Cortical motor output decreases after neuromuscular fatigue induced by electrical stimulation of the plantar flexor muscles.

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Title: Cortical motor output decreases after neuromuscular fatigue induced by electrical stimulation of the plantar flexor muscles.
Authors: Alexandre, F., Derosiere, G., Papaiordanidou, M., Billot, M., Varray, A.
Source: Acta Physiologica. May2015, Vol. 214 Issue 1, p124-134. 11p.
Subjects: Neuromuscular diseases, Brain stimulation, Electrophysiology, Flexor muscles, Somatosensory cortex, Oxyhemoglobin
Abstract: Aim Neuromuscular electrical stimulation ( NMES) causes early onset of neuromuscular fatigue. Peripheral electrophysiological explorations suggest that supra-spinal alterations are involved through sensitive afferent pathways. As sensory input is projected over the primary somatosensory cortex (S1), S1 area involvement in inhibiting the central motor drive can be hypothesized. This study assessed cortical activity under a fatiguing NMES protocol at low frequency. Methods Twenty healthy males performed five NMES sequences of 17 trains over the plantar flexors (30 Hz, 4 s on/6 s off). Before and after each sequence, neuromuscular tests composed of maximal voluntary contractions ( MVCs) were carried out. Cortical activity was assessed during MVCs with functional near-infrared spectroscopy over S1 and primary motor (M1) areas, through oxy- [HbO] and deoxy-haemoglobin [HbR] variation. Electrophysiological data (H-reflex during MVC, EMG activity and level of voluntary activation) were also recorded. Results MVC torque significantly decreased after the first 17 NMES trains ( P < 0.001). The electrophysiological data were consistent with supra-spinal alterations. In addition, [HbO] declined significantly during the protocol over the S1 and M1 areas from the first 17 NMES trains (P < 0.01 and P < 0.001 respectively), while [HbR] increased (P < 0.05 and P < 0.01 respectively), indicating early decline in cortical activity over both primary cortical areas. Conclusions The declining cortical activity over the M1 area is highly consistent with the electrophysiological findings and supports motor cortex involvement in the loss of force after a fatiguing NMES protocol. In addition, the declining cortical activity over the S1 area indicates that the decreased motor output from M1 is not due to increased S1 inhibitory activity. [ABSTRACT FROM AUTHOR]
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Database: Psychology and Behavioral Sciences Collection
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Abstract:Aim Neuromuscular electrical stimulation ( NMES) causes early onset of neuromuscular fatigue. Peripheral electrophysiological explorations suggest that supra-spinal alterations are involved through sensitive afferent pathways. As sensory input is projected over the primary somatosensory cortex (S1), S1 area involvement in inhibiting the central motor drive can be hypothesized. This study assessed cortical activity under a fatiguing NMES protocol at low frequency. Methods Twenty healthy males performed five NMES sequences of 17 trains over the plantar flexors (30 Hz, 4 s on/6 s off). Before and after each sequence, neuromuscular tests composed of maximal voluntary contractions ( MVCs) were carried out. Cortical activity was assessed during MVCs with functional near-infrared spectroscopy over S1 and primary motor (M1) areas, through oxy- [HbO] and deoxy-haemoglobin [HbR] variation. Electrophysiological data (H-reflex during MVC, EMG activity and level of voluntary activation) were also recorded. Results MVC torque significantly decreased after the first 17 NMES trains ( P < 0.001). The electrophysiological data were consistent with supra-spinal alterations. In addition, [HbO] declined significantly during the protocol over the S1 and M1 areas from the first 17 NMES trains (P < 0.01 and P < 0.001 respectively), while [HbR] increased (P < 0.05 and P < 0.01 respectively), indicating early decline in cortical activity over both primary cortical areas. Conclusions The declining cortical activity over the M1 area is highly consistent with the electrophysiological findings and supports motor cortex involvement in the loss of force after a fatiguing NMES protocol. In addition, the declining cortical activity over the S1 area indicates that the decreased motor output from M1 is not due to increased S1 inhibitory activity. [ABSTRACT FROM AUTHOR]
ISSN:17481708
DOI:10.1111/apha.12478