Biomechanics of Spine Pain


“If philosophy and science don’t agree, one is wrong. Which?”


  • TWO (or perhaps three) TYPES OF DISC DEGENERATION


Muscular dysfunction elicited by creep of lumbar viscoelastic tissue. Solomonow M, Baratta RV, Zhou BH, Burger E, Zieske A, Gedalia A. J Electromyogr Kinesiol. 2003 Aug;13(4):381-96.

“20 min of static as well as cyclic flexion under load control and during 7 h of rest following the flexion. It was shown that the creep developed in the viscoelastic tissues during the 20 min of static or cyclic flexion did not fully recover over the 7 h of following rest.

My comments:

From what I have gathered, Mosche Solomonow’s work is preeminent in what appears to be the early onset of acute spine pain. This study showed that just 20 minutes of sustained or repeated spine flexion stretching was enough to cause inflammation in the posterior collagenous tissues of the spine resulting in reactive muscle spasms that peaked 6-7 hours later. Which would be one explanation why spine stretches might initially be relieving of pain, only to cause more muscle spasms hours later as the stretch (likely some of which is more flexion) only further damages the collagenous tissues of the spine.  

Neuromuscular manifestations of viscoelastic tissue degradation following high and low risk repetitive lumbar flexion. Solomonow M. J Electromyogr Kinesiol. 2012 Apr;22(2):155-75.

“The hypothesis is forwarded that static and repetitive (cyclic) lumbar flexion-extension and the associated repeated stretch of the various viscoelastic tissues (ligaments, fascia, facet capsule, discs, etc.) causes micro-damage in their collagen fibers followed by an acute inflammation, triggering pain and reflexive muscle spasms/hyper-excitability. Continued exposure to activities, over time, converts the acute inflammation into a chronic one, viscoelastic tissues remodeling/degeneration, modified motor control strategy and permanent disability. Changes in lumbar stability are expected during the development of the disorder.”

“A series of experimental data from in-vivo feline is reviewed and integrated with supporting evidence from the literature to gain a valuable insight into the multi-factorial development of the disorder. Prolonged cyclic lumbar flexion-extension at high loads, high velocities, many repetitions and short in between rest periods induced transient creep/laxity in the spine, muscle spasms and reduced stability followed, several hours later, by an acute inflammation/tissue degradation, muscular hyper-excitability and increased stability.”

My comments:

This is a fascinating paper, which along with others, goes along to demonstrate that excessive spine flexion, both repetitive and sustained damages the collagenous tissues on the posterior aspect of the spine. That damage causes inflammation and “reactive muscle spasms” that increase stability of the spine and would help allow the spine to heal, except when people think the spasms themselves are the source of pain. They stretch them out to relieve them, with the same stretch being flexion that further damages the spine. The damage sustained in this study would probably best be understood in the category of acute back or neck pain, before continued spine flexion and flexion/extension cycles resulted in disc bulging and herniations that would then cause more severe pain and destabilize the spine.


Prolapsed intervertebral disc. A hyperflexion injury 1981 Volvo Award in Basic Science. Adams MA, Hutton WC. Spine (Phila Pa 1976). 1982 May-Jun;7(3):184-91.

My comments:

This was the first study to produce a prolapsed disc (or disc herniation) in laboratory conditions. Before that, physicians knew disc herniations occurred as they were seen on operating tables. But when they tried to induce them in a lab, rather than injuring the disc, the forces of flexion or compression ended up fracturing the vertebrae instead. Though this study succeeded herniating 26 out of 61 discs with a combination of spine flexion and compression, it was still considered “non-physiologic” as the discs that prolapsed had to be flexed beyond what is considered normally possible in everyday life (by 1 to 6 degrees) before compressive stress was applied. They specifically noted that prolonged flexion stretching prior to a heavy lift could stretch the ligaments allowing normal flexion angles to be exceeded, possibly resulting in a disc herniation.

Interestingly they noted that once the disc herniated they were never able to get the extruded disc material back into the disc, saying it was “like trying to push toothpaste back into the tube.”

