Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized, among the others, by muscle weakness. PD patients reach lower values of peak torque during maximal voluntary contractions but also slower rates of torque development (RTD) during explosive contractions. The aim of this study was to better understand how an impairment in structural/mechanical (peripheral) factors could explain the difficulty of PD patients to raise torque rapidly. Participants (PD patients and healthy matched controls) performed maximum voluntary explosive fixed-end contraction of the knee extensor muscles during which dynamic muscle shape changes (in muscle thickness, pennation angle, and belly gearing: the ratio between muscle belly velocity and fascicle velocity), muscle-tendon unit (MTU) stiffness and EMG activity of the vastus lateralis (VL) were investigated. Both the affected (PDA) and less affected limb (PDNA) were investigated in patients. Control participants reached higher values of peak torque and showed a better capacity to express force rapidly compared to patients (PDA and PDNA). EMG activity was observed to differ between patients (PDA) and controls, but not between controls and PDNA. This suggests a specific neural/nervous effect on the most affected side. On the contrary, MTU stiffness and dynamic muscle shape changes were found to differ between controls and patients, but not between PDA and PDNA. Both sides are thus similarly affected by the pathology. The higher MTU stiffness in PD patients is likely responsible for the impaired muscle capability to change in shape which, in turn, negatively affects the torque rise.

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