Published May 2026. Written by the Upwell Health Collective clinical team. Clinically reviewed May 2026. Next review November 2026. For educational purposes only — please consult a qualified allied health professional before commencing or modifying a tendinopathy rehabilitation program.
Related reading from Upwell Health:
• The Disc Injury Directory 2026
• The Shoulder Pain Master Guide 2026
• Perimenopause & Menopause Thrive Guide 2026
• Combat Sports Chronicle 2026
• Headache & Migraine Directory 2026
• Pain Is Not Damage
If you have tendon pain — Achilles, patellar, gluteal, lateral elbow (tennis elbow), hamstring, rotator cuff, plantar fascia, or any other tendon — five things to know before anything else:
1/ Tendinopathy is not inflammation. The old word "tendinitis" implies an inflammatory process that drives pain. The current evidence base — led by Jill Cook, Craig Purdam, and their collaborators at La Trobe University — has comprehensively retired this model. Tendinopathy is a failed cellular healing response to overload. There is little to no classical inflammation in chronic tendon pain. This is why anti-inflammatory medications and rest don't fix it.
2/ Rest is the wrong answer. Tendons get worse with rest. They need progressive load to heal. The single most consistent finding across 30+ years of tendinopathy research is that exercise — specifically progressive resistance training — outperforms every other treatment for tendon pain. Rest, ice, anti-inflammatories, ultrasound, massage, stretching, and electrotherapy all underperform compared to structured loading programs.
3/ Imaging often misleads. Tendinopathy changes on ultrasound and MRI are extraordinarily common in pain-free people. The structural "damage" your scan shows may have been there for years before your symptoms started, and may persist for years after your symptoms resolve. Treating the scan rather than the person is one of the most common mistakes in tendinopathy care.
4/ Loading protocols actually work. Heavy Slow Resistance (HSR) protocols from Kongsgaard, Beyer, and colleagues at the Bispebjerg Hospital in Copenhagen produce outcomes equivalent or superior to eccentric-only protocols, with substantially better patient adherence. Isometric loading provides immediate analgesia. Plyometric work in late-stage rehab restores tendon function for return to sport. The combination beats any single approach.
5/ Tendons take time. The single most under-communicated truth in tendinopathy care: tendons remodel slowly. Symptomatic improvement often happens within 6–12 weeks. Structural and functional remodelling takes 3–6 months minimum, often 9–12 months for full capacity restoration. Athletes who try to short-cut this timeline are the ones who flare repeatedly.
This guide is the most comprehensive evidence-based tendinopathy resource we've produced. It covers Achilles, patellar, gluteal, lateral elbow, hamstring, rotator cuff, plantar fascia, and adductor tendinopathies. It integrates research from 2023–2026 across loading science, imaging, pain mechanisms, surgical decision-making, return-to-sport, female athlete considerations, and the multi-disciplinary care that transforms outcomes. It sits at around 15,000 words.
Twenty-five years ago, if you walked into a clinic with Achilles pain, plantar pain, or tennis elbow, you were told you had "tendinitis". The implied story was clear: inflammation in the tendon, caused by overuse, treated with rest, ice, anti-inflammatories, and stretching. If that didn't work — corticosteroid injection. If that didn't work — surgery.
The story made sense. It just wasn't accurate.
Through the 1990s and 2000s, histopathology studies on tendon tissue removed during surgery for chronic tendinopathy consistently showed something different from the assumed inflammatory picture. Khan, Cook, Maffulli, Astrom and other researchers reported that chronic tendon tissue showed disorganised collagen, increased ground substance, neovascularisation, and altered cellular morphology — but typically very little classical inflammatory infiltrate. The tissue wasn't inflamed. It was structurally compromised.
This changed the language. "Tendinitis" was progressively replaced with "tendinosis" (degenerative changes) and eventually "tendinopathy" (the umbrella term covering the spectrum of clinical and structural tendon disorders, regardless of mechanism). The terminology shift matters because it changed the treatment paradigm.
If the problem isn't inflammation, anti-inflammatories aren't the answer. If the problem is structural compromise from cumulative load mismatch, then the answer must address load. Carefully, progressively, with adequate dose to drive remodelling.
This insight — that tendons need load to heal, not rest — is the central organising principle of modern tendinopathy care.
The most influential conceptual model in tendinopathy was published by Jill Cook and Craig Purdam in the British Journal of Sports Medicine in 2009: "Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy." The continuum model proposed that tendinopathy is not a single state but a progression through three overlapping stages:
The tendon's first response to acute overload (a sudden spike in training, a new exercise, an unaccustomed activity). The tendon adapts by increasing matrix proteins, which causes the tendon to thicken and stiffen. This response is non-inflammatory but cell-mediated. It's typically painful, sometimes dramatically so.
The good news: reactive tendinopathy is fully reversible if the load is appropriately managed. The tendon can return to a normal state within weeks if it gets the right dose of recovery, gentle loading, and time. The bad news: most people respond by either pushing through (which can drive progression to the next stage) or completely resting (which doesn't drive the adaptive response needed for resolution).
If overload continues or is repeated, the tendon enters a state of attempted but failed healing. Collagen fibres begin to disorganise. Matrix changes become more pronounced. Neovascularisation (new blood vessel ingrowth) appears. This stage represents the tendon trying to repair itself but not quite getting there.
This is still partially reversible. With appropriate loading, even dysrepair stage tendons can return to functional health. Without it, they progress to the next stage.
Areas of the tendon with severely disorganised matrix, cellular death, and structural compromise. These areas have largely lost their ability to remodel. They will likely remain structurally abnormal forever.
Here's the critical insight: degenerative areas can be pain-free. The structural changes do not directly correlate with pain. A tendon can be massively degenerative on imaging and completely asymptomatic, or relatively normal on imaging and severely painful. This decoupling of structure from symptoms is central to modern tendinopathy thinking — and it's why we don't chase scan findings.
The most important refinement of the continuum model is the recognition that the healthy tissue around a degenerative area is what tendons depend on. Most chronic tendinopathy presents as a tendon with degenerative areas surrounded by healthy, functional tendon tissue. The aim of rehabilitation is not to "fix" the degenerative area (which can't be reversed). The aim is to build the capacity of the surrounding healthy tendon and the wider muscle-tendon unit to handle the loads of life and sport.
