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Background In the last two decades, lower-limb exoskeletons have been developed to assist human standing and locomotion. One of the ongoing challenges is the cooperation between the exoskeleton balance support and the wearer control. Here we present a cooperative ankle-exoskeleton control strategy to assist in balance recovery after unexpected disturbances during walking, which is inspired on human balance responses. Methods We evaluated the novel controller in ten able-bodied participants wearing the ankle modules of the Symbitron exoskeleton. During walking, participants received unexpected forward pushes with different timing and magnitude at the pelvis level, while being supported (Exo-Assistance) or not (Exo-NoAssistance) by the robotic assistance provided by the controller. The effectiveness of the assistive strategy was assessed in terms of (1) controller performance (Detection Delay, Joint Angles, and Exerted Ankle Torques), (2) analysis of effort (integral of normalized Muscle Activity after perturbation onset); and (3) Analysis of center of mass COM kinematics (relative maximum COM Motion, Recovery Time and Margin of Stability) and spatio-temporal parameters (Step Length and Swing Time). Results In general, the results show that when the controller was active, it was able to reduce participants’ effort while keeping similar ability to counteract and withstand the balance disturbances. Significant reductions were found for soleus and gastrocnemius medialis activity of the stance leg when comparing Exo-Assistance and Exo-NoAssistance walking conditions. Conclusions The proposed controller was able to cooperate with the able-bodied participants in counteracting perturbations, contributing to the state-of-the-art of bio-inspired cooperative ankle exoskeleton controllers for supporting dynamic balance. In the future, this control strategy may be used in exoskeletons to support and improve balance control in users with motor disabilities.

Balance control is important for mobility, yet exoskeleton research has mainly focused on improving metabolic energy efficiency. Here we present a biomimetic exoskeleton controller that supports walking balance and reduces muscle activity. Humans restore balance after a perturbation by adjusting activity of the muscles actuating the ankle in proportion to deviations from steady-state center of mass kinematics. We designed a controller that mimics the neural control of steady-state walking and the balance recovery responses to perturbations. This controller uses both feedback from ankle kinematics in accordance with an existing model and feedback from the center of mass velocity. Control parameters were estimated by fitting the experimental relation between kinematics and ankle moments observed in humans that were walking while being perturbed by push and pull perturbations. This identified model was implemented on a bilateral ankle exoskeleton. The exoskeleton provided 30% of the estimated ankle moment during steady-state and perturbed walking. Across twelve subjects, exoskeleton support reduced calf muscle activity in steady-state walking by 19 % with respect to a minimal impedance controller. Proportional feedback of the center of mass velocity improved balance support after perturbation. Muscle activity is reduced in response to push and pull perturbations by 10 and 16 % and center of mass deviations by 9 and 18% with respect to the same controller without center of mass feedback. Our control approach implemented on bilateral ankle exoskeletons can thus effectively support steady-state walking and balance control and therefore has the potential to improve mobility in balance-impaired individuals.

Cerebral hypoxic vasodilation is poorly understood in humans, which undermines the development of therapeutics to optimize cerebral oxygen delivery. Across four investigations (total n = 195) we investigated the role of nitric oxide (NO) and hemoglobin-based S-nitrosothiol (RSNO) and nitrite ([Formula: see text]) signaling in the regulation of cerebral hypoxic vasodilation. We conducted hemodilution (n = 10) and NO synthase inhibition experiments (n = 11) as well as hemoglobin oxygen desaturation protocols, wherein we measured cerebral blood flow (CBF), intra-arterial blood pressure, and in subsets of participants trans-cerebral release/uptake of RSNO and [Formula: see text]. Higher CBF during hypoxia was associated with greater trans-cerebral RSNO release but not [Formula: see text], while NO synthase inhibition reduced cerebral hypoxic vasodilation. Hemodilution increased the magnitude of cerebral hypoxic vasodilation following acute hemodilution, while in 134 participants tested under normal conditions, hypoxic cerebral vasodilation was inversely correlated to arterial hemoglobin concentration. These studies were replicated in a sample of polycythemic high-altitude native Andeans suffering from excessive erythrocytosis (n = 40), where cerebral hypoxic vasodilation was inversely correlated to hemoglobin concentration, and improved with hemodilution (n = 6). Collectively, our data indicate that cerebral hypoxic vasodilation is partially NO-dependent, associated with trans-cerebral RSNO release, and place hemoglobin-based NO signaling as a central mechanism of cerebral hypoxic vasodilation in humans.