Jefferson Curl Part 2
The Case Against…
Check out part one if just picking this up. It will get you up to speed why we are looking into the Jefferson Curl (JC) or loaded flexion.
Today we are making an evidenced based case against the JC using Dr. Sacket’s criteria, which includes best available research, clinical expertise, and patient values.
First off… What is a herniated disc?
Drake and McGill (2008) found that the nucleus (center of the disc) is pushed through the inner layer of the annulus (outer layer). Over time, the annulus is delaminated and the nucleus finds it way through. Occasionally this can push into a nerve root causing pain down the leg or along certain distributions.
Now we know what a herniated disc is, let us move onto other matters. Mainly dead pigs.
Dr. McGill’s pig tissue experiments are just a single data point in the case against loaded flexion. As well, it is a way they can test a single variable with identical spines. There are also many other studies… Here are some of the highlights…
The infamous pig study…
Callaghan and McGill (2001) took pig spines and attempted to see what would cause a disc injury. The spine was taken 35% past neutral and repeated. It was found that there was greater chance of severe disc injury with repeated bouts of flexion/extension and low levels of compression versus significantly more axial loaded compression alone. This was the first time a biomechanics study modeled what has been seen clinically and in everyday life.
Before you say pig tissue isn’t human tissue… here is a study that correlates the similarity of pig tissue to human tissue Yingling et al. (1999)
Of course this tissue isn’t alive, but again, just one data point as we will see.
Wade et al. (2014) looked at the microstructure of the disc under repeated loading. This study basically showed that disc failure occurred with flexion and high compression rate. Also it showed more force was required in both neutral and flexed to fracture the endplate than it does to cause disc failure. Key point: the disc in this study was the limiting tissue in both flexion and neutral.
A prospective cohort study done with an N of 861 workers over three years by Hoogendoorn et al. (2000) showed there was an increased risk of low back pain with increased amounts of flexion and rotation. There are many other studies that show increased back pain with occupational required flexion. For example, here and here.
So if you’re counting, (and I know you are) we have animal studies and a prospective cohort study showing a strong link to disc herniation through repetitive flexion. If that was all we had, then that would still be pretty strong… But wait there’s more!
Solomonow (2012) showed that repeated loaded flexion/extension cycles and static postures induced laxity. This study used live cats (in-vivo) and showed that repeated flexion/extension with high loads and little rest period produced ligament creep/laxity that produced high amounts of cytokines (inflammatory factors) several hours later. Side note… There’s your reasoning for why exercise X didn’t hurt at the time, and then pain doubled you over later.
But back to the study…
Sub-failure damage could be the source of inflammation and then inflammation could be the reason for further degradation of the surrounding tissues.
Here’s another from D’Ambrosia et al. (2010) showing pro inflammation factors appeared after repeated bouts of flexion. This was even seen with very light weights. Furthermore, rest may be the largest contributing factor to whether or not inflammatory markers were released. Continuing exercise on the same ligament/tendon/collagen structure can aggravate a minor inflammatory response and turn over to chronic.
Sounds like deadlifts/snatches/kipping pull-ups for time isn’t such a good idea?
So mechanically we are stronger in a neutral position. There is not a single study that shows the human spine or animal model is stronger in a position of flexion. As well, athletically we see amazing feats being pulled off in a “neutralish” position. So why even load up spinal flexion. Power should be driven from the hips, not the spine. Stability is created in the spine, and power is transferred down the chain to extremities.
But Coach Sommer has never had a problem with this move…
Sure. I take him at his word. But we have to understand the sample of athletes Coach has been dealing with. Safe to say elite level gymnasts have different morphologies than an NFL player or couch potato for that matter. A wider lumbar disc will herniate faster with repeated flexion. Compare this with a slender gymnasts with decreased diameter of discs. This gymnast sample of population can probably tolerate more repetitive flexion. Here’s a study by Yates et al. (2010) that showed disc shape was predictive of herniation direction.
Time of day matters as well. When getting out of bed, first thing in the morning, the disc is at maximum hydration. Therefore, the disc has more resistance to flexion. Training flexion has a higher chance for increased delamination and possible herniation. In a occupational study by Snook et al. (1998) showed that decreasing early morning flexion decreased back pain related claims.
The larger picture here, is we don’t know your spine (unless you have x-ray eyes) and there are so many variables that play into spine health. A single exercise with the risk the JC carries doesn’t seem to make sense in a risk/reward evaluation.
All the research aside lets look at some simple, and clinical reasoning… The common sense highway if you will…
- If you want to lengthen your hamstrings, first I would seriously question if this needs to be done. That is a conversation for another day. Second we have way better options to get after hamstrings than to chance the injury mechanism of repeated flexion.
- If you want to increase the flexibility/segmentation of your low back and your multi-segmental flexion isn’t perfect then adding weight is a serious mistake. I don’t care how small the load is. You better have a flawless toe touch with perfect segmentation prior to trying the JC.
- By performing this move your low back muscles will get stronger. Now doubt about it… But what we don’t know is if the disc can adapt to the forces being placed on it. Although discs are collagen and can be remodeled, the inner portion of the annulus is insensate. So you may be getting stronger, but have no idea that the disc is beginning to delaminate from the inside out. Our rate limiting tissue is the disc… And we have no idea if the next flexion cycle is the last for that particular segment.
So we have biomechanical animal studies (both en-vivo and in-vitro), epidemiology, histology, morphology, and just plain ole common sense. Dr. Sacket would have to agree, this is a pretty strong case.
BUT… and there’s a BIG BUT…
Can we effectively dose loaded spinal flexion in order to create resiliency in the disc? AND can we train an injury provoking mechanism to decrease chance of the injury?
Check out part 3 where I go over the case for loaded flexion.[/fusion_text]