Achilles tendon: muscle structure and injury rehabilitation


In previous articles, Matt Lancaster explored a range of training strategies to enhance running robustness and manage the often-difficult transition from injury back to full training. In the final article of this series he addresses the particular challenge of managing Achilles tendon injuries

Tendon injuries constitute about 30% of all running injuries (1). For many recreational runners, a painful, swollen Achilles tendon can lead to months of frustration while for elite athletes, an Achilles tendon injury can become an obstacle to successful performance, and in the worst cases, result in the premature ending of a sporting career.
What is clear is that no single hypothesis or theory adequately provides a succinct, unifying explanation of the problem, while similarly there is no magic cure. Simplistically, the problem may be a unique combination of many components (pathology, pain, the way you move), meaning that management of it should also be based on individual considerations.

Tendon structure, function and regulation

The Achilles tendon is a thick white cord, which emerges from the soleus and gastrocnemius muscles of the calf and inserts into the calcaneum, or heel bone. The tendon fibres are grouped in bundles while the entire tendon is surrounded by connective tissue, called the paratenon (see figure 1). At a microscopic level, tendons consist of cells – tenocytes and tenoblasts – embedded in an extracellualar matrix (ECM).

Tendon Structure

Collagen type I fibres account for the majority of the dry mass of the ECM. These fibres are surrounded by a mass of small proteins and water, collectively referred to as ‘ground substance’ (2). Blood supply to tendons is adequate, though limited, while nerve supply is also sparse but able to provide important feedback, primarily concerning tendon tension (3).

Tendons play a vital role in running, providing elastic energy to help us bound along. This is best illustrated by considering the ultimate biological bounders, kangaroos, who have been shown to actually decrease their oxygen consumption as they increase their hopping speed between 7 km/h and 22 km/h (4). This efficiency is attributed to the storage and recycling of elastic energy within the kangaroos’ long and compliant Achilles tendons (4, 5). Subsequent investigations have found that in order for energy to be stored in a stretched tendon, the attached muscular fibres must generate sufficient tension to resist most of the combined muscle-tendon length change (5).

While we do not run with the super-efficiency of kangaroos, as with bounding, running is dependent on the intrinsic properties of our Achilles tendon (an overly compliant tendon may not be advantageous to athletic performance), calf muscle work to tension the tendon and the ability of our nervous system to coordinate ‘feed-forward motor activity’ and ‘proprioceptive feedback’.

The structure and function of our tendons is regulated in response to loading through a process known as ‘mechanotransduction’, described in PP262. Regular runners may develop thicker tendons over a number of years (6) while at key resistance training thresholds (possibly as high as 95% maximum voluntary contraction or 5% tendon strain), anabolic conditions lead to up-regulation of collagen and a subsequent increase in tendon stiffness (7, 8).
Ground substance proteins such as tenascin-C, which contribute to tendon elasticity, are also regulated in a dose-dependant manner in response to heavy loading (9, 10). Tendon stiffness decreases with age, though this can be ameliorated with resistance training, while adaptation in response to loading may be less apparent in women than men (11, 12).


Historically, the term ‘tendonitis’ has been used to describe overuse tendon injuries. However, analysis of supposedly inflamed tendons reveals an absence of inflammatory cells and chemicals, and the term ‘tendinopathy’ is now used to describe pathological changes associated with Achilles tendon injury (13). Within the umbrella of tendinopathy, the majority of runners suffering Achilles pain will exhibit pathological changes referred to as tendinosis.
Tendinosis can be confirmed with ultrasound imaging. However, the amount of tendinosis seen on imaging does not reflect the amount of pain someone experiences; some people will show signs of tendinosis on imaging without ever having experienced any pain! Moreover, symptom improvement is not necessarily reflected by positive changes on imaging. It is tempting to suggest that tendinosis represents a weakening of the tendon and that the pain is associated with overstrain of the remaining fibres. The reality however, is that the scientific evidence does not support this.


The source of tendon pain remains somewhat elusive, though perhaps significantly the in-growth of new nerves is known to be sensitive to pain chemicals (14). Successful rehabilitation has been related to abolition of the new vessels and nerves while ongoing pain occurs with persistence of the vessels (15). However, non-painful tendons can also exhibit increased vascularity, particularly following exercise and the specificity of the vascular and nerve in-growth to tendon pain is not entirely clear (16).

Finally, it is worth considering that pain is not merely a local tissue phenomenon and that the central nervous system plays a role in all pains. Recent experiments suggest that tendon pain may provoke a greater susceptibility to central nervous system changes than pain originating from other tissues (17).

Musculoskeletal dysfunction

Many theories abound concerning why people develop Achilles tendon injuries. Many of these consider intrinsic risks, such as biomechanics or dysfunctional movement characteristics. While a study in a group of military recruits showed that plantarflexor strength of less than 50N.m and excessive dorsiflexion excursion (greater than nine degrees) were linked with development of Achilles tendon problems, the reality is that there is little valid support for the majority of commonly considered risk factors (18).

