Neuromuscular Electrical Stimulation and Anabolic Signaling in Patients with Stroke
Stroke results in limited ability to produce voluntary muscle contraction and movement on one side of the body, leading to further muscle wasting and weakness. Neuromuscular electrical stimulation is often used to facilitate involuntary muscle contraction; however, the effect of neuromuscular electr...
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Veröffentlicht in: | Journal of stroke and cerebrovascular diseases 2017-12, Vol.26 (12), p.2954-2963 |
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description | Stroke results in limited ability to produce voluntary muscle contraction and movement on one side of the body, leading to further muscle wasting and weakness. Neuromuscular electrical stimulation is often used to facilitate involuntary muscle contraction; however, the effect of neuromuscular electrical stimulation on muscle growth and strengthening processes in hemiparetic muscle is not clear. This study examined the skeletal muscle anabolic response of an acute bout of neuromuscular electrical stimulation in individuals with chronic stroke and healthy older adults.
Eleven individuals (59.8 ± 2.7 years old) were divided into a chronic stroke group (n = 5) and a healthy older adult control group (n = 6). Muscle biopsies were obtained before and after stimulation from the vastus lateralis of the hemiparetic leg for the stroke group and the right leg for the control group. The neuromuscular electrical stimulation protocol consisted of a 60-minute, intermittent stimulation train at 60 Hz. Phosphorylation of mammalian target of rapamycin and ribosomal protein S6 kinase beta-1 were analyzed by Western blot.
An acute bout of neuromuscular electrical stimulation increased phosphorylation of mammalian target of rapamycin (stroke: 56.0%; control: 51.4%; P = .002) and ribosomal protein S6 kinase beta-1 (stroke: 131.2%; control: 156.3%; P = .002) from resting levels to post-neuromuscular electrical stimulation treatment, respectively. Phosphorylated protein content was similar between stroke and control groups at both time points.
Findings suggest that paretic muscles of patients with chronic stroke may maintain ability to stimulate protein synthesis machinery in response to neuromuscular electrical stimulation. |
doi_str_mv | 10.1016/j.jstrokecerebrovasdis.2017.07.019 |
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Eleven individuals (59.8 ± 2.7 years old) were divided into a chronic stroke group (n = 5) and a healthy older adult control group (n = 6). Muscle biopsies were obtained before and after stimulation from the vastus lateralis of the hemiparetic leg for the stroke group and the right leg for the control group. The neuromuscular electrical stimulation protocol consisted of a 60-minute, intermittent stimulation train at 60 Hz. Phosphorylation of mammalian target of rapamycin and ribosomal protein S6 kinase beta-1 were analyzed by Western blot.
An acute bout of neuromuscular electrical stimulation increased phosphorylation of mammalian target of rapamycin (stroke: 56.0%; control: 51.4%; P = .002) and ribosomal protein S6 kinase beta-1 (stroke: 131.2%; control: 156.3%; P = .002) from resting levels to post-neuromuscular electrical stimulation treatment, respectively. Phosphorylated protein content was similar between stroke and control groups at both time points.
Findings suggest that paretic muscles of patients with chronic stroke may maintain ability to stimulate protein synthesis machinery in response to neuromuscular electrical stimulation.</description><identifier>ISSN: 1052-3057</identifier><identifier>EISSN: 1532-8511</identifier><identifier>DOI: 10.1016/j.jstrokecerebrovasdis.2017.07.019</identifier><identifier>PMID: 28823492</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Aged ; Case-Control Studies ; Electric Stimulation Therapy ; Female ; Humans ; Male ; Middle Aged ; mTORC1 ; Muscle Contraction ; Muscle Strength ; Neuromuscular ; Neuromuscular Junction - metabolism ; Neuromuscular Junction - physiopathology ; Paresis - diagnosis ; Paresis - metabolism ; Paresis - physiopathology ; Paresis - therapy ; paretic ; Phosphorylation ; Quadriceps Muscle - innervation ; Quadriceps Muscle - metabolism ; Ribosomal Protein S6 Kinases, 70-kDa - metabolism ; Signal Transduction ; skeletal muscle ; stimulation ; stroke ; Stroke - diagnosis ; Stroke - metabolism ; Stroke - physiopathology ; Stroke - therapy ; TOR Serine-Threonine Kinases - metabolism ; Treatment Outcome</subject><ispartof>Journal of stroke and cerebrovascular diseases, 2017-12, Vol.26 (12), p.2954-2963</ispartof><rights>2017 National Stroke Association</rights><rights>Copyright © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c404t-cbe13cb84196b23d7e803d6cd3291e88e1d7abc5f4f973e62ca8c893f138f223</citedby><cites>FETCH-LOGICAL-c404t-cbe13cb84196b23d7e803d6cd3291e88e1d7abc5f4f973e62ca8c893f138f223</cites><orcidid>0000-0001-8871-1787</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2017.07.019$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3549,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28823492$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mettler, Joni A.</creatorcontrib><creatorcontrib>Bennett, Sydney M.</creatorcontrib><creatorcontrib>Doucet, Barbara M.</creatorcontrib><creatorcontrib>Magee, Dillon M.</creatorcontrib><title>Neuromuscular Electrical Stimulation and Anabolic Signaling in Patients with Stroke</title><title>Journal of stroke and cerebrovascular diseases</title><addtitle>J Stroke Cerebrovasc Dis</addtitle><description>Stroke results in limited ability to produce voluntary muscle contraction and movement on one side of the body, leading to further muscle wasting and weakness. Neuromuscular electrical stimulation is often used to facilitate involuntary muscle contraction; however, the effect of neuromuscular electrical stimulation on muscle growth and strengthening processes in hemiparetic muscle is not clear. This study examined the skeletal muscle anabolic response of an acute bout of neuromuscular electrical stimulation in individuals with chronic stroke and healthy older adults.
