Achilles tendinopathy

Achilles Tendinopathy


According to the literature this common, debilitating lower limb condition is the 2nd most common sporting injury (after the knee). It affects 9% of recreational runners and up to 5% of elite athletes, possibly ending a professional athlete’s career. It affects mainly long to middle distance runners, and those runners who have suddenly increased their distance and/or intensity. Sport is not the only predisposing factor as many non-recreational people may encounter the condition. This blog shall discuss injury to the mid-portion of the AT, although the subject of Achilles tendinopathy is so complex it is worthy of a book.


The Achilles tendon (AT) is easily the strongest and largest tendon in the human body. It can stretch by up 6% during running but its breaking strain where rupture can occur is around 9%. It varies in length and thickness averaging 15cm long, and around 2cm at the midsection, and it joins the calf muscles, gastrocnemius and soleus to the calcaneum. A 3rd muscle plantaris also joins in the medial aspect of the tendon, although this muscle is small and not always present. Where the fibres of these muscles insert into the tendon may be pertinent to the cause of injury; the gastrocnemius inserts into the lateral aspect and the soleus fibres insert into the medial aspect. The mid portion of the AT has a poor blood supply, which precludes it to injury and slow recovery from injury. It is surrounded by the paratendon, a protective sheath which too is prone to injury.

Tendons are made up of collagen (mostly type I). Collagen is arranged as fibrils which are grouped as bundles, but these bundles do not run the length of the tendon. They are connected/ embedded in a proteoglycan-water matrix. These fibrils are wavy (crimped), which become straightened with loading, thus allowing for flexibility.  Tendons have poor blood supply, and therefore oxygen consumption is low and as such they are able to transfer loads and endure strain for long periods without fatigue, ischaemia, cell death and failure. However, this means tendons have poor /prolonged healing times once damaged.


Being viscoelastic, tendons transmit forces from the muscles to the bone. Interestingly tendons are more deformable at low loads and capable of storing more energy, but they are stiffer at high loads/strain and capable of transferring greater loads. This is interesting in that the AT is the main structure for storing energy and releasing it in running, hopping and jumping.

Tendons act like springs; their viscoelastic properties enable storage of energy which can be released in walking, hopping and running. The amount of energy released varies in the literature from 16% to 35%. It has previously been shown that the AT releases 1.3 J/step during walking, and up to 38 J per jump during continuous, one-legged hopping. Bosch suggests that the gastrocnemius has an important role in the energy release and the muscle is most active when the knee is extended during midstance in running.

For a given force, energy storage is proportional to elongation – meaning a stiffer tendon will stretch less and store less energy. Considering that it has been demonstrated that AT stiffness is higher in trained compared with untrained runners and changes in AT stiffness are associated with changes in running economy, more highly trained runners should have a lower capacity for AT energy storage/release. The authors suggest that a stiff tendon unit means the muscles (triceps surae) contract less and as such less energy is wasted. Stored energy release is not fixed during ground contact and will be different between rear and mid/forefoot strikers.

It has previously been shown that the AT releases 1.3 J/step during walking and up to 38J per jump during continuous, one-legged hopping. In the latter case, estimated AT forces during hopping approached 5,000 N, the same as for a 70kg man running at middle distance pace – enough to stretch the tendon by 6%. The AT is capable of loads of up to 12x body weight in running, and a 1cm cross sectional sized tendon can bear up to 100kg. The average ultimate tensile strength of the human Achilles tendon (in caderavic specimens aged over 57 years) is only 1189 N. This means that the AT can work beyond its natural breaking point! Repeated loading / training will increase the production of Type I collagen and the overall size and strength of tendons.

A tendon is perfectly elastic so long as the strain does not exceed 4%, after which the viscous range commences. Elasticity is a time-independent phenomenon, while viscosity is a time-dependent phenomenon against force. So long as the strain /lengthening does not exceed 4% the AT behaves in an elastic manner returning to its original length upon unloading. Microscopic failure will start to occur after the strain exceeds 4% and at around 8-10% molecular slippage and damage occurs, causing possible rupture. During fast running the AT will stretch by 5%.

Excessive loading during physical activity/running, or repeated frequent micro trauma from non-uniform stress without allowing for active repair will result in inflammation of the paratendon and then degradation of the tendon. In excessive loading/exercise collagen is laid down but with only half of the (pridinolone) cross links being formed.

The muscle-tendon unit needs time to adapt to the increased loading – especially eccentric loading of the triceps surae at initial foot contact. If the foot also pronates then the tendon is exposed to further risk. Greatest risk of rupture occurs with sudden high loads placed obliquely on the tendon.