Mechanism of disc rupture. A preliminary report. Gordon SJ, Yang KH, Mayer PJ, Mace AH Jr, Kish VL, Radin EL. Spine (Phila Pa 1976). 1991 Apr;16(4):450-6.

“Fourteen vertebral motion segments with intact posterior elements were loaded repetitively at 1.5 Hz in a combination of flexion (7 degrees), rotation (less than 3 degrees), and compression (1,334 N) for an average of 6.9 hours (range, 3.0-13.0 hours) in a materials testing machine. Loading was terminated when reaction force leveled off for more than 1 hour. Ten discs failed through annular protrusions, and four failed by nuclear extrusion through annular tears, supporting the hypothesis that intervertebral disc prolapse is peripheral in origin.”

My comments:

This is the study where they first figured it out how disc herniations happen in real life. Mild to moderate compression, combined with spine flexion herniated a disc. The average number of cycles in this study was 36,750, which is a large number and why many people get away with bad habits for so long, then wonder what happened. If you assume the spine is loaded like in this study, say 20 times per day, it would fail in 18837.5 days or just over 5 years. Of course in living rather than cadaver tissue there will be some healing going on which would likely prolong ultimate failure substantially. Also some discs failed in as few as 16,290 cycles while others lasted 70,200 so there’s considerable variability, which could be explained by prior disc damage or genetics.

What’s most interesting to me is that it wasn’t figured out until 1991 that the cause of posterior disc herniations was repeated spine flexion. And yet, though I graduated physical therapy school in 1999 I didn’t learn about this until 2008 when reading Stuart McGill’s book Low Back Disorders.

Intervertebral disc herniation: studies on a porcine model exposed to highly repetitive flexion/extension motion with compressive force. Clin Biomech (Bristol, Avon). 2001 Jan;16(1):28-37. Callaghan JP, McGill SM.

My comments:

This was one of the earlier studies done that really figured out how spinal discs herniate and built upon the prior work of Gordon et al.  Gordon was one of the first to be able to reliably produce lumbar herniations in the lab through a combination of compression, and repeated spine flexion and rotation. It’s interesting because prior to this, researchers were unable to get spines to herniate in the lab like they would see clinically with patients.  Callaghan and McGill did so with just flexion and extension with varying levels of compression. What they found was with just 260 Newtons (N) of compression there were no disc herniations in 83700 cycles. At 867 N all discs herniated with an average of 70550 cycles. With 1472 N 3 out of 4 discs failed with a disc herniation while the 4th failed with an end plate failure, with an average of only 34974 cycles.  What both studies found was that discs didn’t herniate from large forces, but rather high repetitions of moderate loads. There are about 4.4 Newtons in a pound and 9.8 N per kg.


Human lumbar spine creep during cyclic and static flexion: creep rate, biomechanics, and facet joint capsule strain. Little JS, Khalsa PS. Ann Biomed Eng. 2005 Mar;33(3):391-401. [free full text]

“Both SLF and RLF resulted in significantly increased intervertebral motion, as well as significantly increased FJC strains at the L3-4 to L5-S1 joint levels. These parameters remained increased after the 20-min recovery. Creep during SLF occurred significantly faster than creep during RLF. The moment relaxation rate function was able to accurately predict the creep rate of the lumbar spine at the single moment tested. The data suggest that SLF and RLF result in immediate and residual laxity of the joint and stretch of the FJC, which could increase the potential for LBP.”

“Although the muscles are the primary contributors to lumbar stiffness during motion, the reflexive activation of the multifidi and longissimus muscles is significantly decreased during sustained or repetitive motion, resulting in creep of the viscoelastic tissues of the spine. Lumbar creep is believed to result in a laxity developed across the intervertebral joint and a subsequent desensitization of the afferents in the ligaments, capsules, and discs.”

“However it has been shown that prolonged and cyclic loading of the spine decreases the reflexive muscle activity and results in spasms of the paraspinal muscles.”

