Loading For Tendinopathies: The Complete Guide (Achilles, Patellar, Gluteal, Proximal Hamstring, Sever's & Osgood-Schlatter's)

The most common mistake people make with tendinopathy is resting it. They stop running, stop squatting, stop loading — and for a few days, maybe even a couple of weeks, it feels better. So they go back to what they were doing. And it comes back. Sometimes worse. This cycle — pain, rest, improvement, return, pain — is the defining feature of undertreated tendinopathy, and it happens because rest addresses the symptom without touching the underlying pathology.

This guide covers everything you need to know about loading for tendinopathy — the mechanism, the models, the protocols, and the specific progressions for each major tendinopathy we see at PRT. Whether you're a runner dealing with insertional Achilles pain, an athlete with patellar tendinopathy, or a parent whose kid has been told to "just rest" their Sever's disease — this is the most useful thing you'll read on the topic.

Section 1: What Is Tendinopathy, Really?

Tendinopathy is not tendinitis. The "-itis" suffix implies inflammation, and while inflammation may play a role in early-stage tendon pain, the dominant pathological process in most clinical presentations is degenerative — a failure of the tendon's collagen matrix to maintain its structural integrity under load. Understanding this distinction changes everything about how you treat it.

The most clinically useful framework for understanding tendinopathy is the Cook & Purdam Continuum Model (2009), which describes tendon pathology across three stages:

1. Reactive Tendinopathy

An acute, non-inflammatory proliferative response to overload. The tendon thickens to reduce stress per unit area. This stage is reversible. It occurs most commonly with a sudden increase in training load — a runner who doubles their weekly mileage in two weeks, or an athlete returning from a deload. The key clinical indicator is a relatively recent onset (days to a few weeks) in response to an identifiable load spike.

2. Reactive-on-Degenerative Tendinopathy

A reactive response superimposed on an already compromised tendon. This is the most common presentation in clinical practice. The tendon has pre-existing degenerative changes — disorganised collagen, increased ground substance, neovascularisation — and reacts to a new load challenge. These patients often describe years of intermittent symptoms with good periods and bad periods. Prognosis is good with appropriate loading but takes longer than reactive-only presentations.

3. Degenerative Tendinopathy

Large areas of degeneration with failed healing response. This stage is largely irreversible, but the surrounding tissue can be loaded and strengthened to compensate. The degenerative portion of the tendon is essentially inert — it will not remodel — but loading the healthy tissue around it improves overall tendon capacity and reduces symptoms. This is why surgery for chronic degenerative tendinopathy has such mixed outcomes: you can remove the degenerate tissue but the loading deficits remain.

Why does this matter clinically? Because the stage determines the approach. Reactive tendons need load management — reduce the provocative load, maintain other loading. Degenerative tendons need progressive heavy loading to drive adaptation in the remaining healthy tissue. Treating a degenerative tendinopathy like a reactive one — prolonged rest, passive treatment, avoiding all load — is one of the most common and most costly clinical errors.

Section 2: Why Loading Is The Treatment

Tendons are mechanosensitive structures. They adapt to load — they remodel their collagen architecture in response to mechanical stimulus. Without load, that stimulus disappears, and the tendon does not maintain its structural integrity. This is why immobilisation produces rapid tendon degeneration, and why prolonged rest is not a treatment for tendinopathy — it is the mechanism of its persistence.

The mechanotransduction pathway works as follows: mechanical load on the tendon activates tenocytes (tendon cells), which upregulate collagen synthesis and initiate matrix remodelling. The stimulus needs to be sufficient (heavy enough), appropriate in character (tensile vs compressive — more on this shortly), and progressive over time. A tendon loaded correctly over 8–12 weeks will have measurably improved structural properties on imaging and clinically meaningful reductions in pain and disability.

Passive treatment — massage, dry needling, shockwave, acupuncture — produces symptom relief through neurological mechanisms (pain gate, central sensitisation, neovascular ablation) without driving structural adaptation. This is useful in the short term for pain management but produces no lasting structural change on its own. The evidence base for every passive modality shows short-term benefit only. The evidence base for loading shows long-term structural remodelling.

This does not mean passive treatment has no role — it does, and we'll cover it in Section 7. But it means passive treatment without progressive loading is a symptom management strategy, not a rehabilitation strategy.

Section 3: The Compression vs Tensile Distinction — The Most Important Thing Your Practitioner Might Not Have Told You

This is the clinical concept that separates effective tendinopathy management from ineffective tendinopathy management, and most patients have never heard it.

