Similar scaling of contralateral and ipsilateral cortical responses during graded unimanual force generation.

Hemibody movements are strongly considered as being under the control of the contralateral hemisphere of the cerebral cortex. However, some neuroimaging studies have found a bilateral activation of either the primary sensori-motor (SM1) areas or the rostral prefrontal cortex (PFC), during unimanual tasks. More than just bilateral, the activation of these areas was found to be symmetrical in some studies. However, the symmetrical response remains strongly controversial notably for handgrip force generations. We therefore aimed to examine the bilateral SM1 and rostral PFC area activations in response to graded submaximal force generation during a unilateral handgrip task. Fifteen healthy subjects performed 6 levels of force (ranging from 5 to 50% of MVC) during a handgrip task. We concomitantly measured the activation of bilateral SM1 and rostral PFC areas through near-infrared spectroscopy (NIRS) and the electromyographic (EMG) activity of the bilateral flexor digitorum superficialis (FDS) muscles. Symmetrical activation was found over the SM1 areas for all the investigated levels of force. At the highest level of force (i.e., 50% of MVC), the EMG of the passive FDS increased significantly and the ipsilateral rostral PFC activation was found more intense than the corresponding contralateral rostral PFC activation. We suggest that the visuo-guided control of force levels during a handgrip task requires the cross-talk from ipsi- to contralateral SM1 to cope for the relative complexity of the task, similar to that which occurs during complex sequential finger movement. We also propose alternative explanations for the observed symmetrical SM1 activation including (i) the ipsilateral corticospinal tract and (ii) interhemispheric inhibition (IHI) mechanism. The increase in EMG activity over the passive FDS could be associated with a release of IHI at 50% of MVC. Finally, our results suggest that the greater ipsilateral (right) rostral PFC activation may reflect the greater demand of attention required to control the motor output at high levels of force.

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

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.