In middle-aged people, poor performance of a combined battery of six lower limb strength and jumping tests (see figure 2) has been demonstrated to be consistent with people suffering with Achilles tendinopathy, suggesting musculoskeletal dysfunction could present a target for clinical action (19). However, the same researchers have found that persistent aberrant lower limb function does not preclude full symptomatic recovery and return to normal sporting activity (20).
Poor performance in a particular strength, hopping or jumping test has a relatively low association to Achilles tendinopathy. However, poor performance of all six tests above is closely related (> 90%) to Achilles tendinopathy.

Combination Tests


Variations of a particular collagen gene (COL5A1), as well as changes within the tenascin-C gene have been linked with an increased prevalence of Achilles tendon injuries(21). This fits comfortably with our understanding of tendon regulation and healing. However, these genetic markers do not provide a diagnostic tool and development of Achilles tendon problems remains dependent upon gene-gene or gene-environment interaction.

Alfredson’s heel-drop exercise

In 1998 a Swedish orthopaedic surgeon published excellent results for a group of patients with Achilles tendinosis who undertook a specific 12-week eccentric calf loading rehabilitation programme (summarised in table 1) (22). The subjects all experienced a dramatic reduction in pain, a significant increase in calf strength and returned to full running.

Table 1

It is worth noting that the experimental group consisted of middle-aged recreational athletes with a long history of symptoms and there is less evidence indicating how to best load more acute presentations in younger athletes. Indeed ten years after Alfredson’s original article there is still a dearth of research demonstrating the effectiveness of eccentric loading over other forms of active loading such as concentric exercise or stretching (23).More recent studies have found that eccentric loading increases collagen deposition in tendinotic tendons, suggesting a healing response (24, 25). Perhaps of greater significance is the apparent disappearance of the vascular in-growth in people who respond favourably to loading and it is possible that the effectiveness of the program is due to the direct effect on pain rather than tendon healing or an increase in calf muscle strength (15).

Consistent with the running specific approach taken in PP issues 259 and 262, the rationale behind Alfredson’s Protocol can be considered as part of an overall return to running strategy.

Active loading

Active loading has the potential to affect your pain and the intrinsic structure and function of the Achilles tendon as well as the calf muscles. It seems reasonable that any approach should involve high-repetition loading into a degree of discomfort, which is progressed by adding weight, as the discomfort becomes less. As pain improves, loading can be used to target other components of your particular presentation.

In healthy tendons, intrinsic stiffness is best increased by high-resistance work. While the loading threshold required to increase collagen deposition in injured tendons is lower than that required in healthy tendons there is little evidence of the threshold required to enhance intrinsic tendon stiffness in injured tendons (25). Nevertheless, it may be that some degree of high load work (such as six-second isometric calf holds into fatigue using a leg press) can augment the pain gains made by a high repetition, lower load rehabilitation programme.

Good calf capacity appears to be important for both tensioning the tendon and taking a fair share of the strain associated with running and the loading strategy can be tailored to address the overriding calf muscle deficit, such as inadequate force generating properties or insufficient local muscular endurance. Initial loading will probably produce a good deal of delayed muscle soreness but calf muscles generally recover quickly and as you adapt you will be surprised at the amount of work you can do.


An inability to run may reflect the consequence of pain, inhibition and a subsequent inability to coordinate leg-spring function as much as it does the presence of tendinosis. During periods of acute loading intolerance, isolated ankle movements and moderate resistance work (eg exercise bands for multidirectional ankle and foot movement) may provide a normal stimulus to help promote appropriate function and limit sensory pain stimuli.

As pain subsides, regaining effective motor control of the calf-Achilles complex and more globally the leg-spring function is crucial to successfully returning to running. Skipping and low intensity hopping drills can provide an appropriate introduction to running specific drills and ultimately plyometric stretch-shorten activities. Plyometric activities represent a high load tendon challenge and progressing too quickly can lead to considerable exacerbation of pain, which may take some time to subside. If you are adding dynamic loading activities it may be wise to reduce other loading exercises to appropriately manage the overall tendon load.


A short period of rest from running during the initial acute painful phase followed by a specific loading programme is sensible. However, the tendon loading and coordinative challenge of running suggest that running should become a central component of your rehabilitation strategy and indeed there is scientific support for continuing to run during rehabilitation, as long as the pain does not exceed moderate intensity (26). Accepting a tolerable amount of running discomfort may also help avoid the negative tendon and muscle consequences of protracted rest. The margins are vague, however, and the line between acceptable discomfort and disabling pain is very individual.

Running progression should be measured and symptoms monitored over a 24-hour period. Reintroduce comfortable tempo running and progress either running time or distance carefully. Our muscle-tendon unit works harder to generate stiffness on soft surfaces, and it may be that running on harder surfaces initially is advantageous. Speed, intensity and spikes (for track runners) should be introduced gradually, with careful evaluation of symptoms.

Loading is not the only form of management for Achilles tendon injuries. However, without adequate tolerance to loading, few runners can enjoy or succeed at their sport. In light of the complexity of tendon injuries, appropriate loading should be considered a central part of any wise management strategy.

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