Corticospinal excitability of tibialis anterior and soleus differs during passive ankle movement

Abstract

The purpose of this study was to assess corticospinal excitability of soleus (SOL) and tibialis anterior (TA) at a segmental level during passive ankle movement. Four experimental components were performed to assess the effects of passive ankle movement and muscle length on corticospinal excitability (MEP/ M max ) at different muscle lengths, subcortical excitability at the level of lumbar spinal segments (LEP/ M max ), intracortical inhibition (SICI) and facilitation (ICF), and H -reflex in SOL and TA. In addition, the degree of fascicle length changes between SOL and TA was assessed in a subpopulation during passive ankle movement. Fascicles shortened and lengthened with joint movement during passive shortening and lengthening of SOL and TA to a similar degree ( p < 0.001). Resting motor threshold was greater in SOL compared to TA ( p ≤ 0.014). MEP/ M max was facilitated in TA during passive shortening relative to the static position ( p ≤ 0.023) and passive lengthening ( p ≤ 0.001), but remained similar during passive ankle movement in SOL ( p ≥ 0.497), regardless of muscle length at the point of stimulus ( p = 0.922). LEP/ M max (SOL: p = 0.075, TA: p = 0.071), SICI (SOL: p = 0.427, TA: p = 0.540), and ICF (SOL: p = 0.177, TA: p = 0.777) remained similar during passive ankle movement. H -reflex was not different across conditions in TA ( p = 0.258), but was reduced during passive lengthening compared to shortening in SOL ( p = 0.048). These results suggest a differential modulation of corticospinal excitability between plantar and dorsiflexors during passive movement. The corticospinal behaviour observed might be mediated by an increase in corticospinal drive as a result of reduced afferent input during muscle shortening and appears to be flexor-biased.

Corticospinal responses during passive shortening and lengthening of tibialis anterior and soleus in older compared to younger adults

“…The firing of muscle spindle afferents increases proportionally to the magnitude of the muscle stretch, but remains low during muscle shortening (Matthews, ). This behaviour influences corticospinal responses; in both upper and lower limb musculature, it has been shown that passive shortening and lengthening are accompanied by increased and decreased corticospinal excitability, respectively (Lewis & Byblow, ; Lewis, Byblow, & Carson, ; Škarabot et al., ). However, the magnitude of change in corticospinal excitability with passive movement might still depend on the muscle investigated (Chye, Nosaka, Murray, Edwards, & Thickbroom, ; Škarabot et al., ), with no modulation having been shown for soleus (SOL) in contrast to tibialis anterior (TA; Škarabot et al., ).…”

“…This behaviour influences corticospinal responses; in both upper and lower limb musculature, it has been shown that passive shortening and lengthening are accompanied by increased and decreased corticospinal excitability, respectively (Lewis & Byblow, ; Lewis, Byblow, & Carson, ; Škarabot et al., ). However, the magnitude of change in corticospinal excitability with passive movement might still depend on the muscle investigated (Chye, Nosaka, Murray, Edwards, & Thickbroom, ; Škarabot et al., ), with no modulation having been shown for soleus (SOL) in contrast to tibialis anterior (TA; Škarabot et al., ). Our recent work showed that passive ankle movement does not influence intracortical inhibitory or facilitatory neurons, or subcortical excitability, thus suggesting that modulation of corticospinal excitability with passive muscle length changes is mediated by the cortical neurons (Škarabot et al., ).…”

“…However, the magnitude of change in corticospinal excitability with passive movement might still depend on the muscle investigated (Chye, Nosaka, Murray, Edwards, & Thickbroom, ; Škarabot et al., ), with no modulation having been shown for soleus (SOL) in contrast to tibialis anterior (TA; Škarabot et al., ). Our recent work showed that passive ankle movement does not influence intracortical inhibitory or facilitatory neurons, or subcortical excitability, thus suggesting that modulation of corticospinal excitability with passive muscle length changes is mediated by the cortical neurons (Škarabot et al., ). Based on primate data, information regarding changes in muscle length is integrated directly into the primary motor cortex via group II afferents, or indirectly into the sensorimotor cortex via Ia afferents mediated by inhibitory interneurons (Hore, Preston, & Cheney, ).…”

“…These muscles were chosen due to their integral role in locomotion (TA; Byrne, O'Keeffe, Donnelly, & Lyons, ) and postural stability (SOL; Capaday, Lavoie, Barbeau, Schneider, & Bonnard, ). The experimental set‐up was replicated from recent work in our laboratory investigating a similar research question in younger adults (Škarabot et al., ). To allow for a direct comparison between young and older adults and importantly characterise any age‐related alterations in function, previously published data from young individuals were pooled, and re‐analysed (Škarabot et al., ).…”

“…The experimental set‐up was replicated from recent work in our laboratory investigating a similar research question in younger adults (Škarabot et al., ). To allow for a direct comparison between young and older adults and importantly characterise any age‐related alterations in function, previously published data from young individuals were pooled, and re‐analysed (Škarabot et al., ).…”