Tendinopathy - Load to Explode

THE TAKEAWAYS

● PROGRESSIVE LOADING SCHEMES ARE REQUIRED TO TREAT TENDINOPATHY. THE INTENSITY OF THESE PROTOCOLS WILL VARY BASED ON THE PATIENT, LEVEL OF PREVIOUS TRAINING, PAIN TOLERANCE, AND VARIOUS OTHER FACTORS.

●  WHILE PROGRESSIVE LOADING SHOULD CONTINUE THROUGHOUT THE PROGRAMMING, ENERGY STORAGE & RELEASE, AND COMPRESSIVE LOADS NEED TO BE ADDED IN EVENTUALLY IF THE DEMANDS OF THE PATIENTS SPORT REQUIRE IT.

● PAIN REQUIRES EDUCATION, AND IS SOMETHING THAT CAN BE TOLERATED, BUT THE AMOUNT MAY VARY FROM PATIENT TO PATIENT. 

● WE DO NOT AIM INTERVENTIONS AT PATHOLOGIC TENDONS AS RESEARCH HAS SUGGESTED THIS TISSUE CANNOT BE RECOVERED. INSTEAD, STRATEGIES ARE AIMED AT BUILDING A ROBUST TENDON WITH THE REMAINING NON-PATHOLOGIC TISSUE. 

● STRETCHING AND MASSAGE ARE ULTIMATELY INEFFECTIVE IN TREATING TENDINOPATHY

INTRO

“Tendinopathy, tendinitis, tendinosis” these are all words that are tossed around the rehabilitation world, many times interchangeably. These words, while all implying something is occurring at the level of the tendon, cannot be swapped in and out at a whim. Elements of our tendon rehabilitation will depend partially on the pathophysiology of the injury which is different in each case above. The objective of this article is to outline the current concepts in tendon rehabilitation management and treatment.

THE CURRENT CONTINUUM

At the time of this writing in 2019, we still do not fully understand how pathology begins in the tendon, though we have some ideas. Previous hypotheses about pathology involve an inflammatory origin & tendon collagen tearing. While tendon collagen tearing as a primary driver has now been all but disproved, the idea of inflammatory mediators playing a role continues to be prevalent, though not at the formerly described levels. The current model, rather than delineating separate stages of tendon pathology, describes the process as more of a continuum. It is also predicated on the idea that the tenocytes are tied closely to the collagen matrix of the tendon, which allows them to sense and respond to load.

THE STAGES

Reactive Tendinopathy

In this initial stage of tendon pathology, an injury, such as excessive acute loading or direct blow, causes a non-traditional inflammatory response. Non-traditional implies that we may not see the common redness, swelling, and tenderness. We will see an uptick in non-collagen proteins such as glycosaminoglycans which will draw fluid into the tendon. This may help increase the area of the tendon helping to distribute force. This phase is seen as normal and reversible, with minimal long-term damage or collagen disorganization.

Tendon Dysrepair

This phase begins as the reactive phase is drawn out for longer than an acute period or at an intense enough stimulus. In this stage, collagen disruption will begin to occur which will augment force transmission and nerve signaling. An increase in type III collagen synthesis will begin to occur which has less tensile strength and more collagen disorganization than type I which is the primary component of the tendon. We will also see a proliferation of nerve and vascular structures, which will most likely not influence levels of pain as previously thought.

Degenerative Tendinopathy

Further progression from the dysrepair stage will bring us to the degenerative portion of tendinopathy. As we move into these portions of tendon pathology, current literature shows that we cannot reverse the pathologic state of the tendon.

Reactive on Degenerative Tendinopathy

This was included in the continuum model to describe a phase of injury where an acute overload response that is normally seen in reactive tendinopathy occurs in a more chronic degenerative state. This phase of tendinopathy is where we will see a vast majority of our patients.

 WHY SHOULD I CARE ABOUT PATHOLOGY ANYWAY?

