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Lumbar Intervertebral Disk Degeneration in Athletes was recently published in the American Journal of Sports Medicine.¹ The researchers found that competitive (participated in their sport for longer than five years and more than 3 times per week)baseball and swimming athletes have a higher incidence of lumbar intervertebral disc degeneration than other athletes (basketball, kendo, soccer, and running) and non-athletes. The study participants were in college and averaged only 19 years old.

Baseball players and swimmers were approximately 2.8 times more likely than non-athletes to have lumbar intervertebral disc degeneration. Compared with other athletes that were only 0.67 – 1.6 times more likely than non-athletes to have lumbar intervertebral disc degeneration.

Let’s explore why this might occur.

In order for a disc to degenerate load on the disc must exceed it’s capacity. Since capacity is likely the same across all of the studied groups we will examine the sport specific lumbar loads.

Baseball: Except for pitchers the largest lumbar loads will occur with batting. Batting is movement that involves forces near voluntary maximum and end range of lumbar rotation (particularly with deceleration at the end of the swing).

There are an average of 38 at bats per team, divided among 9 players gives us 4.2 at bats per player. Let’s guess there is an average of 5 swings per at bat. This leaves us with 21 bat swings per game. Batting practice will of course have a far greater number of swings. In any event, I feel it is safe to consider baseball a low repetition high load activity. Since some of these loads are occurring at the end range of rotation, with very high forces and over a very short period of time the potential for disc injury is great.

Swimming: Since the freestyle stroke is the most common let’s examine this. The perfect freestyle stroke involves almost pure axial rotation. While the pelvis and shoulders are intended to move as a unit there is some rotation that occurs in the lumbar spine. This motion however does not even come close to end range. It is occurring well within a very small portion of the physiological range near neutral.

There are two primary loads on the lumbar spine:

1.       Propulsive Contraction: the propulsion necessary for kicking is provided primarily by the psoas major muscle. If you examine the vector forces of the psoas you will see there is a large compressive component on the lumbar spine (see figure). This force is occurring in an alternating (left-right) highly repetitive fashion during the entire workout.  A large contributor to arm propulsion is the latissimus dorsi. This lat contraction also places a fairly large compressive component on the lumbar spine. Since all muscular contraction pulls with equal force on origin and insertion the psoas and lat contractions necessarily produce as much compressive force on the lumbar spine as propulsive force.

Psoas contraction produces both compressive and shear loads on the lumbar spine. The compressive load is large. Ac: Acetabulum

2.       Stability Contraction: The remaining core muscles (lumbar erectors, abdominals [all 4 pairs], transversospinales group and quatratus lumborum) contract to provide additional stability to maintain near lumbar neutral. This is necessary to counteract the propulsive contractions that are alternating unilateral and produce rotational forces. The sum of the core muscle vectors is largely compressive on the lumbar spine.

Combining the propulsive and stability forces likely means the compressive load on the lumbar spine exceeds the total force of propulsion. (You only need the lumbar stability forces to exceed the pectoralis major contribution to propulsion to arrive at this conclusion- and I think that is a more than fair assessment.)

One might conclude that these forces are occurring in near lumbar neutral and should not pose much of a problem. However, as tissue is subjected to sustained loads, particularly in one posture, the failure tolerance goes down (see figure).  This is why it is bad to sit for long periods of time and why we tend to automatically shift to different positions while sitting- we are load shifting to manage our failure tolerance.

As load is applied over time biological tissues fatigue lowering the injury threshold (failure tolerance). This is know as a fatigue curve.

I find it interesting that the top two sports studied produce lumbar disc degeneration for very different reasons. Baseball is a high load, end range, short time activity while swimming is a moderate load, neutral position, sustained time activity. This highlights the idea that degeneration is a result of load exceeding capacity whether it be due to acute high loads or sustained low loads.

