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Recent studies suggest that transitory blood flow restriction (BFR) may improve the outcomes of training from anatomical (hypertrophy) and neural control perspectives. Whilst the chronic consequences of BFR on local metabolism and tissue adaptation have been extensively investigated, its acute effects on motor control are not yet fully understood. In this study, we compared the neuromechanical effects of continuous BFR against non-restricted circulation (atmospheric pressure—AP), during isometric elbow flexions. BFR was achieved applying external pressure either between systolic and diastolic (lower pressure—LP) or 1.3 times the systolic pressure (higher pressure—HP). Three levels of torque (15, 30, and 50% of the maximal voluntary contraction—MVC) were combined with the three levels of pressure for a total of 9 (randomized) test cases. Each condition was repeated 3 times. The protocol was administered to 12 healthy young adults. Neuromechanical measurements (torque and high-density electromyography—HDEMG) and reported discomfort were used to investigate the response of the central nervous system to BFR. The investigated variables were: root mean square (RMS), and area under the curve in the frequency domain—for the torque, and average RMS, median frequency and average muscle fibres conduction velocity—for the EMG. The discomfort caused by BFR was exacerbated by the level of torque and accumulated over time. The torque RMS value did not change across conditions and repetitions. Its spectral content, however, revealed a decrease in power at the tremor band (alpha-band, 5–15 Hz) which was enhanced by the level of pressure and the repetition number. The EMG amplitude showed no differences whilst the median frequency and the conduction velocity decreased over time and across trials, but only for the highest levels of torque and pressure. Taken together, our results show strong yet transitory effects of BFR that are compatible with a motor neuron pool inhibition caused by increased activity of type III and IV afferences, and a decreased activity of spindle afferents. We speculate that a compensation of the central drive may be necessary to maintain the mechanical output unchanged, despite disturbances in the afferent volley to the motor neuron pool.

Understanding how motor units (MUs) contribute to skeletal mechanical force is crucial for unraveling the underlying mechanism of human movement. Alterations in MU firing, contractile and force-generating properties emerge in response to physical training, aging or injury. However, how changes in MU firing and twitch properties dictate skeletal muscle force generation in healthy and impaired individuals remains an open question. In this work, we present a MU-specific approach to identify firing and twitch properties of MU samples and employ them to decode musculoskeletal function in vivo. First, MU firing events were decomposed offline from high-density electromyography (HD-EMG) of six lower leg muscles involved in ankle plantar-dorsi flexion. We characterized their twitch responses based on the statistical distributions of their firing properties and employed them to compute MU-specific activation dynamics. Subsequently, we decoded ankle joint moments by linking our framework to a subject-specific musculoskeletal model. We validated our approach at different ankle positions and levels of activation and compared it with traditional EMG-driven models. Our proposed MU-specific formulation achieves higher generalization across conditions than the EMG-driven models, with significantly lower coefficients of variation in torque predictions. Furthermore, our approach shows distinct neural strategies across a large repertoire of contractile conditions in different muscles. Our proposed approach may open new avenues for characterizing the relationship between MU firing and twitch properties and their influence on force capacity. This can facilitate the development of targeted rehabilitation strategies tailored to individuals with specific neuromuscular conditions.

Background: Data loss in wearable sensors is an inevitable problem that leads to misrepresentation during diabetes health monitoring. We systematically investigated missing wearable sensors data to get causal insight into the mechanisms leading to missing data. Methods: Two-week-long data from a continuous glucose monitor and a Fitbit activity tracker recording heart rate (HR) and step count in free-living patients with type 2 diabetes mellitus were used. The gap size distribution was fitted with a Planck distribution to test for missing not at random (MNAR) and a difference between distributions was tested with a Chi-squared test. Significant missing data dispersion over time was tested with the Kruskal–Wallis test and Dunn post hoc analysis. Results: Data from 77 subjects resulted in 73 cleaned glucose, 70 HR and 68 step count recordings. The glucose gap sizes followed a Planck distribution. HR and step count gap frequency differed significantly (p < 0.001), and the missing data were therefore MNAR. In glucose, more missing data were found in the night (23:00–01:00), and in step count, more at measurement days 6 and 7 (p < 0.001). In both cases, missing data were caused by insufficient frequency of data synchronization. Conclusions: Our novel approach of investigating missing data statistics revealed the mechanisms for missing data in Fitbit and CGM data.

