Affiliations: [a] School of Sport, Exercise and Health Sciences, Loughborough University, Loughborough, UK | [b] School of Health Professions, University of Plymouth, Plymouth, UK | [c] Department of Sport & Exercise Science, University of Bedfordshire, Bedfordshire, UK
Correspondence:
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Corresponding author: Dr. Jonathan P. Folland, School of Sport, Exercise & Health Sciences, Loughborough University, Ashby Road, Loughborough, Leicestershire, LE11 3TU, UK. Tel.: +44 0 1509 226334; Fax: +44 0 1509 226301; E-mail: j.p.folland@lboro.ac.uk
Abstract: The specific neuromuscular mechanisms for compromised muscle strength with PD, and the improvement that occurs with medication, have not been clearly delineated. This study assessed knee extension and flexion strength of PD patients whilst on and off medication and examined the neural mechanisms responsible for any changes. Ten idiopathic PD patients were assessed whilst on and off medication (⩾ 12-h after drug withdrawal), ∼ 7 days apart. Isometric strength of the knee extensors and flexors was assessed, and the interpolated twitch technique used to measure activation of the knee extensors. Surface EMG was also used to measure neural drive to the agonists and antagonists. Without medication isometric strength of the knee extensors (7%) and flexors (11%) was impaired and the interpolated twitch technique revealed activation of the knee extensors was reduced (8%, P = 0.005). Maximum agonist amplitudes for nkee extension and flexion were unchanged off-medication (0.59 < P < 0.77). The agonist and antagonist EMG-force relationships, and the maximum antagonist EMG, were unaffected by medication withdrawal. The decrease in knee extension strength when PD patients were off medication was due to reduced activation of the agonist muscle, rather than any change in antagonist co-activation, and these changes were associated with reduced locomotory performance.