Other Studied Sports: Basketball, Kendo (a Japanese sword fighting martial art) and soccer all involve:

1.       Highly varied motions: load is distributed among various tissues and various parts of the disc.

2.       Don’t regularly involve extremes of lumbar range: there are no large end range forces.

3.       Include periods of varied intensity: allows relative recovery of failure tolerance.

Running was the only sport to demonstrate a reduced incidence of lumbar disc degeneration compared with the non-athlete group, although this result did not reach statistical significance. However, I find this result particularly interesting. The propulsive forces with running involve the glutes, quads, hamstrings and adductor magnus- none of these muscles provide compressive forces on the lumbar spine. The lumbar spine is loaded by gravity, core contraction and psoas major. The psoas major contraction is minimal as this is relatively unloaded and only contracts to cycle through unresisted hip flexion. The net result is the spine is loaded in near neutral and not subjected to sustained compressive stability forces. In fact, it’s plausible the pumping effect from weight bearing to non-weight bearing with each stride provides hydration/nutrients to the disc and loads/unloads the disc evenly. In my experience most back pain caused by running is actually a result of problems accumulated by sitting all day and then going for a run. In other words, running is not the underlying source of load but rather the activity that reveals the problem.

Conclusions:

1. Sport and health are very different things. Sport involves repetitive high loads that often cause degeneration even at relatively young ages. Sport does not equal optimal health because it breaks the rule of moderation.

2. Compressive forces from propulsion and stability are often overlooked. Vector analysis provides an excellent conceptual framework to appropriately assess tissue load.

3. The clinical application of basic physics (i.e. failure tolerance) is invaluable in understanding human dysfunction.

William F. Brady, DC, CSCS

Dr. William Brady is the founder of Integrative Diagnosis, an educational program that unifies diagnosis and guides treatment of musculoskeletal disorders. Seminar information is available at www.integrativediagnosis.com. Be sure and check out our new online program.

1. http://ajs.sagepub.com/cgi/content/abstract/37/1/149

Copyright 2009 Integrative Diagnosis LLC

Hypoxic Fibrous Adhesion Pathway
There are four critical steps in the hypoxic production of fibrous adhesion.

1. Repeated or sustained contraction of skeletal muscle results in decreased intracellular oxygen concentrations.
2. Decreased oxygen concentrations leads to the production of oxygen free radicals.
3. Oxygen free radicals are very fast, specific and sensitive triggers for attraction and replication of fibroblasts.
4. Increasing fibroblast density leads to increased collagen production and other ultrastructural changes forming fibrous adhesion.

Howlett et al1 demonstrated in single skeletal muscle fibers that the rate of fall in intracellular oxygen concentration is dependent on contraction frequency. Increasing contraction frequency resulted in progressively larger drops in oxygen concentration. In a similar study Kindig et al2 demonstrated that longer contraction duration also resulted in decreased oxygen concentrations.
Fletcher et al3 determined that hypoxia triggers the production of oxygen free radicals which cause normal peritoneal fibroblasts to produce fibrous adhesion. Exposure of fibroblasts to hypoxia resulted in an irreversible increase in TGF-B1 and type I collagen. This reaction could be prevented by adding free radical scavengers. Their findings support the link between hypoxia, free radical production and the development of adhesion.

Other researchers have further demonstrated the relationship between low oxygen levels and the proliferation of fibroblasts4 as well as oxygen free radicals providing a very fast, specific and sensitive trigger for fibroblast proliferation5. It has even been demonstrated that fibroblasts themselves release oxygen free radicals, potentially creating positive feedback for further increasing fibroblast density.
Murrell et al. confirmed that increased cell density of fibroblasts is the critical factor in fibrotic conditions that leads to fibrous adhesion6.

Further support of the dual pathway to fibrous adhesion production is seen in cases of radiation toxicity. Radiation has long been used to destroy tumors. However, the radiation also damages healthy tissue. Of particular interest is microvascular injury that leads to an early inflammatory process and a delayed (3-12 month) fibroproliferative process7. Free radical production secondary to radiation treatment has been implicated in causing muscular fibrosis8.

