Study Design Experimental Study Objectives To characterize the specific hindlimb electromyographic (EMG) patterns in response to muscle stretch and to measure the applied forces during stretching in the rat model of moderate SCI. Setting Kentucky Spinal Cord Injury Research Center, Louisville, KY, USA Methods Female Sprague Dawley rats (n=4) were instrumented for telemetry-based EMG recording (right Rectus Femoris and Biceps Femoris) and received a moderate T10 spinal cord injury (SCI). The major hindlimb muscle groups were stretched using our clinically modeled protocol. The EMG responses were recorded biweekly for 8 weeks. The forces applied during stretching were measured using a custom-designed glove. Locomotor function was assessed using the BBB Open Field Locomotor Scale, 3D kinematics and gait analysis. Results Three main EMG patterns in response to stretch were identified: clonic-like, air-stepping and spasms. Torques applied during stretching ranged from 0.8–6 N*cm, and did not change significantly over the weeks of stretching. Two stretching sessions a week did not result in a significant disruption to locomotor function. Conclusions Stretching evokes EMG patterns in rats similar to those reported in humans including clonus and spasms. The torques used during stretching are comparable, based on the ratio of torque to body weight, to the few previously published studies that measured the forces and/or torques applied by physical therapists when stretching patients. Future studies are warranted to fully explore the impact of muscle stretch on spinal cord function after injury. Sponsorship DoD, KSCHIRT, NIH

Spinal cord injury (SCI) is a devastating condition that results in whole‐body dysfunction, notably cardiovascular (CV) disruption and disease. Injury‐induced destruction of autonomic pathways in conjunction with a progressive decline in physical fitness contribute to the poor CV status of SCI individuals. Despite the wide use of exercise training as a therapeutic option to reduce CV dysfunction, little is known about the acute hemodynamic responses to the exercise itself. We investigated CV responses to an exercise challenge (swimming) following both high and low thoracic contusion to determine if the CV system is able to respond appropriately to the challenge of swimming. Blood pressure (BP) telemetry and echocardiography were used to track the progression of dysfunction in rodents with T3 and T10 SCI (n = 8 each) for 10 weeks postcontusion. At 1 week postinjury, all animals displayed a drastic decline in heart rate (HR) during the exercise challenge, likely a consequence of neurogenic shock. Furthermore, over time, all groups developed a progressive inability to maintain BP within a narrow range during the exercise challenge despite displaying normal hemodynamic parameters at rest. Echocardiography of T10 animals revealed no persistent signs of cardiac dysfunction; T3 animals exhibited a transient decline in systolic function that returned to preinjury levels by 10 weeks postinjury. Novel evidence provided here illustrates that incomplete injuries produce hemodynamic instability that only becomes apparent during an exercise challenge. Further, this dysfunction lasts into the chronic phase of disease progression despite significant recovery of hindlimb locomotion and cardiac function.

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