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Purpose The objective was to examine the impact of non-postural muscle fatigue on anticipatory postural control, during postural perturbations induced by platform translations. The experimental setup investigated the central changes caused by fatigue without the potential confounding influence of peripheral fatigue within the postural muscles. Methods Fatigue induced in forearm muscles by a maximal handgrip contraction has been previously shown to influence forearm force production for 10 min, reduce ankle plantarflexion force for 1 min and create measureable central fatigue for 30 s. The peak-to-peak anterior/posterior displacement of the center of mass and center of pressure (COP) and muscle activity were measured during the postural perturbation tasks performed before the fatigue protocol and for 10 min post-fatigue. Results The fatigue protocol decreased the peak-to-peak COP displacement from 128.0 ± 12.3 mm pre-fatigue to 81.9 ± 7.8 mm post-fatigue during the forwards platform translation ( p  < 0.05) and from 133.8 ± 12.0 to 89.2 ± 7.9 mm during the backwards translation ( p  < 0.05). The fatigue protocol also caused the tibialis anterior (TA pre-fatigue = −0.25 ± 0.04 s, TA post-fatigue = −0.41 ± 0.02 s, p  = 0.001) and medial gastrocnemius muscles (MG pre-fatigue = −0.39 ± 0.03 s, MG post-fatigue = −0.48 ± 0.02 s, p  = 0.028) to be recruited significantly earlier relative to the pre-fatigue condition. Conclusion This experimental setup ensured that peripheral fatigue did not develop in the postural muscles; therefore, a general fatigued-induced modification of the postural strategy is proposed as the origin of the postural changes and delayed recovery.

Context: With regard to intermittent training exercise, the effects of the mode of recovery on subsequent performance are equivocal. Objective: To compare the effects of 3 types of recovery intervention on peak torque (PT) and electromyographic (EMG) activity of the knee extensor muscles after fatiguing isokinetic intermittent concentric exercise. Design: Crossover study. Setting: Research laboratory. Patients or Other Participants: Eight elite judo players (age = 18.4 ± 1.4 years, height = 180 ± 3 cm, mass = 77.0 ± 4.2 kg). Intervention(s): Participants completed 3 randomized sessions within 7 days. Each session consisted of 5 sets of 10 concentric knee extensions at 80% PT at 120°/s, with 3 minutes of recovery between sets. Recovery interventions were passive, active, and electromyostimulation. The PT and maximal EMG activity were recorded simultaneously while participants performed isokinetic dynamometer trials before and 3 minutes after the resistance exercise. Main Outcome Measure(s): The PT and maximal EMG activity from the knee extensors were quantified at isokinetic velocities of 60°/s, 120°/s, and 180°/s, with 5 repetitions at each velocity. Results: The reduction in PT observed after electromyo-stimulation was less than that seen after passive ( P < .001) or active recovery ( P < .001). The reduction in PT was less after passive recovery than after active recovery ( P < .001). The maximal EMG activity level observed after electromyostimulation was higher than that seen after active recovery ( P < .05). Conclusions: Electromyostimulation was an effective recovery tool in decreasing neuromuscular fatigue after high-intensity, intermittent isokinetic concentric exercise for the knee extensor muscles. Also, active recovery induced the greatest amount of neuromuscular fatigue.

Spinal cord injury leads to severe locomotor deficits or even complete leg paralysis. Here we introduce targeted spinal cord stimulation neurotechnologies that enabled voluntary control of walking in individuals who had sustained a spinal cord injury more than four years ago and presented with permanent motor deficits or complete paralysis despite extensive rehabilitation. Using an implanted pulse generator with real-time triggering capabilities, we delivered trains of spatially selective stimulation to the lumbosacral spinal cord with timing that coincided with the intended movement. Within one week, this spatiotemporal stimulation had re-established adaptive control of paralysed muscles during overground walking. Locomotor performance improved during rehabilitation. After a few months, participants regained voluntary control over previously paralysed muscles without stimulation and could walk or cycle in ecological settings during spatiotemporal stimulation. These results establish a technological framework for improving neurological recovery and supporting the activities of daily living after spinal cord injury. Spatially selective and temporally controlled stimulation of the spinal cord, together with rehabilitation, results in substantial restoration of locomotor function in humans with spinal cord injury.