Some of you may be thinking “Who cares if the pathology is predicated on inflammatory cells, tendon collagen tearing, or tenocyte mediated load responses? I just want to treat my patients!” The reason that pathology plays a prominent role in treating tendinopathy is because the response to two of the mechanisms listed above is usually to REST. When there is a major inflammatory event or massive collagen tearing at the Achilles Tendon, often there is a substantial period of rest and unloading to allow for inflammation to subside and collagen to heal respectively. While in those instances this response may be justified in a load mediated tendinopathy, a gradual return to a progressive loading program is supported by the current research. Tendons require load to help maintain their structure.

 HOW DO WE DIAGNOSE TENDINOPATHY?

5 Key Markers:

·      Related to overload

·      Must be localized

·      Load dependent increases in pain

·      Worse with energy storage and release loads

·      Increased pain the day after high loads

Palpation is an invalid mechanism of determining tendinopathy and should not be used to confirm diagnosis. Often tendons will remain sore to palpation following treatment of tendinopathy and return to sport regardless. Remember, palpation pain is not correlated with symptoms or findings on imaging.

  “TREAT THE DONUT NOT THE HOLE”

This is a common phrase that has been thrown around since the current continuum has gained more widespread acclaim. What this is implying is that once a tendon moves into late dysrepair or degenerative phases. The potential to reverse the pathologic tendon structure is no longer believed to be possible. Fortunately for our patients, with the appropriate rehabilitation we are able to restore function and diminish pain regardless. Sean Docking et al. in 2015 found that in both a pathologic achilles and patella tendon there was more tissue with good collagen structure than in a normal tendon. This is believed to be adaptation on the part of our pathologic tendon and provides us with the ability to PROGRESSIVELY reload the tendons without fear of injury. The phrase “treat the donut not the hole” is a convenient analogy we can use to express to our patients that we are not looking to treat the pathologic portion of the tendon, or the hole, and that we are aiming to target the remainder of the donut making it has robust as possible. This analogy is simple to understand and can help alleviate possible underlying fear of rupture or further injury with loading. REMEMBER, while it is okay to load a tendon that is degenerative, it must be done with an appropriate dosage and in a gradually progressive manner

  

SO, WE NEED TO LOAD IT … HOW EXACTLY DO WE DO THAT?

Another preconceived notion about tendinopathy was that it responded primarily to eccentric loading. Although eccentric loading can play a role in tendinopathy treatment, it is no longer considered the end-all intervention strategy to address the pathology. Below we will discuss some common loading strategies implemented in tendinopathy.

Eccentrics

A landmark study by Alfredson et al. in 1998 studied an eccentric training load protocol (3 x 15 eccentric heel raises, 2 x per day) over 12 weeks in 15 recreational athletes with chronic Achilles tendinosis. His comparison group was 15 recreational athletes who underwent more conventional physical therapy which included rest, orthotic, anti-inflammatories, etc. The control group eventually all underwent surgical intervention to address the tendinosis. This study had minimal control for volume, intensity, RPE of the loads, and training protocols between groups. Similarly, it followed a very specific subset of patients, the recreational runner. Following the study there was minimal significant difference between the groups aside from eccentric strength, which was the primary mechanism of training in the study group. Regardless of this fact, the takeaway from the article became that eccentric training was the primary way to treat tendinopathy. The problem with this is that while eccentric strength training can be considered a viable option when comparing to conservative treatment, alternative loading protocols were not considered and variables not taken into consideration. The positive aspects of this article were that it helped to drive the movement towards loading as a more conservative method for treating tendinopathy over surgical intervention, as well as a faster recovery time to pre-injury levels for the non-surgical group.1