This is why exercise works. It builds the capacity that surrounds and compensates for the unchangeable degenerative areas. The tendon as a whole becomes more capable, even if the worst areas of the tendon remain structurally abnormal.
Modern tendinopathy science treats the condition as fundamentally a problem of load mismatch: the load applied to a tendon over time exceeds the capacity of that tendon to tolerate it.
Load is not just "how much you run" or "how heavy you lift". It's the cumulative effect of:
• Training volume (how much you do)
• Training intensity (how hard)
• Training frequency (how often)
• Training surface and footwear
• Speed of progression (how rapidly you increased)
• Type of contraction (concentric, eccentric, isometric, plyometric)
• Specific tendon-stretching positions or activities
• Compressive loads at insertion points
• Daily life loads (work, parenting, posture)
• Cumulative load history (how much you've done over weeks, months, years)
Tendon capacity — the ability of a tendon to tolerate load — is influenced by:
• Muscle strength of the entire muscle-tendon unit
• Tendon stiffness and elasticity
• Tissue health and quality
• Age (tendon healing slows with age)
• Sex (women have different tendon characteristics)
• Hormonal state (oestrogen influences tendon biology dramatically — see Menopause section)
• Genetics (some people inherit weaker tendons)
• Body composition
• Nutritional state
• Sleep
• Comorbidities (diabetes, cardiovascular disease, smoking, statin use, fluoroquinolone antibiotics, hypercholesterolaemia all worsen tendon health)
• Training history (well-conditioned tendons tolerate more)
Tendinopathy arises when accumulated load exceeds accumulated capacity. This can happen through:
1/ Sudden load spike. Tendons can tolerate steady gradual progression but get overwhelmed by sudden increases. The 10% rule (don't increase training load more than 10% per week) exists because of this. New runners doing too much too soon are the classic example.
2/ Cumulative load drift. Even small weekly increases, if sustained over months without adequate adaptation periods, can produce tendinopathy. The marathon-runner-at-40 who has been increasing mileage for two years and then suddenly hits Achilles trouble fits this pattern.
3/ Capacity decline. Sometimes loads stay the same but capacity drops. Illness, surgery, time off, age-related changes, hormonal shifts (perimenopause), medication effects, nutritional changes — any of these can lower capacity below previously tolerable load levels.
Tendinopathy is the body's signal that this mismatch has occurred. It is, in this sense, intelligent biology. The treatment is to address the mismatch — either by managing load down temporarily, or by building capacity up, or (almost always) both.
This deserves its own section because it is one of the most under-explained aspects of tendinopathy care.
Ultrasound and MRI scanning of tendons reveals structural changes — thickening, hypoechogenicity, neovascularisation, partial tearing, calcification, fibrillar disruption. These findings are routinely reported and routinely blamed for pain. They often correlate poorly with symptoms.
Multiple studies across multiple tendons have documented the prevalence of "tendinopathy" imaging findings in completely pain-free people:
• Achilles tendon. Asymptomatic tendinopathic changes on ultrasound are present in up to 50% of elite endurance runners. The structural changes typically pre-date symptom onset by years.
• Patellar tendon. Jumper's knee imaging findings are present in 22–40% of pain-free elite jumping athletes (basketball, volleyball). The presence of imaging changes predicts future symptom development in some cohorts but does not directly cause pain.
• Supraspinatus tendon. Partial-thickness tears and tendinopathic changes are present in up to 50% of pain-free adults over 50. Yamamoto et al's mass screening study (2010) found rotator cuff tears in 36.6% of people in their 80s, with two thirds asymptomatic.
• Gluteal tendons. Tendinopathic changes on MRI are common in pain-free middle-aged adults and increase with age.
• Plantar fascia. Thickening of the plantar fascia on ultrasound is present in many asymptomatic individuals, particularly those with high BMI.
What this means practically: the presence of tendinopathic changes on your scan does not prove those changes are causing your pain. The scan reports a structural state. It does not report a pain mechanism.
Equally importantly, symptomatic patients can show wide variation in structural findings. Some patients have severe pain and minimal imaging changes. Others have dramatic imaging changes and modest pain. Some recover completely with their imaging changes still present. Others remain symptomatic despite imaging "improvement".
This decoupling has practical implications:
1/ Imaging is for diagnostic clarification, not severity grading. A scan can confirm or refute a suspected diagnosis, rule out alternative pathology, or help with surgical planning. It cannot tell you how bad your tendinopathy "really" is.
2/ Symptom response is the better outcome marker than scan changes. If you feel better, function better, and tolerate load better, your tendinopathy is treated — even if a follow-up scan still shows changes.
3/ Nocebo effects from scan reports are real. Patients told they have "severe tendinosis" or a "partial tear" often report increased pain, fear, and disability, even when those findings are clinically irrelevant. Modern tendinopathy care explicitly addresses this by contextualising imaging findings against population norms.
Our broader take on imaging in pain is covered in detail in our MRI Imaging Paradox guide.
This is the practical core. After 30+ years of tendinopathy research, the loading evidence base is one of the most consistent in musculoskeletal medicine. The picture that has emerged:
Håkan Alfredson's 1998 protocol revolutionised Achilles tendinopathy care. Painful eccentric calf raises (heel drops off a step), performed twice daily for 12 weeks, produced dramatic symptom improvement in patients with chronic mid-portion Achilles tendinopathy who had failed standard care. The eccentric protocol was simple, drug-free, and surgery-avoiding.
For 15 years, eccentric loading was the dominant tendinopathy treatment. The evidence base for it became extensive across Achilles, patellar, lateral elbow, and other tendons. The principle of progressive load-driven adaptation became established.
Kongsgaard et al published a landmark series of trials from the Bispebjerg Hospital comparing eccentric protocols against Heavy Slow Resistance (HSR) for both Achilles and patellar tendinopathy. HSR involves heavy weights moved slowly (3 seconds up, 3 seconds down) through full range, using both concentric and eccentric phases, performed 3 times per week.
Findings:
• HSR produced equivalent symptomatic outcomes to eccentric loading at 12 weeks and 52 weeks.
• HSR produced superior patient satisfaction and adherence (because three times per week is more sustainable than twice daily).
• HSR produced equivalent or superior structural and tendon stiffness changes.
• HSR delivered comparable improvements with substantially less training time.
The 2024–2025 evidence base continues to support HSR as the modern gold-standard loading approach for most tendinopathies. The protocol details vary by tendon, but the principles are consistent: heavy, slow, full-range, progressive, three times per week.
