Research Review By Dr. Demetry Assimakopoulos©


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Date Posted:

February 2014

Study Title:

The Challenge of Managing Tendinopathy in Competing Athletes


Cook JL & Purdam CR

Author's Affiliations:

Department of Physiotherapy, School of Primary Health Care, Monash University, Melbourne, Victoria, Australia; Department of Physical Therapies, Australian Institute of Sport, Canberra, Australian Capital Territory, Australia.

Publication Information:

British Journal of Sports Medicine 2014; 48: 506-509.

Background Information:

Tendinopathies are extremely common in athletic populations, especially during the competitive season when loads are tremendously high. With this comes frustration, on the part of the athlete and healthcare provider, as these injuries can be detrimental to the performance of athletes who make their living from performing ballistic, high speed activities. Often, tendinopathies are not an easy fix, and do not resolve over the course of a competitive season.

In cases such as these, the only recourse is to plan and execute a comprehensive rehabilitation program that attempts to increase the tendon’s ability to absorb load. The problem with this statement is that, such a comprehensive program is, to quote Dr. Cook “…incompatible with ongoing participation in competitive sport.” So what do we do? The following review attempts to give clinicians some insight into the management of tendinopathies during in-season play.


Features and Biology of Tendon Pain:

It is safe to say that tendon pain is provoked tremendously by loading. It is unusual for the tendon to trigger pain without load, or to be painful at rest or while sleeping, unless there is an associated metabolic or seronegative clinical condition.

While a multitude of studies have been published in recent years on the anatomy, biology and physiology of tendon pain, these topics still remain poorly understood. Research suggests that abnormal tendon cells generate signaling neuropeptides, and the receptors for epinephrine, acetylcholine, glutamate, substance P and TNF-alpha. Up-regulation of these neuropeptides produce a local response, increasing vascular and tenocyte responses. They may also cause a neural response and provoke pain.

There is a general disagreement in the current literature concerning the potential for neuronal ingrowth that occurs with tendon injury. Most of the innervation appears to come from sympathetic fibers, as opposed to sensory. However, there can be nerves that have a combined sensory and sympathetic function. Also, an increase in the number of NMDA (glutamate) and neurokinin-1(substance P) receptors have been found in some tendinopathies. Additionally, some degree of central sensitization and a reduction in the centrally mediated descending inhibition is theorized to contribute to the overall perception of pain. Thus, both local (tendinous) and central factors contribute to the pain associated with tendinopathy.

The Continuum Model:

This model stipulates that there are three stages of tendinopathy that occur in a linear, temporal fashion:
  1. Reactive
  2. Disrepair
  3. Degenerative
(Writers note: the authors provide the reader with no definitive means of determining which stage a particular athlete is in). Multistage pathology may be the most common presentation in season, where an athlete with an underlying degenerative tendinopathy presents to a manual therapist with a flare up of a past injury. This type of injury is otherwise known as a reactive on degenerative tendinopathy. The changes in the mechanical properties of the tendon after injury (mainly stiffness and elasticity) at the interface between areas of different tendon pathology may create an environment for degenerative tendons to become reactive in previously unaffected portions of the tendon.

Load and Tendon Pathology:

It seems as though athletes who can effectively, efficiently and repeatedly store and release energy (i.e. jump high, great agility, and so on) are more likely to develop tendinopathies. It is likely not only due to their capacity to store large amounts of energy, but also to genetics, as it has been shown that endurance runners are likely to have the TT allele of the Col5A1 gene, which has previously been associated with tendinopathy. Gender also seems to be an intrinsic factor in the development of tendinopathy, as men are twice as likely to develop tendinopathies, compared to women.

With this being said, biologic tissues have the capacity to adapt over time to increase their load tolerance and energy absorption. This adaptation occurs due to increased tendon stiffness and an increase in matrix protein production. The response to load appears to be greater in pathological tissues.

Management Considerations:

Management of In-Season Tendinopathy:

Often, tendinopathies emerge due to a mismatch between the tendon’s load-bearing capacity and load placed on a tendon, most notably through a substantial and/or sudden change in load during activities. A tendinopathic response is triggered if the magnitude or temporal distribution exceeds the tendon’s threshold.

With reactive tendinopathies, the key intervention should be to reduce the activation and/or sensitization of tenocytes. This may cause a reduction in cytokine and neuropeptide release, and proteoglycan deposition in the matrix. Then, appropriately progressed loads are needed for the tendon to maintain and/or remodel the matrix.

A very high total load, a combination of a number of small overloads in series, a rapid increase in total load and excessive tensile loading are all major factors in the genesis of a reactive tendinopathic response. Additionally, eccentric loading regimes performed alongside high training loads have been demonstrated to create tendinopathies, and should be avoided in season. Also, reducing compressive loads and decreasing the combination of repetitive compression and tensile loads (shear) is important. Simple changes such as the reduction of stretching, particularly for insertional/entheseal lesions of the hamstrings, adductors and Achilles, can be helpful. A direct blow to a tendon, say with a ball or kick from an opponent, can induce a large reactive response that can take weeks to settle.

A number of clinical/orthopedic tests can be used to monitor tendon pain. Both low load and high load tests can be used:
  • Achilles: single leg heel raise (low); hop (high)
  • Patellar tendon: decline squat (low); high single leg jump or landing from a height (high)
  • Hamstring: single leg bent knee bridge (low); single leg dead lift (high)
  • Gluteal: single leg stance (low); hop (high)
Friction or firm massage to a painful and reactive tendon can be provocative to the tendon and peritendinous structures, in spite of the fact that these therapies have been shown to stimulate protein production in animal models. Still, it is suggested that these therapies be saved for a more degenerative presentation.

