Tendinopathies: Part 2 — Tendon Loading & Movement Patterning
TL;DR
Loading the tendon is a major part of the rehab process for tendinopathies. As previously mentioned, we walk the line of tendon capacity, progressively nudging the tendon’s threshold upwards. We must be aware that tendon loading is not linear and that different exercises load the tendon differently.
For many years, there has been debate about which tendon protocol is best — an isometric, eccentric or concentric-based program. It seems none are better than the other. The key is to load the tendon using heavy, slow-resistance programming.
Here, we are loading the tendon for around 30 seconds, which happens to be the required time spent under tension for the tendon to access its viscoelastic properties. The relaxation of the stiffened tendon via the elastic transition of the tendon forces the protected, degenerated area to become loaded. Assuming the load is tolerable, the loading of the degenerated area may induce the proliferation of adequate tendon architecture and create a path to pre-injury tendon loading.
In my mind, effective movement patterning may be the missing step in tendon rehab. The modification of symptoms with movement patterning could suggest we are offloading the tendon in a dynamic setting. When a patient presents to the clinic, I look at the area of complaint from a different perspective — there is too much force going into this area… how can we change that?
When combing through the literature, the inconclusiveness of the pathogenesis of tendinopathy bothered me. Discussions suggested that thin and stiff tendons were to blame, yet there was no clear correlation between having a small cross-sectional area of the tendon and the presence of tendinopathy. This drove me bananas!
Movement in the lower limb is cyclical, meaning the joints of the hip, knee, and ankle are all engineered to transition through active ranges of motion. So, what happens if this range is decreased? I think it would be reasonable to suggest that there is a focality of biomechanical force. This reduction in force distribution may cause a localization of force, which may produce an artificially thin tendon. Over time, this can cause the tendon to become stiffer and, thus, brittle. The potential result of an overloaded environment is the presentation of tendinosis or tendinitis.
The fun part of tendinous injuries is finding positions that modify the symptoms that the sensitized tendon experiences. This is also a precarious game of trying not to ruin someone’s perception of self. In the grand scheme of things, movement likes to flow in the path of least resistance. If we can expand someone’s range of motion (active particularly) and pattern through different movements, can we disperse the force and offload the grumpy area?
More below!
Tendon Loading
Load is simultaneously the thing that makes a tendon better and worse. Too little load and the tendon won’t adapt. In fact, an underloaded tendon will likely degenerate further. Too much load and the tendon will flare up. You will need to manage a beautifully painful dance of optimal loading for progression, and as you’ll soon see, other contributors determine when a load is too much(1,2). (See below)
Adaptation pushes the curve to the right, making the tendon more resilient at tolerating higher loads. Maladaptation pushes the curve to the left causing the inverse. (Docking, 2019)
One theory about the development of tendinopathy states that a tendon that is brittle is more susceptible to injury. In my eyes (I use glasses), tendon injury looks something like this…
The tendon repetitively becomes damaged; this damage can be deemed degeneration, and the loading potential is compromised. We now have a tendon that is degenerating; force still needs to transmit through the area, and thus, we load ill-prepared tendinous tissue surrounding the area of degeneration.
In the world of biomechanics, tissue is brittle if it is thin and stiff. A particular challenge with tendinous tissue being stiff is that it feels very springy. Herein lies the red herring for athletes: as the tendon becomes weaker or more degenerated, it stiffens the area around the weakened area as a protective mechanism. The springiness is transient and may be pain-free at the start of an activity, but as we progressively load past tissue tolerance… watch out!
Here is where an example might make sense: Our very good pal, Jimmothy, has had ongoing tendon pain for about a month now. He’s had a couple of good days in a row and decides to go on a run. Much to Jimmothy’s surprise, he’s feeling quite springy on his feet (pump fake).
During the run, it doesn’t take long for the brittle tissue in his tendon to start becoming symptomatic. This is where we need to understand progressive, graded exposure to activity, along with the Demar Derozan-esque pump fake that tendinopathies throw at their victims. “Wow — excellent amount of doom and gloom, Austin. Thanks for this blog”.
Let’s get to percolating. If a brittle tendon (thin and stiff) can progress into a problematic tendon, how can we rehab/prehab a tendon to be the opposite? Well, reader, I’m glad you asked. Let me give you some background information quickly, not entirely because it’s useful but because it gives context… and because this coffee has me buzzing.
If we look at professional sports leagues that have experienced lockouts, we see a trend — a reasonable proportion of soft tissue injuries, particularly muscular strains. A potential reason is these athletes have an abnormal/sub-optimal pre-season routine. Of concern, their heavy slow resistance component may be diminished(3,4). We know that these programs are great for tendon health. They allow the body to utilize the viscoelastic (via Young’s modulus) properties of the tendon to store energy.
The result for these locked-out athletes is decreased tendinous deformation(axial stretch) under load, and the outcome is higher demand on the contractile muscle (particularly in decelerating limbs) and boom muscle strain. Force demand and tissue capacity = injury.