Heavy Slow Resistance

More recently, papers have been looking more closely at the loading protocols being utilized and different intensity variables. Beyer et al. in 2015 compared the widely used eccentric protocol with a heavy slow resistance loading scheme. The primary difference between heavy slow resistance (HSR) and eccentric training is concentric phase and brief isometric element in the heavy slow resistance protocol. The results of the paper demonstrated no significant difference between the groups’ function/pain following the interventions, but greater short-term satisfaction with the treatment program in the HSR group. This may be due to the average weekly time spent performing interventions, 308 min/wk for the eccentric group compared to 107 min/wk for the HSR group, or increased variability in the training protocol. This paper outlined that the type of contraction—eccentric vs. concentric—was less important than previously established in the Alfredson paper.2 Similarly, Kongsgaard et al. found comparative short term (12 weeks) results when comparing corticosteroid, eccentric protocol, and heavy slow resistance in treating patella tendinopathy. At 6 months follow up corticosteroid injection efficiency had diminished while the eccentric and heavy slow resistance protocols remained comparable and effective.3 Further, Malliaras et al. performed a systematic review in 2013 comparing Alfredson’s eccentric protocol with Silbernagel’s eccentric-concentric and HSR. They concluded that “the review identified limited (Achilles) and conflicting (Patellar) evidence that clinical outcomes are superior with eccentric loading compared with other loading programmes, questioning the currently entrenched clinical approach to these injuries. There is equivalent evidence for Silbernagel combined (Achilles) and greater evidence for HSR loading (Patellar).”4

DID WE ACTUALLY FIGURE ANYTHING OUT? ARE WE MISSING ANYTHING?

An important factor that has been established is that the progressive intensity of the load is as important as the type of contraction being performed at this time. As you can see from the above studies—which are only a few of many—the type of contraction is not as important as once previously thought, since the HSR protocol contained concentric contractions showed a similar effect to an entirely eccentric based protocol. This does not mean you should go throw 200 pounds on the back of an older patient coming into your office with a reactive on degenerative tendinopathy, but that you need to find the right entry point to provide higher intensity loads to our different populations and you have the option to use all types of muscular contraction at your disposal. While these studies have shown the ability to strengthen muscle and address the series elastic component of the tendon, they are not the whole picture. A primary component that is missing from these studies is the ability of the tendon to adapt to energy storage loads or compressive loads that are required for the fast, explosive loads and compression seen at tendon insertion respectively. Another component not really emphasized here is the potential for utilizing high load isometrics to produce an analgesic effect in earlier stage tendinopathy, or, with more fearful patients, to help with pain management.

 

PLYOMETRICS!

Plyometrics are a huge part of tendinopathy rehabilitation that is not discussed in the previous eccentric and HSR protocols. They play a critical part in returning an athlete to sport and for recreational fitness enthusiasts, should their mode of exercise require it. The important thing to remember is that plyometrics will require high energy storage load & release capabilities and are provocative in nature. For this reason, they need to be dosed appropriately, slowly, and progressively. For example, a box jump from a static position will emphasis a concentric contraction with a small eccentric component at the high landing point on the box. On the other hand, a counter movement box jump will call into effect the stretch shortening cycle and elastic properties of the muscle/tendon to a much higher degree. Similarly, a drop jump will focus more on the eccentric component of the movement. Surface heights also play an impact on the intensity of the movement, with high landings requiring less eccentric load than landings on low surfaces or the ground. Understanding how to progress difficulty and demand here is important to adding plyometric training and avoiding re-entering the reactive phase.

CAN WE TALK A LITTLE BIT ABOUT PAIN?

Pain and associated loss of function are often the main drivers that sends patients into our clinics. The exact nociceptive drivers of tendinopathy pain in our reactive and reactive on degenerative clients is still not 100% percent clear. In Dr. Jill Cook’s Tendon & Sport presentation on tendinopathy she elaborates on how pathology on imaging is not tied directly to tendon pain. She notes that if we were to randomly sample and ultrasound/MRI a grouping of people, many would have signs of tendon pathology but remain asymptomatic. She goes on to note that tendinopathy pain in the lower extremity does not seem to be centrally sensitized (though the research is not definitive here by any means) and appears to be generated from a local nociceptive driver. And while it was previously thought that an increase in neovascularization in the deep mid-portion of the tendon may correlate to increased pain, these nerves have actual turned out to be sympathetic in nature, not sensory. Sensory nerves that are primarily located in the periphery or membranous sheath of the tendon or peri-tendon are most likely responsible for tendinopathy-based pain.5

 

JILL COOK RECOMMENDATIONS FOR REHABBING TENDINOPATHY

BACK TO PAIN… SHOULD WE AVOID IT?