Obstacle avoidance during locomotion is essential for safe, smooth locomotion. Physiological studies regarding muscle synergy have shown that the combination of a small number of basic patterns produces the large part of muscle activities during locomotion and the addition of another pattern explains muscle activities for obstacle avoidance. Furthermore, central pattern generators in the spinal cord are thought to manage the timing to produce such basic patterns. In the present study, we investigated sensory-motor coordination for obstacle avoidance by the hindlimbs of the rat using a neuromusculoskeletal model. We constructed the musculoskeletal part of the model based on empirical anatomical data of the rat and the nervous system model based on the aforementioned physiological findings of central pattern generators and muscle synergy. To verify the dynamic simulation by the constructed model, we compared the simulation results with kinematic and electromyographic data measured during actual locomotion in rats. In addition, we incorporated sensory regulation models based on physiological evidence of phase resetting and interlimb coordination and examined their functional roles in stepping over an obstacle during locomotion. Our results show that the phase regulation based on interlimb coordination contributes to stepping over a higher obstacle and that based on phase resetting contributes to quick recovery after stepping over the obstacle. These results suggest the importance of sensory regulation in generating successful obstacle avoidance during locomotion.

Breathing is a well-described, vital and surprisingly complex behaviour, with behavioural and physiological outputs that are easy to directly measure. Key neural elements for generating breathing pattern are distinct, compact and form a network amenable to detailed interrogation, promising the imminent discovery of molecular, cellular, synaptic and network mechanisms that give rise to the behaviour. Coupled oscillatory microcircuits make up the rhythmic core of the breathing network. Primary among these is the preBötzinger Complex (preBötC), which is composed of excitatory rhythmogenic interneurons and excitatory and inhibitory pattern-forming interneurons that together produce the essential periodic drive for inspiration. The preBötC coordinates all phases of the breathing cycle, coordinates breathing with orofacial behaviours and strongly influences, and is influenced by, emotion and cognition. Here, we review progress towards cracking the inner workings of this vital core.

Bioresorbable electronic stimulators are of rapidly growing interest as unusual therapeutic platforms, i.e., bioelectronic medicines, for treating disease states, accelerating wound healing processes and eliminating infections. Here, we present advanced materials that support operation in these systems over clinically relevant timeframes, ultimately bioresorbing harmlessly to benign products without residues, to eliminate the need for surgical extraction. Our findings overcome key challenges of bioresorbable electronic devices by realizing lifetimes that match clinical needs. The devices exploit a bioresorbable dynamic covalent polymer that facilitates tight bonding to itself and other surfaces, as a soft, elastic substrate and encapsulation coating for wireless electronic components. We describe the underlying features and chemical design considerations for this polymer, and the biocompatibility of its constituent materials. In devices with optimized, wireless designs, these polymers enable stable, long-lived operation as distal stimulators in a rat model of peripheral nerve injuries, thereby demonstrating the potential of programmable long-term electrical stimulation for maintaining muscle receptivity and enhancing functional recovery. Bioresorbable electronic stimulators can deliver electrical stimulation in rodents to enhance functional muscle recovery after nerve injury. Here, the authors present a bioresorbable dynamic covalent polymer that enables reliable, long-lived operation of soft, stretchable devices of this type.