I bet you’re wondering why there was no tendon injury in this case — their tendons had a reduced capacity to deform underload, they were not brittle. Therefore, the weakest point in the chain was the muscle tissue.
Alright, now I hope you have a general idea of what’s going on because I have no idea what’s happening. Let’s ask another question: How can we load the tendon adequately to facilitate the adaptation of its architectural makeup? We will have to spend a ton of time progressively loading the tendon.
We need to spend at least 30–35 seconds transmitting force through the affected tendon. That time frame is so important because we can force the tendon to “relax” or transition towards more of an elastic tissue. In doing so, we avoid the tendon’s current protective mechanism to remain stiff, especially near the degenerated portion. THIS IS KEY. WE NEED TO ATTEMPT TO LOAD THE AREA THAT IS DEGENERATED(5).
Doing this may facilitate the proliferation of cellular remodeling within the tendon and allow for better force transmission. Without the relaxation response of the tendon, we are simply loading around the degenerated portion of the tendon. Since there is no tension being transmitted through the compromised area of the tendon, the degenerated area experiences compression(6). To clarify this theory, think of a balloon. The latex experiences tension (the non-degenerated tendon), and the air within the balloon is compressed (the degenerated part of the tendon).
Unfortunately for tissues in the body, the avoidance of parental disappointment is not what motivates their career choice. Musculoskeletal tissues communicate and thus respond to mechanical stimulus through a process called mechanotransduction. The compression that occurs at the tendon level facilitates the production of type 2 collagen(7), which is found heavily in joint cartilage. I think we can agree cartilage (cushion and glide) and tendons (force transmission and movement) have very different functions. The next challenge is that a tendon is most susceptible to damage when an area is compressed and tensioned simultaneously. Overload in the area experiencing both tension and compression may result in type-3 collagen production, which is weaker and more heavily vascularized/innervated (potential to feel it more)— voila a pathological tendon(7). Therefore, establishing an intentional approach to load the tissues adequately to match their functional demand will be imperative to facilitate the appropriate adaptation.
Lastly, there has historically been an emphasis on eccentric and isometric loading, with most practitioners arbitrarily relying on eccentric rehab a la The Alfredson protocol. In a nutshell, heavy, slow resistance is the strategy that should be employed when attempting to rehab a tendinopathy. This can be done isometrically, concentrically and/or eccentrically. The most important caveat to mention here is the initial integration of isometric exercise is beneficial for pain reduction and thus can be optimized to do so.
Movement Patterns
You just spent the last couple of minutes reading about how we need to load a tendon, and I’m about to explain how we can think about offloading it. (Seems a wee bit cuckoo-bananas — but welcome to my brain).
I noted, but did not explain, that when we have an increased force demand without adequate tissue capacity, we subject ourselves to injury. As I mentioned in my first blog, many of the issues I see are of “mysterious” conception, meaning there was no obvious mechanism of injury. So we can think about this as a chronic accumulation of force(microtrauma) which, over time, has reduced the tissue’s capacity to manage what the person believed to be a tolerable force.
This is multifaceted because recovery and hormones play a big factor, but I want to focus on movement patterns. What we do know is that the common tendon patient finds that the offloaded tendon feels better. So now we tango… How can we load and offload the tendon simultaneously? The incorporation of movement patterning with adequate tendon loading can help us with this waltz.
I had an epiphany in the middle of November. I was incredibly lost in the tendinopathy sauce. I focused on one theory that suggested that a tendon is predisposed to tendinopathy if it is thin and stiff. Oddly, the crucial window for growth of tendon cross-sectional area occurs in adolescence. Why don’t most people with inactive developmental years have tendinopathies? There are also instances where someone has an “adequate” cross-sectional area of the tendon, but they have tendinopathy. Something is not adding up — how can we have what appears to be a viable tendon, but it has undergone a degenerative process? Or conversely, why isn’t my office filled with thin-tendon folk?
What I think might be happening is an inadequacy of movement in which force is being improperly distributed through the tendon. What I am trying to suggest is that the lack of fluid motion in the absence of a high level of tissue capacity can cause tendinopathy to develop. This is because force can not be distributed cyclically through the tendinous tissue and, as a result, artificially creates a thin (only a small area takes the largest concentration of force) and stiff tendon. There is the potential that the tendon was simply overloaded, but that doesn’t ooze the same kind of sexy.
I’d like to make it seem like I’m not totally blowing sh*t out of my ass. A study was published in 2021 that intended to examine patellar tracking and biomechanics in populations with and without tendinopathy. What mugs me off about some studies that look to collect anthropometric or biomechanical data on movement is that they do not examine the joint in the closed chain or under a load that could expose movement tendencies. This 2021 study used a step-down task to look at the dynamic loading of the lower limb — so I’m less grumpy.
Aside: An interesting read on the topic of movement assessment is a 2017 paper on the validity of functional movement screening (FMS) and how its usefulness is clouded by its lack of loading to expose movement aberrations — this also applies to outcomes of therapy(8). What I’m saying is, that it’s great you can have a stunning bodyweight squat, but if you want to squat 350 lbs, what does a bodyweight squat really tell you? Answer: How well they drop it low at the club.