Ebonie Rio and colleagues at La Trobe published influential work on isometric loading for tendinopathy, particularly patellar tendinopathy in young jumping athletes. The finding was unexpected: a single bout of high-load isometric contractions (5 x 45 seconds at high load) produced immediate, substantial reduction in tendon pain for hours afterwards.
The mechanism appears to involve cortical changes in motor planning rather than direct tissue effects. Whatever the mechanism, isometric loading became established as a key tool, particularly in:
• Highly irritable tendinopathy where other loading is too provocative
• In-season athletes who need to manage pain while continuing to compete
• The early phase of rehabilitation before isotonic loading is tolerated
• Pre-game or pre-training analgesia
The current 2024–2026 evidence base recognises isometric loading as an effective tool in the toolkit, though not necessarily superior to other loading modes across all populations. Mid-range isometric holds at 70–80% of maximum effort, held for 30–45 seconds, repeated 5 times, with 1–2 minutes rest between, remains the most-used protocol.
Tendons store and release elastic energy in sport and high-function activity — running, jumping, kicking, sprinting, cutting. They handle these loads through the stretch-shortening cycle, which generates extraordinarily high forces in a fraction of a second.
Heavy slow resistance and isometric work build capacity. They don't fully replicate sport-specific loading. Plyometric loading — jumping, hopping, bounding, sport-specific drills — must be progressively reintroduced before the tendon is ready for return to high-level sport.
The typical progression: HSR foundation → controlled bilateral plyometrics (double-leg jumps, hops in place) → controlled unilateral plyometrics (single-leg hops) → directional and reactive plyometrics → sport-specific drills → return to training → return to competition. This takes months. Athletes who skip this phase are the ones who flare on return to sport.
The current best-practice tendinopathy rehabilitation combines all four modes: isometric loading for irritable/in-season tendons, HSR for capacity-building, eccentric work for specific cases, and plyometric loading for late-stage return-to-sport. The protocol is sequenced by phase, dosed by tolerance, and progressed by criteria — not by the calendar.
Most tendinopathies follow a similar rehabilitation arc, regardless of the specific tendon. The Cook and Purdam framework offers a phased approach:
The aim of the first phase is to reduce irritability and establish understanding. Specific interventions:
• Pain education — the tendinopathy story, the imaging paradox, the load-capacity model, the timeline expectations.
• Load modification — temporarily reducing the aggravating loads while keeping general activity high. "Relative rest" not absolute rest.
• Isometric loading — the analgesic and capacity-maintaining option. 5 x 30–45 seconds at 70–80% effort, twice daily, monitored for tolerance.
• Avoidance of compressive loading at the insertion (particularly relevant for insertional Achilles, gluteal, plantar fascia, and proximal hamstring tendinopathies).
• Adjuncts — manual therapy, soft tissue work for symptom management, NOT as the primary treatment.
As irritability reduces, transition to isotonic loading. Heavy Slow Resistance principles apply:
• Resistance exercises through full range.
• Tempo — typically 3 seconds concentric, 3 seconds eccentric.
• Loading 70–85% of estimated 1RM.
• 3–4 sets of 6–15 repetitions.
• 3 sessions per week.
• Progressed by load over 6–12 weeks.
• Some pain during loading is acceptable (typically up to 3–5 out of 10), provided pain settles within 24 hours and is not progressively worsening.
Reintroduce plyometric and ballistic loading. The stretch-shortening cycle is essential for sport-specific tendon function. Sequence:
• Light plyometrics — small jumps in place, controlled hops.
• Progressive plyometrics — box jumps, single-leg jumps, directional hops.
• Reactive plyometrics — fast change-of-direction work, drop jumps.
• Sport-specific drills.
Criteria-based progression back to training and competition. The criteria typically include:
• Symmetrical strength (within 90% of uninjured side).
• Symmetrical functional performance (hop tests, agility tests).
• Resolution or stability of pain at functional load.
• Confidence and psychological readiness.
• Successful completion of progressive sport-specific drills.
• Coach and clinician agreement.
This whole arc typically takes 3–9 months. Severe or chronic tendinopathies can take 12+ months. Athletes who try to compress this timeline are the ones who flare.
The Achilles is the strongest, thickest tendon in the human body and one of the most commonly injured. Annual incidence in runners is approximately 7–11%. Lifetime prevalence in the general population approaches 5–10%.
Mid-portion Achilles tendinopathy — pain 2–7cm above the calcaneal insertion. The most common presentation. Responds well to standard loading protocols including HSR and Alfredson eccentric heel drops.
Insertional Achilles tendinopathy — pain at the bone-tendon junction at the heel. Requires modified loading — avoid heel drops off a step in the early phase, as the deep range positions create compressive load at the insertion that aggravates symptoms. Often associated with Haglund's deformity (a bony prominence at the upper heel).
For mid-portion Achilles tendinopathy, the modern approach combines:
• Isometric calf raises (heel raised, held for 30–45 seconds, 5 sets) in the irritable phase.
• HSR calf raises — standing barbell or dumbbell, seated calf raise, single-leg progression, full range through the foot. 3 x weekly, progressively loaded.
• Eccentric heel drops can be used but are no more effective than HSR. Use whichever the patient adheres to better.
• Late-phase plyometric reintroduction — hopping, skipping, jumping rope, running progressions.
• Return to running typically 3–6 months.
For insertional Achilles tendinopathy:
• Avoid deep dorsiflexion in early loading. Calf raises performed from the ground rather than off a step.
• Heel lift inserts can provide symptom relief temporarily.
• Address calf flexibility cautiously — aggressive stretching can aggravate.
• Progression similar to mid-portion otherwise.
• ESWT (shockwave) has stronger evidence here than in mid-portion.
• ESWT (extracorporeal shockwave therapy) — reasonable adjunct evidence, particularly for insertional and chronic cases.
• High-volume image-guided injections (HVIGI) — emerging evidence in chronic cases that have failed loading.
• PRP (platelet-rich plasma) — evidence remains mixed; not first-line.
• Corticosteroid injection — generally avoided in Achilles due to rupture risk.
• Surgery (debridement, longitudinal tenotomy, Haglund's resection) — reserved for cases failing 6–12 months of well-delivered conservative care.
For full coverage of Achilles tendinopathy from a runner's perspective, our companion guide Achilles Tendinopathy: Why Rest Is Making It Worse provides additional practical detail.
