Tuesday 21st August 2018

Altered muscle activation patterns shown to cause hamstring injuries- a guide to correction


In a study comparing those who have suffered hamstring injuries with uninjured controls researchers found those injured had an altered neurological control that increased the cumulative load on the muscle.  The authors suggest that screening for this issue could be used for prevention, and that for correction one should focus on exercises that control movement. 

The research findings are highly significant, but their recommendations appear to be unpractical and flawed.  Screening for such neurological control abnormalities would not be practical in a clinic setting, and research has shown that corrective exercises do not correct such abnormal neurological control.  We discuss the more practical alternative approach of identifying the potential causes of such neurological abnormalities.  These can easily be screened for in clinical practice, and addressed both for prevention and rehabilitation.

What the study found

A study of sports people used surface electromyography (EMG) to compare the neurological control of those who had suffered hamstring injuries with normal controls.  They found that those injured had abnormal sensorimotor neurological control of their muscles, specifically the activation timings of their muscles were altered.  The authors speculate that this places a higher cumulative load on the hamstrings, noting that previous research has shown such abnormal sensorimotor control has been shown to increase the risk of hamstring injuries, and has also been associated with lower back pain, sacroiliac injuries and knee injuries. 

The implications

The identification of a causative factor for hamstring and other injuries allows for possible screening and preventative measures.  Furthermore, this abnormal sensorimotor function needs to be seriously considered with rehabilitation.  By increasing the load on the hamstrings such abnormal sensorimotor control would hinder healing and predispose to further re-occurrences.  

Screening for the issues

How does one screen for such sensorimotor abnormalities?  For the study the researchers analysed EMG readings.  Such investigations though are probably not practical in a typical clinic at the moment.   However, it may be an option in elite sports settings. 

Exercises do not correct these abnormailities

Without providing any supporting evidence the authors suggest that such sensorimotor abnormalities be remedied by focusing on controlled movement with exercises.  However, as discussed in our research summary "Exercises shown to not correct abnormal muscle activation patterns" previous research showed that such exercises failed to alter a similar abnormal pattern associated with neck pain.  Thus, this approach will likely not work.  

An alternative practical solution

The strategy
To find a practical solution one needs to look what causes of such sensorimotor changes.  Detecting these rather than the effect could provide a practical way to screen for this problem.  Further, if these causes could be treated this could enable effective correction.

Influences on sensorimotor control
It is important to understand that most sensorimotor control is mediated subconsciously by the central nervous system.  This system receives information from sensors in the muscles, connective tissues and other parts of the body and uses this to produce postures and movements that maximise balance while minimising pain and the stress on tissues.  Any issue that requires compensation or causes abnormal sensory feedback has the potential to cause an alteration to this sensorimotor control.

Articular dysfunction
Abnormal articular function is discussed in our research summary “Adding manual therapies directed at improving function produces far superior results".  Such dysfunction can alter sensorimotor control by providing abnormal sensory feedback, and by creating issues that require compensation.  The research trialed exercises alone versus similar exercises combined with interventions aimed at restoring normal function.  The main intervention was joint adjustments / manipulations designed to help normalise joint function.  The trial results showed that combining the interventions to normalise function produced clearly superior results. 

Trigger points and altered activation patterns
As discussed in our research summary “Latent (Pain Free) Trigger Points Alter Neurological Control of Shoulder Movement Causing Damage, Impingement and Injury" in a trail of latent (pain free) myofascial trigger points “trigger points" in the shoulder girdle muscles it was found that when trigger points were present the muscle activation patterns were altered.  The de-activation (treatment) of these trigger points was found to normalise the muscle activation patterns.  In other research it was found that the presence of a trigger point in a muscle caused the muscle to quickly fatigue and become painful, with EMG showing adjoining muscles to be quickly recruited.  It appears that the central nervous system adjusts it's motor control to compensate for the poor of function and potential pain from the muscle containing the trigger point.  

Other influences
Articular dysfunction and trigger points are likely extremely common causes of abnormal sensorimotor control, but there are undoubtedly others.

The solution
As previously discussed, it is not practical to screen for abnormal sensorimotor function in a clinical setting, and the cause would need to be addressed anyway.  The practical solution for both prevention and the rehabilitation of injury appears to be to screen for and correct articular dysfunction, trigger points, and any other potential causative issues.  This article is not suggesting that exercises not be used, rather that the actual cause of abnormal sensorimotor control should be addressed so the central nervous system can control them appropriately.


Sole, G., Milosavljevic, S., Nicholson, H., & Sullivan, S. J. (2012). Altered muscle activation following hamstring injuries. Br J Sports Med46(2), 118-123.

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