Anyways, back to this 2021 study… They noticed that symptomatic patellar tendons had (statistically significant) excess lateral mobility in the patella and increased ankle external rotation during a dynamic step-down task. So now here is a correlation — increased lateral mobility of the patella, increased external rotation of the ankle, and tendinopathy presentation(9).
This is where my brain goes: as we transition into a landing, we should transition our foot from a supinated (rigid lever) to a pronated (cushion) position. What is required at the ankle is the internal rotation of the tibia and internal rotation of the hip. If neither can happen, our foot does not adequately pronate. There is little dissipation of force into soft tissue (cushioning) and likely little dispersion of tensile stress throughout the patellar tendon. Over time, we may expose ourselves to potential tissue overload and failure.
Maybe a bit of movement clarification is in order here. My thought process is that the hip joint, for whatever reason, does not cycle through “normal” anatomical internal and external rotation. From a tension standpoint, this can potentially explain the lateral mobility and external rotation bias of the ankle, as noted by the study.
My modness might seem a little more plausible with a study that corroborates the presented theory above. Grau et. al studied females with patellar tendinopathy attempting to understand a potential biomechanical cause of their tendon injury. The difference they found between control and patellar tendinopathy patients was eccentric overuse of the quads, lack of control of pronation (via increased pronation velocity), and lack of joint coordination(10). My thought is that these findings suggest there is a lack of control of active ranges of motion in the lower kinetic chain in patients with patellar tendon issues.
As mentioned in previous blogs — joints act, and muscles react. In the scenario where the hip intends to rotate internally, and there is a lack of internal hip range, the hip external rotators will begin contracting earlier than is optimal (in a way prematurely). If we then consider where the major hip external rotators attach, it happens to be on the lateral side of the leg and into the IT band. It is plausible that the lateral mobility of the patella is the result of diminished internal rotation in the lower limb — as is the external rotation of the ankle.
The fun part of tendinous injuries is finding positions that modify the symptoms that their sensitized tendon experiences. This is also a precarious game of trying not to ruin someone’s perception of self and make them think they are a terrible mover. I think in the grand scheme of things, movement likes to flow in the path of least resistance. If we can expand someone’s range of motion (active particularly) and pattern through different movements, can we disperse the force and offload the grumpy area?
Sorry about taking so long with this one.
With Love,
Austin
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Docking, S. I., & Cook, J. (2019). How do tendons adapt? Going beyond tissue responses to understand positive adaptation and pathology development: A narrative review. Journal of musculoskeletal & neuronal interactions, 19(3), 300–310.
Volpi A, Haselman W, Photopoulos C, Banffy M. Regular-Season Injury Rates in the National Football League After an Attenuated Preseason Due to COVID-19. Orthopaedic Journal of Sports Medicine. 2022;10(11). doi:10.1177/23259671221133776
Waldén, M., Ekstrand, J., Hägglund, M. et al. Influence of the COVID-19 Lockdown and Restart on the Injury Incidence and Injury Burden in Men’s Professional Football Leagues in 2020: The UEFA Elite Club Injury Study. Sports Med — Open 8, 67 (2022). https://doi.org/10.1186/s40798-022-00457-4
Atkinson, T. S., Ewers, B. J., & Haut, R. C. (1999). The tensile and stress relaxation responses of human patellar tendon varies with specimen cross-sectional area. Journal of biomechanics, 32(9), 907–914.
Baar, K. (2019). Stress Relaxation and Targeted Nutrition to Treat Patellar Tendinopathy. International Journal of Sport Nutrition and Exercise Metabolism, 29(4), 453–457. Retrieved Jan 3, 2024, from https://doi.org/10.1123/ijsnem.2018-0231
Docking, S., Samiric, T., Scase, E., Purdam, C., & Cook, J. (2013). Relationship between compressive loading and ECM changes in tendons. Muscles, ligaments and tendons journal, 3(1), 7–11. https://doi.org/10.11138/mltj/2013.3.1.007
Frost, D. M., Beach, T. A., Campbell, T. L., Callaghan, J. P., & McGill, S. M. (2017). Can the Functional Movement Screen™ be used to capture changes in spine and knee motion control following 12 weeks of training?. Physical Therapy in Sport, 23, 50–57.
Lazaro, R. M., Souza, R. B., & Luke, A. C. (2021). Patellar mobility and lower limb kinematics during functional activities in individuals with and without patellar tendinopathy. The Knee, 30, 241–248. https://doi.org/10.1016/j.knee.2021.04.002
Grau, S., Maiwald, C., Krauss, I., Axmann, D., Janssen, P., & Horstmann, T. (2008). What are causes and treatment strategies for patellar-tendinopathy in female runners? Journal of Biomechanics, 41(9), 2042–2046. https://doi.org/10.1016/j.jbiomech.2008.03.005