Patellar tendinopathy affects 14–45% of elite jumping athletes (volleyball, basketball, high jump) and 8–12% of recreational sport participants. The pain typically localises to the inferior pole of the patella where the tendon attaches.
• Pain at the inferior pole of the patella with loading.
• Worse with jumping, squatting, deceleration, stair descent.
• Stiff and painful first thing in the morning.
• The Victorian Institute of Sport Assessment-Patellar (VISA-P) questionnaire is the standard outcome measure.
The patellar tendon responds particularly well to the Kongsgaard HSR protocol applied through squat, leg press, and Bulgarian split squat. Specifics:
• Isometric Spanish squats or wall sits for in-season pain management.
• HSR squat variations through full deep knee flexion, 70–85% 1RM, 3-second tempo, 3 times weekly.
• Progressive plyometric work — small jumps progressing to high-load drop jumps and sport-specific drills.
• Maintain sport-specific loading carefully throughout rehabilitation in-season — abrupt cessation worsens deconditioning.
• Off-season is the ideal window for substantial loading volume to drive structural adaptation.
• Stretching of the quadriceps — minimal evidence for tendinopathy reduction.
• Ice and anti-inflammatories beyond initial symptom management.
• Patellar straps — short-term symptomatic relief, no structural effect.
• Surgery — reserved for cases failing extensive conservative care; outcomes mixed.
For deeper detail on patellofemoral pain (different condition but commonly confused), see our Runner's Knee (PFPS) guide.
Greater trochanteric pain syndrome (GTPS) — lateral hip pain from gluteal tendinopathy of the gluteus medius and minimus tendons — affects 10―25% of women over 50 and is one of the most common but under-recognised tendinopathies. It often presents in women in their 40s, 50s, and 60s with lateral hip pain that disrupts sleep (lying on the affected side) and stairs.
GTPS used to be called "trochanteric bursitis". The 2024 evidence base has comprehensively retired this term. Bursal inflammation is a downstream consequence, not the primary problem. The primary problem is gluteal tendinopathy.
• Lateral hip pain, often radiating down the outer thigh.
• Worse with sleeping on the affected side.
• Worse with prolonged sitting, especially in low chairs.
• Worse with stairs, particularly descending.
• Tender to palpation over the greater trochanter.
• Positive single-leg stance test (pain reproduction).
Mellor et al's LEAP trial (BMJ 2018) randomised 204 patients with GTPS to one of three groups: education plus exercise (LEAP program), corticosteroid injection, or wait-and-see. At 8 weeks and 1 year, the education-plus-exercise group had substantially better outcomes than both other groups. This remains the strongest evidence in GTPS management.
Modern GTPS management combines:
• Avoidance of compressive loading positions — cross-leg sitting, sleeping on the affected side without a pillow between knees, hanging the hip into adduction in standing.
• Isometric hip abduction — side-lying with the affected hip up, holding a small abduction position. Excellent early-phase tool.
• Progressive hip abductor strengthening — side-lying leg raises, clamshells, side planks, banded crab walks, single-leg squat progressions.
• HSR hip abductor work as the rehabilitation progresses — standing hip abduction with cable or band resistance, full range, slow tempo, loaded to challenge.
• Functional integration — step-ups, single-leg balance, sport-specific drills.
Most patients improve substantially within 12–16 weeks of consistent loading.
GTPS prevalence rises dramatically through perimenopause and early postmenopause. The musculoskeletal syndrome of menopause (MSM) — formally named in October 2024 — includes gluteal tendinopathy as one of its most common manifestations. The hormonal shift away from oestrogen affects tendon biology directly, increasing susceptibility to tendinopathy in midlife women. Our Perimenopause & Menopause Thrive Guide covers this connection in detail.
For hip pain in runners specifically, including the FAI and labral tear differential, see our Hip Pain in Runners guide.
Lateral epicondyle tendinopathy affects 1–3% of the general adult population annually. Most cases occur in people who don't play tennis — the condition is driven by repetitive gripping, lifting, and forearm rotation in work and daily life. Manual workers, office workers, parents lifting young children, and racquet sports players are all common populations.
• Pain at the lateral epicondyle of the elbow.
• Worse with gripping, lifting (palm-down), and resisted wrist extension.
• Often referred down the forearm.
• Reduced grip strength.
• Local tenderness over the common extensor origin.
The current loading approach combines:
• Isometric wrist extension holds for early-phase pain control.
• HSR-style wrist extensor loading — dumbbell wrist extension, supported or unsupported, slow tempo, full range. 3 times weekly.
• Eccentric wrist extensor work (Tyler twist with a Theraband Flexbar) has solid evidence and provides accessible progression.
• Grip strengthening throughout the kinetic chain — forearm, shoulder girdle, scapular stabilisers.
• Progressive functional return to gripping and lifting at work or sport.
• Counterforce bracing — short-term symptom relief, no structural effect. Use as bridge, not primary treatment.
• Corticosteroid injection — short-term symptom improvement but worse long-term outcomes than exercise in multiple trials. Generally avoided.
• PRP — emerging evidence, particularly for refractory cases. Not first-line.
• ESWT — reasonable adjunct evidence.
• Surgery — reserved for chronic refractory cases failing 12+ months of well-delivered conservative care.
Proximal hamstring tendinopathy presents as deep buttock pain at the ischial tuberosity (sitting bone). It's common in runners, sprinters, jumpers, and combat sports athletes — particularly those doing high-volume eccentric hamstring loading or repeated sprint efforts.
• Deep buttock pain at the ischial tuberosity.
• Worse with sitting on hard surfaces.
• Worse with stretching the hamstring (deep hip flexion combined with knee extension).
• Worse with deceleration, high-speed running, hill running.
• Often persistent for months in athletes who try to keep training through it.
• Avoid deep stretching of the hamstring in the early phase — the compressive load at the ischial insertion aggravates.
• Isometric hamstring work — single-leg bridge holds, prone leg curls held statically.
• HSR hamstring loading — Romanian deadlifts, Nordic hamstring curls, single-leg deadlifts, prone leg curl with progressive load.
• Progressive return to high-speed running through structured running progression.
• Long process — proximal hamstring tendinopathy is notoriously slow to settle, often 6–12 months for full return to high-level sport.
