Voluntary activation failure contributes more to plantar flexor weakness than antagonist coactivation and muscle atrophy in chronic stroke survivors

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 (r(2) = 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.

Disturbances of motor unit rate modulation are prevalent in muscles of spastic-paretic stroke survivors

“…Although increases in antagonist coactivation have been observed poststroke (Trumbower et al 2010), it is unlikely that antagonist coactivation played a role in the observed saturation in firing profiles in the current study, as coactivation ratios of the antagonist elbow extensor and elbow flexor muscles were similar across muscle types during the voluntary ramp contractions. This agrees with previous findings in which antagonist coactivation did not contribute to muscle weakness poststroke (Klein et al 2010).…”

“…Firing rate slopes that were Յ0.5 pps/s, despite increasing force, were considered as impaired rate modulation. Because the force profile during the voluntary ramp contractions may not adequately represent the descending drive equally in the different muscle types (Fellows et al 1994;Klein et al 2010;Madhaven et al 2011), we performed a secondary analysis in which we used the firing rate profile of the higher-threshold unit instead of the peak force as an index of the descending drive. Furthermore, because maximal firing rates may be variable poststroke (Hu et al 2012), we used the peak of the smoothed lower-threshold unit's firing rate profile instead of the average of three spikes surrounding the first maximum firing rate as the start of the saturation in firing rates.…”

“…Impairments in voluntary activation of the involved limb have been observed poststroke (Madhaven et al 2011) and have been suggested to contribute to muscle weakness of the involved limb in stroke survivors (Klein et al 2010). Although the mechanisms for voluntary activation failure are not well understood (Gandevia et al 2001), reduced drive from disrupted corticospinal tracts (Berardelli et al 1987) may play a role in the observed saturation in firing profiles.…”

The role of the ipsilesional side in the rehabilitation of post-stroke subjects

“…In cases of central nervous system lesion, like stroke, the plantar flexor muscles are more prone to activation failure than the proximal muscles (i.e. quadriceps) (Klein et al, 2010). Specifically, the behaviour of the soleus as a postural muscle may reveal postural control dysfunction more evidently, since uniarticular muscles are thought to be more affected by central influences than by peripheral influences (Kautz et al, 2005).…”

Ankle antagonist coactivation in the double-support phase of walking: Stroke vs. healthy subjects

“…Electrodes were placed in muscles midbelly according to anatomical references (Cheng et al 2004;Klein et al 2010). The ground electrodes were placed over each patella.…”