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

1. Canosa-Carro, L., Bravo-Aguilar, M., Abuín-Porras, V., Almazán-Polo, J., García-Pérez-de-Sevilla, G., Rodríguez-Costa, I., López-López, D., Navarro-Flores, E., & Romero-Morales, C. (2022). Current understanding of the diagnosis and management of the tendinopathy: An update from the lab to the clinical practice. Disease-a-Month, 68(10), 101314. https://doi.org/10.1016/j.disamonth.2021.101314

2. 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.

3. 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

4. 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

5. 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.

6. 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

7. 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

8. 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.

9. 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

10. 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

Tendinopathy: Part 1 — What is a Tendon Injury?

TL;DR

Have you ever woken up and felt a horrible ache in your patellar or Achilles tendon — usually after doing a ton of work the day before? How about pain at the sole of your foot in the morning with your first few steps? If the answer is yes, you may have a tendinous injury!

Well, buckle up… because this is a hefty topic! At first, I didn’t realize just how dense and inconclusive the literature is surrounding these types of injuries — which might be a good explanation as to why clinically tendinous injuries are so tricky to treat.

Tendinopathy (tendon-based injuries) can present in two ways. The first is acute tendonitis, which usually includes red-hot sensations, swelling and pain. The second is chronic tendinosis, which has no inflammation but consists of a dull ache with the potential for flare-ups (nagging tendon pain).

The literature points to five factors that can influence tendon pathology: load, movement patterns, recovery, metabolism, and genetics. I will focus on tendon loading and movement patterns.

Having tendinopathy can feel akin to the world ending — every step or movement with that limb is painful. You get tossed from your routine, and maybe worst of all, you wake up and immediately feel discomfort. The sh*t part about tendinopathy is that while rest tends to make the boo-boo feel better, an unloaded tendon will only get worse.

This is where we play my favourite game of “How much can we do until we flare up?”. As annoying as this sounds (and is), flare-ups are informative from a therapeutic point of view as they can establish a tolerability threshold.

The pathogenesis of tendinopathies is a fairly muddy topic. In general, we understand that a damaged and painful tendon is one that is experiencing a tendinopathy (itis or osis). The predominant theory is that tendons are predisposed to tendinopathy if they are thin and stiff (which makes them brittle). This change to tendon elasticity may predispose them to micro-traumas that, over time, without adequate recovery, may result in degeneration and symptoms.

Part of tendon pathology is a stiffening of the tendon, a protective mechanism that shields the compromised area of the tendon. This stiffening will result in two issues: disproportionately low symptoms at below-threshold loads and additional spring at the start of an activity/movement.

The first issue is something I explain to every athlete I work with. Just because you have little to no symptoms while navigating your low-impact daily life (haha this sounds like a roast) does not mean that you are ready to get cooking on the court, field, road, or trails. We do know that tendon loading does not follow a linear path, meaning running is exponentially more taxing on the tendon than walking is.

The second issue is of maddening potential — you go out for a run, your tendon is proper stiff and thus bouncy. You are flying… until maybe 10–15 minutes into the run. There is some relaxation of that stiffened tendinous tissue, and then we are back to loading that degenerated part of the tendon.

From a rehabilitation perspective, symptomatic flare-ups are informative and, in my mind, necessary. Flare-ups can help establish where the threshold for the tendon is — this can be from a load, volume or intensity view. Furthermore, we can begin to establish how modifiable factors such as diet and hormones can impact how the symptoms present.

Alcohol and poor dietary conditions can change the systemic inflammatory profile, potentially creating an environment that, at the very least, increases the sensitivity of soft tissue such as the tendon. Hormones, particularly in females, can change the stiffness of soft tissue and the production of collagen in the body. Therefore, the same adequate load to achieve adaptation on day one post-menstrual cycle may cause a symptomatic flare-up on day 20 post-menstrual cycle.

I think that understanding why a flare-up may have occurred is very powerful for a patient. Being able to anticipate when an action may lead to additional symptoms or preemptively modify loading to mitigate the risk of a flare-up might help to reduce the mental catastrophization that occurs with chronic tendinopathies.

Tendinopathies — Part 1 — What in Tarnation?

In the theme of spooky season, I decided to write about one of the spookiest of chronic musculoskeletal complaints: tendon pain. (I know what you’re thinking, “This story was published in November”). Well, sike! November turned into December very quickly. “December is not that spooky.” Well, grab yourself a candle, dim the lights and dust off the Ouija board because we need to set the ambiance for this blog.

