Tongue motor function is crucial in a wide range of basic activities and its impairment affects quality of life. The electrophysiological assessment of the tongue relies primarily on needle electromyography, which is limited by its invasiveness and inability to capture the concurrent activity of the different tongue muscles. This work aimed at developing an intraoral grid for high-density surface electromyography (HDsEMG) to non-invasively map the electrical excitation of tongue muscles. We developed a grid of 4 x 8 electrodes deposited over an adhesive 8-μm thick polyurethane membrane. The testing protocol was conducted on 7 healthy participants and included functional tasks (vowels articulation and tongue movements) aimed at activating different regions of the tongue. The electrical stability of contact was assessed by measuring electrode-tongue impedances before and after the tasks. The spatial amplitude distribution of global EMG and single motor unit action potentials (MUAPs) was characterized. Electrode-tongue impedance magnitude showed no significant changes in the pre-post comparison (58±46kΩ vs. 67±58kΩ at 50Hz). Contact stability was confirmed by the quality of the signals that allowed to quantify spatiotemporal characteristics of muscle activation during the different tasks. The analysis of the spatial distribution of individual MUAPs amplitude showed that they were confined to relatively small areas on the tongue surface (range: 0.5cm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> – 3.9cm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> ). A variety of different spatiotemporal MUAP patterns, likely due to the presence of different muscle compartments with different fiber orientations, were observed. Our results demonstrate that the developed electrode grid enables HDsEMG acquisition from the tongue during functional tasks, thus opening new possibilities in tongue muscle assessment both at global and single motor unit level.

After a stroke, antagonist muscle activation during agonist command impedes movement. This study compared measurements of antagonist muscle activation using surface bipolar EMG in the gastrocnemius medialis (GM) and high-density (HD) EMG in the GM and soleus (SO) during isometric submaximal and maximal dorsiflexion efforts, with knee flexed and extended, in 12 subjects with chronic hemiparesis. The coefficients of antagonist activation (CAN) of GM and SO were calculated according to the ratio of the RMS amplitude during dorsiflexion effort to the maximal agonist effort for the same muscle. Bipolar CAN (BipCAN) was compared to CAN from channel-specific (CsCAN) and overall (OvCAN) normalizations of HD-EMG. The location of the CAN centroid was explored in GM, and CAN was compared between the medial and lateral portions of SO. Between-EMG system differences in GM were observed in maximal efforts only, between BipCAN and CsCAN with lower values in BipCAN (p < 0.001), and between BipCAN and OvCAN with lower values in OvCAN (p < 0.05). The CAN centroid is located mid-height and medially in GM, while the CAN was similar in medial and lateral SO. In chronic hemiparesis, the estimates of GM hyperactivity differ between bipolar and HD-EMGs, with channel-specific and overall normalizations yielding, respectively, higher and lower CAN values than bipolar EMG. HD-EMG would be the way to develop personalized rehabilitation programs based on individual antagonist activations.

The CNS may produce the same endpoint trajectory or torque profile with different muscle activation patterns. What differentiates these patterns is the presence of co-contraction, which does not contribute to effective torque generation but allows to modulate joints' mechanical stiffness. While it has been suggested that the generation of force and the modulation of stiffness rely on separate pathways, a characterization of the differences between the synaptic inputs to motor neurons (MNs) underlying these tasks is still missing. In this study, participants co-activated the same pair of upper-limb muscles, i.e., the biceps brachii and the triceps brachii, to perform two functionally different tasks: limb stiffness modulation or endpoint force generation. Spike trains of MNs were identified through decomposition of High-Density EMGs collected from the two muscles. Cross-correlogram showed a higher synchronization between MNs recruited to modulate stiffness, while cross-muscle coherence analysis revealed peaks in the beta-band, which is commonly ascribed to a cortical origin. These peaks did not appear during the co-activation for force generation, thus suggesting separate cortical inputs for stiffness modulation. Moreover, a within-muscle coherence analysis identified two subsets of MNs that were selectively recruited to generate force or regulate stiffness. This study is the first to highlight different characteristics, and probable different neural origins, of the synaptic inputs driving a pair of muscles under different functional conditions. We suggest that stiffness modulation is driven by cortical inputs which project to a separate set of MNs, supporting the existence of a separate pathway underlying the control of stiffness.

Predictors and mitigators of strain injuries have been studied in sprint‐related sports. While the rate of axial strain, and thus running speed, may determine the site of muscle failure, muscle excitation seemingly offers protection against failure. It seems therefore plausible to ask whether running at different speeds changes the distribution of excitation within muscles. Technical limitations undermine however the possibility of addressing this issue in high‐speed, ecological conditions. Here we circumvent these limitations with a miniaturized, wireless, multi‐channel amplifier, suited for collecting spatio‐temporal data and high‐density surface electromyograms (EMGs) during overground running. We segmented running cycles while 8 experienced sprinters ran at speeds close to (70% and 85%) and at (100%) their maximum, over an 80 m running track. Then we assessed the effect of running speed on the distribution of excitation within biceps femoris (BF) and gastrocnemius medialis (GM). Statistical parametric mapping (SPM) revealed a significant effect of running speed on the amplitude of EMGs for both muscles, during late swing and early stance. Paired SPM revealed greater EMG amplitude when comparing 100% with 70% running speed for BF and GM. Regional differences in excitation were observed only for BF however. As running speed increased from 70% to 100% of the maximum, a greater degree of excitation was observed at more proximal BF regions (from 2% to 10% of the thigh length) during late swing. We discuss how these results, in the context of the literature, support the protective role of pre‐excitation against muscle failure, suggesting the site of BF muscle failure may depend on running speed.

Biofeedback based on electromyograms (EMGs) has been recently proposed to reduce exaggerated postural activity. Whether the effect of EMG biofeedback on the targeted muscles generalizes to – or is compensated by – other muscles is still an open question we address here. Fourteen young individuals were tested in three 60 s standing trials, without and with EMG-audio feedback: (i) collectively from soleus and medial gastrocnemius and (ii) from medial gastrocnemii. The Root Mean Square (RMS) of bipolar EMGs sampled from postural muscles bilaterally was computed to assess the degree of activity and postural sway was assessed from center of pressure (CoP). In relation to standing naturally, EMG-audio feedback from soleus and medial gastrocnemii decreased plantar flexors’ activity (∼10%) at the cost of increased amplitude of tibialis anterior (∼5%) and vasti muscles (∼20%) accompanied by a posterior shift of the mean CoP position. However, EMG-audio feedback from medial gastrocnemii reduced only plantar flexors’ activity when compared to standing. Current results suggest the EMG biofeedback has the potential to reduce calf muscles’ activity without loading other postural muscles especially when using medial gastrocnemii as feedback source, with implications on postural training aimed at assisting individuals in activating more efficiently postural muscles during standing.