The Location of Peak Upper Trapezius Muscle Activity During Submaximal Contractions is Not Associated With the Location of Myofascial Trigger Points: New Insights Revealed by High-density Surface EMG
The authors present novel findings in the field of myofascial pain and trigger points that make use of recent advances in high-density surface electromyography (HDsEMG). HDsEMG was used over the trapezius muscle to assess the location of peak EMG average rectified value (ARV). The location of peak ARV was compared between individuals with and without myofascial pain, in addition to assessing the relationship between the location of peak ARV and that of the palpated myofascial trigger point (MTrP). EMG outcomes were evaluated during isometric shoulder elevation ramp contractions to either 15% or 60% of maximal voluntary contraction (MVC). The authors report a significant caudal shift in the location of the peak ARV in individuals with myofascial pain versus asymptomatic controls; however, they were unable to demonstrate a relationship between the location of peak ARV and the location of the trapezius MTrP. The authors suggest these findings support a change in motor control in individuals with myofascial pain.
There are a few potentially significant observations that should be addressed to assist with the interpretation of these findings. Firstly, the findings of this study contrast with previous research suggesting that MTrP exhibit increased EMG activity characterized by increased baseline and/or spontaneous endplate activity.1 In the present study, however, 6 of 13 MTrP were located either outside of the HDsEMG electrode array (Fig. 5) or along its border. The potential impact of this on the reliability of EMG recordings, peak ARV calculations, and/or the lack of correspondence between peak ARV and MTrP location was not addressed. A larger sample size could have addressed this potential limitation.
Figure 2 illustrates the ARV peak position (cm) for both groups and it appears that the initial ARV peak positions are significantly different between groups for each MVC target (15% and 60%). In particular, differences exist in both the initial position and direction of movement during the initial ramp contraction in both 15% and 60% MVC contractions for asymptomatics. It is unclear whether this was expected or whether this was unaccounted for in the analysis. Initial peak positions are not presented in Figure 4, making it difficult for the reader to interpret the findings in a physiological context. Furthermore, variability in baseline EMG activity existed between symptomatics and asymptomatics and we are unsure as to how the authors addressed this in their analysis. Normalizing their findings to baseline, for example, would enable group comparisons; otherwise, it is unclear whether these effects were a function of motor control adaptations or simply due to baseline differences.
Finally, similar to previous work by Holtermann et al,2 which demonstrates nonuniform activation of the upper trapezius during intense ramp contractions, the authors also report nonuniform activation of the upper trapezius muscle characterized by a caudal shift in the location of peak EMG amplitude recordings during the 60% MVC contraction, but not the 15% MVC. In line with Holtermann and colleagues, it is possible that these findings may simply be due to the increased muscle activations evoked in the 60% MVC group, and not motor control adaptations. The absence of nonuniform contraction at 15% MVC is justified as “probably due to the limited force modulation requested during this task”; it would have been interesting if the authors provided their perspectives on potential physiological explanations for these muscle activation differences observed between the low and high MVC groups.
We would otherwise like to commend the authors for this interesting and important work, which provides a basis for further research into the poorly understood area of motor control in myofascial pain syndrome.