Human motor fatigability as evoked by repetitive movements results from a gradual breakdown of surround inhibition. / Baechinger, Marc; Lehner, Rea; Thomas, Felix; Hanimann, Samira; Balsters, Joshua; Wenderoth, Nicole.

In: eLife, Vol. 8, e46750, 16.09.2019, p. 1-30.

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Human motor fatigability as evoked by repetitive movements results from a gradual breakdown of surround inhibition. / Baechinger, Marc; Lehner, Rea; Thomas, Felix; Hanimann, Samira; Balsters, Joshua; Wenderoth, Nicole.

In: eLife, Vol. 8, e46750, 16.09.2019, p. 1-30.

Research output: Contribution to journalArticle

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Baechinger, Marc ; Lehner, Rea ; Thomas, Felix ; Hanimann, Samira ; Balsters, Joshua ; Wenderoth, Nicole. / Human motor fatigability as evoked by repetitive movements results from a gradual breakdown of surround inhibition. In: eLife. 2019 ; Vol. 8. pp. 1-30.

BibTeX

@article{d6902de1c91244f08c222ecef026bcf9,
title = "Human motor fatigability as evoked by repetitive movements results from a gradual breakdown of surround inhibition",
abstract = "Motor fatigability emerges when demanding task are executed over an extended period of time. Here, we used repetitive low-force movements that cause a gradual reduction in movement speed (or “motor slowing”) to study the central component of fatigability in healthy adults. We show that motor slowing is associated with a gradual increase of net excitability in the motor network and, specifically, in primary motor cortex (M1), which results from overall disinhibition. Importantly, we link performance decrements to a breakdown of surround inhibition in M1, which is associated with high coactivation of antagonistic muscle groups. This is consistent with the model that a loss of inhibitory control might broaden the tuning of population vectors such that movement patterns become more variable, ill-timed and effortful. We propose that the release of inhibition in M1 is an important mechanism underpinning motor fatigability and, potentially, also pathological fatigue as frequently observed in patients with brain disorders. ",
keywords = "Fatigue, motor slowing, repetitive movements, functional magnetic resonance imaging, electrophysiology, Transcranial magnetic stimulation",
author = "Marc Baechinger and Rea Lehner and Felix Thomas and Samira Hanimann and Joshua Balsters and Nicole Wenderoth",
year = "2019",
month = sep,
day = "16",
doi = "10.7554/eLife.46750",
language = "English",
volume = "8",
pages = "1--30",
journal = "eLife",
issn = "2050-084X",
publisher = "eLife Sciences Publications",

}

RIS

TY - JOUR

T1 - Human motor fatigability as evoked by repetitive movements results from a gradual breakdown of surround inhibition

AU - Baechinger, Marc

AU - Lehner, Rea

AU - Thomas, Felix

AU - Hanimann, Samira

AU - Balsters, Joshua

AU - Wenderoth, Nicole

PY - 2019/9/16

Y1 - 2019/9/16

N2 - Motor fatigability emerges when demanding task are executed over an extended period of time. Here, we used repetitive low-force movements that cause a gradual reduction in movement speed (or “motor slowing”) to study the central component of fatigability in healthy adults. We show that motor slowing is associated with a gradual increase of net excitability in the motor network and, specifically, in primary motor cortex (M1), which results from overall disinhibition. Importantly, we link performance decrements to a breakdown of surround inhibition in M1, which is associated with high coactivation of antagonistic muscle groups. This is consistent with the model that a loss of inhibitory control might broaden the tuning of population vectors such that movement patterns become more variable, ill-timed and effortful. We propose that the release of inhibition in M1 is an important mechanism underpinning motor fatigability and, potentially, also pathological fatigue as frequently observed in patients with brain disorders.

AB - Motor fatigability emerges when demanding task are executed over an extended period of time. Here, we used repetitive low-force movements that cause a gradual reduction in movement speed (or “motor slowing”) to study the central component of fatigability in healthy adults. We show that motor slowing is associated with a gradual increase of net excitability in the motor network and, specifically, in primary motor cortex (M1), which results from overall disinhibition. Importantly, we link performance decrements to a breakdown of surround inhibition in M1, which is associated with high coactivation of antagonistic muscle groups. This is consistent with the model that a loss of inhibitory control might broaden the tuning of population vectors such that movement patterns become more variable, ill-timed and effortful. We propose that the release of inhibition in M1 is an important mechanism underpinning motor fatigability and, potentially, also pathological fatigue as frequently observed in patients with brain disorders.

KW - Fatigue

KW - motor slowing

KW - repetitive movements

KW - functional magnetic resonance imaging

KW - electrophysiology

KW - Transcranial magnetic stimulation

U2 - 10.7554/eLife.46750

DO - 10.7554/eLife.46750

M3 - Article

VL - 8

SP - 1

EP - 30

JO - eLife

JF - eLife

SN - 2050-084X

M1 - e46750

ER -