Stroke Increases Ischemia-related Decreases in Motor Unit Discharge Rates

Following stroke, hyperexcitable sensory pathways, such as the group III/IV afferents that are sensitive to ischemia, may inhibit paretic motor neurons during exercise. We quantified the effects of whole leg ischemia on paretic vastus lateralis motor unit firing rates during sub-maximal isometric contractions. Ten chronic stroke survivors (>1 year post stroke) and 10 controls participated. During conditions of whole leg occlusion, the discharge timings of motor units were identified from decomposition of high-density surface EMG signals during repeated sub-maximal knee extensor contractions. Quadriceps resting twitch responses and near infrared spectroscopy measurements of oxygen saturation as an indirect measure of blood flow were made. There was a greater decrease in paretic motor unit discharge rates during the occlusion compared with the controls (average decrease for stroke and controls, 12.3±10.0% and 0.1±12.4%; p<0.001). The motor unit recruitment thresholds did not change with the occlusion (stroke: without occlusion 11.68±5.83%MVC vs with occlusion 11.11±5.26%MVC; control: 11.87±5.63 %MVC vs 11.28±5.29 %MVC). Resting twitch amplitudes declined similarly for both groups in response to whole leg occlusion (stroke: 29.16±6.88 Nm vs 25.75±6.78 Nm; control: 38.80±13.23 Nm vs 30.14±9.64 Nm). Controls had a greater exponential decline (lower time constant) in oxygen saturation blood flow as compared to the stroke group (stroke time constant: 22.90±10.26 min vs. control time constant: 5.46±4.09 min, p<0.001). Ischemia of the muscle resulted in greater neural inhibition of paretic motor units compared with controls and may contribute to deficient muscle activation post stroke.