Proceedings of The Physiological Society

King's College London (2009) Proc Physiol Soc 14, PC32

Poster Communications

Strength and neural activation of the knee joint musculature in Parkinson’s Disease: Effects of medication.

J. P. Folland1, B. Haas2, P. C. Castle3

1. School of Sport & Exercise Sciences, Loughborough University, Loughborough, United Kingdom. 2. School of Health Professions, University of Plymouth, Plymouth, United Kingdom. 3. School of Physical Education and Sports Science, University of Bedfordshire, Plymouth, United Kingdom.

The muscle weakness that occurs with Parkinson’s disease (PD) appears to be largely attenuated with medication (principally dopaminergic agonists; Brown et al. 1997), but the specific neuromuscular mechanisms for compromised muscle strength with PD, and the improvement that occurs with medication, have not been clearly delineated. This study compared the knee extension and flexion strength of PD patients on and off medication, and assessed the associated changes in agonist and antagonist neural activation. Ten patients with idiopathic PD (8 men, 2 women. Mean ± SD: age, 63 ± 15 yr; body mass, 76 ± 14 kg, Hoehn-Yahr scale, 1.9 ± 0.8) completed a familiarisation session and two main trials randomly assigned as, on medication (ON) and off medication (OFF, 12 hours after drug withdrawal). Knee joint muscle function of both legs was assessed unilaterally with an isometric strength testing chair at knee and hip joint angles of 90°. Force was measured with a strain gauge perpendicular to the tibia, and surface electromyography (Bagnoli-4, Delsys, USA) was collected from the rectus femoris, vastus lateralis, biceps femoris and semitendinosus. Peak knee extension and flexion force was determined with a series of maximal voluntary contractions (MVCs). EMG root mean square (RMS) was measured during a 500 ms epoch around peak force and during a stable segment of sub-maximal knee extensions at 20, 40, 60 and 80% of peak force. The interpolated twitch technique was applied to a second series of knee extension MVCs with single square-wave pulses (constant current, 50 μs duration; DS7AH, Digitimer Ltd, UK) delivered percutaneously to evoke supramaximal twitches before and during each MVC. Impaired locomotory performance (‘Up and Go’ and ‘5 m walk’ times) confirmed a greater severity of movement disorder when off medication. Isometric strength of the knee extensors (ON, 410 ± 103 vs OFF, 381 ± 86 N; Paired t, P=0.03) and flexors (ON, 165 ± 37 vs OFF, 149 ± 37 N; Paired t, P=0.09) was reduced without medication. Maximum voluntary activation of the knee extensors, assessed with the interpolated twitch technique, was reduced by a similar magnitude (7.5%) after withdrawal of medication (ON, 86.7 ± 10.2 vs OFF, 80.3 ± 12.6%; Paired t, P=0.005). Without medication, maximum agonist EMG amplitudes for knee extension and flexion were 13 and 7% lower, respectively, but these effects were not significant (Paired t, 0.59≤P≤0.77). During knee extension contractions the agonist and antagonist EMG-force relationships, and the maximum antagonist EMG, were unaffected by medication withdrawal. In conclusion, the decrease in knee extension strength when PD patients were off medication was entirely due to reduced neural drive to the agonist muscle, rather than any change in antagonist activation, and these changes were associated with reduced locomotory performance.

Where applicable, experiments conform with Society ethical requirements