Firing duration of masseter motor units during prolonged low-level contractions q M. Farella a,b,d,⇑ , M.E. De Oliveira a , L.M. Gallo a , T. Läubli c , L. Tomatis c , C. Müller c , R. Obrenovic a , S. Palla a a Clinic for Masticatory Disorders, Removable Prosthodontics, and Special Care Dentistry, University of Zürich, Zürich, Switzerland b Discipline of Orthodontics, Department of Oral Sciences, University of Otago, Dunedin, New Zealand c Center for Organizational and Occupational Health Sciences, Swiss Federal Institute of Technology Zürich (ETH), Zürich, Switzerland d Discipline of Orthodontics, Department of Dental, Oral, and Maxillo-Facial Sciences, University of Naples, Naples, Italy article info Article history: Accepted 14 May 2011 Available online 18 July 2011 Keywords: Electromyography Masticatory muscles Motor units Decomposition software Orofacial pain highlights  This study represents the first attempt to track motor unit action potentials in the masseter muscle dur- ing a low-intensity isometric contraction lasting 30 min.  In this experiment, motor unit action potentials were automatically identified and decomposed, thus minimising the risk of introducing examiner biases.  The majority of motor units in the masseter muscle are either sporadically or intermittently active dur- ing prolonged low-level biting contractions, but some motor units are continuously active. abstract Objective: The study aimed to determine whether motor units (MUs) of the masseter muscle can be con- tinuously active during a prolonged low-level sustained contraction. Methods: Intramuscular fine-wire EMG activity was recorded unilaterally from the masseter muscles of 13 pain-free volunteers (mean age ± SD = 26.7 ± 7.7 years), during low-level biting tasks performed for 30 min. The stored intramuscular EMG signals were decomposed into individual MU action-potential trains using long-term decomposition software. Depending on relative duration of the MU activity, MUs were classified as sporadically (<50% of the time), intermittently (50% 6 time 6 95%), or continu- ously active (>95% of the time). Results: The overall number of MUs identified during the low-level biting task was 203. Of these, nine continuously active MUs (4.4%) were found in six of the 13 subjects investigated, whereas 50 intermittent MUs (24.6%) were found in 12 subjects. The remaining MUs (71.0%) were sporadically active and were found in all of the subjects investigated. Conclusion: The majority of masseter MUs is sporadically or intermittently active during prolonged low- level contractions, but some of them can also be continuously active. Significance: Sustained clenching efforts may be accompanied by continuous activity of a few selected muscle fibres. Ó 2011 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. 1. Introduction The causes of muscle pain are still largely unknown. There is some evidence that the pathogenesis of muscle pain, especially of chronic pain, involves multiple mechanisms at the level of the muscles and the peripheral and central nervous system. However, it is still unclear what exactly activates the peripheral muscle nociceptors and induces muscle hyperalgesia. Stimuli may include either peripheral chemical or mechanical agents or trigger points activity in addition to reactive or even primary central mechanisms that may lead, for example, to neurogenic inflammation (Benoliel et al., 2011). Muscle pain, as in case of work-related myalgia, is a complex phenomenon including physical and psychosocial factors. It is commonly manifested in occupational settings that demand pro- longed static and/or highly repetitive loads, often at low amplitude. These conditions can provoke tissue damage with subsequent nociceptor activation and muscle pain. Indeed, local tissue damage or metabolic alterations have been observed in the muscles of patients with work-related myalgia. The tissue alterations include cytochrome-c oxidase deficiency, low capillary-to-fibre area ratio, impaired blood flow and reperfusion injury, Ca ++ accumulation, 1388-2457/$36.00 Ó 2011 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.clinph.2011.05.017 q Data were collected at Swiss Federal Institute of Technology Zürich (ETH), Switzerland. ⇑ Corresponding author at: Department of Oral Sciences, University of Otago, P.O. Box 647, Dunedin 9054, New Zealand. Tel.: +64 3 479 5852; fax: +64 3 479 7070. E-mail address: mauro.farella@otago.ac.nz (M. Farella). Clinical Neurophysiology 122 (2011) 2433–2440 Contents lists available at ScienceDirect Clinical Neurophysiology journal homepage: www.elsevier.com/locate/clinph