

• Jump rope

• Running progressions

Phase 6: Return to Function

Gradually expose patients to the demands of work or sport.

• Cutting

• Sprinting

• Climbing

• Occupational tasks

• Sport-specific drills

Progress should be guided by tendon irritability—not simply by the calendar. Monitor pain during activity, symptoms afterward, and especially the tendon's response the following morning.

Remember that some tendons dislike compression as much as tensile loading. Insertional Achilles, gluteal, and proximal hamstring tendinopathies are common examples where compressive positions may need to be modified early before being progressively reintroduced.

Finally, don't just rehab the tendon.

Rehab the person.

Training errors, sleep, metabolic health, medications (such as fluoroquinolones or repeated corticosteroid exposure), recovery, fear of movement, and overall conditioning all influence tendon outcomes.

Clinical Reality

Tendon rehab has spent forty years chasing the next breakthrough.

We chased inflammation.

We chased degeneration.

We chased eccentric exercise.

We chased PRP.

We chased stem cells.

We chased shockwave.

Every few years we discover another miracle.

Then a decade later we quietly move on.

Through every fad, one principle has survived.

Progressive loading.

Not because it's exciting.

Not because it sells courses.

Because that's how tendons have always adapted.

The tendon never changed.

We did.

-the Pissed-Off PT- like, subscribe, share-

References

• Alfredson H, Pietilä T, Jonsson P, Lorentzon R. Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. Am J Sports Med. 1998.

• Beyer R, Kongsgaard M, Hougs Kjær B, et al. Heavy slow resistance versus eccentric training as treatment for Achilles tendinopathy. Am J Sports Med. 2015.

• Cook JL, Purdam CR. Is tendon pathology a continuum? Br J Sports Med. 2009.

• Dean BJF, Dakin SG, Millar NL, Carr AJ. Review: Emerging concepts in the pathogenesis of tendinopathy. Surgeon. 2016.

• Docking SI, Cook JL. Pathological tendons maintain sufficient aligned fibrillar structure on ultrasound tissue characterization to explain why they can still load. Br J Sports Med. 2019.

• Khan KM, Cook JL, Kannus P, Maffulli N, Bonar SF. Time to abandon the "tendinitis" myth. BMJ. 2002.

• Kjaer M, Langberg H, Heinemeier K, et al. From mechanical loading to collagen synthesis, structural changes and function in human tendon. Scand J Med Sci Sports. 2009.

• Magnusson SP, Kjaer M, Langberg H. The impact of loading, unloading, ageing and injury on the human tendon. J Physiol. 2010.

• Wang JHC. Mechanobiology of tendon. J Biomech. 2006;39:1563-1582.

• Khan KM, Scott A. Mechanotherapy: How physical therapists' prescription of exercise promotes tissue repair. Br J Sports Med. 2009.

• Screen HRC, Berk DE, Kadler KE, Ramirez F, Young MF. Tendon functional extracellular matrix. J Orthop Res. 2015.