Personalization of gait neuroprosthetics is paramount to ensure their efficacy for users, who experience severe limitations in mobility without an assistive device. Our goal is to develop assistive devices that collaborate with and are tailored to their users, while allowing them to use as much of their existing capabilities as possible. Currently, personalization of devices is challenging, and technological advances are required to achieve this goal. Therefore, this paper presents an overview of challenges and research directions regarding an interface with the peripheral nervous system, an interface with the central nervous system, and the requirements of interface computing architectures. The interface should be modular and adaptable, such that it can provide assistance where it is needed. Novel data processing technology should be developed to allow for real-time processing while accounting for signal variations in the human. Personalized biomechanical models and simulation techniques should be developed to predict assisted walking motions and interactions between the user and the device. Furthermore, the advantages of interfacing with both the brain and the spinal cord or the periphery should be further explored. Technological advances of interface computing architecture should focus on learning on the chip to achieve further personalization. Furthermore, energy consumption should be low to allow for longer use of the neuroprosthesis. In-memory processing combined with resistive random access memory is a promising technology for both. This paper discusses the aforementioned aspects to highlight new directions for future research in gait neuroprosthetics.

Trans-spinal direct current stimulation (tsDCS) provides a non-invasive, clinically viable approach to potentially restore physiological neuromuscular function after neurological impairment, e.g., spinal cord injury (SCI). Use of tsDCS has been hampered by the inability of delivering stimulation patterns based on the activity of neural targets responsible to motor function, i.e., α-motor neurons (α-MNs). State of the art modeling and experimental techniques do not provide information about how individual α-MNs respond to electrical fields. This is a major element hindering the development of neuro-modulative technologies highly tailored to an individual patient. For the first time, we propose the use of a signal-based approach to infer tsDCS effects on large α-MNs pools in four incomplete SCI individuals. We employ leg muscles spatial sampling and deconvolution of high-density fiber electrical activity to decode accurate α-MNs discharges across multiple lumbosacral segments during isometric plantar flexion sub-maximal contractions. This is done before, immediately after and 30 min after sub-threshold cathodal stimulation. We deliver sham tsDCS as a control measure. First, we propose a new algorithm for removing compromised information from decomposed α-MNs spike trains, thereby enabling robust decomposition and frequency-domain analysis. Second, we propose the analysis of α-MNs spike trains coherence (i.e., frequency-domain) as an indicator of spinal response to tsDCS. Results showed that α-MNs spike trains coherence analysis sensibly varied across stimulation phases. Coherence analyses results suggested that the common synaptic input to α-MNs pools decreased immediately after cathodal tsDCS with a persistent effect after 30 min. Our proposed non-invasive decoding of individual α-MNs behavior may open up new avenues for the design of real-time closed-loop control applications including both transcutaneous and epidural spinal electrical stimulation where stimulation parameters are adjusted on-the-fly.

Postinhibitory excitation is a transient overshoot of a neuron's baseline firing rate following an inhibitory stimulus and can be observed in vivo in human motoneurons. However, the biophysical origin of this phenomenon is still unknown and both reflex pathways and intrinsic motoneuron properties have been proposed. We hypothesized that postinhibitory excitation in motoneurons can be facilitated by hyperpolarization-activated inward currents (h-currents). Using an electrical circuit model, we investigated how h-currents can modulate the postinhibitory response of motoneurons. Further, we analyzed the spike trains of human motor units from the tibialis anterior muscle during reciprocal inhibition. The simulations revealed that the activation of h-currents by an inhibitory postsynaptic potential can cause a short-term increase in a motoneuron's firing probability. This result suggests that the neuron can be excited by an inhibitory stimulus. In detail, the modulation of the firing probability depends on the time delay between the inhibitory stimulus and the previous action potential. Further, the postinhibitory excitation's strength correlates with the inhibitory stimulus's amplitude and is negatively correlated with the baseline firing rate as well as the level of input noise. Hallmarks of h-current activity, as identified from the modeling study, were found in 50% of the human motor units that showed postinhibitory excitation. This study suggests that h-currents can facilitate postinhibitory excitation and act as a modulatory system to increase motoneuron excitability after a strong inhibition.