Date of Award

Spring 2012

Document Type

Thesis

Degree Name

Master of Arts (MA)

Department

Biomedical Engineering

First Advisor

Allison S. Hyngstrom

Second Advisor

Brian D. Schmit

Third Advisor

Sandra S. Hunter

Abstract

Stroke causes paresis in leg muscles, such as the knee extensors, that significantly impairs motor control and function during tasks such as walking. Reduced endurance and increased kinematic asymmetries during walking over time indicate paretic musculature may fatigue more quickly than non-paretic musculature. The primary purpose of this study was to identify abnormalities in neuromuscular fatigue (reduction in force over time) of the paretic knee extensors and associate them with motor performance.

We investigated the effects of repeated six second isometric submaximal (30% of maximum voluntary contraction) knee extensor fatiguing contractions on task failure and motor performance in ten chronic stroke subjects and compared them to ten, healthy controls. A systematic criterion determined task failure. We recorded knee extensor torque, stretch reflex responses, surface electromyography (EMG) of agonist (rectus femoris and vastus medialis) and antagonist (medial hamstring) knee extensor muscles, and muscle fiber conduction velocity (CV) of the vastus lateralis muscle as interpretive measures of neuromuscular fatigue. A power spectral density analysis of the intermittent target torque estimated the effect of fatigue on force fluctuations. Two isometric submaximal torque tracking tasks performed before and after fatigue provided direct measures of fatigue on force variability and error. Stroke subjects failed the fatiguing task significantly sooner than control subjects. In controls, averaged rectified EMG amplitude significantly increased and CV significantly reduced with fatigue, while no changes occurred in stroke. Fatigue caused a spectral shift toward higher force fluctuation frequencies in control but not stroke subjects. Time to task failure in stroke subjects negatively correlated with their walking speed. Additionally, pre-fatigue torque variability and error was greater in stroke than control subjects, and increased significantly with fatigue.

In summary, paretic knee extensors have increased neuromuscular fatigability of the paretic knee extensors which relates to walking speed. The interpretative measures suggest that central factors may contribute more to time-to-task failure as compared to peripheral (muscular factors) in stroke survivors. Performance data demonstrate pre and post-fatigue impairments in sub-maximal force regulation. Taken together, these data demonstrate previously un-described impairments in paretic knee extensor force generation and regulation that could contribute to motor dysfunction post stroke.

Available for download on Sunday, May 25, 2014

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