Therapeutic loading, such as sustained isometric fatiguing muscle contractions, should be introduced early on, even in reactive tendinopathies, as total removal of tendon load is catabolic for a tendon. This type of load results in mechanical hypoalgesia and increased pressure pain threshold in human subjects (1), and should be completed in the mid-to-inner range of the muscle-tendon unit to reduce compression. They should be repeated several times/day, utilizing 4-5 sets of 40-60 second holds. Keep in mind that clinicians need to tailor treatments to the patient in front of them, and as such, can reduce the volume of training by decreasing holding time and repetitions/day if indicated.

Management should also focus on creating optimal distribution and absorption of energy across multiple joints and the athlete’s kinetic chain. For example, restricted ankle dorsiflexion in landing can increase the load on the patellar tendon, thus leading to patellar tendinopathy. Additionally, gluteal strengthening, calf strengthening and landing re-education may be necessary to optimize energy absorption across all major joints or segments. This approach can be utilized early in the management cycle, providing symptomatic gains as the troubled tendon is offloaded.

Ultrasound tissue characterization of tendons can help to monitor athletes who are predisposed to injury, as tendon pathology can exist for years and never actually cause pain. Research into this imaging modality has shown that it is quite capable of detecting a tissue response to load. However, more research is needed to confirm this assertion.

It is also possible to use pharmaceutical interventions to decrease pain through inhibiting cell activation and proliferation. Ibuprofen, naproxen, indeomethacin, celecoxib and TNF-alpha use have been shown to decrease tenocyte activation. Additionally, doxycycline, green tea and omega-3 supplementation may be appropriate; however, the efficacy is variable.

Corticosteroid injection has the capacity to significantly inhibit cell activity and proliferation, and is effective in achieving quick recovery in a profoundly reactive tendon. While considerable literature exists suggesting that corticosteroid injection is inappropriate for the treatment of tendinopathy, the author stated that in her opinion, corticosteroid injections do have a place in the health care system for the management of tendinopathy. She also states that in the research setting, corticosteroids may have been used inappropriately, and even during the incorrect stage of tendinopathy (degenerative), without satisfactory load management and rehabilitation needed to rebuild the loading capacity of the tendon. While these injections are capable of reducing pain, simply allowing the patient to go back to playing is problematic: firstly, only few oral analgesics are strong enough to control tendon pain after the injection is performed; secondly, injectable agents are often diffused into nearby structures and can affect the athletes capacity to play and protect nearby joints; lastly, loading an injured tendon maximally when pain free appears to make the injury progressively worse.

Surgical intervention is not commonly utilized during a season, as it requires approximately 6-9 months of rehabilitation. While this is true, Alfredson (2) and Willberg (3) developed surgical methods for the Achilles and patellar tendons, respectively, that require a post-operative rehabilitation regimen as short as 6 weeks, which makes their method a viable option for in-season management of cases where all conservative care have been exhausted. However, only performing surgery, without addressing the contributing factors of load capacity, does not create an environment for a good long term outcome.

Adjunct treatments such as extracorporeal shockwave, supportive strapping, bracing, orthoses, footwear and other equipment choices should be considered in the management of an athlete with tendinopathy during the regular season, and may provide enough support to allow for satisfactory athletic function. However, it is important to note that while shockwave therapy can help relieve pain for several weeks, it can also be disruptive to tendon tissue.

Ultimately, managing athletes is about attempting to prevent injuries by identifying at-risk athletes, individualizing training methods, monitoring changes in pain and the immediate adjustment of loads when needed. Additionally, maintaining functional loads relevant to the sport during the offseason is important so as to decrease the possibility for deconditioning of the injured tendon and is vehemently suggested.

It is also important to consider the kinetic chain in the management of tendinopathies, so as to optimally distribute the absorption of energy across multiple joints. An example of this is the association between decreased ankle dorsiflexion and patellar tendinopathy; not having enough ankle dorsiflexion has the potential to overload the patellar tendon. Building on this example of patellar tendinopathy, gluteal strengthening, calf strengthening and landing re-education to increase the load distribution across the kinetic chain is also important. This type of management can be performed early on in the treatment process and can help to considerably offload an injured tendon.

Managing tendinopathies in season is difficult and complex. The clinician needs to understand how to stage pathology, determine one’s response to load, and understand which loads are affecting the tendon, extrinsically and intrinsically. Complementary interventions may be useful in improving pain and function, but might not be able to change tendon load capacity. Intratendinous treatments such as surgery are more likely to produce exacerbation and are not recommended in season when ongoing performance is expected.

Study Methods:

No methods were stated, as this was an opinion piece; an exposition of the current literature on this topic.

Study Strengths / Weaknesses

  • Rigorous citing for further personal research
  • The authors state exactly when a discussed topic is simply their clinical opinion.
  • No inclusion/exclusion criteria
  • No analysis was performed, as this was an editorial piece, not a systematic review.

Additional References:

  1. Fallon K, Purdam C, Lovell G, et al. A ‘polypill’ for acute tendon pain in athletes with tendinopathy? J Sci Med Sport 2008; 11: 235–8.
  2. Alfredson H. Ultrasound and Doppler-guided mini-surgery to treat midportion Achilles tendinosis: results of a large material and a randomised study comparingtwo scraping techniques. Br J Sports Med 2011; 45: 407–10.
  3. Willberg L, Sunding K, Forssblad M, et al. Sclerosing polidocanol injections or arthroscopic shaving to treat patellar tendinopathy/jumper’s knee? A randomised controlled study. Br J Sports Med 2011; 45: 411–15.