Skeletal muscle has a robust capacity for regeneration following injury. However, few if any effective therapeutic options for volumetric muscle loss are available. Autologous muscle grafts or muscle transposition represent possible salvage procedures for the restoration of mass and function but these approaches have limited success and are plagued by associated donor site morbidity. Cell-based therapies are in their infancy and, to date, have largely focused on hereditary disorders such as Duchenne muscular dystrophy. An unequivocal need exists for regenerative medicine strategies that can enhance or induce de novo formation of functional skeletal muscle as a treatment for congenital absence or traumatic loss of tissue. In this review, the three stages of skeletal muscle regeneration and the potential pitfalls in the development of regenerative medicine strategies for the restoration of functional skeletal muscle in situ are discussed.

Injured peripheral nerves but not central nerves have the capacity to regenerate and reinnervate their target organs. After the two most severe peripheral nerve injuries of six types, crush and transection injuries, nerve fibers distal to the injury site undergo Wallerian degeneration. The denervated Schwann cells (SCs) proliferate, elongate and line the endoneurial tubes to guide and support regenerating axons. The axons emerge from the stump of the viable nerve attached to the neuronal soma. The SCs downregulate myelin-associated genes and concurrently, upregulate growth-associated genes that include neurotrophic factors as do the injured neurons. However, the gene expression is transient and progressively fails to support axon regeneration within the SC-containing endoneurial tubes. Moreover, despite some preference of regenerating motor and sensory axons to “find” their appropriate pathways, the axons fail to enter their original endoneurial tubes and to reinnervate original target organs, obstacles to functional recovery that confront nerve surgeons. Several surgical manipulations in clinical use, including nerve and tendon transfers, the potential for brief low-frequency electrical stimulation proximal to nerve repair, and local FK506 application to accelerate axon outgrowth, are encouraging as is the continuing research to elucidate the molecular basis of nerve regeneration.

Krabbe disease (KD) is a neurodegenerative disorder caused by the lack of β- galactosylceramidase enzymatic activity and by widespread accumulation of the cytotoxic galactosyl-sphingosine in neuronal, myelinating and endothelial cells. Despite the wide use of Twitcher mice as experimental model for KD, the ultrastructure of this model is partial and mainly addressing peripheral nerves. More details are requested to elucidate the basis of the motor defects, which are the first to appear during KD onset. Here we use transmission electron microscopy (TEM) to focus on the alterations produced by KD in the lower motor system at postnatal day 15 (P15), a nearly asymptomatic stage, and in the juvenile P30 mouse. We find mild effects on motorneuron soma, severe ones on sciatic nerves and very severe effects on nerve terminals and neuromuscular junctions at P30, with peripheral damage being already detectable at P15. Finally, we find that the gastrocnemius muscle undergoes atrophy and structural changes that are independent of denervation at P15. Our data further characterize the ultrastructural analysis of the KD mouse model, and support recent theories of a dying-back mechanism for neuronal degeneration, which is independent of demyelination.

The spinal cord is a fascinating structure that is responsible for coordinating movement in vertebrates. Spinal motor neurons control muscle activity by transmitting signals from the spinal cord to diverse peripheral targets. In this study, we profiled 43,890 single-nucleus transcriptomes from the adult mouse spinal cord using fluorescence-activated nuclei sorting to enrich for motor neuron nuclei. We identified 16 sympathetic motor neuron clusters, which are distinguishable by spatial localization and expression of neuromodulatory signaling genes. We found surprising skeletal motor neuron heterogeneity in the adult spinal cord, including transcriptional differences that correlate with electrophysiologically and spatially distinct motor pools. We also provide evidence for a novel transcriptional subpopulation of skeletal motor neuron (γ*). Collectively, these data provide a single-cell transcriptional atlas ( http://spinalcordatlas.org ) for investigating the organizing molecular logic of adult motor neuron diversity, as well as the cellular and molecular basis of motor neuron function in health and disease. Blum et al. performed single-nucleus RNA sequencing of the adult mouse spinal cord. This analysis revealed heterogeneity in the autonomic and skeletal motor systems and provides a resource to study motor neurons in health and disease.