Motor Compensation During Lower Limb Pedaling After Stroke

Long-term motor dysfunction in the lower limb is common after stroke. One potential contributor is motor compensation, a behavior in which functions originally performed by the paretic limb are performed by the non-paretic limb. Compensation in chronic stroke may contribute to long-term motor dysfunction by limiting functional ability, impairing future recovery, and eliciting maladaptive neuroplasticity. The purpose of this dissertation was to describe the impact of compensation on motor function and brain activation during lower limb pedaling and identify elements that produce this behavior. To achieve this purpose, we evaluated muscle activation and motor performance when compensation was prevented. During unilateral pedaling, paretic muscle activation increased but motor performance deteriorated. During bilateral uncoupled pedaling, paretic muscle activation further increased. However, subjects were unable to coordinate movements of the legs, and motor performance further deteriorated. These results suggest that compensation improves motor performance but limits paretic motor output. Because motor performance was worse during bilateral uncoupled than unilateral pedaling, impaired interlimb coordination may be a primary factor leading to compensation. As a follow-up, we determined whether altered interlimb spinal reflex pathways contribute to impaired interlimb coordination after stroke. Interlimb cutaneous reflexes were elicited during pedaling, and we assessed whether the amplitude was altered. Interlimb reflex was altered, particularly in bifunctional muscles and at pedaling transitions. Reflex alterations were correlated with impairments in interlimb coordination and compensation. These data suggest that stroke-related changes in interlimb reflex pathways undermine interlimb coordination. Finally, we assessed whether altered motor commands and performance, such as seen with compensation, are related to decreased pedaling-related brain activation after stroke. Brain activation was measured during volitional pedaling and during passive pedaling, when between-group differences were minimized. Between-group differences in brain activation persisted during passive pedaling, suggesting that altered motor commands and pedaling performance do not account for reduced brain activation after stroke. Overall, these studies provide insight into rehabilitative interventions that may decrease long-term motor dysfunction in the lower limb after stroke. One potential strategy is to enhance paretic muscle activity by preventing compensation while simultaneously employing efforts to improve interlimb coordination, possibly by manipulating interlimb reflex pathways

Task Failure during Exercise to Exhaustion in Normoxia and Hypoxia Is Due to Reduced Muscle Activation Caused by Central Mechanisms While Muscle Metaboreflex Does Not Limit Performance

To determine whether task failure during incremental exercise to exhaustion (IE) is principally due to reduced neural drive and increased metaboreflex activation eleven men (22±2 years) performed a 10s control isokinetic sprint (IS; 80 rpm) after a short warm-up. This was immediately followed by an IE in normoxia (Nx, PIO2:143 mmHg) and hypoxia (Hyp, PIO2:73 mmHg) in random order, separated by a 120 min resting period. At exhaustion, the circulation of both legs was occluded instantaneously (300 mmHg) during 10 or 60s to impede recovery and increase metaboreflex activation. This was immediately followed by an IS with open circulation. Electromyographic recordings were obtained from the vastus medialis and lateralis. Muscle biopsies and blood gases were obtained in separate experiments. During the last 10s of the IE, pulmonary ventilation, VO2, power output and muscle activation were lower in hypoxia than in normoxia, while pedaling rate was similar. Compared to the control sprint, performance (IS-Wpeak) was reduced to a greater extent after the IE-Nx (11% lower P<0.05) than IE-Hyp. The root mean square (EMGRMS) was reduced by 38 and 27% during IS performed after IE-Nx and IE-Hyp, respectively (Nx vs. Hyp: P<0.05). Post-ischemia IS-EMGRMS values were higher than during the last 10s of IE. Sprint exercise mean (IS-MPF) and median (IS-MdPF) power frequencies, and burst duration, were more reduced after IE-Nx than IE-Hyp (P<0.05). Despite increased muscle lactate accumulation, acidification, and metaboreflex activation from 10 to 60s of ischemia, IS-Wmean (+23%) and burst duration (+10%) increased, while IS-EMGRMS decreased (-24%, P<0.05), with IS-MPF and IS-MdPF remaining unchanged. In conclusion, close to task failure, muscle activation is lower in hypoxia than in normoxia. Task failure is predominantly caused by central mechanisms, which recover to great extent within one minute even when the legs remain ischemic. There is dissociation between the recovery of EMGRMS and performance. The reduction of surface electromyogram MPF, MdPF and burst duration due to fatigue is associated but not caused by muscle acidification and lactate accumulation. Despite metaboreflex stimulation, muscle activation and power output recovers partly in ischemia indicating metaboreflex activation has a minor impact on sprint performance

