Achilles Tendinopathy

Achilles tendinopathy is a common overuse condition involving structural changes in the Achilles tendon, often resulting from repetitive mechanical loading. Although frequently seen in athletes, particularly runners and jumping sport participants, it also occurs in non-athletic individuals. The condition may present with or without partial tendon tearing and is associated with mechanical overload, decreased flexibility, and impaired tendon adaptation.

Pathophysiology and Terminology

Achilles tendinopathy involves progressive changes in the tendon structure, rather than acute inflammation. Histological examination reveals disrupted collagen fiber alignment, increased water-binding molecules such as glycosaminoglycans, and degenerative cellular activity.

The condition does not always follow a traumatic event. Rather, symptoms typically arise when an already-degenerating tendon is stressed beyond its capacity. Subclinical tendon changes can exist before symptoms manifest. The preferred terminology for this condition is “tendinopathy,” which encompasses the pathological continuum described by Cook and Purdam, including:

1. Reactive tendinopathy – a short-term response to acute overload

2. Tendon disrepair – increased matrix disruption with cellular proliferation

3. Degenerative tendinopathy – permanent structural deterioration with limited healing potential

The tendon may progress along or regress through these stages depending on load management and tissue response.

Location Classification

Achilles tendinopathy is classified anatomically as:

• Midportion tendinopathy: affects the tendon body, typically 2–6 cm above the calcaneal insertion

• Insertional tendinopathy: involves the distal tendon-bone interface, often <2 cm from its insertion

Clinically Relevant Anatomy

The Achilles tendon is the strongest tendon in the human body, formed by the convergence of the gastrocnemius and soleus muscles. It inserts onto the calcaneus and functions to transmit muscular force during plantarflexion activities such as walking, running, and jumping.

The tendon is primarily composed of type I collagen, organized in parallel bundles embedded within an extracellular matrix. Proteoglycans and glycosaminoglycans contribute to the ground substance, providing viscoelastic properties. The tendon is surrounded by a paratenon, a loose connective tissue layer that facilitates gliding and provides limited vascular supply.

Notably, the tendon’s blood supply is sparse, especially in the midportion, which contributes to its limited healing potential.

Etiology

Tendon injury is commonly associated with repeated loading beyond the tendon’s capacity. Mechanical stress leads to microtrauma, particularly when load distribution between the gastrocnemius and soleus is non-uniform. Repetitive strain promotes local matrix disorganization, increased protein synthesis, and, if uncorrected, degenerative change.

Contributing factors include:

• Overuse or training errors

• Reduced flexibility

• Poor tendon vascularity

• Metabolic factors (e.g., obesity, diabetes)

• Genetic predisposition (e.g., COL5A1 gene variants)

Overpronation of the foot is a significant biomechanical risk factor, often resulting in altered loading patterns through the Achilles tendon.

Clinical Presentation

A hallmark symptom is morning pain and stiffness, which reflects impaired tendon elasticity after prolonged inactivity. Pain is typically localized 2–6 cm above the calcaneal insertion. Swelling and nodular thickening may be palpable.

Clinical signs include:

• Pain during and after activity

• Local tenderness and thickening on palpation

• Positive arc sign and Royal London Hospital test

• Limited dorsiflexion and calf flexibility

• Possible atrophy of the calf musculature in chronic cases

Diagnostic imaging is not essential but may aid in differential diagnosis. Ultrasound can detect tendon thickening, neovascularization, and disorganization. MRI is useful for complex or unclear cases.

Differential Diagnosis

• Plantar fasciitis

• Calcaneal stress fracture

• Retrocalcaneal bursitis

• Posterior ankle impingement

• Sural nerve entrapment

• Deep vein thrombosis

• Sever’s disease (in adolescents)

• Partial tendon rupture

Examination

Assessment includes:

• Subjective history: onset, aggravating activities, training changes

• Objective evaluation: inspection for swelling or deformity, strength testing, and range of motion

• Palpation: localized tenderness and thickening

• Functional testing: single-leg heel raises, hop tests

• Posture and biomechanics: including pronation, arch height, and leg alignment

Validated outcome measures include the VISA-A questionnaire, the Foot and Ankle Ability Measure (FAAM), and the Lower Extremity Functional Scale (LEFS).

Physiotherapy Management

Education and Load Modification

Complete rest is discouraged. Instead, patients should modify activity to stay within a tolerable pain threshold while continuing progressive rehabilitation. Patient education includes:

• The role of mechanical loading in tendon adaptation

• Realistic expectations for symptom progression

• Identification and modification of risk factors (e.g., footwear, BMI)

Biomechanical Optimization

A comprehensive biomechanical assessment is recommended. Foot orthotics may provide short-term relief in acute cases and moderate benefit in chronic stages. Taping strategies may assist with symptom control but are supported primarily by expert opinion.

Progressive Tendon Loading

The foundation of treatment is controlled mechanical loading, aimed at restoring the tendon’s ability to store and release energy efficiently. This typically progresses through three stages:

Phase 1: Isometric Loading

Isometric exercises (e.g., static heel raises) help reduce pain and maintain tendon load tolerance. These may be performed using both limbs or single-limb variations depending on tendon irritability.

Phase 2: Isotonic Loading

Once pain subsides, isotonic calf raises are introduced to rebuild strength. Both seated and standing variations target different muscle groups. Heavy slow resistance (HSR) training can be used to further increase tendon and muscular capacity.

Phase 3: Energy Storage and Release

This phase includes plyometric and hopping exercises to simulate sports-specific loading and restore tendon spring mechanics. These exercises should only be introduced when pain is minimal and strength is normalized.

Adjunct Therapies

Adjunct treatments should support, not replace, exercise therapy. Options include:

• Manual therapy: Joint mobilization for joint restrictions (limited evidence)

• Shockwave therapy: May reduce symptoms in chronic cases; low-energy protocols are preferred

• Dry needling: May be used with ultrasound guidance in chronic, thickened tendons

• Iontophoresis: Limited use in acute cases only

• Sclerotherapy: May target neovascularization in recalcitrant cases

• Night splints: May offer benefit in acute cases, not recommended in chronic stages

• PRP injections: No clear evidence of benefit over placebo

• Surgical options: Considered only when conservative treatment fails; includes percutaneous tenotomy, debridement, or newer minimally invasive procedures (e.g., Zadek osteotomy)

Summary

Achilles tendinopathy is a degenerative overuse condition that responds best to progressive mechanical loading. Early diagnosis, activity modification, and targeted rehabilitation are key to restoring tendon function. Adjunct therapies may be used for symptom management but should not replace exercise-based interventions.

Rehabilitation must address not only the tendon itself but the entire kinetic chain contributing to load distribution. Evidence supports the use of heavy, slow resistance training and energy storage exercises to return the tendon to full function. While recovery timelines vary, adherence to a structured program significantly improves long-term outcomes.