A major contributor to impaired locomotion post-stroke is abnormal phasing of paretic muscle activity, but the mechanisms remain unclear. Previous studies have shown that, in the paretic limb of people post-stroke, Group Ia reflexes are abnormally elevated and fail to decrease in amplitude during locomotion. Hence, we hypothesized that inappropriate muscle phasing may be associated with enhanced transmission in the monosynaptic Group Ia afferent pathway. Soleus (SO) H-reflexes were used to examine transmission in the Group Ia afferent pathway to SO motor neurons during pedaling, a locomotor task in which abnormal muscle phasing is evident. Our hypothesis predicted that H-reflexes would be elevated during the flexion phase of pedaling where inappropriate SO activity occurs. H-reflexes were elicited in paretic (n = 13) and neurologically intact (NI, n = 26) individuals at 11 different positions in the pedaling cycle and during tonic plantar flexion at comparable limb positions and levels of SO EMG. In both groups, SO H-reflexes were smaller during pedaling as compared to matched tonic plantar flexion. In the NI group, but not the paretic group, SO H-reflex amplitude was significantly modulated across the pedaling cycle. H-reflexes were large during extension and small during flexion. Reduced H-reflex modulation post-stroke was associated with the level of neuromuscular impairment as indicated by Fugl-Meyer score. However, regardless of impairment level, stroke subjects displayed H-reflex suppression during the flexion phase of pedaling. After correcting for the level of background muscle activity, H-reflexes were found to be larger in paretic as compared to NI individuals, regardless of the phase of the pedaling cycle. We conclude that Group Ia afferent transmission is enhanced in the paretic SO of people post-stroke as compared to NI individuals. However, contrary to our hypothesis, enhanced transmission in the Group Ia monosynaptic spinal pathway is not specifically associated with extraneous extensor muscle activity during the flexion phase of pedaling and is unlikely to account for abnormal locomotor muscle phasing post-stroke. This result is important because it suggests that, despite the presence of hyperactive monosynaptic reflexes post-stroke, this impairment may not make an important contribution to abnormal locomotor muscle activity.
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