Tendon pain can be a nightmare (ooky spooky, of course) for people. Tendon pain can be felt as a deep discomfort in a fairly inert tissue. Tendinopathy can present acutely as very inflamed and painful or chronically as a dull ache, which has the potential to flare into something more akin to the acute phase (swollen and painful).

People get trapped in this horror-iffic cycle of pain, partial recovery and then re-aggravation. In most cases, the underlying tissue issue has never been resolved, and the person is using symptom resolution as a guide to returning to full activity.

At this point, we can queue the theatrics — patients plead with their practitioners, their spirituality, and even the poor employee at the boutique running shoe store who only wants to correct pronation — “Why me?!?!” they ask.

This can be a tricky little question to answer, but in short, it’s multifactorial. My hope is that by the end of this blog, you will have more confidence in the management plan for your condition and less reliance on retail employees.

As a performance-based practitioner, I hate telling people not to move. Imagine you run 40km a week, and some stupid idiot says, “Yeah, you’re probably going to want to stop that”. The person has no fracture, strain, or other traumatic soft tissue tear. Their only issue is that after their run, they have tendon pain.

I mean, sure, stop running! The tendon pain will no longer hurt after runs, but eventually, it may start hurting after walks (current literature illustrates a modification in load, not cessation — silly goose). I’m not out here trying to fearmonger, but the reality with a tendon is that a strong tendon is a loaded tendon.

I’ll get more into what exactly is happening to the tendon, but from my perspective, it’s a wee bit silly not to address the tendon and make it more resilient to the activity the person wants to do while they continue to do it (in some capacity).

What is a tendinopathy?

Tendinopathies are, as their name suggests, tendinous injuries. We have two categories of common tendinopathies seen in the clinic:

1. Acute tendonitis — this is when your tendon is hot, red, and severely painful to load.

2. Chronic tendinopathy or tendinosis — this is where we see the most tendinous degeneration.

You may learn that this person had tendonitis previously, and their tendon was never the same after. From a tissue perspective, what the heck is going on? Well, acute tendonitis is the presence of tendon damage with inflammation. Tendinosis is tendon damage and pain without inflammation. The current theory around tendinosis is that it results from cumulative microtrauma(1,2).

This is where I’m at:

A great way to break down the pathogenesis or the cause of tendinopathies and, ultimately, the treatment is to subdivide the factors that contribute to tendon inflammation and degeneration (and, conversely, their healing and strengthening).

The literature consistently discusses five factors: load, recovery, movement patterns, metabolism, and genetics. This is a good time to mention tendinopathies are a pain in the ass. The common characteristic with many tendinopathy patients is what I like to call the cycle of madness (modness if you prefer the British grime vernacular). They’re mod/mad for a few reasons.

The first is that the length of time it takes to properly rehab a tendon is frustrating — up to a year! The next is the classic, “My sh*t feels pretty good right now. I’m going to do the thing that initially set off my injury at a pre-injury intensity”. The truth of the matter is that no injury has a linear recovery curve; there will be flare-ups, and this is especially true for tendons.

We will get into loading and movement patterns next week!

With Love,

Austin

Up next:

Part 2: Tendon Loading & Movement Patterns

1. Canosa-Carro, L., Bravo-Aguilar, M., Abuín-Porras, V., Almazán-Polo, J., García-Pérez-de-Sevilla, G., Rodríguez-Costa, I., López-López, D., Navarro-Flores, E., & Romero-Morales, C. (2022). Current understanding of the diagnosis and management of the tendinopathy: An update from the lab to the clinical practice. Disease-a-Month, 68(10), 101314. https://doi.org/10.1016/j.disamonth.2021.101314

2. 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.

Unwrapping Back Pain: Finding a Balance of Stability, Mobility, & Strength

Stability — TL;DR

Does your core strength actually decrease the likelihood that you’ll have lower back pain? Many people come into the clinic with various back complaints and admit to having a subjectively weak core. The term neutral spine has become the victim of misinterpretation, people tend to view a spinal extension bias as neutral. No spinal movement is innately bad, spines like to move and were engineered to do so. Reliance on the passive structures of the spine — ligaments, joint capsules, discs — for support is silly, we should train our core muscles to support the spine. Positioning of the abdomen is the first movement pattern I try and solve. The goal is to relatively align the diaphragms(the pelvic floor and the diaphragm) in parallel. This balances the tension on the front and the back of the abdomen. The next thing I care about is breathing while they maintain this tension. Many lose tension when instructed to breathe, which is a problem given we breathe … all the time. Lastly, rehabbing only in the sagittal plane is a wee bit silly. Our limbs are not located midline, therefore, any unilateral challenge we place on ourselves involves a rotational action and rotational reaction - guess what provides the rotational reaction?