Tendons experience two types of mechanical load: tensile load (the tendon being pulled along its length) and compressive load (the tendon being compressed against a bone or other structure). These two load types have fundamentally different effects on tendon pathology depending on where the tendon inserts and what stage of pathology is present.

The Achilles tendon is the best clinical example. The mid-portion of the Achilles (2–6cm above the calcaneal insertion) is a tensile loading zone — it responds well to eccentric and heavy slow resistance loading. The insertional Achilles (at the bone-tendon junction) is also subject to compressive load when the heel moves into dorsiflexion — the tendon wraps around the calcaneus and gets compressed against it.

This is why the famous Alfredson eccentric heel drop protocol — dropping the heel below the level of the step — which is extremely effective for mid-portion Achilles tendinopathy, is contraindicated for insertional Achilles tendinopathy. The heel drop increases compressive load on the insertion. Using it for insertional presentations will provoke the tendon and drive pathology, not resolve it.

The same principle applies to gluteal tendinopathy (compressed against the greater trochanter in hip adduction — avoid crossing legs, sitting with hip adducted), proximal hamstring tendinopathy (compressed at the ischial tuberosity in hip flexion — avoid aggressive hamstring stretching), and patellar tendinopathy (compressed at the inferior pole in deep knee flexion). Knowing which load type is provocative for which location is the foundation of an effective protocol.

Section 4: How To Choose The Right Load

There are three loading types used in tendinopathy rehabilitation, each appropriate at different stages and for different presentations:

Isometric Loading

A sustained muscle contraction with no joint movement. The tendon is loaded without change in length. Research by Rio et al. (2015) demonstrated that isometric contractions at 70% MVC held for 45 seconds reduce cortical inhibition and produce immediate analgesic effects in patellar tendinopathy. This makes isometrics the first-line loading approach for irritable tendons — they provide sufficient mechanical stimulus to drive tenocyte activity without the dynamic load that provokes reactive responses. Start here with reactive presentations, high irritability, or in-season athletes who need pain management for competition.

Heavy Slow Resistance (HSR)

The primary driver of tendon structural adaptation. Heavy load (3–5RM range), performed slowly (typically 3 seconds concentric, 3 seconds eccentric), through full available range, 3 times per week. Beyer et al. (2015) demonstrated that HSR produces equivalent outcomes to eccentric-only protocols for mid-portion Achilles tendinopathy with higher patient satisfaction and compliance. The mechanism is superior collagen synthesis stimulus at heavy loads — lighter loads do not produce adequate tenocyte activation for structural remodelling. Progress load every 1–2 weeks as tolerated using the pain monitoring rules below.

Energy Storage Loading

Plyometric and spring-like loading — the load type most closely resembling sport. Hopping, jumping, bounding, sprinting. This is the final stage of rehabilitation before return to sport, and the one most commonly skipped. A tendon that has been successfully loaded through HSR but has not been exposed to energy storage loading is not prepared for the demands of running or court sports. Introduce energy storage loading only once pain is consistently ≤2/10 during HSR and there is no reactivity in the 24 hours following loading sessions.

Pain Monitoring Rules

The VISA score and pain monitoring rules from Cook & Purdam provide clear load progression guidance: pain during loading should remain ≤3/10. Pain after loading should return to baseline within 24 hours. If pain exceeds 3/10 during or takes longer than 24 hours to settle, the load was too high and should be reduced. This framework allows progressive overload without driving reactivity — it is not "no pain, no gain" but it is not "avoid all pain" either.

Section 5: Protocol Breakdowns

Insertional Achilles Tendinopathy

Location: At the calcaneal insertion. Worst in the morning, eases with warm-up, worsens with increased load. Provocative: dorsiflexion end range (heel drops below step level), barefoot walking, hills.

Protocol: Isometric calf raises on a flat surface (not off a step) — 5 x 45 seconds at 70% effort, daily. Progress to heavy slow resistance heel raises on flat ground, double leg first, progressing to single leg. Never load the tendon in dorsiflexion. A small heel lift (6–10mm) worn during rehabilitation reduces compressive load at the insertion and should be considered in the early stages. Return to running on flat surfaces before hills or track.

Mid-Portion Achilles Tendinopathy

Location: 2–6cm above the insertion. Diffuse thickening palpable. Provocative: high-speed loading, long runs, hills. NOT provoked by passive dorsiflexion.

Protocol: Eccentric heel drops off a step OR heavy slow resistance heel raises (evidence equivalent — use HSR for better compliance). Start double leg, add load via weight vest or barbell. 3 sets x 15 reps, progress to 4 x 8 with added load over 12 weeks. Alfredson's original eccentric protocol (3 x 15 twice daily) remains valid. Energy storage phase begins at week 8–10 with double-leg hops progressing to single-leg.