Clinical Importance
Understanding of the hypoxic fibrous adhesion pathway should encourage clinicians to see musculoskeletal disorders in a new light. The presence of fibrous adhesion should be considered in any MS disorder that involves sustained or repeated muscular contraction.
Poor or prolonged postures, repetitive motions and athletic pursuits can cause fibrous adhesions to be produced in the absence of inflammation, trauma or surgery.
Many conditions exist (mensciod entrapment, disc derangement, altered axis of rotation etc.) that cause protective muscular hypertonicity. Hypertonicity is a state of sustained contraction that could, over time, trigger the hypoxic fibrous adhesion pathway. Fibrous adhesion would then be an additional pathology to address with specific treatment tactics.

Diagnosis of Fibrous Adhesion
Surgeons often report visualizing fibrous adhesions during surgical procedures. As a diagnostic method this is reliable but highly invasive.
Diagnostic ultrasound can be used to diagnose the presence of fibrous adhesions. This is non-invasive and has the added benefit of visualizing motion as well. The drawbacks to diagnostic ultrasound include sensitivity (large areas of fibrous adhesion are necessary to discriminate from healthy tissue) and expense.
Adhesions can be identified by limited ranges of motion. Of course this is non-specific to adhesion and therefore best used as pre and post treatment assessment combined with other techniques.
Skilled palpation is extremely useful in identifying fibrous adhesion9. The only difficulty with palpation is that it requires about two years of consistent effort and training from a dedicated provider to be reliable. Instrument assisted palpation can be helpful in certain tissues as well.

Conclusion
Fibrous adhesions can be produced via hypoxic mechanisms without trauma or inflammation.
Since fibrous adhesion can develop from sustained or repeated muscle contraction they may occur as frequently as other common MS disorders such as weakness and joint dysfunction. Therefore, fibrous adhesion should be considered in the diagnostic workup of most MS complaints. For long term effectiveness treatment tactics must be geared directly toward the reduction of adhesion, when present.

Note: This is a brief clinical review, not an exhaustive literature review. There is a lot of good research to support these claims not cited here. No idea is permanent. I welcome your thoughts and comments.

William Brady, DC, CSCS

DrWilliamBrady@gmail.com

Special thanks to Dr. Mike Leahy, the developer of ART®, who first introduced me to this concept more than 10 years ago.

References:
1. Howlett RA et al. Intracellular PO2 kinetics at different contraction frequencies in Xenopus single skeletal muscle fibers. J Appl Physiol. 2007 Apr;102(4):1456-61.
2. Kindig CA et al. Effect of contractile duration on intercellular PO2 kinetics in Xenopus single skeletal myocytes. J Appl Physiol.2005 May;98(5):1639-45.
3. Fletcher NM et al. Hypoxia-generated superoxide induces the development of the adhesion phenotype. Free Radic Biol Med. 2008 August 15; 45(4): 530–536.
4. Falanga V et al. Low oxygen stimulates proliferation of fibroblasts seeded as single cells. J Cell Physiol. 1993 Mar;154(3):506-10
5. Murrell GC et al. Modulation of fibroblast proliferation by oxygen free radicals. Biochem J 1990;265:659-665.
6. Murrell GC et al. Dupuytren’s contracture. Fine structure in relation to aetiology. J Bone Joint Surg Br. 1989 May;71(3):367-73.
7. Wang J et al. Significance of endothelial dysfunction in the pathogenesis of early and delayed radiation enteropathy. World J Gastroenterol. 2007 Jun 14;13(22):3047-55.
8. Wegrowski J et al. (1987)in The Control of Tissue Damage, vol. 2, pp. 39-42, Elsiver, Amsterdam.
9. Leahy PM. (1996) in Active Release Techniques, pp.21-29, Aactive Release Techniques LLC, Colorado Springs CO.