Abstract
There is a significant influence of muscle fatigue on the coupling of antagonistic muscles while patients with post-stroke spasticity are characterized by abnormal antagonistic muscle coactivation activities. This study was designed to verify whether the coupling of antagonistic muscles in patients with post-stroke spasticity is influenced by muscle fatigue. Ten patients with chronic hemipare and spasticity and 12 healthy adults were recruited to participate in this study. Each participant performed a fatiguing isometric elbow flexion of the paretic side or right limb at 30% maximal voluntary contraction (MVC) level until exhaustion while surface electromyographic (sEMG) signals were collected from the biceps brachii (BB) and triceps brachii (TB) muscles during the sustained contraction. sEMG signals were divided into the first (minimal fatigue) and second halves (severe fatigue) of the contraction. The power and coherence between the sEMG signals of the BB and TB in the alpha (8–12 Hz), beta (15–35 Hz), and gamma (35–60 Hz) frequency bands associated with minimal fatigue and severe fatigue were calculated. The coactivation ratio of the antagonistic TB muscle was also determined during the sustained fatiguing contraction. The results demonstrated that there was a significant decrease in maximal torque during the post-fatigue contraction compared to that during the pre-fatigue contraction in both stroke and healthy group. In the stroke group, EMG-EMG coherence between the BB and TB in the alpha and beta frequency bands was significantly increased in severe fatigue compared to minimal fatigue, while coactivation of antagonistic muscle increased progressively during the sustained fatiguing contraction. In the healthy group, coactivation of the antagonistic muscle showed no significant changes during the fatiguing contraction and no significant coherence was found in the alpha, beta and gamma frequency bands between the first and second halves of the contraction. Therefore, the muscle fatigue significantly increases the coupling of antagonistic muscles in patients with post-stroke spasticity, which may be related to the increased common corticospinal drive from motor cortex to the antagonistic muscles. The increase in antagonistic muscle coupling induced by muscle fatigue may provide suggestions for the design of training program for patients with post-stroke spasticity.
Highlights
The ability of the central nervous system to appropriately control agonistic and antagonistic muscles is a key mechanism to maintain body coordination during human voluntary movements and postural adjustments, which can be damaged by post-stroke spasticity (Tamburella et al, 2017)
The wilcoxon test was used to compare the differences in the significant coherence integrals, and the results revealed that significant coherence integral results in both the alpha (P = 0.018) and beta (P = 0.005) frequency bands were significantly higher during the second half of the fatiguing contraction compared to those during the first half of the contraction
We found that the intermuscular coherences between the antagonistic biceps brachii (BB) and triceps brachii (TB) muscles in the alpha and beta frequency bands were significantly increased during the second half of the contraction compared to those during the first half of the contraction in the stroke group
Summary
The ability of the central nervous system to appropriately control agonistic and antagonistic muscles is a key mechanism to maintain body coordination during human voluntary movements and postural adjustments, which can be damaged by post-stroke spasticity (Tamburella et al, 2017). Spasticity is a common complication of stroke and affects up to 40% of patients with hemiplegia (Wissel et al, 2013) It results from the decreased inhibition or facilitation of hypertonia after stroke as a result of motor impairment (Wang et al, 2018). Neuromuscular fatigue has the tendency to arise when performing physical activities after stroke, which has received little attention in clinical rehabilitation research (Boudarham et al, 2014). It can be defined as a reversible reduction in the neuromuscular system’s capacity to generate force or power (Vollestad, 1997), which encompasses a number of changes occurring at both the central and peripheral levels (Enoka et al, 2011; Wang et al, 2017). Whether neuromuscular fatigue influences the control of antagonist muscles in patients with post-stroke spasticity remains unclear
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