Rose, M. J. | Search bioRxiv

bioRxiv2026

Effects of Ankle Stiffness on Total Leg Kinematics, Mechanics, and Muscle Activation during Walking

PurposeAnkle stiffness can be altered by normal aging, bone and joint pathology, and treatments such as orthoses or surgical joint fusion. The effects of ankle stiffness on gait are not yet well understood but may be crucial for understanding how these pathologies and treatments influence body mechanics. The objective of this work was to investigate how isolated changes in stiffness applied in parallel with the ankle impact lower-limb kinematics, kinetics, joint work, and muscle activation during walking in individuals without lower-limb pathology. MethodsNine young adults without lower-limb pathology wore an adjustable-stiffness ankle exoskeleton and walked at 31 different conditions of ankle spring stiffness, neutral angle, and treadmill incline. We recorded motion capture data, ground reaction forces, and muscle activation, and analyzed the resultant data for trends as a function of ankle stiffness. ResultsExoskeleton-side ankle range of motion decreased and asymmetry increased across all joints as ankle stiffness increased, primarily due to decreased plantarflexion at toe-off. The 30 Nm/rad spring stiffness condition led to a minimum in mean exoskeleton-side muscle activation and hip joint work, but increased kinematic asymmetry. ConclusionOur results suggest that there may exist a range of stiffnesses at the lower end of typically-studied values that can reduce muscle activation and joint work during walking, though at the cost of kinematic symmetry. These findings provide a deeper understanding of how ankle stiffness influences gait mechanics, with potential applications in wearable devices, clinical rehabilitation, and assistive technology.

bioengineering↗

bioRxiv2023

Evidence for peripheral and central actions of codeine to dysregulate deglutition in the anesthetized cat

Systemic administration of opioids has been associated with aspiration and swallow dysfunction in humans. We speculated that systemic administration of codeine would induce dysfunctional swallowing and that this effect would have a peripheral component. Experiments were conducted in spontaneously breathing, anesthetized cats. The animals were tracheotomized and electromyogram electrodes were placed in upper airway and chest wall respiratory muscles for recording swallow related motor activity. The animals were allocated into three groups: vagal intact (VI), cervical vagotomy (CVx), and supra-nodose ganglion vagotomy (SNGx). A dose response to intravenous codeine was performed in each animal. Swallowing was elicited by injection of 3 ml of water into the oropharynx. The number of swallows after vehicle was significantly higher in the VI group than in SNGx. Codeine had no significant effect on the number of swallows induced by water in any of the groups. However, the magnitudes of water swallow-related EMGs of the thyropharyngeus muscle were significantly increased in the VI and CVx groups by 2-4 fold in a dose-related manner. In the CVx group, the geniohyoid muscle EMG during water swallows was significantly increased. There was a significant codeine dose-related increase in spontaneous swallowing in each group. The spontaneous swallow number at the 10 mg/kg dose of codeine was significantly larger in the CVx than that in the SNGx groups. During water-evoked swallows, intravenous codeine increased upper airway motor drive in a dose-related manner, consistent with dysregulation. The appearance of spontaneous swallowing in response to codeine in all groups supports a central action of this drug on the swallow pattern generator and also is consistent with dysregulation. At the highest dose of codeine, the reduced spontaneous swallow number in the SNGx group relative to CVx is consistent with a peripheral excitatory action of codeine either on pharyngeal/laryngeal receptors or in the nodose ganglion itself.

physiology↗