“…any movement performed subsequent to lumbar creep, while the intervertebral joints are lax and the muscle activity is reduced, could be mechanically unstable and have a greater potential to result in injury.”

“The rate of creep was faster during static flexion compared to cyclic flexion.”

“Older specimens have been shown to creep further in flexion than younger specimens and recover more slowly.”

My comments:

I thought this study was particularly interesting, because while they showed that spine flexion stretches do increase spine flexion range of motion, and that range of motion increases reactive muscle spasms, the ability of your nerves to sense while your muscles provide adequate support to prevent injury lessens over time. And that prolonged stretch is worse than repetitive stretch. Which fits with my experience taking yoga classes, where I felt the more gentle or restorative “Hatha” yoga classes felt worse on my spine than the more aggressive fitness-oriented vinyasa flows. I felt both brought the spine into too much flexion and extension, but the slower Hatha classes held you there longer, and didn’t do very much at all to build muscular fitness to protect the spine. The vinyasa flows still stretched the spine too much, but they didn’t hold those stretches as long, thus being less harmful, and they did more to build total body fitness, which is very much a good thing. And that’s part of what got me thinking about developing my own Spinal Flow Yoga™, where I fully eliminated what I think are harmful spine stretches, while amping up the total body fitness aspects in a progressive way.


Disc prolapse: evidence of reversal with repeated extension. Scannell JP, McGill SM. Spine (Phila Pa 1976). 2009 Feb 15;34(4):344-50.

In this study they tested the theory (Physiotherapist Robin McKenzie’s theory) that if spine flexion causes herniated discs backward, then spine extension should heal the disc by pushing the nucleus back forward.

Previous research has established that repeated flexion can create disc prolapse, the question here is whether repeated extension can reverse the process.
The C3/4 segments of 18 porcine cervical spines were dissected and potted in cups. Specimens were preloaded, then axially compressed (1472 N), and repeatedly rotated in either pure flexion or combined flexion and side flexion at a rate of 0.5 degrees /s. Specimens that prolapsed were axially compressed and repeatedly and rotated into extension.
Based on a blinded radiologist’s review of the radiograph images, all 18 specimens contained healthy discs before testing, but after testing 2 of the 18 specimens had endplate fractures, whereas 11 of the 18 specimens had prolapsed. Prolapsed nucleus was reduced in 5 of the 11 prolapsed specimens after the reversal testing, whereas the remaining 6 did not change. Subclassification analysis revealed that the prolapsed discs that centralized had significantly less disc height loss (P < 0.01). Neither the classification of the herniation (circumferential or radial) nor the angle of lordosis of the specimens was linked to the behavior of the specimens.

My comments:

They did 5400 to 10,800 of pure flexion, or 900 to 2700 reps of flexion combined with side bending, both combined with 1472 Newtons of compression to accelerate disc protrusion with a lesser disc height loss that comes with pure flexion. With an attempt to reverse the damage with repeated extension with lesser compressive force of only 260 N. As noted in the abstract, the extension worked to help reverse the disc protrusion about half the time (5/11). Average disc height loss of the discs for which prolapse reversed was about 42%, and for those it did not reverse disc hight loss averaged about 68%. After the reversal procedure (repeated extension) disc height loss was ~37% when it worked and 55% when it didn’t. So it seems that the extension can help if the disc isn’t that damaged yet from the flexion stretch, but if there was more disc height loss, the extension didn’t help. Interestingly, even when the extension worked, the discs were left 37% flatter than they were prior to the procedure so it would be hard to argue that all the damage was reversed. Also the nature of spine flexion induced damage includes tearing and separating of the collagen fibers in the outer annulus containing the nucleus. Such that even if spine extension was able to physically push the nuclear back to the center, it seems unlikely that I would stay there for long if flexion resumed, due to already present breach of the annular wall.