While there doesn’t seem to be a definitive answer on this, something to consider would be chronic pain load. For example, it is acceptable to raise a patient’s pain level from 3/10 – 5/10 during a session if the pain does not remain for a prolonged period of time. The patient should also previously been educated and comfortable with increasing their pain level.

Similarly, Jason Eure DPT, when speaking on the Clinical Athlete podcast, speaks about the possibility of implementing a once daily test or 24-hour load response test to determine symptom reactivity following sessions. For example, if an eccentric step-down causes tendon pain that brings your patient into therapy and you begin a progressive loading protocol, you can replicate that movement each day to test the reactivity of the tendon to your programming. So, if the patient wakes up at 8 AM each day and performs the step-down test we should not be seeing dramatic spikes in their pain levels the day following treatment sessions. Alternatively, over the weeks the test can also be used to track progress and improved accommodation to load of the tendon.6

Prior experiences with physical therapy and pain may play a large factor in determining comfort levels when moving into pain. Patients who have previously experienced significant pain in PT with poor outcomes, or have fear avoidance beliefs about moving, may require a deeper building of therapeutic alliance, a little more education, and a prolonged period in the isometric phase prior to shifting into a more progressive loading protocol. It is our responsibility as clinicians to educate that in some cases—not all—pain is not an accurate reflection of damage. Remember that each person in front of you is an individual, N = 1. The approach you take must consider social and psychological factors at play, regardless of where the evidence points biomechanically. If you thrust your evidence-based beliefs on someone, load them up irresponsibly without their consent or proper education, and cause them to experience pain, you may just lose them as a patient. Worse off, this may send them down an unnecessary surgical route or further their fear catastrophizing habits.

 

WHAT TYPE OF EDUCATION SHOULD WE BE PROVIDING TO OUR PATIENTS?

●       Set the right expectations! Treating a tendinopathy is a lengthy process (months) and requires dedication to the protocol to see through the to the finish line.

●       Pain—if explained correctly and does not cause a chronic effect—can be pushed into during a loading program at the patient’s tolerance.

●       The rehabilitation of a tendinopathy will often hit peaks and valleys as improvement occurs and testing of tendon capacity is implemented. This should be discussed early on so that setbacks do not drive fear, doubt, or inconsistency with programming.

●       Education regarding the increased cross sectional area of good tissue in a pathologic tendon is important to help quell any fearful beliefs that tendon rupture may occur during a loading protocol.

●       Perception of tightness is often a symptom of tendinopathy. Commonly, stretching is something patients seek out to address tightness, but in the case of tendinopathy compression with tensile, loading may flare up tendon issues and does not address loading adaptations we are looking for in our program.

?CITATIONS

1.    Alfredson, H, et al. “Heavy-Load Eccentric Calf Muscle Training for the Treatment of Chronic Achilles Tendinosis.” American Journal of Sports Medicine. Volume 26(3), June 1998, 360 – 366.

2.    Beyer, R, et al. “Heavy Slow Resistance Versus Eccentric Training as Treatment for Achilles Tendinopathy: A Randomized Control Trial.” American Journal of Sports Medicine. Volume 43(7), July 2015, 1704 – 1711.

3.    Konsgaard, M, et al. “Corticosteroid Injections, Eccentric Decline Squat Training, and Heavy Slow Resistance Training in Patellar Tendinopathy.” Scandinavian Journal of Medicine & Science in Sports. Vol 19(6), December 2009, 790 – 802.

4.    Malliaras, P, et al. “Achilles and Patellar Tendinopathy Loading Programmes: a Systematic Review Comparing Clinical Outcomes and Identifying Potential Mechanisms for Effectiveness.” Sports Medicine. Volume 43(4), April 2013, 267 – 286.

5.    Cook, Jill. “Tendon & Sport”. November 2017.

6.    Eure, Jason. “Came for the Tendinopathy but Stayed for the Donuts.” Clinical Athlete, August 2017.