Cadence and range of motion modulate pedal force in a rat model of motorized cycling after spinal cord injury.

Abstract

Motorized cycling (MC) can be utilized post-spinal cord injury (SCI) in patients who lack the strength and/or stability to participate in traditional physical exercise interventions. MC has been applied with the goal of improving locomotor function or cardiovascular health in both human and animal models of SCI. However, a discrepancy exists between the results of human and animal studies of MC, particularly regarding cardiovascular outcomes. Despite the abundance of studies in both humans and animals, the mechanism behind the improvements in cardiovascular function following MC are poorly understood. We posited that increased venous return during MC is likely due to the skeletal muscle pump, where muscle activity during MC would be triggered by stretch reflexes. As stretch reflexes are dependent on both rate and length of muscle stretch, we hypothesized that cycling cadence and crank length could modulate muscle activity and therefore hindlimb loading during cycling. Initial studies testing the development of the instrumented pedals noted spasticity that was represented in the force traces, and a filtering technique was developed to separate spastic from non-spastic forces. Results using this technique combined with EMG of a knee flexor and extensor suggest that higher cadences (≥30 RPM) increased RMS EMG and non-spastic forces, while lower cadences (≤15 RPM) increased spastic forces. Furthermore, large spastic events were associated with a decrease in BP, while high cadence cycling with limited spasticity appeared to elevate BP and HR above baseline levels. These results suggest that MC in rats may constitute a mild eccentric training regimen; clinical translation may therefore be dependent on the ability to reflexively generate muscle contraction in patients during cycling

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