I’ve met one of the primary researchers in this paper (Stuart McGill) and asked him if he started recommending repeated back extension to his exercise program in light of this study. He said he still didn’t, because he thought the repeated extension would eventually result in arthritis of the facet joints of the spine. Rather, he thought laying flat on one’s stomach with the head raised either on two fists or, at most, up on elbows (Sphinx pose in yoga) and staying in that position for as long as 15 minutes would likely have the same positive effect without repeatedly stressing the facet joints of the spine.


Extent of nucleus pulposus migration in the annulus of porcine intervertebral discs exposed to cyclic flexion only versus cyclic flexion and extension. Balkovec C, McGill S. Clin Biomech (Bristol, Avon). 2012 Oct;27(8):766-70.

Repeated flexion of an intervertebral disc has been identified as a mechanism to produce posterior herniations. Repeated extension under certain conditions has also been shown to cause the nucleus of partially herniated discs to reverse and migrate anteriorly. While research shows that the nucleus pulposus migrates anteriorly in extension and infiltrates the annulus posteriorly in flexion, it is not known if a cycle of flexion followed by a cycle of extension produces more or less annular damage compared to pure flexion alone.

Two groups of porcine spinal motion segments were exposed to either repeated flexion with extension or just repeated flexion. Digitized photographs of dissected specimens enhanced with a radio-opaque blue dye enabled the quantification of the area of annulus infiltrated with nucleus pulposus.

Specimens exposed to both flexion and extension showed significantly more annular damage and axial creep compared to those exposed to flexion alone.

It would appear that while flexion alone can still cause nucleus pulposus to track through the annulus of an intervertebral disc, the effects are compounded when it is followed by a subsequent cycle of extension. Thus, movements which require both repetitive flexion and extension, have the potential to produce more annular damage than those which require merely flexion.

“Cyclic extension has been shown to assist in return return of nucleus (Scannel and McGill 2009), but there may be a cost of more annulus damage. Perhaps static extension as opposed to repeated cyclic extension may be more helpful by producing less trauma — this remains to be seen.”

My comments:

This is one the the reasons why I really like, and really trust Stuart McGills research. Based on the their 2009 study where extension was able to partially reverse flexion induced disc damage with repeated extension, it was a good question to wonder what would happen if you just alternated the stress one for one rather waiting until the spine had been flexed thousands of times. And rather than trying to prove a preconceived point, they just tested it, reported what happened and adjusted his treatment protocol based on real outcomes. Which I think is a considerably more effective strategy than coming up with a treatment plan first, then trying to prove that it works, because that’s where all sorts of bias kicks in.

In both groups they did 10,000 cycles, either of pure spine flexion, or flexion alternated with extension, both with 1500 Newtons of compression. With pure flexion the nucleus tracked rearward on average 4.5 mm, while alternating flexion with extension the nucleus tracked rearward 53% more, 6.9mm. So it seems the spine is a lot like a wire coat hanger. The further back and forth you bend it, and the more times you do so, the faster it snaps.


The direction of progressive herniation in porcine spine motion segments is influenced by the orientation of the bending axis. Aultman CD, Scannell J, McGill SM. Clin Biomech (Bristol, Avon). 2005 Feb;20(2):126-9. 

Matched cohorts (nu=16) of porcine cervical spine (C3/4 and C5/6) motion segments were potted in aluminum cups and bent at an angle of 30 degrees to the sagittal plane flexion axis while under a sustained compressive load of 1472 N.

The direction of bending motion affected the tracking pattern of the nucleus through the annular fibres in a predictable pattern. Specifically, bending the motion segments at an angle of 30 degrees to the left of the sagittal plane flexion axis biased the movement of the nucleus toward the posterior right side of the disc in 15 of the 16 specimens.