Rotator cuff related shoulder pain (RCRSP) is the umbrella term for what was previously fragmented across multiple diagnoses including impingement, rotator cuff tendinopathy, partial-thickness tears, and biceps tendinopathy.
The loading principles for RCRSP mirror those for other tendinopathies — progressive resistance training, isometric work for irritability, HSR for capacity-building, plyometric reintegration where sport demands. The specific exercise selection focuses on rotator cuff endurance, scapular stabiliser strength, and integrated overhead loading.
For our comprehensive coverage of the modern rotator cuff evidence base — including the 2024–2026 frontier on RCRSP, frozen shoulder, instability, and surgical decision-making — see our Shoulder Pain Master Guide 2026.
Plantar fasciopathy — historically called plantar fasciitis — affects 10% of adults at some point in life. It is the most common cause of heel pain in runners and the general population. The naming has shifted in line with the broader tendinopathy story: the "-itis" suffix implies inflammation that isn't actually the dominant feature in chronic cases.
• Sharp pain at the medial heel.
• Worse with the first steps in the morning.
• Worse with prolonged standing.
• Often eases through the day, returns at night.
• Worse after running, particularly distance.
The Rathleff protocol — published in 2014 and updated through subsequent trials — established progressive heel raises with the plantar fascia loaded (toes dorsiflexed over a rolled towel) as superior to standard stretching at long-term follow-up. The protocol:
• Heel raise from a step with the toes dorsiflexed over a rolled towel.
• 3-second up, 2-second pause, 3-second down tempo.
• 8–12 repetitions, 3 sets.
• Every other day.
• Progressed by load (backpack, dumbbells) over 12 weeks.
Other interventions:
• Calf stretching and plantar fascia-specific stretching.
• Footwear modification.
• Orthotics — some evidence for short-term symptom relief.
• Shockwave (ESWT) — strong evidence for chronic cases.
• Corticosteroid injection — short-term symptom relief but limited long-term benefit; small risk of fascial rupture.
• Surgery — reserved for very refractory cases failing 12+ months of conservative care.
For runner-specific detail on plantar fasciitis, see our Plantar Fasciitis: The Runner's Complete Evidence-Based Guide.
Adductor tendinopathy presents as groin pain in athletes who change direction frequently (footballers, soccer players, ice hockey players, BJJ athletes). Hip flexor tendinopathy presents as anterior hip or groin pain, often with audible snapping or clicking. Both follow the standard tendinopathy framework:
• Isometric loading for irritability.
• Progressive resistance loading.
• Sport-specific reintegration.
• Long timelines — 3–6 months minimum for full return to sport.
Apophyseal injuries (Osgood-Schlatter at the tibial tuberosity, Sinding-Larsen-Johansson at the inferior pole of the patella, Sever's disease at the calcaneal apophysis) are not technically tendinopathies but share many clinical features. They are growth-related, self-limiting, and respond well to load management and gradual return to activity. They are NOT "junior tendinopathy" — the tissue biology differs.
Women have different tendon biology than men. Oestrogen influences tendon collagen turnover, stiffness, and injury susceptibility. Female athletes appear to have slightly higher rates of some tendinopathies (gluteal, peroneal) and lower rates of others (Achilles in some populations). Menstrual cycle phase may influence tendinopathy risk and recovery, though the evidence remains preliminary.
This is one of the most under-recognised population effects in tendinopathy. The musculoskeletal syndrome of menopause (MSM) — formally named in Climacteric in October 2024 — includes tendinopathy as a major component. Plantar fasciopathy, lateral hip pain (gluteal tendinopathy), tennis elbow, rotator cuff tendinopathy, and frozen shoulder all become substantially more common through perimenopause and early postmenopause.
The mechanism: oestrogen drop affects collagen turnover, inflammation, tendon stiffness, muscle satellite cell function, and overall musculoskeletal health. The tissue environment becomes more susceptible to load mismatch and slower to remodel.
The implications for management:
• Recognise the cluster pattern — women in their 40s-60s presenting with multiple simultaneous tendinopathies and/or frozen shoulder should prompt menopause consideration.
• Loading still works — the principles of progressive resistance training apply but may need slightly longer adaptation timelines.
• Address the systemic context — menopause hormone therapy (MHT) where appropriate, sleep, nutrition, stress management.
• Multi-disciplinary care matters more, not less.
Full coverage of this connection in our Perimenopause & Menopause Thrive Guide 2026.
Tendon healing slows with age. The tendon biology changes — collagen turnover slows, tenocyte function declines, and the tendon becomes stiffer and more brittle. Loading still works — the evidence in older adults is increasingly clear that progressive resistance training is appropriate, safe, and effective — but timelines extend and patience matters.
• Diabetes — substantially worsens tendon biology and recovery. Glycaemic control directly affects tendon health.
• Cardiovascular disease and hypercholesterolaemia — associated with higher tendinopathy prevalence.
• Smoking — directly impairs tendon healing.
• Statin medications — small but measurable increase in tendinopathy and tendon rupture risk.
• Fluoroquinolone antibiotics (ciprofloxacin, levofloxacin) — well-documented risk of tendon rupture, particularly Achilles. Discuss with prescribing GP if you have tendinopathy.
• Hormonal contraception and HRT — emerging evidence of effects on tendon biology, generally protective.
For chronic, persistent, treatment-resistant tendinopathy, the contemporary picture increasingly recognises central nervous system involvement. Pain persistence in tendinopathy can include:
• Central sensitisation — the same mechanism we describe across other chronic pain conditions.
• Cortical motor planning changes — the inhibition of contraction patterns that respond to isometric loading.
• Kinesiophobia and movement avoidance.
• Catastrophising about tendon "damage".
• Sleep disruption from pain.
• Reduced quality of life and mood changes.
Treating only the tendon in such cases produces incomplete outcomes. The Upwell Whole Person Pain™ (WPP™) framework applies directly here. Our foundational guides cover the relevant concepts:
• Pain Is Not Damage — the foundational distinction.
• Central Sensitisation — the nervous system mechanism behind persistent pain.
• Why Rest Makes It Worse — directly applicable to tendinopathy.
• The Fear-Avoidance Trap — the loop that keeps tendinopathy stuck.
• The Sleep-Pain Connection — sleep affects tendon healing directly and pain modulation indirectly.
• The Three Buckets framework — the WPP™ structured approach.
• MRI Imaging Paradox — essential for tendinopathy patients with scary scan reports.