Patellar Tendinopathy (Jumper's Knee)

Location: inferior pole of the patella. Provocative: jumping, landing, deep squatting, prolonged sitting. Classic presentation: pain at the start of activity that warms up, returns after.

Protocol: Isometric wall sits (70° knee flexion, 70% effort, 5 x 45 seconds) for immediate pain relief and irritability management. Progress to heavy slow resistance leg press and Spanish squats (feet planted, shin vertical — minimises compressive load at the inferior pole). Avoid deep squats, leg extensions past 60° of knee flexion, and aggressive quad stretching in the early stages. Return to jumping only after completing full HSR progression.

Gluteal Tendinopathy

Location: greater trochanter attachment of gluteus medius/minimus. Often misdiagnosed as trochanteric bursitis (frequently co-exists). Provocative: sitting cross-legged, lying on the affected side, hip adduction in walking (especially stairs), stretching the ITB.

Protocol: Education on compressive load positions is as important as exercise. Avoid hip adduction in sitting and standing. Sleep with a pillow between knees. Exercise: isometric hip abduction against a wall, progressing to lateral band walks, single-leg press, and heavy slow resistance hip abduction. Stretching the ITB (which applies compressive load across the trochanteric bursa and tendon) is contraindicated. This is another case where the exercise patients are most commonly given — ITB stretching — makes the condition worse.

Proximal Hamstring Tendinopathy

Location: ischial tuberosity. Provocative: sitting (especially on hard surfaces), uphill running, hip flexion under load. The classic presentation: a runner who can run but cannot sit comfortably afterward.

Protocol: Isometric hamstring contractions in a non-provocative range (hip in slight extension). Avoid aggressive hamstring stretching — it applies compressive load at the ischial tuberosity and consistently drives flare-ups. Progress to heavy slow resistance deadlifts with a limited hip flexion range, progressing range as symptoms allow over 12–16 weeks. Nordic hamstring curls introduced late in the program. This is one of the longer rehabilitation timelines — expect 16–24 weeks to full running capacity.

Section 6: Paediatric Apophysitis — Sever's Disease & Osgood-Schlatter's

Apophysitis is fundamentally different from adult tendinopathy and must be treated differently. In skeletally immature athletes, the weakest point in the muscle-tendon-bone chain is not the tendon — it is the apophysis, the growth plate at the tendon attachment. Sever's disease (calcaneal apophysitis) and Osgood-Schlatter's disease (tibial tubercle apophysitis) occur when the tensile load from the Achilles and patellar tendons respectively exceeds the tolerance of the growth plate during periods of rapid growth.

For parents: this is not a serious injury and does not cause long-term damage. It is a growth-related overuse condition that resolves with skeletal maturity. The goal is symptom management and load modification — not complete rest, which leads to deconditioning and a painful return to sport.

Management: Load modification (reduce provocative volumes while maintaining conditioning through swimming, cycling, resistance training). Heel lifts for Sever's to reduce Achilles tension on the calcaneal apophysis. Soft tissue work to the calf and quad complex to reduce tendon tension at the apophysis. Strengthening the surrounding musculature to distribute load away from the apophysis.

Shockwave is contraindicated in paediatric apophysitis.

Shockwave therapy delivers high-energy acoustic waves to tissue. The evidence for shockwave in adult tendinopathy is reasonable (discussed in Section 7). In paediatric patients with open growth plates, shockwave is absolutely contraindicated — the acoustic energy can damage the apophysis and has been associated with growth disturbance. If a practitioner recommends shockwave for a child with Sever's or Osgood-Schlatter's, seek a second opinion.

Section 7: Adjunct Modalities — Where They Fit

Shockwave Therapy

The best-supported adjunct modality for chronic mid-portion and insertional Achilles tendinopathy, patellar tendinopathy, and proximal plantar fasciopathy. The proposed mechanism includes neovascular disruption, stimulation of collagen synthesis, and cortical pain modulation. Short-term to medium-term evidence is solid. It should be used alongside loading programs, not instead of them. It will not produce structural adaptation without loading — it reduces the pain that limits loading, which is valuable but secondary to the loading program itself.

Dry Needling

Useful for managing associated muscle guarding and trigger point activity in the muscle belly proximal to the tendon. The evidence for needling directly into the tendon is mixed — some protocols show short-term benefit for neovascular disruption (similar mechanism to shockwave) but the tendon itself has relatively poor needle-specific mechanotransduction. We use it primarily for calf, quad, glute, and hamstring trigger point management to reduce the load contribution to the tendon.

