Motor cortex plasticity response to acute cardiorespiratory exercise and intermittent theta-burst stimulation is attenuated in premanifest and early Huntington’s disease
Abstract Huntington’s disease (HD) mouse models suggest that cardiovascular exercise may enhance neuroplasticity and delay disease signs, however, the effects of exercise on neuroplasticity in people with HD are unknown. Using a repeated-measures experimental design, we compared the effects of a sin...
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Nature Portfolio
2022-01-01
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Series: | Scientific Reports |
Online Access: | https://doi.org/10.1038/s41598-021-04378-2 |
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author | Sophie C. Andrews Dylan Curtin James P. Coxon Julie C. Stout |
author_facet | Sophie C. Andrews Dylan Curtin James P. Coxon Julie C. Stout |
author_sort | Sophie C. Andrews |
collection | DOAJ |
description | Abstract Huntington’s disease (HD) mouse models suggest that cardiovascular exercise may enhance neuroplasticity and delay disease signs, however, the effects of exercise on neuroplasticity in people with HD are unknown. Using a repeated-measures experimental design, we compared the effects of a single bout of high-intensity exercise, moderate-intensity exercise, or rest, on motor cortex synaptic plasticity in 14 HD CAG-expanded participants (9 premanifest and 5 early manifest) and 20 CAG-healthy control participants, using transcranial magnetic stimulation. Measures of cortico-motor excitability, short-interval intracortical inhibition and intracortical facilitation were obtained before and after a 20-min bout of either high-intensity interval exercise, moderate-intensity continuous exercise, or rest, and again after intermittent theta burst stimulation (iTBS). HD participants showed less inhibition at baseline compared to controls. Whereas the control group showed increased excitability and facilitation following high-intensity exercise and iTBS, the HD group showed no differences in neuroplasticity responses following either exercise intensity or rest, with follow-up Bayesian analyses providing consistent evidence that these effects were absent in the HD group. These findings indicate that exercise-induced synaptic plasticity mechanisms in response to acute exercise may be attenuated in HD, and demonstrate the need for future research to further investigate exercise and plasticity mechanisms in people with HD. |
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language | English |
last_indexed | 2024-12-13T13:46:17Z |
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spelling | doaj.art-dc899624c21f42869b3faac61925cc4d2022-12-21T23:43:26ZengNature PortfolioScientific Reports2045-23222022-01-0112111110.1038/s41598-021-04378-2Motor cortex plasticity response to acute cardiorespiratory exercise and intermittent theta-burst stimulation is attenuated in premanifest and early Huntington’s diseaseSophie C. Andrews0Dylan Curtin1James P. Coxon2Julie C. Stout3School of Psychological Sciences and Turner Institute for Brain and Mental Health, Monash UniversitySchool of Psychological Sciences and Turner Institute for Brain and Mental Health, Monash UniversitySchool of Psychological Sciences and Turner Institute for Brain and Mental Health, Monash UniversitySchool of Psychological Sciences and Turner Institute for Brain and Mental Health, Monash UniversityAbstract Huntington’s disease (HD) mouse models suggest that cardiovascular exercise may enhance neuroplasticity and delay disease signs, however, the effects of exercise on neuroplasticity in people with HD are unknown. Using a repeated-measures experimental design, we compared the effects of a single bout of high-intensity exercise, moderate-intensity exercise, or rest, on motor cortex synaptic plasticity in 14 HD CAG-expanded participants (9 premanifest and 5 early manifest) and 20 CAG-healthy control participants, using transcranial magnetic stimulation. Measures of cortico-motor excitability, short-interval intracortical inhibition and intracortical facilitation were obtained before and after a 20-min bout of either high-intensity interval exercise, moderate-intensity continuous exercise, or rest, and again after intermittent theta burst stimulation (iTBS). HD participants showed less inhibition at baseline compared to controls. Whereas the control group showed increased excitability and facilitation following high-intensity exercise and iTBS, the HD group showed no differences in neuroplasticity responses following either exercise intensity or rest, with follow-up Bayesian analyses providing consistent evidence that these effects were absent in the HD group. These findings indicate that exercise-induced synaptic plasticity mechanisms in response to acute exercise may be attenuated in HD, and demonstrate the need for future research to further investigate exercise and plasticity mechanisms in people with HD.https://doi.org/10.1038/s41598-021-04378-2 |
spellingShingle | Sophie C. Andrews Dylan Curtin James P. Coxon Julie C. Stout Motor cortex plasticity response to acute cardiorespiratory exercise and intermittent theta-burst stimulation is attenuated in premanifest and early Huntington’s disease Scientific Reports |
title | Motor cortex plasticity response to acute cardiorespiratory exercise and intermittent theta-burst stimulation is attenuated in premanifest and early Huntington’s disease |
title_full | Motor cortex plasticity response to acute cardiorespiratory exercise and intermittent theta-burst stimulation is attenuated in premanifest and early Huntington’s disease |
title_fullStr | Motor cortex plasticity response to acute cardiorespiratory exercise and intermittent theta-burst stimulation is attenuated in premanifest and early Huntington’s disease |
title_full_unstemmed | Motor cortex plasticity response to acute cardiorespiratory exercise and intermittent theta-burst stimulation is attenuated in premanifest and early Huntington’s disease |
title_short | Motor cortex plasticity response to acute cardiorespiratory exercise and intermittent theta-burst stimulation is attenuated in premanifest and early Huntington’s disease |
title_sort | motor cortex plasticity response to acute cardiorespiratory exercise and intermittent theta burst stimulation is attenuated in premanifest and early huntington s disease |
url | https://doi.org/10.1038/s41598-021-04378-2 |
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