Eleven individuals (59.8 ± 2.7 years old) were divided into a chronic stroke group (n = 5) and a healthy older adult control group (n = 6). Muscle biopsies were obtained before and after stimulation from the vastus lateralis of the hemiparetic leg for the stroke group and the right leg for the control group. The neuromuscular electrical stimulation protocol consisted of a 60-minute, intermittent stimulation train at 60 Hz. Phosphorylation of mammalian target of rapamycin and ribosomal protein S6 kinase beta-1 were analyzed by Western blot.
An acute bout of neuromuscular electrical stimulation increased phosphorylation of mammalian target of rapamycin (stroke: 56.0%; control: 51.4%; P = .002) and ribosomal protein S6 kinase beta-1 (stroke: 131.2%; control: 156.3%; P = .002) from resting levels to post-neuromuscular electrical stimulation treatment, respectively. Phosphorylated protein content was similar between stroke and control groups at both time points.
Findings suggest that paretic muscles of patients with chronic stroke may maintain ability to stimulate protein synthesis machinery in response to neuromuscular electrical stimulation.</description><subject>Aged</subject><subject>Case-Control Studies</subject><subject>Electric Stimulation Therapy</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>mTORC1</subject><subject>Muscle Contraction</subject><subject>Muscle Strength</subject><subject>Neuromuscular</subject><subject>Neuromuscular Junction - metabolism</subject><subject>Neuromuscular Junction - physiopathology</subject><subject>Paresis - diagnosis</subject><subject>Paresis - metabolism</subject><subject>Paresis - physiopathology</subject><subject>Paresis - therapy</subject><subject>paretic</subject><subject>Phosphorylation</subject><subject>Quadriceps Muscle - innervation</subject><subject>Quadriceps Muscle - metabolism</subject><subject>Ribosomal Protein S6 Kinases, 70-kDa - metabolism</subject><subject>Signal Transduction</subject><subject>skeletal muscle</subject><subject>stimulation</subject><subject>stroke</subject><subject>Stroke - diagnosis</subject><subject>Stroke - metabolism</subject><subject>Stroke - physiopathology</subject><subject>Stroke - therapy</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Treatment Outcome</subject><issn>1052-3057</issn><issn>1532-8511</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkE1LxDAQhoMorq7-BelRhK6ZpB_pUWX9gEWF9R7SZLpmbRtNWsV_b5ZVT16EgQnhyTuZh5AzoDOgUJyvZ-swePeCGj3W3r2rYGyYMQrljMaCaoccQM5ZKnKA3XimOUs5zcsJOQxhTSlALvJ9MmFCMJ5V7IAs73H0rhuDHlvlk3mLevBWqzZZDraLd4N1faJ6k1z0qnat1cnSrnrV2n6V2D55jAD2Q0g-7PAc32y-d0T2GtUGPP7uU_J0PX-6uk0XDzd3VxeLVGc0G1JdI3BdiwyqombclCgoN4U2nFWAQiCYUtU6b7KmKjkWTCuhRcUb4KJhjE_J6Tb21bu3EcMgOxs0tq3q0Y1BQsVpxQvGN-jlFtXeheCxka_edsp_SqBy41au5V9u5catpLFi2JScfM8b6w7Nb8SPzAgstgDGpd8tehl0lKPRWB-1SuPsf-Z9AVv-mqg</recordid><startdate>201712</startdate><enddate>201712</enddate><creator>Mettler, Joni A.</creator><creator>Bennett, Sydney M.</creator><creator>Doucet, Barbara M.</creator><creator>Magee, Dillon M.</creator><general>Elsevier Inc</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>7X8</scope><orcidid>https://orcid.org/0000-0001-8871-1787</orcidid></search><sort><creationdate>201712</creationdate><title>Neuromuscular Electrical Stimulation and Anabolic Signaling in Patients with Stroke</title><author>Mettler, Joni A. ; Bennett, Sydney M. ; Doucet, Barbara M. ; Magee, Dillon M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c404t-cbe13cb84196b23d7e803d6cd3291e88e1d7abc5f4f973e62ca8c893f138f223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Aged</topic><topic>Case-Control Studies</topic><topic>Electric Stimulation Therapy</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>mTORC1</topic><topic>Muscle Contraction</topic><topic>Muscle Strength</topic><topic>Neuromuscular</topic><topic>Neuromuscular Junction - metabolism</topic><topic>Neuromuscular Junction - physiopathology</topic><topic>Paresis - diagnosis</topic><topic>Paresis - metabolism</topic><topic>Paresis - physiopathology</topic><topic>Paresis - therapy</topic><topic>paretic</topic><topic>Phosphorylation</topic><topic>Quadriceps Muscle - innervation</topic><topic>Quadriceps Muscle - metabolism</topic><topic>Ribosomal Protein S6 Kinases, 70-kDa - metabolism</topic><topic>Signal Transduction</topic><topic>skeletal muscle</topic><topic>stimulation</topic><topic>stroke</topic><topic>Stroke - diagnosis</topic><topic>Stroke - metabolism</topic><topic>Stroke - physiopathology</topic><topic>Stroke - therapy</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mettler, Joni A.