Construction of a Test Bench for the Development of Experimental Methods for the Reproduction of Road Induced Vibrations During Indoor Cycling

Il lavoro svolto si è focalizzato sul concepimento e sulla costruzione di un banco prova per la riproduzione delle vibrazioni indotte dalle diverse tipologie di strade, su una bicicletta. Dopo la fase progettuale e realizzativa e dopo aver collaudato e funzionalità del banco prova il lavoro si è focalizzato su test comparativi fra uno stelo per manubrio rigido e uno ammortizzato al fine di comparare le grandezze fondamentali quali funzione di trasferimento, accelerazioni e Confort index

Afferent information modulates spinal network activity in vitro and in preclinical animal models

Primary afferents are responsible for the transmission of peripheral sensory information to the spinal cord. Spinal circuits involved in sensory processing and in motor activity are directly modulated by incoming input conveyed by afferent fibres. Current neurorehabilitation exploits primary afferent information to induce plastic changes within lesioned spinal circuitries. Plasticity and neuromodulation promoted by activity-based interventions are suggested to support both the functional recovery of locomotion and pain relief in subjects with sensorimotor disorders. The present study was aimed at assessing spinal modifications mediated by afferent information. At the beginning of my PhD project, I adopted a simplified in vitro model of isolated spinal cord from the newborn rat. In this preparation, dorsal root (DR) fibres were repetitively activated by delivering trains of electrical stimuli. Responses of dorsal sensory-related and ventral motor-related circuits were assessed by extracellular recordings. I demonstrated that electrostimulation protocols able to activate the spinal CPG for locomotion, induced primary afferent hyperexcitability, as well. Thus, evidence of incoming signals in modulating spinal circuits was provided. Furthermore, a robust sensorimotor interplay was reported to take place within the spinal cord. I further investigated hyperexcitability conditions in a new in vivo model of peripheral neuropathic pain. Adult rats underwent a surgical procedure where the common peroneal nerve was crushed using a calibrated nerve clamp (modified spared nerve injury, mSNI). Thus, primary afferents of the common peroneal nerve were activated through the application of a noxious compression, which presumably elicited ectopic activity constitutively generated in the periphery. One week after surgery, animals were classified into two groups, with (mSNI+) and without (mSNI-) tactile hypersensitivity, based on behavioral tests assessing paw withdrawal threshold. Interestingly, the efficiency of the mSNI in inducing tactile hypersensitivity was halved with respect to the classical SNI model. Moreover, mSNI animals with tactile hypersensitivity (mSNI+) showed an extensive neuroinflammation within the dorsal horn, with activated microglia and astrocytes being significantly increased with respect to mSNI animals without tactile hypersensitivity (mSNI-) and to sham-operated animals. Lastly, RGS4 (regulator of G protein signaling 4) was reported to be enhanced in lumbar dorsal root ganglia (DRGs) and dorsal horn ipsilaterally to the lesion in mSNI+ animals. Thus, a new molecular marker was demonstrated to be involved in tactile hypersensitivity in our preclinical model of mSNI. Lastly, we developed a novel in vitro model of newborn rat, where hindlimbs were functionally connected to a partially dissected spinal cord and passively-driven by a robotic device (Bipedal Induced Kinetic Exercise, BIKE). I aimed at studying whether spinal activity was influenced by afferent signals evoked during passive cycling. I first demonstrated that BIKE could actually evoke an afferent feedback from the periphery. Then, I determined that spinal circuitries were differentially affected by training sessions of different duration. On one side, a short exercise session could not directly activate the locomotor CPG, but was able to transiently facilitate an electrically-induced locomotor-like activity. Moreover, no changes in reflex or spontaneous activity of dorsal and ventral networks were promoted by a short training. On the other side, a long BIKE session caused a loss in facilitation of spinal locomotor networks and a depression in the area of motor reflexes. Furthermore, activity in dorsal circuits was long-term enhanced, with a significant increase in both electrically-evoked and spontaneous antidromic discharges. Thus, the persistence of training-mediated effects was different, with spinal locomotor circuits being only transiently modulated, whereas dorsal activity being strongly and stably enhanced. Motoneurons were also affected by a prolonged training, showing a reduction in membrane resistance and an increase in the frequency of post-synaptic currents (PSCs), with both fast- and slow-decaying synaptic inputs being augmented. Changes in synaptic transmission onto the motoneuron were suggested to be responsible for network effects mediated by passive training. In conclusion, I demonstrated that afferent information might induce changes within the spinal cord, involving both neuronal and glial cells. In particular, spinal networks are affected by incoming peripheral signals, which mediate synaptic, cellular and molecular modifications. Moreover, a strong interplay between dorsal and ventral spinal circuits was also reported. A full comprehension of basic mechanisms underlying sensory-mediated spinal plasticity and bidirectional interactions between functionally different spinal networks might lead to the development of neurorehabilitation strategies which simultaneously promote locomotor recovery and pain relief

