Trigger Points And A Sympathetic State

In last week’s blog article I discussed the role that soft tissue therapy can play in recovery and helping to raise the athlete’s stress resistance.  In doing so, I referenced two articles that looked at trigger point therapy and its effects on the autonomic nervous system, as measured by heart rate variability.  Today, I wanted to expand a bit on trigger points and their relationship to a sympathetic state as this information is helpful to further enhance our understanding of the role soft tissue therapy can play in the training and sports performance arena.

Trigger Points – An integrated Hypothesis

Before going into how the sympathetic system and trigger points are related it is best to first explain the hypothesis of what is going on, or more appropriately, what we think is going on when there is a trigger point.  I emphasize the word think because no one is really sure and there are a variety of hypotheses out there, one of which being that there is no such thing as a trigger point at all and really all that is taking place is just entrapment of nerves (although this doesn’t completely explain many of the random referral patterns that have been known to take place when a trigger point is compressed and also, as we will see later in the article, the biochemical environment and the local sympathetic state would be a potential player in the irritation and/or compression of the nerves anyway).  I wrote trigger point 101 a little over three years ago as a way to give some basic information about what trigger points are and how we can treat them and while I may explain some of the info in there differently these days (it was three years ago!) I still think that there is some basic stuff in there that will help people better understand this phenomenon.

While there are a number of hypotheses out there probably the most accepted is the “integrated hypothesis” as explained by McPartland and Simons:

“The ‘integrated hypothesis’ regarding the etiology of myofascial trigger points states that each trigger point has a sensory component, a motor component, and an autonomic component.  The hypothesis encompasses local myofascial tissue, the CNS, and systemic biomechanical factors.”

This integrated hypothesis is all encompassing and works to explain how trigger points form, what happens when they form, why they feel painful, and how the nervous system comes into play.  This hypothesis includes many things such as:

  • Excessive muscle contraction will compress local sensory nerves and blood vessels decreasing local blood supply of oxygen
  • What there is pain when the trigger point is provoked
  • Elevations of protons, bradykinin, serotonin, substance P, norepinephrine, calcitonin, and TNF-a in the area of the trigger point
  • The localized sweating, vasoconstriction, and pilomotor activity (goosebumps) when a trigger point is provoked

Putting all of this together we begin to understand the mulifaceted nature of trigger points and understand that there is more to it than just the myofascial system.  The nervous system, the endocrine system, and in fact all systems of the body will play a role (although the nervous system is really in the driver’s seat).

Looking Further Into The Nervous System

Shah and colleagues have conducted a few studies which looked specifically at the biochemical milieu of trigger points.  When looking at trigger points in the upper trapezius of subjects in one of three groups – (1) Normal/no neck pain/no trigger points; (2) Latent/no neck pain/latent trigger points; (3) Active/cervical pain of <3 months duration/Active trigger points present – what they found was that those with active trigger points, when compared to the other two groups, had:

  • A lower threshold of local tenderness (confirmed by a pressure algometer)
  • Greater amounts of bradykinin, substance P, TNF-a, serotonin, norepinephrine, calcitonin gene-related peptide
  • Significantly lower pH

An additional finding this group of researchers made was that a variety of inflammatory mediators (e.g., neuropeptides, catecholamines, and cytokines) were found to be elevated in the area of the active trigger point.  Also, the biochemical milieu in a site remote to the active trigger point (they used the gastrocnemius as the site remote to the active trigger point in the upper trapezius) was lower than in the active site; however, when compared to that of the latent and normal groups, it was found that the active group’s biochemical milieu was significantly higher in the remote location.  The researchers noted that this may suggest potential central sensitization.  I look at this information in the context of an athlete who is overtrainined or overstressed and pushing towards sympathetic dominance where the internal environment is reflecting this hormonal shift.

Finally, another point that Shah et al. note is that, in association with elevated sympathetic activity, increased levels of norepinephrine have been implicated in their role of depressed feedback control of muscle length and increased spontaneous electrical activity at motor enplates, thus hinting at norepinephrine’s potential role in the pathophysiology of trigger points and myofascial pain syndromes.

Conclusions and Practical Applications

Placing this information and the information from last week’s article into context we can begin to piece together a much broader picture of the ways in which out autonomic state can have an influence over the myofascial system thus inhibiting the way we move and perform.

Using this information we can further enhance an athlete’s recovery, either from injury or from competition/training, by figuring out ways to influence the nervous system in order to get what we want in the training or therapy program.  Soft tissue therapy may be one potential way to influence this state but it is, of course, not the only way.

Finally, another way to help athletes with their overall program is to make them aware of things that can perpetuate trigger points – and it should come as no surprise that most of these things are also nervous system irritants - such as:

  • Overuse
  • Overtraining
  • Nutritional deficiencies
  • Poor sleep
  • High amounts of stress (psychological or physical)
  • Drug use
  • Tobacco and nicotine (getting baseball players to stop using smokeless tobacco should be a high priority)
  • High amounts of caffeine intake (small amounts should not be a problem; however, high amounts of caffeine like we see in many college athletes who live on things like coffee, diet soda, and red bull is going to provoke a sympathetic environment)
  • Prolonged postures (IE, sitting)…as they say, “movement is medicine”

In the end it really comes down to educating your athletes/clients/patients and developing a well rounded program that addresses their needs and is appropriately managed to ensure that the program is doing what you want it to do.

References

McPartland JM, Simons DG. Myofascial Trigger Points: Translating Molecular Theory into Manual Therapy. J Manual & manipulative Therapy 2006; 14(4): 232-239.

Shah JP, Gilliams, EA. Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis: An application of muscle pain concepts to myofascial pain syndrome. JBMT 2008; 12: 371-384.

Shah JP, et al. An in vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle. J Appl Physiol 2005; 99: 1977-1984.

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