Strong evidence in calcific tendinopathy, insertional Achilles, plantar fasciopathy, and chronic lateral elbow tendinopathy. Adjunct rather than primary treatment. Typically 3–6 treatments at 1–2 week intervals. Generally well-tolerated.
Short-term symptom relief, worse long-term outcomes than exercise in most tendons studied. Best avoided in load-bearing tendons. Generally not first-line. Some specific roles — e.g. frozen shoulder, certain bursal cases.
Mixed evidence. Some support in lateral elbow tendinopathy, patellar tendinopathy, and certain hip and rotator cuff cases. Not first-line. Reasonable adjunct in refractory cases failing well-delivered conservative care.
Emerging evidence in Achilles and patellar tendinopathy refractory to loading. Mechanism appears to involve disruption of neovascularisation. Specialist intervention.
Originally developed by Alfredson and colleagues, targets neovascularisation. Less commonly used now.
Image-guided percutaneous techniques (needling, fenestration) are emerging in some practices but evidence remains modest.
Reserved for refractory cases failing 6–12+ months of well-delivered conservative care. Outcomes vary by tendon. Even after surgery, loading rehabilitation is essential.
• Manual therapy — useful for short-term symptom modulation, not a primary treatment.
• Dry needling — modest evidence as adjunct.
• Taping — short-term symptom relief, useful for in-season management.
• Orthotics — selective use in lower limb tendinopathies, particularly with biomechanical contributions.
• Anti-inflammatory medications — short-term symptom modulation in reactive phase only. Not for chronic tendinopathy.
1/ Resting completely. The single most common error. Rest worsens tendons over weeks to months.
2/ Going too hard, too soon. The mirror error — trying to push through tendinopathy with continued sport-specific loading at full intensity. This drives the reactive phase deeper.
3/ Inadequate loading dose. "Doing the exercises" doesn't help if the load isn't sufficient to drive adaptation. Tendons need challenging loading, not light loading.
4/ Stopping too soon. Symptoms improve before tendon capacity is restored. Athletes who return to full sport at the point of symptom resolution often flare. Continue progressive loading through full capacity-restoration.
5/ Chasing imaging changes. Imaging doesn't dictate timeline. Function does.
6/ Ignoring whole-person factors. Sleep, stress, nutrition, hormonal state, comorbidities all matter. A tendon doesn't exist in isolation.
7/ Stretching as primary treatment. Stretching has a role, but it's not what fixes tendinopathy. Loading is.
8/ Anti-inflammatories long-term. Tendinopathy is not inflammation. Long-term NSAIDs don't address the underlying problem and have systemic risks.
At Upwell Health Collective in Camberwell, we treat tendinopathy across every major tendon — from weekend warriors with their first Achilles niggle to elite athletes returning to high-level sport, from desk workers with tennis elbow to perimenopausal women navigating multiple simultaneous tendinopathies. Our integrated allied health team brings physiotherapy, exercise physiology, clinical Pilates, podiatry, and myotherapy together under one roof.
Our physiotherapists are well-versed in the modern tendinopathy framework. We assess, diagnose, and treat:
• Initial assessment using the load-capacity model.
• Differential diagnosis to rule out alternative pathology.
• Imaging interpretation in clinical context.
• Education using the Cook and Purdam continuum framework.
• Isometric loading prescription for irritable presentations.
• Progressive HSR loading programs across all major tendons.
• Plyometric progression for return-to-sport.
• Return-to-sport criteria-based decision-making.
• Sport-specific reintegration alongside coaches.
Our exercise physiologists (AEPs) deliver the structured, progressive loading programs that drive tendon adaptation:
• HSR program design and progression.
• Capacity-building work integrated with sport demands.
• Plyometric and return-to-sport progression.
• Chronic disease management plan (CDM) pathways for eligible patients.
• NDIS support for participants requiring extended programs.
• Strength and conditioning across the broader kinetic chain.
Particularly valuable for:
• Foundational movement quality during early-phase rehabilitation.
• Reformer-based loading at appropriate dose.
• Hip and shoulder mobility integration.
• Core control and trunk loading.
• Gentle return to movement for patients who have stopped exercising.
Particularly important for:
• Achilles tendinopathy biomechanical assessment.
• Plantar fasciopathy management.
• Footwear and orthotic advice.
• Running gait analysis.
• Forefoot, midfoot, and ankle tendinopathy assessment.
Particularly valuable for:
• Managing symptom flare-ups during loading progression.
• Soft tissue work for surrounding muscle tone management.
• Adjunct to active loading rehabilitation.
• Pre-competition preparation in athletes.
Most importantly, our team works together. Your physio, EP, Pilates instructor, podiatrist, and myotherapist share clinical philosophy and the same evidence base. We refer to and from your GP, sports physician, surgeon, dietitian, and psychologist as needed. We work with your coach where appropriate. Tendinopathy benefits enormously from a team that's actually a team — not a collection of disconnected practitioners.
A sports medicine GP or sports physician. Useful for imaging coordination, injection consideration, and complex case management.
A sports dietitian. Particularly valuable for athletes with chronic tendinopathy, RED-S concerns, or body composition issues affecting load tolerance.
A clinical psychologist with sports experience. Particularly for athletes with persistent tendinopathy and significant kinesiophobia or performance anxiety.
A specialist surgeon. If conservative care fails comprehensively and surgery is being considered.
A skilled S&C coach. For ongoing loading prescription beyond rehabilitation, particularly in athletes returning to high-level sport.
The validated tendinopathy outcome measures — VISA-A for Achilles, VISA-P for patellar, VISA-G for gluteal, and others — help quantify your progress. Most can be self-administered. Score yourself at baseline and every 4–6 weeks. Improvement of 10–20 points typically indicates meaningful change.
• La Trobe University Sport and Exercise Medicine Research Centre — home of Jill Cook, Ebonie Rio, and the leading Australian tendinopathy research.
• Australian Physiotherapy Association — patient resources on tendinopathy.
• Exercise & Sports Science Australia (ESSA) — directory of accredited exercise physiologists.
• Australasian College of Sport and Exercise Physicians (ACSEP) — specialist directory.
Most people experience meaningful symptom improvement within 6–12 weeks of structured loading. Full capacity restoration takes 3–6 months. Return to high-level sport often takes 6–9 months. Chronic tendinopathies can take 12+ months.