“Callaghan and McGill (2001) determined that posterior disc herniations are consistently created with repetitive flexion under modest static compressive forces. Their data suggest that disc herniation are an injury  that can result from cumulative bending trauma after only 5870 cycles of flexion/extension while under a compressive load of only 867 N [195 lb or 88 kg]

My comments:

In this study McGill’s group did much the same spine flexion tests, with 1472 N [150 kg] compressive force but combined with a 30 degree side bend to the left for just 6000 cycles. And just like a jelly donut, compression towards the left got the jelly (or nucleus pulposus) to herniate back to the right 94% of the time. One, who really likes stretching, might be inclined to then say, “instead of side bending repeatedly to one side you should alternatively side bend to the other.” However, seeing as alternating flexion with extension stretch increased the rate of herniation 53% as cited above, alternating right side flexion with left, would very likely only accelerate damage as well. So the real solution (to lessen spine degenerative stress) would be to stretch the spine (in any direction) less frequently, less intensely, and or combined with less compressive force.


Intervertebral disc degeneration: evidence for two distinct phenotypes. Adams MA, Dolan P. J Anat. 2012 Dec;221(6):497-506. [free full text] 

“We review the evidence that there are two types of disc degeneration. ‘Endplate-driven’ disc degeneration involves endplate defects and inwards collapse of the annulus, has a high heritability, mostly affects discs in the upper lumbar and thoracic spine, often starts to develop before age 30 years, usually leads to moderate back pain, and is associated with compressive injuries such as a fall on the buttocks. ‘Annulus-driven’ disc degeneration involves a radial fissure and/or a disc prolapse, has a low heritability, mostly affects discs in the lower lumbar spine, develops progressively after age 30 years, usually leads to severe back pain and sciatica, and is associated with repetitive bending and lifting.”

“Research into disc degeneration is expanding rapidly, as large population studies have shown a strong dose-related association between intervertebral disc degeneration and back pain or sciatica. The association is notoriously variable, however, because some previous studies on smaller selected groups found little or no association between some aspects of disc degeneration and pain.”

“Evidently, certain features of disc degeneration are often painful, but not in all cases, and other features are rarely if ever painful.”

“…several biochemical changes in degenerated discs, such as proteoglycan and water loss, appear to be more or less inevitable with advancing age, and have little or no direct association with pain…”

“‘Disc degeneration’ can be likened to accelerated ageing”

“The biochemical and functional changes of ageing are exaggerated (or accelerated) in some discs, particularly those in the lower lumbar spine.”

“The result is a vicious circle of frustrated healing and repeated re-injury which characterise disc degeneration”

“Degenerated human discs lose height at a rate of approximately 3% per year, whereas normal discs lose <1% per year. Annulus height largely determines the separation of adjacent neural arches, so disc-narrowing causes severe compressive loading of the apophyseal joints, which in turn can lead to osteoarthritis. Disc height loss also slackens intervertebral ligaments and subsequent re-stabilisation by means of vertebral body marginal osteophytes.”

My comments:

This paper is of the better synthesis of what’s going on with regards to the causes of low back pain. It came out 5 years prior to American Physician’s Association paper regarding the treatment of acute, sub-acute and chronic low back pain, for which one gets the impression that nobody has a clue about what causes, or what one should do for low back pain. Adams and Dolan don’t have a lot to say about treatment here, but they sure nail the causes, describe the process of degeneration in detail, and shed light on why some of the confusion is there.

The basic gist of the paper is that there is some normal age related disc degeneration that is generally not painful. Then there is accelerated disc degeneration related to vertical disc herniations, vertebral end plate damage, Schmorl’s nodes and compressive injuries, which usually affect the middle back that are somewhat painful. The third type is the posterior disc protrusion injuries, annulus damage, secondary to  spine flexion forces that are highly painful and most related to your lower back pain and sciatica. This is in complete accordance with other bio-mechanics research I have read, probably because the conclusions are based on all that research.


Lumbar spine endplate fractures: Biomechanical evaluation and clinical considerations through experimental induction of injury. Curry WH, Pintar FA, Doan NB, Nguyen HS, Eckardt G, Baisden JL, Maiman DJ, Paskoff GR, Shender BS, Stemper BD. J Orthop Res. 2016 Jun;34(6):1084-91.

