Electronic Thesis and Dissertation Repository

Degree

Doctor of Philosophy

Program

Kinesiology

Supervisor

Dr. Charles L. Rice

Abstract

Diabetes mellitus (DM) imparts vascular and metabolic stressors that cause damage and dysfunction to the human nervous system. The disorder associated with this dysfunction is termed diabetic polyneuropathy (DPN). Although DPN has been associated with muscle weakness and atrophy, the extent of its impacts on the neuromuscular system is not well understood. The five studies presented in my thesis investigated how DPN affects the neuromuscular system in humans, from the motor neuron to skeletal muscle contractile properties, using a combination of electromyography (EMG), dynamometry and magnetic resonance imaging (MRI) techniques.

The purpose of Studies 1 and 2 was to determine whether the neurogenic loss of motor units underlies the muscle weakness and atrophy associated with DPN, and to investigate how these changes may differ in an upper and lower limb muscle. I determined DPN patients feature reduced motor unit estimates (MUNEs) compared to controls, and progression of motor unit loss in DPN may follow a length-dependent pattern.

The purpose of Study 3 was to assess the stability of neuromuscular transmission in patients with DPN compared with healthy controls, using a novel set of electrodiagnostic parameters obtained via quantitative EMG. I determined DPN patients have less stable neuromuscular transmission, and the feature intermittent conduction failure at a relatively low contraction intensity.

The purpose of Study 4 was to investigate skeletal muscle contractile properties and morphology in DPN patients associated with the severity of muscle denervation. I determined DPN patients possess slowed muscle, with greater proportional amounts of non-contractile muscle tissue compared to controls.

The purpose of Study 5 was to explore the fatigability of DPN patients during a sustained, maximal voluntary contraction (MVC). I determined DPN patients have less endurance than controls, and their increased fatigability may be associated with neuromuscular transmission failure.

Overall these foundational explorations greatly expand our knowledge of how DPN can impact the neuromuscular system in humans. Furthermore, the studies contained within my thesis may help direct further useful studies and strategies to understand, and direct clinical support in those with DPN.


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