Exercise effects in Huntington disease
Huntington disease (HD) is a relentlessly progressive neurodegenerative disorder with symptoms across a wide range of neurological domains, including cognitive and motor dysfunction. There is still no causative treatment for HD but environmental factors such as passive lifestyle may modulate disease...
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| Veröffentlicht in: | Journal of neurology 2017, Vol.264 (1), p.32-39 |
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| creator | Frese, Sebastian Petersen, Jens A. Ligon-Auer, Maria Mueller, Sandro Manuel Mihaylova, Violeta Gehrig, Saskia M. Kana, Veronika Rushing, Elisabeth J. Unterburger, Evelyn Kägi, Georg Burgunder, Jean-Marc Toigo, Marco Jung, Hans H. |
| description | Huntington disease (HD) is a relentlessly progressive neurodegenerative disorder with symptoms across a wide range of neurological domains, including cognitive and motor dysfunction. There is still no causative treatment for HD but environmental factors such as passive lifestyle may modulate disease onset and progression. In humans, multidisciplinary rehabilitation has a positive impact on cognitive functions. However, a specific role for exercise as a component of an environmental enrichment effect has been difficult to demonstrate. We aimed at investigating whether endurance training (ET) stabilizes the progression of motor and cognitive dysfunction and ameliorates cardiovascular function in HD patients. Twelve male HD patients (mean ± SD, 54.8 ± 7.1 years) and twelve male controls (49.1 ± 6.8 years) completed 26 weeks of endurance training. Before and after the training intervention, clinical assessments, exercise physiological tests, and a body composition measurement were conducted and a muscle biopsy was taken from M. vastus lateralis. To examine the natural course of the disease, HD patients were additionally assessed 6 months prior to ET. During the ET period, there was a motor deficit stabilization as indicated by the Unified Huntington’s Disease Rating Scale motor section score in HD patients (baseline: 18.6 ± 9.2, pre-training: 26.0 ± 13.7, post-training: 26.8 ± 16.4). Peak oxygen uptake (
V
˙
O
2
peak
) significantly increased in HD patients (∆
V
˙
O
2
peak
= +0.33 ± 0.28 l) and controls (∆
V
˙
O
2
peak
= +0.29 ± 0.41 l). No adverse effects of the training intervention were reported. Our results confirm that HD patients are amenable to a specific exercise-induced therapeutic strategy indicated by an increased cardiovascular function and a stabilization of motor function. |
| doi_str_mv | 10.1007/s00415-016-8310-1 |
| format | Article |
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V
˙
O
2
peak
) significantly increased in HD patients (∆
V
˙
O
2
peak
= +0.33 ± 0.28 l) and controls (∆
V
˙
O
2
peak
= +0.29 ± 0.41 l). No adverse effects of the training intervention were reported. Our results confirm that HD patients are amenable to a specific exercise-induced therapeutic strategy indicated by an increased cardiovascular function and a stabilization of motor function.</description><identifier>ISSN: 0340-5354</identifier><identifier>EISSN: 1432-1459</identifier><identifier>DOI: 10.1007/s00415-016-8310-1</identifier><identifier>PMID: 27747393</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Bicycling - physiology ; Bicycling - psychology ; Body Mass Index ; Cognition & reasoning ; Cognitive ability ; Dementia ; Exercise ; Exercise Therapy - methods ; Hospitals ; Humans ; Huntington Disease - genetics ; Huntington Disease - physiopathology ; Huntington Disease - psychology ; Huntington Disease - therapy ; Huntingtons disease ; Male ; Maximum oxygen consumption ; Medicine ; Medicine & Public Health ; Middle Aged ; Motor Activity - physiology ; Neurology ; Neuropsychological Tests ; Neuroradiology ; Neurosciences ; Original Communication ; Oxygen Consumption - physiology ; Physical Endurance - physiology ; Physical fitness ; Psychiatric Status Rating Scales ; Severity of Illness Index ; Treatment Outcome ; Verbal learning</subject><ispartof>Journal of neurology, 2017, Vol.264 (1), p.32-39</ispartof><rights>Springer-Verlag Berlin Heidelberg 2016</rights><rights>Journal of Neurology is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-b82d8098b22b36f1294feb7f1b86b0fc80c09573dc97a7c573b4dcf9e1fc73a43</citedby><cites>FETCH-LOGICAL-c405t-b82d8098b22b36f1294feb7f1b86b0fc80c09573dc97a7c573b4dcf9e1fc73a43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00415-016-8310-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00415-016-8310-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27747393$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Frese, Sebastian</creatorcontrib><creatorcontrib>Petersen, Jens A.