“Twenty lumbar motion segments were compressed to failure. Two methods were used in the preparation of the lumbar motion segments. Group 1 (n = 7) preparation maintained pre-test sagittal lordosis, whereas Group 2 (n = 13) specimens had a free-rotational end condition for the cranial vertebra, allowing sagittal rotation of the cranial vertebra to create parallel endplates. Five Group 1 specimens experienced posterior vertebral body fracture prior to endplate fracture, whereas two sustained endplate fracture only. Group 2 specimens sustained isolated endplate fractures. Group 2 fractures occurred at approximately 41% of the axial force required for Group 1 fracture”

My comments:

Putting it into simpler English, this paper found that discs can be herniated vertically by compression, generally not due to posture or exercise technique, but more so trauma (like falls or accidents.) To test this, they took human lumbar cadaver spine segments and applied increasing axial (compressive) force to lumbar discs until they broke. They did one group of discs aligned neutral (preserving the normal lordotic arch, which is in fact some extension) thus preserving the normal wedge shape of the lumbar disc. The other group did so with the discs fixed in flexion (representing a rounded, slouched, non-neutral posture) in which the same axial force was then applied. The interesting finding was that the neutral spine position was largely protective such that only 2 of the 7 spine segments had endplate failures, while 5 out of the 7 vertebral bodies themselves failed first. In the flexed spine group, all the endplates failed first and failure was at 3703 Newtons, which was less than half of the force absorbed by the neutral spine vertebral segments, which didn’t fail until force reached 8442 Newtons. That’s a 128% increase in compression strength just by keeping the spine neutral.

It’s clear per other studies that posterior disc herniations are caused by repeated spine flexion, which is accelerated with lumbar twisting, and worsened when alternating spine flexion with extension stretches. As such, maintaining neutral spine during the bulk of daily activities and exercise appears ultimately protective. What this paper adds is that the same neutral spine position that is protective against posterior disc herniations also lessens risk of endplate fractures and vertical disc herniations. That’s what one might call a pretty cool coincidence.


In vivo remodeling of intervertebral discs in response to short- and long-term dynamic compression. Wuertz K, Godburn K, MacLean JJ, Barbir A, Donnelly JS, Roughley PJ, Alini M, Iatridis JC. J Orthop Res. 2009 Sep;27(9):1235-42. 

“We conclude that dynamic compression is consistent with a notion of “healthy” loading that is able to maintain or promote matrix biosynthesis without substantially disrupting disc structural integrity. A slow accumulation of changes similar to human disc degeneration occurred when dynamic compression was applied for excessive durations, but this degenerative shift was mild when compared to static compression, bending, or other interventions that create greater structural disruption.”

This paper looked at 2 weeks of 1.5 hours of compression loading per day vs 8 hours. They found 1.5 hours (likened to working out) preferable to 8 hours (likened to heavy labor) for disc health, but both being better than static bending, which I have discussed at length in relation to spine flexion. However, the comparison I thought most interesting here was that the dynamic loading of 1 hz (1 impulse per second) was also healthier than static compression, where the compressive load just sits on the spine. The latter I think is what people do to themselves when they learn that sitting in spine flexion is bad for the back. Which is using firm but prolonged contractions of their spine extensor muscles to maintain a neutral spine when sitting in chairs (or on a ball) with poor lumbar support, compressing their spines for as long as they can manage. Thus I think it’s much more beneficial to get a better chair and properly adjust, or add lumbar support to your chairs you have, so that you can relax your spine while sitting and working. Akin to having your cake and eat it too, thus maintaining the neutral spine, without the concomitant spine extensor compression weighing down on your back. In standing this is usually less of an issue because if you have good standing posture you can align your hips over your feet, shoulders over your hips, and your head over your shoulders. Thus lessening muscle contractile compressive forces, which is the reason why that’s taught when “centering” in Spinal Flow™ – a slightly modified version of Tadasana.

Chad Reilly, Physical Therapist and developer of Spinal Flow Yoga™


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