Reflex excitation of muscles during human walking

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Reflex excitation of muscles during human walking. / Nielsen, Jens Bo; Sinkjær, Thomas.

In: Advances in Experimental Medicine and Biology, Vol. 508, 2002, p. 369-375.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Nielsen, JB & Sinkjær, T 2002, 'Reflex excitation of muscles during human walking', Advances in Experimental Medicine and Biology, vol. 508, pp. 369-375. https://doi.org/10.1007/978-1-4615-0713-0_42

APA

Nielsen, J. B., & Sinkjær, T. (2002). Reflex excitation of muscles during human walking. Advances in Experimental Medicine and Biology, 508, 369-375. https://doi.org/10.1007/978-1-4615-0713-0_42

Vancouver

Nielsen JB, Sinkjær T. Reflex excitation of muscles during human walking. Advances in Experimental Medicine and Biology. 2002;508:369-375. https://doi.org/10.1007/978-1-4615-0713-0_42

Author

Nielsen, Jens Bo ; Sinkjær, Thomas. / Reflex excitation of muscles during human walking. In: Advances in Experimental Medicine and Biology. 2002 ; Vol. 508. pp. 369-375.

Bibtex

@article{96b8517365d543d0bfa099bf3f221fc1,
title = "Reflex excitation of muscles during human walking",
abstract = "Sensory activity may contribute to the control of human walking in two different ways. It may contribute to the pre-programmed drive to the motoneurones and to the reactions to unexpected external perturbations. Some recent findings in relation to these two different roles of sensory activity will be reviewed. When unloading the ankle plantarflexors in the stance phase of walking a drop in the soleus EMG activity is seen at a latency of around 60 ms. This drop is likely caused by the removal of the contribution of Gp II afferents from the ankle plantarflexors to the motoneuronal drive. When stretching plantarflexor muscles in the stance phase three reflex responses are generally observed. These responses may be caused by the spinal monosynaptic Ia reflex pathway, a spinal Gp II pathway and a transcortical reflex pathway, respectively. The reflex responses are modulated with the background EMG activity and may not be evoked in the swing phase when the plantarflexors are not active. In contrast, stretch of the ankle dorsiflexor muscles evoke relatively small responses in the swing phase when these muscles are active, but very large responses in the stance phase when the muscles are silent. Part of these responses may have a transcortical nature. These findings illustrate the complexity with which sensory input may contribute to the ongoing muscle activity during walking and may also mediate adequate responses to sudden external perturbations.",
author = "Nielsen, {Jens Bo} and Thomas Sinkj{\ae}r",
year = "2002",
doi = "10.1007/978-1-4615-0713-0_42",
language = "English",
volume = "508",
pages = "369--375",
journal = "Advances in Experimental Medicine and Biology",
issn = "0065-2598",
publisher = "Springer",

}

RIS

TY - JOUR

T1 - Reflex excitation of muscles during human walking

AU - Nielsen, Jens Bo

AU - Sinkjær, Thomas

PY - 2002

Y1 - 2002

N2 - Sensory activity may contribute to the control of human walking in two different ways. It may contribute to the pre-programmed drive to the motoneurones and to the reactions to unexpected external perturbations. Some recent findings in relation to these two different roles of sensory activity will be reviewed. When unloading the ankle plantarflexors in the stance phase of walking a drop in the soleus EMG activity is seen at a latency of around 60 ms. This drop is likely caused by the removal of the contribution of Gp II afferents from the ankle plantarflexors to the motoneuronal drive. When stretching plantarflexor muscles in the stance phase three reflex responses are generally observed. These responses may be caused by the spinal monosynaptic Ia reflex pathway, a spinal Gp II pathway and a transcortical reflex pathway, respectively. The reflex responses are modulated with the background EMG activity and may not be evoked in the swing phase when the plantarflexors are not active. In contrast, stretch of the ankle dorsiflexor muscles evoke relatively small responses in the swing phase when these muscles are active, but very large responses in the stance phase when the muscles are silent. Part of these responses may have a transcortical nature. These findings illustrate the complexity with which sensory input may contribute to the ongoing muscle activity during walking and may also mediate adequate responses to sudden external perturbations.

AB - Sensory activity may contribute to the control of human walking in two different ways. It may contribute to the pre-programmed drive to the motoneurones and to the reactions to unexpected external perturbations. Some recent findings in relation to these two different roles of sensory activity will be reviewed. When unloading the ankle plantarflexors in the stance phase of walking a drop in the soleus EMG activity is seen at a latency of around 60 ms. This drop is likely caused by the removal of the contribution of Gp II afferents from the ankle plantarflexors to the motoneuronal drive. When stretching plantarflexor muscles in the stance phase three reflex responses are generally observed. These responses may be caused by the spinal monosynaptic Ia reflex pathway, a spinal Gp II pathway and a transcortical reflex pathway, respectively. The reflex responses are modulated with the background EMG activity and may not be evoked in the swing phase when the plantarflexors are not active. In contrast, stretch of the ankle dorsiflexor muscles evoke relatively small responses in the swing phase when these muscles are active, but very large responses in the stance phase when the muscles are silent. Part of these responses may have a transcortical nature. These findings illustrate the complexity with which sensory input may contribute to the ongoing muscle activity during walking and may also mediate adequate responses to sudden external perturbations.

UR - http://www.scopus.com/inward/record.url?scp=0036354989&partnerID=8YFLogxK

U2 - 10.1007/978-1-4615-0713-0_42

DO - 10.1007/978-1-4615-0713-0_42

M3 - Journal article

C2 - 12171132

AN - SCOPUS:0036354989

VL - 508

SP - 369

EP - 375

JO - Advances in Experimental Medicine and Biology

JF - Advances in Experimental Medicine and Biology

SN - 0065-2598

ER -

ID: 237411510