Peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation

Abstract Maximal-rate rhythmic repetitive movements cannot be sustained for very long, even if unresisted. Peripheral and central mechanisms of fatigue, such as the slowing of muscle relaxation and an increase in M1-GABAb inhibition, act alongside the reduction of maximal execution rates. However, m...

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Autores principales: Elena Madinabeitia-Mancebo, Antonio Madrid, Antonio Oliviero, Javier Cudeiro, Pablo Arias
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/cbb6327e4d9846a2a0c4cda1f4781a81
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spelling oai:doaj.org-article:cbb6327e4d9846a2a0c4cda1f4781a812021-12-02T10:49:34ZPeripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation10.1038/s41598-020-80743-x2045-2322https://doaj.org/article/cbb6327e4d9846a2a0c4cda1f4781a812021-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-80743-xhttps://doaj.org/toc/2045-2322Abstract Maximal-rate rhythmic repetitive movements cannot be sustained for very long, even if unresisted. Peripheral and central mechanisms of fatigue, such as the slowing of muscle relaxation and an increase in M1-GABAb inhibition, act alongside the reduction of maximal execution rates. However, maximal muscle force appears unaffected, and it is unknown whether the increased excitability of M1 GABAergic interneurons is an adaptation to the waning of muscle contractility in these movements. Here, we observed increased M1 GABAb inhibition at the end of 30 s of a maximal-rate finger-tapping (FT) task that caused fatigue and muscle slowdown in a sample of 19 healthy participants. The former recovered a few seconds after FT ended, regardless of whether muscle ischaemia was used to keep the muscle slowed down. Therefore, the increased excitability of M1-GABAb circuits does not appear to be mediated by afferent feedback from the muscle. In the same subjects, continuous (inhibitory) and intermittent (excitatory) theta-burst stimulation (TBS) was used to modulate M1 excitability and to understand the underlying central mechanisms within the motor cortex. The effect produced by TBS on M1 excitability did not affect FT performance. We conclude that fatigue during brief, maximal-rate unresisted repetitive movements has supraspinal components, with origins upstream of the motor cortex.Elena Madinabeitia-ManceboAntonio MadridAntonio OlivieroJavier CudeiroPablo AriasNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Elena Madinabeitia-Mancebo
Antonio Madrid
Antonio Oliviero
Javier Cudeiro
Pablo Arias
Peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation
description Abstract Maximal-rate rhythmic repetitive movements cannot be sustained for very long, even if unresisted. Peripheral and central mechanisms of fatigue, such as the slowing of muscle relaxation and an increase in M1-GABAb inhibition, act alongside the reduction of maximal execution rates. However, maximal muscle force appears unaffected, and it is unknown whether the increased excitability of M1 GABAergic interneurons is an adaptation to the waning of muscle contractility in these movements. Here, we observed increased M1 GABAb inhibition at the end of 30 s of a maximal-rate finger-tapping (FT) task that caused fatigue and muscle slowdown in a sample of 19 healthy participants. The former recovered a few seconds after FT ended, regardless of whether muscle ischaemia was used to keep the muscle slowed down. Therefore, the increased excitability of M1-GABAb circuits does not appear to be mediated by afferent feedback from the muscle. In the same subjects, continuous (inhibitory) and intermittent (excitatory) theta-burst stimulation (TBS) was used to modulate M1 excitability and to understand the underlying central mechanisms within the motor cortex. The effect produced by TBS on M1 excitability did not affect FT performance. We conclude that fatigue during brief, maximal-rate unresisted repetitive movements has supraspinal components, with origins upstream of the motor cortex.
format article
author Elena Madinabeitia-Mancebo
Antonio Madrid
Antonio Oliviero
Javier Cudeiro
Pablo Arias
author_facet Elena Madinabeitia-Mancebo
Antonio Madrid
Antonio Oliviero
Javier Cudeiro
Pablo Arias
author_sort Elena Madinabeitia-Mancebo
title Peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation
title_short Peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation
title_full Peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation
title_fullStr Peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation
title_full_unstemmed Peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and M1 neuromodulation
title_sort peripheral-central interplay for fatiguing unresisted repetitive movements: a study using muscle ischaemia and m1 neuromodulation
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/cbb6327e4d9846a2a0c4cda1f4781a81
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