</creatorcontrib><creatorcontrib>Ligon-Auer, Maria</creatorcontrib><creatorcontrib>Mueller, Sandro Manuel</creatorcontrib><creatorcontrib>Mihaylova, Violeta</creatorcontrib><creatorcontrib>Gehrig, Saskia M.</creatorcontrib><creatorcontrib>Kana, Veronika</creatorcontrib><creatorcontrib>Rushing, Elisabeth J.</creatorcontrib><creatorcontrib>Unterburger, Evelyn</creatorcontrib><creatorcontrib>Kägi, Georg</creatorcontrib><creatorcontrib>Burgunder, Jean-Marc</creatorcontrib><creatorcontrib>Toigo, Marco</creatorcontrib><creatorcontrib>Jung, Hans H.</creatorcontrib><title>Exercise effects in Huntington disease</title><title>Journal of neurology</title><addtitle>J Neurol</addtitle><addtitle>J Neurol</addtitle><description>Huntington disease (HD) is a relentlessly progressive neurodegenerative disorder with symptoms across a wide range of neurological domains, including cognitive and motor dysfunction. There is still no causative treatment for HD but environmental factors such as passive lifestyle may modulate disease onset and progression. In humans, multidisciplinary rehabilitation has a positive impact on cognitive functions. However, a specific role for exercise as a component of an environmental enrichment effect has been difficult to demonstrate. We aimed at investigating whether endurance training (ET) stabilizes the progression of motor and cognitive dysfunction and ameliorates cardiovascular function in HD patients. Twelve male HD patients (mean ± SD, 54.8 ± 7.1 years) and twelve male controls (49.1 ± 6.8 years) completed 26 weeks of endurance training. Before and after the training intervention, clinical assessments, exercise physiological tests, and a body composition measurement were conducted and a muscle biopsy was taken from M. vastus lateralis. To examine the natural course of the disease, HD patients were additionally assessed 6 months prior to ET. During the ET period, there was a motor deficit stabilization as indicated by the Unified Huntington’s Disease Rating Scale motor section score in HD patients (baseline: 18.6 ± 9.2, pre-training: 26.0 ± 13.7, post-training: 26.8 ± 16.4). Peak oxygen uptake (
V
˙
O
2
peak
) significantly increased in HD patients (∆
V
˙
O
2
peak
= +0.33 ± 0.28 l) and controls (∆
V
˙
O
2
peak
= +0.29 ± 0.41 l). No adverse effects of the training intervention were reported. Our results confirm that HD patients are amenable to a specific exercise-induced therapeutic strategy indicated by an increased cardiovascular function and a stabilization of motor function.</description><subject>Bicycling - physiology</subject><subject>Bicycling - psychology</subject><subject>Body Mass Index</subject><subject>Cognition & reasoning</subject><subject>Cognitive ability</subject><subject>Dementia</subject><subject>Exercise</subject><subject>Exercise Therapy - methods</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Huntington Disease - genetics</subject><subject>Huntington Disease - physiopathology</subject><subject>Huntington Disease - psychology</subject><subject>Huntington Disease - therapy</subject><subject>Huntingtons disease</subject><subject>Male</subject><subject>Maximum oxygen consumption</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Motor Activity - physiology</subject><subject>Neurology</subject><subject>Neuropsychological Tests</subject><subject>Neuroradiology</subject><subject>Neurosciences</subject><subject>Original Communication</subject><subject>Oxygen Consumption - physiology</subject><subject>Physical Endurance - physiology</subject><subject>Physical fitness</subject><subject>Psychiatric