Soft Tissue Work

Manual therapy, massage, and instrument-assisted soft tissue mobilisation to the muscle belly reduce tendon load by improving muscle extensibility and reducing tension at the tendon attachment. Useful early in the program and before loading sessions to improve tissue quality. Does not produce structural tendon adaptation — see the pattern here. Every passive modality has a role in symptom management and preparation for loading. None of them are the treatment.

Section 8: Nutrition For Tendon Healing

Tendon remodelling is a metabolic process — it requires raw material as well as mechanical stimulus. The nutritional evidence base for tendinopathy, while not as extensive as the loading evidence, is worth incorporating.

Collagen + Vitamin C

Shaw et al. (2017) demonstrated that 15g of hydrolysed collagen with 50mg of Vitamin C, taken 60 minutes before exercise, significantly increased collagen synthesis markers compared to placebo. The mechanism: Vitamin C is a required co-factor for prolyl hydroxylase, an enzyme critical in collagen cross-linking. The amino acid precursors from hydrolysed collagen (glycine, proline, hydroxyproline) are bioavailable in circulation at the time of loading, providing substrate for synthesis. This is not a supplement to take at any time — the pre-exercise timing is mechanistically important.

Protein

Adequate total protein is foundational. Target 1.6–2.2g/kg/day for an athlete in active rehabilitation. Leucine-rich sources (whey, meat, eggs) are preferred for their superior mTOR activation and protein synthesis stimulus. Under-eating total protein is extremely common in injured athletes and directly impairs tissue healing capacity.

Omega-3 Fatty Acids

EPA and DHA reduce the production of pro-inflammatory prostaglandins via competitive inhibition of the arachidonic acid pathway. In the context of tendinopathy, which has a significant central sensitisation component, reducing systemic inflammatory load is clinically useful. Target 2–3g combined EPA/DHA daily from fish oil. Food sources alone are rarely sufficient at therapeutic doses.

Creatine

Creatine monohydrate supports the heavy resistance loading that drives tendon adaptation by increasing phosphocreatine availability for high-intensity efforts. The indirect benefit is the ability to train harder during HSR sessions. 3–5g daily. Loading phase not necessary at maintenance doses. One of the most evidence-supported supplements in existence for muscle and connective tissue.

Conclusion: Load It Properly, Heal It Permanently

Tendinopathy is a loading problem with a loading solution. The continuum model tells you what stage you're at. The compression vs tensile distinction tells you which loads to avoid and which to pursue. The HSR protocol is the primary driver of structural adaptation. Everything else — shockwave, needling, soft tissue work, nutrition — supports the loading program without replacing it.

If you have been told to rest, ice, and hope for the best, you are missing the treatment. If you have been doing exercises that feel good but haven't progressed your load in months, you are missing the stimulus for adaptation. If you are using passive treatment to manage pain between flare-ups without a structured loading progression, you are managing a chronic condition that can be resolved.

At PRT, we assess tendinopathy using the continuum model, identify the compression and tensile demands of your specific presentation, build a load progression matched to your tissue capacity and your sport, and use adjunct modalities strategically to keep you training while you adapt. We see this at both our Scarborough and East York locations.

Book at PRT East York: 1400 O'Connor Drive, Suite 14 — 416-288-0875

Book at PRT Scarborough: 2100 Ellesmere Road, Suite 120 — 416-439-1001

Or book online at prtherapy.janeapp.com

References

Cook, J. L., & Purdam, C. R. (2009). Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British Journal of Sports Medicine, 43(6), 409–416.

Rio, E., Kidgell, D., Purdam, C., Gaida, J., Moseley, G. L., Pearce, A. J., & Cook, J. (2015). Isometric exercise induces analgesia and reduces inhibition in patellar tendinopathy. British Journal of Sports Medicine, 49(19), 1277–1283.

Beyer, R., Kongsgaard, M., Hougs Kjær, B., Øhlenschlæger, T., Kjær, M., & Magnusson, S. P. (2015). Heavy slow resistance versus eccentric training as treatment for Achilles tendinopathy. American Journal of Sports Medicine, 43(7), 1704–1711.

Shaw, G., Lee-Barthel, A., Ross, M. L., Wang, B., & Baar, K. (2017). Vitamin C–enriched gelatin supplementation before intermittent activity augments collagen synthesis. American Journal of Clinical Nutrition, 105(1), 136–143.

Alfredson, H., Pietilä, T., Jonsson, P., & Lorentzon, R. (1998). Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. American Journal of Sports Medicine, 26(3), 360–366.