If we can not stabilize against all the demands placed on our core where does this leave us? The movement will likely occur at the weakest point in the chain — the path of least resistance. The excessive motion and accumulation of forces in that one area can result in a build-up of tension in the surrounding musculature.

Ever heard of recurrent lower back pain? We have an initial flare-up of low back discomfort, we give it time, symptoms may decrease, and we forget about it — until it rears its ugly head again. It’s like scraping a scab off over and over, it gets a little better but we never resolve the underlying issue. You’re going to make me say it — how about we take the opportunity to optimize movement so that forces are shared as equally as possible throughout the system! *We know that low back pain has a high likelihood to reoccur in a person’s lifetime, but we can use rehab and education to make a person more resilient to reoccurrence and aware of management strategies*

Stability

Does your core strength actually decrease the likelihood that you’ll have lower back pain? I find it comedic when patients come into the clinic with back pain and elude to the fact that they know their core is not strong enough. I’m a curious cat so I typically prod, “how do you know?” and typically the answer is well my back gets sore after I do an activity. I find it interesting that the average patient understands the fundamental role of the core musculature, they can associate a weak core with the risk of developing discomfort, but they do not prioritize its training. As practitioners, we can get … lazy … simply prescribing McGill’s “large and in-charge” 3 exercises — bird dogs, side planks, and crunches. I think these exercises have value, but they are not the only exercises that should be prescribed! Obviously, other practitioners think their value is monumental given the amount of “Try these 3 exercises to forever rid yourself of any back pain for the rest of your life” videos on social media. So we know the importance of core strength and stability, but do we train it to be functional?

This is where I am at:

More often than not we are fixated on where the spine is in space. Practitioners hold on to the term neutral spine like Smeagle held on to The One Ring. Neutral spine has been misinterpreted, the common neutral spine assumption is an anti-flexed spine. I was guilty of having this view. No spinal movement is innately bad — flexion, extension, rotation, and lateral flexion are all okay. Yes, repetitive flexion of a porcine spine can cause disc herniations. These porcine spines were stripped of their active contractile components, therefore, we understand that repetitive flexion of an unsupported spinal column can be detrimental to the structural integrity of spinal tissue. We can manage the stress on the passive components of the spine by offloading them with the active tissue (muscle), this is not a mind-blowing statement. I suppose someone could read this bad blog and scoff at the fact that I don’t talk about tissue creep. Tissue creep occurs when people stay in sustained postures for an extended period of time. A big problem with tissue creep is the change in the tissue stiffness of the area that has experienced creep and the change in the proprioception of the area (how the brain perceives that area). You can see how a reduction in tissue stiffness and position sense could predispose you to injury. My solution is the same solution I have for all posture-related questions. What is a good posture in my opinion? A good posture is a variable posture. If a variable posture can not be achieved a proper warmup (this should be done anyway) will be required to stimulate the mechanoreceptors to improve position sense.

As we have established, reliance on passive structures in the spine may predispose you to injury. I think a fair place to start is to observe how someone adds tension to their core. I would say many people simply pressurize their abdomen (the feeling of pushing your belly out). If we are thinking about how we can adequately add tension to the abdomen both dorsally(back) and ventrally(front) we need to think about how to properly position the two diaphragms — the diaphragm … diaphragm and the pelvic floor. Proper parallel alignment of the two diaphragms makes it much easier to adequately apply tension throughout the entirety of the core. Rehab guru Dr. S. Sharmann’s approach might focus more on balancing the positional and functional demands of the core musculature. Nevertheless, the objective remains the same — get the muscles in their best position to perform and coordinate, thus increasing our potential to stabilize. Maybe an easier way to think about this is — I am an Instagram influencer attempting to influence you to look at my glutes. I know a little cheat code, if I extend my lumbar spine I can create the illusion that my badonkadonk is much larger than it truly is. Funny enough, this position is often regarded as one of the safest positions for the spine. If we then think about the length-tension relationship of the core muscles in this extended position. The muscles on the back or dorsum of the person are basically maximally shortened. In contrast, the muscles on the ventral surface or the front are maximally lengthened. The result is that we have little tension on the front of the abdomen, and here is the kicker — force production of muscles is reduced at their maximal ranges of motion, therefore, the capacity for the muscles on the ventral surface of the abdomen to contract is compromised — but(t) I still managed to catch your eye.