Status Rating Scales</subject><subject>Severity of Illness Index</subject><subject>Treatment Outcome</subject><subject>Verbal learning</subject><issn>0340-5354</issn><issn>1432-1459</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkE1LAzEURYMotlZ_gBspCOIm-vI1SZZS6gcU3Og6TDJJmdLO1GQG9N-bMlVEEFwlcM-7j3cQOidwQwDkbQLgRGAgBVaMACYHaEw4o5hwoQ_RGBgHLJjgI3SS0goAVA6O0YhKySXTbIyu5u8-ujr5qQ_Buy5N62b62Ddd3Sy7tplWOSqTP0VHoVwnf7Z_J-j1fv4ye8SL54en2d0COw6iw1bRSoFWllLLikCo5sFbGYhVhYXgFDjQQrLKaVlKl3-WVy5oT4KTrORsgq6H3m1s33qfOrOpk_Prddn4tk-GqEIx4FDQf6D5cE6Ulhm9_IWu2j42-ZBMCUm5oGK3mwyUi21K0QezjfWmjB-GgNn5NoNvk32bnW9D8szFvrm3G199T3wJzgAdgJSjZunjj9V_tn4CkwaH-g</recordid><startdate>2017</startdate><enddate>2017</enddate><creator>Frese, Sebastian</creator><creator>Petersen, Jens A.</creator><creator>Ligon-Auer, Maria</creator><creator>Mueller, Sandro Manuel</creator><creator>Mihaylova, Violeta</creator><creator>Gehrig, Saskia M.</creator><creator>Kana, Veronika</creator><creator>Rushing, Elisabeth J.</creator><creator>Unterburger, Evelyn</creator><creator>Kägi, Georg</creator><creator>Burgunder, Jean-Marc</creator><creator>Toigo, Marco</creator><creator>Jung, Hans H.</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>2017</creationdate><title>Exercise effects in Huntington disease</title><author>Frese, Sebastian ; 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There is still no causative treatment for HD but environmental factors such as passive lifestyle may modulate disease onset and progression. In humans, multidisciplinary rehabilitation has a positive impact on cognitive functions. However, a specific role for exercise as a component of an environmental enrichment effect has been difficult to demonstrate. We aimed at investigating whether endurance training (ET) stabilizes the progression of motor and cognitive dysfunction and ameliorates cardiovascular function in HD patients. Twelve male HD patients (mean ± SD, 54.8 ± 7.1 years) and twelve male controls (49.1 ± 6.8 years) completed 26 weeks of endurance training. Before and after the training intervention, clinical assessments, exercise physiological tests, and a body composition measurement were conducted and a muscle biopsy was taken from M. vastus lateralis. To examine the natural course of the disease, HD patients were additionally assessed 6 months prior to ET. During the ET period, there was a motor deficit stabilization as indicated by the Unified Huntington’s Disease Rating Scale motor section score in HD patients (baseline: 18.6 ± 9.2, pre-training: 26.0 ± 13.7, post-training: 26.8 ± 16.4). Peak oxygen uptake (
V
˙
O
2
peak
) significantly increased in HD patients (∆
V
˙
O
2
peak
= +0.33 ± 0.28 l) and controls (∆
V
˙
O
2
peak
= +0.29 ± 0.41 l). No adverse effects of the training intervention were reported. Our results confirm that HD patients are amenable to a specific exercise-induced therapeutic strategy indicated by an increased cardiovascular function and a stabilization of motor function.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>27747393</pmid><doi>10.1007/s00415-016-8310-1</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0340-5354 |
| ispartof | Journal of neurology, 2017, Vol.264 (1), p.32-39 |
| issn | 0340-5354 1432-1459 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1868304062 |
| source | MEDLINE; SpringerLink Journals |
| subjects | Bicycling - physiology Bicycling - psychology Body Mass Index Cognition & reasoning Cognitive ability Dementia Exercise Exercise Therapy - methods Hospitals Humans Huntington Disease - genetics Huntington Disease - physiopathology Huntington Disease - psychology Huntington Disease - therapy Huntingtons disease Male Maximum oxygen consumption Medicine Medicine & Public Health Middle Aged Motor Activity - physiology Neurology Neuropsychological Tests Neuroradiology Neurosciences Original Communication Oxygen Consumption - physiology Physical Endurance - physiology Physical fitness Psychiatric Status Rating Scales Severity of Illness Index Treatment Outcome Verbal learning |
| title | Exercise effects in Huntington disease |
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