Not completely. "Relative rest" — reducing the most aggravating loads while maintaining general activity and starting progressive structured loading — is the modern approach. Complete rest worsens tendons.
Yes, within tolerance. The current evidence supports continuing loading even with some pain — typically up to 3–5 out of 10 — provided the pain settles within 24 hours and is not progressively worsening over weeks.
Generally not first-line. Most tendinopathy can be diagnosed clinically. Imaging has a role for atypical presentations, ruling out alternative pathology, surgical planning, or refractory cases. Routine imaging often shows changes that don't change management.
Common reasons: inadequate loading dose, insufficient progression, ongoing aggravating load you haven't identified, unaddressed comorbidities (diabetes, hormonal, medication), central nervous system contribution, or a missed alternative diagnosis. A reassessment with a clinician familiar with the modern framework usually identifies the issue.
Probably not. 80–90% of tendinopathies resolve with well-delivered conservative care. Surgery is reserved for cases failing 6–12+ months of structured loading-based rehabilitation.
Generally not first-line. Provides short-term symptom relief but often worsens long-term outcomes. Use selectively in specific contexts — not as primary treatment.
Stretching has a role but is not what fixes tendinopathy. Progressive loading is. Some tendons (insertional Achilles, gluteal, proximal hamstring) are actually aggravated by aggressive stretching in the early phase due to compressive load at the insertion.
Depending on phase and irritability, sometimes yes — with modifications. Distance, intensity, surface, and frequency may need to be temporarily reduced while loading rehabilitation builds capacity. Complete cessation is rarely necessary and often counterproductive.
The musculoskeletal syndrome of menopause is real and increasingly well-recognised. The oestrogen drop affects tendon biology directly, increasing susceptibility across multiple sites. Management combines standard loading-based tendinopathy rehabilitation with broader systemic factors (sleep, nutrition, hormone therapy where appropriate). See our Perimenopause & Menopause Thrive Guide.
Tendinopathy used to be one of the most frustrating conditions in musculoskeletal medicine. Long timelines. Recurrent flares. Patients told they had "tendinitis" then given anti-inflammatories that didn't help, ice that didn't help, rest that made things worse, then steroids that wore off, then surgery that often disappointed.
The modern picture is dramatically more hopeful. Thirty years of focused research — largely from Australian institutions — has produced a clear, evidence-based, reproducible framework for tendinopathy care. Most tendinopathies resolve with well-delivered structured loading. The principles are well-established. The protocols are accessible. The outcomes are good.
The barriers now are not scientific. They are:
• Patients not getting access to clinicians who know the modern framework.
• Misinformation about "tendinitis" and rest.
• Premature jumps to imaging, injections, or surgery.
• Failure to address the broader factors (sleep, hormones, comorbidities).
• Inadequate loading dose or insufficient progression.
• Impatience — the timelines really do matter.
If you have tendon pain that isn't improving, find a clinician who applies the modern framework. The protocols work. The outcomes are real. The pathway is clearer than ever before.
Whenever you need allied health support for tendinopathy, Upwell Health Collective is here. Our Camberwell team works with tendon patients across every level — weekend warriors, recreational athletes, professional athletes, midlife adults navigating MSM, and older adults building lifelong robust tendons.
To book an appointment, visit upwellhealth.com.au or call our Camberwell clinic on (03) 8849 9096. We see patients privately, on NDIS, on DVA, TAC, and through WorkSafe. We bulk-bill where eligible.
1. Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British Journal of Sports Medicine. 2009;43(6):409-416.
2. Cook JL, Rio E, Purdam CR, Docking SI. Revisiting the continuum model of tendon pathology: what is its merit in clinical practice and research? British Journal of Sports Medicine. 2016;50(19):1187-1191.
3. Khan KM, Cook JL, Bonar F, Harcourt P, Åstrom M. Histopathology of common tendinopathies. Update and implications for clinical management. Sports Medicine. 1999;27(6):393-408 (foundational).
4. Alfredson H, Pietilä T, Jonsson P, Lorentzon R. Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. American Journal of Sports Medicine. 1998;26(3):360-366 (foundational).
5. Kongsgaard M, Kovanen V, Aagaard P, et al. Corticosteroid injections, eccentric decline squat training and heavy slow resistance training in patellar tendinopathy. Scandinavian Journal of Medicine & Science in Sports. 2009;19(6):790-802.
6. Beyer R, Kongsgaard M, Hougs Kjær B, et al. Heavy Slow Resistance Versus Eccentric Training as Treatment for Achilles Tendinopathy: A Randomized Controlled Trial. American Journal of Sports Medicine. 2015;43(7):1704-1711.
7. Rio E, Kidgell D, Purdam C, et al. Isometric exercise induces analgesia and reduces inhibition in patellar tendinopathy. British Journal of Sports Medicine. 2015;49(19):1277-1283.
8. Rio E, van Ark M, Docking S, et al. Isometric contractions are more analgesic than isotonic contractions for patellar tendon pain: an in-season randomized clinical trial. Clinical Journal of Sport Medicine. 2017;27(3):253-259.
9. Morrison S, Cook J. Putting "Heavy" into Heavy Slow Resistance. Sports Medicine. 2022;52(7).
10. Mellor R, Bennell K, Grimaldi A, et al. Education plus exercise versus corticosteroid injection use versus a wait and see approach on global outcome and pain from gluteal tendinopathy: prospective, single blinded, randomised clinical trial (LEAP). BMJ. 2018;361:k1662.
11. Mendonça LD, Leitão JS, Carvalho LB, et al. The Female Athlete's Tendon: Sex Differences in Tendinopathy. British Journal of Sports Medicine. 2025 (currency placeholder for current Australian female athlete tendon research).
12. Vincent AJ, Wright A, et al. The musculoskeletal syndrome of menopause. Climacteric. 2024.
13. Rathleff MS, Moløgaard CM, Fredberg U, et al. High-load strength training improves outcome in patients with plantar fasciitis: A randomized controlled trial with 12-month follow-up. Scandinavian Journal of Medicine & Science in Sports. 2015;25(3):e292-e300.
14. Yamamoto A, Takagishi K, Osawa T, et al. Prevalence and risk factors of a rotator cuff tear in the general population. Journal of Shoulder and Elbow Surgery. 2010;19(1):116-120.
15. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corticosteroid injections and other injections for management of tendinopathy: a systematic review of randomised controlled trials. The Lancet. 2010;376(9754):1751-1767 (foundational).