Clearly, the AT can store and release significant amounts of energy, by stretching and contracting repeatedly for long periods of time. Often the AT is functioning just below a threshold where repeated micro trauma occurs and not far below complete failure/rupture. Therefore, it is no surprise this remarkable part of the human anatomy tendon is frequently injured in both athletic populations and the less active.


Intrinsic and Extrinsic Factors

Age; the older we get the greater likelihood of injury. Dehydration of the tendon, changes to the collagen make up and its loss of elastic properties – make it softer and less able to shift loads.  Chronic disease – diabetes mellitus, rheumatoid arthritis, obesity and hypertension, high cholesterol levels, hyperlipidaemia and continued use of Fluoroquinolone antibiotics such as Ciprofloxacin; accounts for 2% of Achilles tendon injury. In these conditions the collagen fibres become disorganised, becoming less able to withstand the loads placed on it. The tendon responds well to stress, and long periods of activity and loading lead to adaptation and increase in the size and strength of any tendon. Exercise promotes collagen turnover and overall synthesis of collagen.  Resistance training will increase tendon stiffness and perpetual running for over 5 years will increase the cross-sectional girth of the tendon making it stronger and less likely to rupture. Inactivity will reduce the strength, stiffness and tensile strength of tendons.

Excessive pronation is associated with Achilles tendinopathy. Pronation, excessive or prolonged may be due to malfunction of foot biomechanics, running on uneven surfaces or from errors in running technique such as over-striding, and/or inadequate core strength. Forefoot strikers will place increased loads through the tendon. Many runners who have converted to minimal footwear and then run in a forefoot striking pattern have encountered AT injury. Forces that place highest stress on the muscle-tendon unit occur during the eccentric muscle contractions, which occur when the foot is plantar flexed at initial contact. Poor foot control at initial contact in walking and running can be exacerbated by imbalances in lower limb muscle control, proprioception and strength. Muscle fatigue may well render the Achilles tendon at risk. Bowing of the tendon from pronation (or supination) has been shown to cause reduced blood flow into the AT, rendering it vulnerable to damage.

Extrinsic factors include footwear. Poor quality, old, or well used running shoes which have bottomed out thus offering inadequate control will often increase the moments that can cause or exacerbate pronation. Compression of the AT from a high or very stiff collar are known to exacerbate or cause tendon damage. Running consistently on hard surfaces and cambered roads may also be a contributing factor, as will a sudden increase in intensity and distance. Minimalist running shoes with a low drop will place more strain on the AT.

Most often, pathology occurs from a culmination of both intrinsic and extrinsic factors.


Prevention / Treatment

The full treatment and prevention practices are not within the scope of this article. However, what may be gleaned from the above is:

The overall health of an individual should be taken into consideration.

Age, and lack of use result in decreased collagen production and turnover decreased water content and increase in collagen crimp angles, meaning tendons lose their elastic properties, becoming compliant and less stiff. Proprioception is also reduced with a compliant tendon thus rendering any tendon more prone to injury, and possible rupture. Sudden large forces at an oblique angle are thought to be the main risk of rupture.

Running form; according to some authors the gastrocnemius being fully extended at mid-stance will enable more energy release from the Achilles, thus improving running economy. Minimising knee flexion at mid-stance could be a consideration when making changes to running form.

Consider for example, a 50-year old runner deciding to suddenly wear minimal footgear and change his/her running style to a forefoot striker would pose a significant risk. Management of risk reduction for the ageing, forefoot striking runner could include technique changes to allow for a more midfoot or low angled foot heel strike position. However, it should be noted that during high angled (foot position) in heel strike running the tendon will be stiffer, and thus less able to absorb energy which can subsequently be released.

Excessive eversion/pronation leads to decreased tendon vascularity. Control and reduction of hindfoot frontal plane motion and velocity using foot orthoses should be given great consideration, in both prevention and treatment of Achilles tendinopathy.

Because negative/eccentric work of the calf muscles produces the most loading therapists should offer Strength and conditioning – including eccentric calf loading exercise as a major part of a rehab programme. If excess pronation is also present then based on anatomy, it is important to improve conditioning and strength of the triceps surae – with emphasis being paid to the soleus muscle. For runners changing to mid-foot/forefoot striking pattern this exercise becomes even more important.

Many clinicians, including ourselves use topical NSAIDs, such as Diclophenac (Voltarol) – yet the pathology of Achilles tendinopathy, as well as plantar fasciosis (fasciitis) is not inflammatory. Any inflammation occurs only in the pre-symptomatic stages of the pathological process. Yet the use of such agents does seem to give some benefit to patients; one would therefore assume their use is for pain management only.



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