Fatigue and muscle activation during submaximal elbow flexion in children with cerebral palsy Aude-Clémence M. Doix a,b , Anette Gulliksen a , Siri M. Brændvik a,c , Karin Roeleveld a, / a Department of Human Movement Science, NTNU, Trondheim, Norway b University of Nice Sophia Antipolis, LAMHESS, EA 6309, 06205 Nice, France c Clinical Services, St. Olavs University Hospital, Trondheim, Norway article info Article history: Received 28 June 2012 Received in revised form 20 December 2012 Accepted 20 December 2012 Keywords: Cerebral palsy Muscle fatigue Muscle activation Motor unit recruitment Submaximal contraction abstract The purpose of this study was to investigate whether children with cerebral palsy (CP), like typically developing peers, would compensate for muscle fatigue by recruiting additional motor units during a sus- tained low force contraction until task failure. Twelve children with CP and 17 typically developing peers performed one submaximal isometric elbow flexion contraction until the task could no longer be sustained at on average 25% (range 10–35%) of their maximal voluntary torque. Meanwhile surface electromyography (EMG) was measured from the biceps brachii and triceps brachii, and acceleration variations of the forearm were detected by an accelerometer. Slopes of the change in EMG amplitude and median frequency and accelerometer variation during time normalised to their initial values were calculated. Strength and time to task failure were similar in both groups. Children with CP exhibited a lower increase in EMG amplitude of the biceps brachii and triceps brachii during the course of the sustained elbow flexion task, while there were no significant group differences in median frequency decrease or acceleration variation increase. This indicates that children with CP do not compensate muscle fatigue with recruitment of additional motor units during sustained low force contractions. Ó 2013 Elsevier Ltd. All rights reserved. 1. Introduction Cerebral palsy (CP) is the most common neurological disorder in children, with a European prevalence of 1.5–3 per 1000 live births (Cans, 2000). CP is a term that encompasses motor or postural impairments caused by injuries in the central nervous system dur- ing early development; from in utero, birth or within the child’s first 2–3 years (Bax et al., 2005). The most common physical symp- toms are spasticity, muscle weakness, decreased control, and fati- gue (Rosenbaum et al., 2007; Rose and McGill, 2005; Jahnsen et al., 2003). Yet, fatigue in CP is often described as a general feeling of weakness (Jahnsen et al., 2003), and, as described later in this introduction, only few reports relate about neuromuscular activa- tion strategies during a fatiguing task in CP. Muscle fatigue is generally defined as a decrease in maximal force capacity induced by sustained or repeated muscular contrac- tions whether or not the task can be maintained (Gandevia, 2001; Enoka and Duchateau, 2008). Muscle fatigue comprises ionic and metabolic changes in the muscle fibre causing impaired action po- tential propagation and excitation–contraction coupling, and changes in the neural – central – drive conducted via the cortico- spinal pathway to alpha motorneurons which innervate muscle fi- bres (Allen et al., 2008; Gandevia, 2001). A decreased propagation velocity over muscle fibre membranes is represented by a decrease in the median/mean frequency of the power density spectrum (MDF) of the electromyogram (EMG) (De Luca, 1997; Farina et al., 2004). When a fatiguing contraction at a constant submaxi- mal force level is sustained, the amplitude of the measured EMG signal increases. Even though the synchronisation of activated mo- tor units (MUs) firing pattern partly accounts for the increment of the EMG signal (Yao et al., 2000) with fatigue, it is widely acknowl- edged that this muscle fatigue is usually compensated by recruit- ment of additional MUs that contribute to the amplitude of the measured signal (Enoka and Duchateau, 2008; De Luca, 1997; Far- ina et al., 2004). One of the main motor impairments in CP widely discussed in literature is muscle weakness. Indeed, reduced strength in children with CP compared to typically developing peers is reported both in the lower (Engsberg et al., 2000; Leunkeu et al., 2010) and the upper (Akataki et al., 1996; Vaz et al., 2006; Smiths-Engelsman et al., 2005) limb. The cerebral lesion in CP alters the neural drive (Mockford and Caulton, 2010), decreasing the number of MUs that can be activated and their maximal firing rate during voluntary contractions (Rose and McGill, 2005). Moreover, in the gastrocne- mius lateralis, the medial hamstring and the iliacus the muscle 1050-6411/$ - see front matter Ó 2013 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.jelekin.2012.12.005 / Corresponding author. E-mail address: karin.roeleveld@svt.ntnu.no (K. Roeleveld). Journal of Electromyography and Kinesiology 23 (2013) 721–726 Contents lists available at SciVerse ScienceDirect Journal of Electromyography and Kinesiology journal homepage: www.elsevier.com/locate/jelekin