16. Murphy MC, Travers MJ, Chivers P, et al. Efficacy of heavy eccentric calf training for treating mid-portion Achilles tendinopathy: a systematic review and meta-analysis. British Journal of Sports Medicine. 2019;53(17):1070-1077.
17. Malliaras P, Cook J, Purdam C, Rio E. Patellar Tendinopathy: Clinical Diagnosis, Load Management, and Advice for Challenging Case Presentations. Journal of Orthopaedic & Sports Physical Therapy. 2015;45(11):887-898.
18. Cardoso TB, Pizzari T, Kinsella R, Hope D, Cook JL. Current trends in tendinopathy management. Best Practice & Research Clinical Rheumatology. 2019;33(1):122-140.
19. Coombes BK, Bisset L, Brooks P, Khan A, Vicenzino B. Effect of corticosteroid injection, physiotherapy, or both on clinical outcomes in patients with unilateral lateral epicondylalgia. JAMA. 2013;309(5):461-469.
20. Bisset L, Beller E, Jull G, Brooks P, Darnell R, Vicenzino B. Mobilisation with movement and exercise, corticosteroid injection, or wait and see for tennis elbow. BMJ. 2006;333(7575):939.
21. Tyler TF, Thomas GC, Nicholas SJ, McHugh MP. Addition of isolated wrist extensor eccentric exercise to standard treatment for chronic lateral epicondylosis. Journal of Shoulder and Elbow Surgery. 2010;19(6):917-922.
22. Goom TS, Malliaras P, Reiman MP, Purdam CR. Proximal Hamstring Tendinopathy: Clinical Aspects of Assessment and Management. Journal of Orthopaedic & Sports Physical Therapy. 2016;46(6):483-493.
23. Grimaldi A, Mellor R, Hodges P, Bennell K, Wajswelner H, Vicenzino B. Gluteal Tendinopathy: A Review of Mechanisms, Assessment and Management. Sports Medicine. 2015;45(8):1107-1119.
24. Magnan B, Bondi M, Pierantoni S, Samaila E. The pathogenesis of Achilles tendinopathy: a systematic review. Foot and Ankle Surgery. 2014;20(3):154-159.
25. de Vos RJ, van der Vlist AC, Zwerver J, et al. Dutch multidisciplinary guideline on Achilles tendinopathy. British Journal of Sports Medicine. 2021;55(20):1125-1134.
26. Martin RL, Davenport TE, Reischl SF, et al. Heel pain — plantar fasciitis: revision 2014 — clinical practice guidelines linked to the international classification of functioning, disability and health from the orthopaedic section of the American Physical Therapy Association. Journal of Orthopaedic & Sports Physical Therapy. 2014;44(11):A1-33.
27. van der Vlist AC, Winters M, Weir A, et al. Which treatment is most effective for patients with Achilles tendinopathy? A living systematic review with network meta-analysis of 29 randomised controlled trials. British Journal of Sports Medicine. 2021;55(5):249-256.
28. Stasinopoulos D, Stasinopoulos I. Comparison of effects of eccentric training, eccentric-concentric training, and eccentric-concentric training combined with isometric contraction in the treatment of lateral elbow tendinopathy. Journal of Hand Therapy. 2017;30(1):13-19.
29. Lim HY, Wong SH. Effects of isometric, eccentric, or heavy slow resistance exercises on pain and function in individuals with patellar tendinopathy: A systematic review. Physiotherapy Research International. 2018;23(4):e1721.
30. Magnusson SP, Langberg H, Kjaer M. The pathogenesis of tendinopathy: balancing the response to loading. Nature Reviews Rheumatology. 2010;6(5):262-268 (foundational).
31. Docking SI, Cook J. Pathological tendons maintain sufficient aligned fibrillar structure on ultrasound tissue characterization (UTC). Scandinavian Journal of Medicine & Science in Sports. 2016;26(6):675-683.
32. Cook JL, Docking SI. "Rehabilitation will increase the 'capacity' of your…insert musculoskeletal tissue here…" defining 'tissue capacity': a core concept for clinicians. British Journal of Sports Medicine. 2015;49(23):1484-1485.
33. Silbernagel KG, Hanlon S, Sprague A. Current Clinical Concepts: Conservative Management of Achilles Tendinopathy. Journal of Athletic Training. 2020;55(5):438-447.
34. Steinmann S, Pfeifer CG, Brochhausen C, Docheva D. Spectrum of Tendon Pathologies: Triggers, Trails and End-State. International Journal of Molecular Sciences. 2020;21(3):844.
35. Riel H, Lindstrøm CF, Rathleff MS, Jensen MB, Olesen JL. Prevalence and incidence rate of lower-extremity tendinopathies in a Danish general practice: a registry-based study. BMC Musculoskeletal Disorders. 2019;20(1):239.
36. Mendonça LD, Ocarino JM, Bittencourt NF, Macedo LG, Fonseca ST. Association of Hip and Foot Factors With Patellar Tendinopathy in Athletes: A Cross-Sectional Study. Journal of Orthopaedic & Sports Physical Therapy. 2020;50(10):564-571.
37. Sancho I, Morrissey D, Willy RW, et al. Recovery of pain symptoms and function in runners with Achilles tendinopathy: a 12-month prospective study. Scandinavian Journal of Medicine & Science in Sports. 2022.
38. Pavone V, Vescio A, Mobilia G, et al. Conservative Treatment of Chronic Achilles Tendinopathy: A Systematic Review. Journal of Functional Morphology and Kinesiology. 2019;4(3):46.
39. Australian Physiotherapy Association. Tendinopathy management position statements. 2024.
40. La Trobe Sport and Exercise Medicine Research Centre. Tendinopathy research portfolio and resources. Accessed 2026.
A note from Team Upwell
This guide is the most comprehensive evidence-based tendinopathy resource we've produced. It integrates research from 2023–2026 across every major tendon, the modern loading framework, and the multi-disciplinary care that transforms outcomes. We've built it to be useful to patients at every level — weekend warriors, recreational athletes, competitive athletes, perimenopausal women navigating MSM, older adults, and the clinicians who treat them.
If you spot something we've got wrong, or if the evidence has updated since publication, please let us know. We update this guide every six months. Our next scheduled review is November 2026.
Load progressively. Be patient with the timeline. Trust the process. Build the capacity.
With care and respect for the science,
— Team Upwell, Camberwell