The Spinal Stability System

Stability of the spinal system is imperative to its function and crucial to protect the spine from injury. The stabilizing system includes the mechanical contributions of passive forces generated by spinal tissues and the surrounding forces generated by active muscular contractions. Okay, I lied. Muscles also provide passive force contributions. Let’s unpack this.

Tissue Characteristics

Active forces are the result of muscular contractions, or muscle shortening. Passive forces come from the material properties of a tissue itself being stretched. The structures of the spine — vertebrae and their attachments to discs, ligaments, etc. — provide some resistance to bending and thus offer passive force contributions.

Let’s use the most fundamental exercise as an example: bicep curls (obviously). Actively contracting your bicep allows you to move your arm through the shortening and lengthening phases of a curl. If you were to:

1. Let your arm hang limp at your side,
2. extend your arm as straight as it can go, and
3. relax your elbow extensor muscles (triceps).

You would notice that your elbow joints spring into slight flexion the second that you relax. This is from the passive tension of your elbow flexor muscles and tendons. The same is true for many muscles and joints in the body, albeit their actions are much less obvious than our simple example.

There’s some funny business between the active and passive force generation capabilities of our spinal systems. The spinal stability hypothesis argues:

There is an inverse compensatory relationship between the stabilizing contributions of the active force generation of muscles and the passive resistive tissue forces [1].

In practical terms, the ‘stiffness’ of your spinal tissues remodels and changes in response to changes in the force production capabilities of the muscles that surround your spine and vice versa. This hypothesis was shown experimentally, where mice with calcified spines (mechanically stiffer) had spinal muscles with reduced stiffness [2]. In other words, the system tries to maintain its level of stability and seems to adapt its properties to do so.

On a more technical note, in the tissue biomechanics world, we quantify the stability of spinal segments by measuring ‘neutral zones’. Neutral zones are regions of low resistance to motion. We’ll use a simple metaphor here: imagine you have a stick, and it’s somewhat hydrated, so you can bend it without it snapping instantly. You can bend the stick a bit in any direction without using too much force — this is the neutral zone. Once you try to bend the stick a lot more, you notice that it begins to take a lot more effort, or force, to continue bending the stick — this means you are no longer in the ‘neutral zone’. A stick that requires more force to bend than another has greater stiffness, or modulus, in biomechanical terms.

So for the stabilizing system to be efficient, small movements from a neutral position must be produced by minimal muscular exertion [1]. And large movements and forces that place the system into its end ranges of motion are met with resistance from our tissues, providing stability. Makes sense, right? We don’t want to require a lot of force to move or bend a little, but we should require way more force to bend or deform a tissue a lot to protect us from injury.

To summarize, our bodies strive to maintain a delicate balance between permissible motion and requisite stability. Changes in the properties of one tissue lead to adaptation in another to compensate. This is happening to all of our spinal tissues right now. The ongoing adaptation is particularly striking for individuals who have sustained spinal injuries and those with back pain.

The adaptive changes don’t stop at our tissues either. Our nervous systems also adjust in response to changes in our spinal function and physiology.

Muscle Activation

Our nervous systems coordinate muscle activity differently once we have back pain. The picture below depicts an experiment where participants flexed (bending forward) to full flexion and then extended back up again. Participants were split into two groups: those who had back pain, those who didn’t [3]. If we examine the rest of the figure below, we’ll see printouts of the electrical activity of a spinal erector muscle — as measured by EMG (electromyography). EMG tells us when a muscle is contracting and how much it is contracting relative to a maximal effort.

If we examine graph A, we can see that there is muscle activity during the flexion and extension phases, but none during the full flexion phase. This is called the flexion relaxation phenomenon, or FRP. The FRP describes the cessation of extensor muscle activity when the trunk is in a full flexed position. This is because the passive forces (or force returned by bending the stick) of spinal tissues are sufficient to support the weight of the trunk in this position.

Graph B shows the same exercise, but this time there is no drop of muscle activity when the participants were fully bent over, no FRP. Guess which group had back pain?

If you guessed group B, then you’re right. Full flexion is a vulnerable position biomechanically — and our systems know it. So, the nervous systems of people with back pain instinctively continue to support the spine with muscular force in situations where a pain-free system would not.

Why does this happen? When our nervous system detects that there is pain or instability in the spinal system, it compensates by stabilizing through additional muscular force production.

If it wasn’t obvious already, this means that it’s extra important for people with LBP to build strength in their posterior chain muscles — because as we’ve just seen, there is additional demand on the muscles of people with back pain.

Thank you all for tuning in to another weekly newsletter!

Best,

Mitch

References

[1] Panjabi et al., 1992: https://pubmed.ncbi.nlm.nih.gov/1490035/

[2] Gsell et al., 2017: https://pubmed.ncbi.nlm.nih.gov/28240653/

[3] Gouteron et al., 2022: https://link.springer.com/article/10.1007/s00586-021-06992-0