Since the book of Basmajian JV, & De Luca CJ entitled Muscles Alive: their functions revealed by electromyography, I have not seen any new interpretation of the influence factors that affect the interpretation of muscle force production. For example, the type of muscle fiber, muscle length, and muscle velocity may influence the association between EMG signal as an electrical and mechanical activity of a muscle.
There has been considerable advancement in all of these areas since Muscles Alive was published, especially with the increased interest in past years of EMG-driven modelling and the like. Numerous relevant publications, from multiple groups and fields, are discoverable through PubMed (and similar search engines).
Dear Professor Kilani,
I have studied the attached article and found it beneficial.
Regards,
Ischemia affects small motor units first and changes the appearance of EMG/force:
http://www.researchgate.net/publication/46427024_Impairment_of_human_soleus_motor_units_during_ischemia/file/d922b4f7c98a38032c.pdf
Article Impairment of human soleus motor units during ischemia
EMG best discribes the extent of motor unit recruitment - which is an indirect indicator of the exerted force,
Coupling EMG with Dynamometry gives you a nice way to quantify force produced by muscle action.
How to use EMG for measuring or training muscles involved with chronic pain?
There are studies that consider the muscle pain and its functional consequences?
Dear Prof. Gurgel,
Well, the so-called pain-adaptation hypothesis suggests that pain results in re-organization of motor control strategy to minimize further damage to injured tissues. It is, therefore, possible that chronic pain sufferers inhibit motor unit recruitment of painful muscles by way of a central mechanism. Such pain-induced modifications of muscle activity may be compensated for by simultaneous elevated antagonist muscle activity or other phasic or deeper muscles, reflecting probably a functional adaptation of muscle coordination. Previously, it has been reported that chronic tension-type headache patients reveal lower EMG output during maximal voluntary contraction as well as sustained contractions. Such a muscular response was considered as a centrally mediated secondary pain response due to chronic pain condition leading to impaired recruitment.
To sum up, since chronic pain can disturb control of motor nervous system by disturbing muscle coordination- the imbalance between agonist and antagonist muscle activities- investigation of antagonist co-activations may supply an enlightening insight into different aspects of muscular adaptation to modified strategies as well as adopted compensatory strategies in different types of muscular pain.
In addition, it has also been reported that many abnormalities found in chronic pain patients, may be induced by pain rather than by primary causative factors; Consequently, evaluation of exact pain mechanisms is complicated in this state. It is, therefore, recommended that some kind of neurophysiological markers would be searched in pain studies before chronification during and outside of spontaneous attacks to find the possible underlying pathology in earlier phase of disease. Such information could be advantageous for intervening new treatment strategies as well as predicting the onset of attacks or estimating the progress of disease.
I do research on chronic tension-type headache sufferers (muscular dysfunction in these patients due to pain) and the foregoing notes are parts of discussion section of my master thesis.
Kind regards,
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