Voluntary activation failure contributes more to plantar flexor weakness than antagonist coactivation and muscle atrophy in chronic stroke survivors
Journal Articles
Overview
Research
Identity
Additional Document Info
View All
Overview
abstract
The contributions of nervous system muscle activation and muscle atrophy to poststroke weakness have not been evaluated together in the same subject. Maximal voluntary contraction (MVC) torque, voluntary activation (twitch interpolation), and electromyographic (EMG) amplitude were determined bilaterally in the plantar flexors of seven chronic stroke survivors (40–63 yr, 24–51 mo poststroke). Volumes of the plantar flexor muscles were determined bilaterally with magnetic resonance imaging (MRI). The mean (±SD) contralesional (paretic) MVC torque was less than one-half of the ipsilesional leg: 56.7 ± 57.4 vs. 147 ± 35.7 Nm ( P = 0.006). Contralesional voluntary activation was only 48 ± 36.9%, but was near complete in the ipsilesional leg, 97 ± 1.9% ( P = 0.01). The contralesional MVC EMG amplitude (normalized to the maximum M-wave peak-to-peak amplitude) of the gastrocnemii and soleus were 36.0 ± 28.5 and 36.0 ± 31.0% of the ipsilesional leg. Tibialis anterior (TA) EMG coactivation was not different between the contralesional (23.2 ± 24.0% of TA MVC EMG) and ipsilesional side (12.3 ± 5.7%) ( P = 0.24). However, TA EMG coactivation was excessive (71%) in one subject and accounted for ∼8% of her weakness based on the estimated antagonist torque. Relative (%ipsilesional leg) plantar flexor and gastrocnemii volumes were 88 ± 6% ( P = 0.004) and 76 ± 15% ( P = 0.01), respectively. Interlimb volume differences of the soleus, deep plantar flexors, and peronei were not significant. Preferred walking speed (0.83 ± 0.33 m/s) was related to the contralesional MVC torque ( r2= 0.57, P = 0.05, N = 7), but the two subjects with the greatest weakness walked faster than three others. Our findings suggest that plantar flexor weakness in mobile chronic stroke survivors reflects mostly voluntary activation failure, with smaller contributions from antagonist activity and atrophy.