</creatorcontrib><creatorcontrib>Bennett, Sydney M.</creatorcontrib><creatorcontrib>Doucet, Barbara M.</creatorcontrib><creatorcontrib>Magee, Dillon M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of stroke and cerebrovascular diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mettler, Joni A.</au><au>Bennett, Sydney M.</au><au>Doucet, Barbara M.</au><au>Magee, Dillon M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuromuscular Electrical Stimulation and Anabolic Signaling in Patients with Stroke</atitle><jtitle>Journal of stroke and cerebrovascular diseases</jtitle><addtitle>J Stroke Cerebrovasc Dis</addtitle><date>2017-12</date><risdate>2017</risdate><volume>26</volume><issue>12</issue><spage>2954</spage><epage>2963</epage><pages>2954-2963</pages><issn>1052-3057</issn><eissn>1532-8511</eissn><abstract>Stroke results in limited ability to produce voluntary muscle contraction and movement on one side of the body, leading to further muscle wasting and weakness. Neuromuscular electrical stimulation is often used to facilitate involuntary muscle contraction; however, the effect of neuromuscular electrical stimulation on muscle growth and strengthening processes in hemiparetic muscle is not clear. This study examined the skeletal muscle anabolic response of an acute bout of neuromuscular electrical stimulation in individuals with chronic stroke and healthy older adults.
Eleven individuals (59.8 ± 2.7 years old) were divided into a chronic stroke group (n = 5) and a healthy older adult control group (n = 6). Muscle biopsies were obtained before and after stimulation from the vastus lateralis of the hemiparetic leg for the stroke group and the right leg for the control group. The neuromuscular electrical stimulation protocol consisted of a 60-minute, intermittent stimulation train at 60 Hz. Phosphorylation of mammalian target of rapamycin and ribosomal protein S6 kinase beta-1 were analyzed by Western blot.
An acute bout of neuromuscular electrical stimulation increased phosphorylation of mammalian target of rapamycin (stroke: 56.0%; control: 51.4%; P = .002) and ribosomal protein S6 kinase beta-1 (stroke: 131.2%; control: 156.3%; P = .002) from resting levels to post-neuromuscular electrical stimulation treatment, respectively. Phosphorylated protein content was similar between stroke and control groups at both time points.
Findings suggest that paretic muscles of patients with chronic stroke may maintain ability to stimulate protein synthesis machinery in response to neuromuscular electrical stimulation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28823492</pmid><doi>10.1016/j.jstrokecerebrovasdis.2017.07.019</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-8871-1787</orcidid></addata></record> |
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subjects | Aged Case-Control Studies Electric Stimulation Therapy Female Humans Male Middle Aged mTORC1 Muscle Contraction Muscle Strength Neuromuscular Neuromuscular Junction - metabolism Neuromuscular Junction - physiopathology Paresis - diagnosis Paresis - metabolism Paresis - physiopathology Paresis - therapy paretic Phosphorylation Quadriceps Muscle - innervation Quadriceps Muscle - metabolism Ribosomal Protein S6 Kinases, 70-kDa - metabolism Signal Transduction skeletal muscle stimulation stroke Stroke - diagnosis Stroke - metabolism Stroke - physiopathology Stroke - therapy TOR Serine-Threonine Kinases - metabolism Treatment Outcome |
title | Neuromuscular Electrical Stimulation and Anabolic Signaling in Patients with Stroke |
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