The Design of an Electro-Mechanical Bicycle for an Immersive Virtual Environment

Roughly 50,000 people are injured in bicycle collisions with motor vehicles each year, approximately 6,000 of these injuries involve children less than 14 years old. To better understand which factors put bicycling children at risk for motor vehicle collisions, researchers at the University of Iowa built a virtual environment that simulates the experience of riding through a town and crossing roads with motor vehicles traffic. The stationary bicycle, the focus of this report, replicates the pedal forces experienced by a rider. The stationary bike also provides the simulator with the bicycle’s velocity and steering angle. This report describes the design of the system, which features a flywheel designed to represent the rider and bike inertia, the mechanical linkages between the rider and an electric motor, and a system to measure steering angles. The bicycle has been built and tested and is currently in use in the virtual environment

Aerospace medicine and biology: A continuing bibliography with indexes (supplement 336)

This bibliography lists 111 reports, articles and other documents introduced into the NASA Scientific and Technical Information System during April 1990. Subject coverage includes: aerospace medicine and psychology, life support systems and controlled environments, safety equipment, exobiology and extraterrestrial life, and flight crew behavior and performance

Investigating the physiological mechanisms of the oxygen consumption \u201cslow component\u201d.

The study of the oxygen consumption (VO2) kinetics is focused on the understanding of how human metabolism adjusts during the transition from a condition of resting/movement to another in order to satisfy the new energetic demand. As an integrated index of pulmonary, cardiovascular and muscles capacity VO2 kinetics have gained progressively increasing interests during the XX and the early XXI centuries. Thanks to the development of new technologies as well as an always increasing community of interested scientists in this subject, the knowledge in this field has been expanded considerably. However, some of the topics related to VO2 kinetics remain debated and call for further research. One of these topics is the loss of efficiency of human locomotion that occurs at the higher metabolic intensities, after the transitory period in which a new steady-state in VO2 should be achieved. This phenomenon is typically called VO2 \u201cslow component\u201d, as representative of a further increase in VO2 after the expected steady-state. The importance of the VO2 slow component lies in its link with exercise tolerance and on the understanding of the adaptations of the human body during physical activity. Therefore, researchers have tried to define the physiological underpinning of the slow component and to develop intervention strategies to reduce its amplitude. Nevertheless, a number of physiological uncertainties regarding the mechanistic bases of the slow component exist and require to be clarified. The purpose of this thesis was to deal with this gap and to study the origins of the VO2 slow component, and the loss of efficiency of locomotion that the slow component represents. In chapter one, a brief explanation of the VO2 response during exercise and the current explanatory theories for the VO2 slow component are provided. In chapter two, the experimental aims of the thesis are explained. Then, the results of four different studies are presented in chapters three, four, five, and six. Finally, chapter seven summarizes the main findings of this research work