Sequela of the ECSS (Part 1: Axial Compression)
In the previous article I described the Extension/Compression Stabilizing Strategy (ECSS) and its origins in detail. While no doubt this stabilizing strategy can be effective, it has many short and long term consequences influencing both injury risk and performance. Over the next several weeks, I will be covering each of these sequela. Today, the focus concerns axial compression of the spine.
In review, the ECSS is a compensatory postural syndrome in which the athlete/patient/client uses hyperactivity of the para-spinal muscles to stabilize the spine in the absence of adequate intra-abdominal pressure (IAP). This results in elevation of the ribcage and forward tilting of the pelvis (anteversion). Both the muscle imbalance and the resulting structural orientation of the pelvis and ribcage have profound, and yet often unappreciated, effects on function, pain, and performance.
It is important for coaches to know the consequences of this common compensatory stabilizing strategy to help get athletes to achieve their maximal physical potential.
Sequela: Axial Compressive Forces (Acute Injury)
Because of their close proximity to the spine, the para-spinal muscles have the capability of producing significant amounts of compression on the spine. Because of this close proximity, the lever arm through which they produce motion is microscopic compared to that of the abdominals, with whom they must work to control positioning of the torso. This means that in order to balance out the abdominals, the amount of force they must produce is massive. The only force in the body capable of mitigating this compressive force is IAP. Optimally, IAP works with the spinal extensors to manage the positioning and movement of the ribcage, spine, and pelvis. Unfortunately, with the ECSS, there is inadequate IAP in the system, which is actually the cause of the problem. So what effect does this massive compression have on the spine itself?
Most notably, this elevated axial spinal compression increases the athlete’s risk for discogenic pain and even disc pathology (e.g. bulge, herniation, sequestration). Disc injuries are of the most common in both the general and athletic populations, often resulting in leaving the sport/activity altogether.
The disc works a lot like a water balloon with a bunch of rubber bands wrapped around it -
really, really strong rubber bands. The water in this analogy is the nucleus pulpous and the rubber bands are the annulus fibrosis (see image 1). When the water balloon (or disc) is
compressed, the fluid within is dispersed outwardly against the rubber bands (annulus fibrosis). The stronger the magnitude of the outward-pushing force (intra-discal pressure), the greater the tension in the surrounding annular fibers. This is how the body absorbs shock.
If the magnitude of the outward-pushing force is too great, or it is maintained for a dangerously long period of time (aka chronic), than damage to the annular fibers ensues. They become permanently stretched (distorted). In medical terms, this permanent stretching of the annular fibers is called a disc bulge or disc herniation. It is obvious that gravity will increase the intra-discal pressure. What is less obvious is that hyperactivity of the spinal extensors also increases the intra-discal pressure, and to a significant degree. I would even go so far as to say that most disc injuries are the result of the intra-discal pressure produced by the spinal extensors themselves and not by gravity.
When someone is using an ECSS, they are maintaining high amounts of tension in their spinal extensors, which places an intense and chronic compressive force on the intervertebral discs, resulting in pathological tension in the annular fibers. Without any movement, because of the increased axial compression produced by the spinal extensors, there is an elevated amount of intra-discal pressure. This places a chronic and acute stress on the annular fibers, both of which insidiously contribute to disc pathology.
All movement of the spine results in changes in magnitude in the intra-discal pressure. (In)famously, if you bend forward, the pressure within the disc rises, which is why most disc injuries occur with flexion. But the pressure also rises if you bend left or right or twist side to side. This is normal. All movement results in undulation of intra-discal pressure and alters the distribution of the tension within the angular fibers. When you bend forward, the nucleus pulpous is pushed backwards, disproportionately increasing the tension in the posterior aspect of the angular fibers. All movements cause both changes in intra-discal pressure and altered distribution of the annular tension. This is why the disc evolved into their current structure, to allow spinal movement whilst protecting the spine from bending and compressive forces that naturally occur with these movements. Without intervertebral discs, our function as a species would be greatly hindered.
In a healthy disc, in an athlete with a normal stabilizing strategy, the disc is capable of handling these naturally occurring changes in intra-discal pressure without permanent distortion. With an ECSS, however, the levels to which the intra-discal pressure reach with normal movement is much greater due to the increased axial compression. Now, with normal bending and twisting of the spine, the tension that results in the annular fibers will often reach pathological levels, which causes permanent distortion (aka disc pathology). Bending forward to pick up your phone off the bench between sets should not herniate your disc. But if your posterior chain is cranked on (ECSS) due to the heavy emphasis you put on it in your training (pun intended), now, when you bend over to pick up your phone, the resulting intra-discal pressure may reach pathological levels. This is how the ECSS contributes to acute disc injury. It increases the intra-discal pressure to levels that can cause pertinent damage to the disc.
Sequela: Axial Compressive Forces (Chronic Pathology)
There is also a long term effect the ECSS has on disc pathology, which admittedly drifts into theoretical waters. Stick with me for 3 minutes and decide for yourself. The ECSS applies a chronic, compressive load on the spine. As discussed above, this increases the intra-discal pressure, which contributes to acute disc injury. But what effect does this chronic load have on the discs long term?
Intervertebral discs get nutrients through a process call imbibition. Imbibition is a squishing and un-squishing of the discs, which moves nutrients in and out between the discs themselves and the surrounding interstitial fluid. During this process, the discs are able to absorb the necessary nutrients to keep them healthy. Think of this like a sponge under water. If you squish the sponge with your hand, the water contained within the sponge will be pushed out. When you release your grip, the water will be pushed back in.
In healthy spines, with good postural stabilizing strategies, imbibition is happening throughout the day concomitantly with each and all of our movements. Each position and each movement will increase or decrease the compressive load on the disc, this allows the interstitial fluid to move in and out of the disc, providing the nutrients it needs to live a long and healthy life. With the ECSS, however, the residual compressive load on the disc is significantly elevated. This reduces the amount of decompression experienced throughout the day. Less decompression equals less nutrients entering the disc via imbibition. Over time, if the disc in consistently getting less nutrients due to the hindered imbibition, then it will “theoretically” develop a nutrient deficiency of sorts. With less nutrients, the disc becomes unhealthy and is unable to handle the normal changes in intra-discal pressure. This leads to early and more rapid degeneration, resulting in early-onset pathology such as degenerative disc disease.
This list of the negative effects the ECSS has on the spine is long. Next week we discus another sequela of the ECSS, hyperextension of the lumbar spine.
- Dr. Richard Ulm