Oh, before I forget. We should know how to breathe. An interesting takeaway from working with patients this last year and a half (internship and practice), is the amount of people who simply hold their breath when doing core exercises. Even when I work with patients on very simple core-setting exercises and ask them to take 3–5 breaths they struggle to maintain core tension while breathing. What you may see is a flaring of the ribs as they attempt to inhale. My mentorship and the Integrated Seminar Series were great for highlighting the importance of being able to breathe with core tension. I’m paraphrasing here but, you don’t want to be an asshole and breathe with your rib cage! If tension can not be maintained while breathing we have a problem. At a minimum, your patient should be able to breathe and stabilize at the same time. If these two actions can not happen in conjunction it suggests they will have to sacrifice one to achieve the other. In the office with their practitioner breathing goes bye-bye, elsewhere breathing might take more precedence.

Hopefully, all of this yappa-yappa has not scared you away, because this is why I think all this mumbo-jumbo is important. A spine that is being held at end-range extension is probably pretty good at resisting pure flexion. The tricky thing is that our limbs are not located perfectly in line with our spine, thus, when loading our limbs biomechanically we insert a rotational demand and require a rotational reaction. In the words of Gary Ward, “Joints act, muscles react”. This is where those sleepy muscles on the front(ventral surface) of the abdomen come into play. The obliques play an important role in controlling the rotational demands placed on the core. There are two challenges now: the suboptimal balancing of the core musculature and the lack of emphasis traditional rehab/prehab/training programs place on rotational control.

My approach is:

1. Can you actually move your spine?

2. Can you actively recruit your abdominal muscles?

3. Can you breathe while those abdominal muscles are turned on?

4. Add the context of movement … do you fall apart when doing various movements (capacity issue)?

Mad respect for the read!

With love,

Austin

My approach

I could bore you and tell you the techniques I use to treat people, however, I do not think that is the best way to describe my approach to neuro-musculoskeletal issues. I think an obvious challenge when departing from school is that the protective membrane that the institution provides is gone. I am currently spending a lot of brainpower trying to understand what I think a good practice looks like and what would excite me to go to work daily. I can tell you for free it was not case report writing. The goal of this blog will be to elaborate on my Instagram posts. I can not stand those really long wordy IG captions, so this is the solution. A blog written by a poor writer, enjoy!

Anyway here is where I am at:

Most injuries that I have seen in practice have no real mechanism of injury. For example, Jimmothy does not typically come into the clinic to tell you that he was hit by a car and his knee was driven medially. *Unfortunate shout out to Nick Chubb and RIP my fantasy team* The history describes a clear potential mechanism that will then guide the physical examination. In Jimmothy’s case, he may have some torn ligaments and require a surgical consult along with pre-hab and rehab.

More often I see something like — Jimmothy comes into the clinic and tells you his knee hurts. Orthopedic tests are unremarkable, he feels some tenderness on the inside of his knee. His pain is usually felt after long bouts of standing and the day after running. The diagnosis is as murky as the physical findings, let us just call it a meniscus irritation. Easy peasy, throw a laser on it and you’re done, thanks for reading. Just kidding this is not Star Wars. Ok let’s rub the knee to make the boo-boo feel better, that may work, but that does not work for me.

What I think we should consider is - how can we optimize movement to dissipate forces. To simplify that statement we could look back to our pal Jimmothy — we can postulate that there is an increased concentration of load causing the tissue of the medial knee to at the very least sensitize. How can we use soft tissue therapies, joint manipulation, and exercise to change the way force is distributed in the body? This is a good time for a shout-out, Dr. Wishloff offered me the opportunity of mentorship. I was able to spend 3 months watching how she was able to treat both the symptoms and the system. For a new practitioner, this was revolutionary and puzzling simultaneously. The inspiration leads you down a path where you want to understand and ask questions like yes their knee hurts but — how is the spine moving? How about the foot? Did you look at the hips? Additional considerations are — does the joint have that range of motion? Is the range of motion full but they can not control the full range? Can they control the full range but lose control at a certain load? To summarize how my approach has rapidly changed over the last few months. The issues I tend to see are chronic mechanical issues, therefore, we may take a mechanical approach via movement-based therapy which can yield a great deal of patient autonomy and also keeps me percolating.

There will be more to follow. Oh, and for you folks who just love strengthening things. Yes, mobility is not always the answer, however, if a tissue is being overloaded- is it not a reasonable first step to try and redistribute the load?