Bed rest and resistive vibration exercise unveil novel links between skeletal muscle mitochondrial function and insulin resistance
Aims/hypothesis Physical inactivity has broad implications for human disease including insulin resistance, sarcopenia and obesity. The present study tested the hypothesis that (1) impaired mitochondrial respiration is linked with blunted insulin sensitivity and loss of muscle mass in healthy young m...
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| Veröffentlicht in: | Diabetologia 2017-08, Vol.60 (8), p.1491-1501 |
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| creator | Kenny, Helena C. Rudwill, Floriane Breen, Laura Salanova, Michele Blottner, Dieter Heise, Tim Heer, Martina Blanc, Stephane O’Gorman, Donal J. |
| description | Aims/hypothesis
Physical inactivity has broad implications for human disease including insulin resistance, sarcopenia and obesity. The present study tested the hypothesis that (1) impaired mitochondrial respiration is linked with blunted insulin sensitivity and loss of muscle mass in healthy young men, and (2) resistive vibration exercise (RVE) would mitigate the negative metabolic effects of bed rest.
Methods
Participants (
n
= 9) were maintained in energy balance during 21 days of bed rest with RVE and without (CON) in a crossover study. Mitochondrial respiration was determined by high-resolution respirometry in permeabilised fibre bundles from biopsies of the vastus lateralis. A hyperinsulinaemic–euglycaemic clamp was used to determine insulin sensitivity, and body composition was assessed by dual-energy x-ray absorptiometry (DEXA).
Results
Body mass (−3.2 ± 0.5 kg vs −2.8 ± 0.4 kg for CON and RVE, respectively,
p
|
| doi_str_mv | 10.1007/s00125-017-4298-z |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_hal_p</sourceid><recordid>TN_cdi_hal_primary_oai_HAL_hal_01613882v1</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1899121362</sourcerecordid><originalsourceid>FETCH-LOGICAL-c449t-6edbc473eac89644f0b7b44a2ab442cdf10800c78f0553a844a77d1632f5bdb13</originalsourceid><addsrcrecordid>eNp1kcFu1TAQRS0Eoo_CB7BBltjAIjB2nNhZlgpopSexAYmd5TgT6tZxip0E6JIvx2leK4TExh7NnLkz9iXkOYM3DEC-TQCMVwUwWQjeqOLmAdkxUfICBFcPyW4tF0zVX4_Ik5QuAaCsRP2YHHFV5bgRO_L7HXY0YpqoCbeBS5NbkC6ujWZyY6D4E6N1CekcFnSehnFBT70LV4m2OP1ADDRdocfJeDrMyXqkg5tGezGGLrqc7Odgb6XWES6kOTcfRplg8Sl51Buf8NnhPiZfPrz_fHpW7D99PD892RdWiGYqauxaK2SJxqqmFqKHVrZCGG7yyW3XM1AAVqoeqqo0Kpek7Fhd8r5qu5aVx-T1pnthvL6ObjDxlx6N02cne73mgNWsVIovK_tqY6_j-H3O36MHlyx6bwKOc9JMNQ3jrKx5Rl_-g16Ocwz5JZo1TEgJlVgF2UbZOKYUsb_fgIFezdSbmXkJqVcz9U3ueXFQntsBu_uOO_cywDcg5VL4hvGv0f9V_QMduaw3</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1914770541</pqid></control><display><type>article</type><title>Bed rest and resistive vibration exercise unveil novel links between skeletal muscle mitochondrial function and insulin resistance</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Kenny, Helena C. ; Rudwill, Floriane ; Breen, Laura ; Salanova, Michele ; Blottner, Dieter ; Heise, Tim ; Heer, Martina ; Blanc, Stephane ; O’Gorman, Donal J.</creator><creatorcontrib>Kenny, Helena C. ; Rudwill, Floriane ; Breen, Laura ; Salanova, Michele ; Blottner, Dieter ; Heise, Tim ; Heer, Martina ; Blanc, Stephane ; O’Gorman, Donal J.</creatorcontrib><description>Aims/hypothesis
Physical inactivity has broad implications for human disease including insulin resistance, sarcopenia and obesity. The present study tested the hypothesis that (1) impaired mitochondrial respiration is linked with blunted insulin sensitivity and loss of muscle mass in healthy young men, and (2) resistive vibration exercise (RVE) would mitigate the negative metabolic effects of bed rest.
Methods
Participants (
n
= 9) were maintained in energy balance during 21 days of bed rest with RVE and without (CON) in a crossover study. Mitochondrial respiration was determined by high-resolution respirometry in permeabilised fibre bundles from biopsies of the vastus lateralis. A hyperinsulinaemic–euglycaemic clamp was used to determine insulin sensitivity, and body composition was assessed by dual-energy x-ray absorptiometry (DEXA).
Results
Body mass (−3.2 ± 0.5 kg vs −2.8 ± 0.4 kg for CON and RVE, respectively,
p
< 0.05), fat-free mass (−2.9 ± 0.5 kg vs −2.7 ± 0.5 kg,
p
< 0.05) and peak oxygen consumption (
V
⋅
O
2
peak
) (10–15%,
p
< 0.05) were all reduced following bed rest. Bed rest decreased insulin sensitivity in the CON group (0.04 ± 0.002 mg kgFFM
−1
[pmol l
−1
] min
−1
vs 0.03 ± 0.002 mg kgFFM
−1
[pmol l
−1
] min
−1
for baseline vs post-CON), while RVE mitigated this response (0.04 ± 0.003 mg kgFFM
−1
[pmol l
−1
] min
−1
). Mitochondrial respiration (oxidative phosphorylation and electron transport system capacity) decreased in the CON group but not in the RVE group when expressed relative to tissue weight but not when normalised for citrate synthase activity. LEAK respiration, indicating a decrease in mitochondrial uncoupling, was the only component to remain significantly lower in the CON group after normalisation for citrate synthase. This was accompanied by a significant decrease in adenine nucleotide translocase protein content.
Conclusions
/
interpretation
Reductions in muscle mitochondrial respiration occur concomitantly with insulin resistance and loss of muscle mass during bed rest and may play a role in the adaptations to physical inactivity. Significantly, we show that RVE is an effective strategy to partially prevent some of the deleterious metabolic effects of bed rest.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-017-4298-z</identifier><identifier>PMID: 28500394</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Absorptiometry, Photon ; Adaptation ; Adenine ; Adult ; Bed Rest ; Body composition ; Body Composition - physiology ; Body mass ; Citrate synthase ; Cross-Over Studies ; Disease resistance ; Dual energy X-ray absorptiometry ; Electron transport ; Energy balance ; Energy Metabolism - physiology ; Environmental Sciences ; Exercise ; Fat-free body mass ; Glucose Clamp Technique ; Human Physiology ; Humans ; Hypotheses ; Immobilization ; Insulin ; Insulin resistance ; Insulin Resistance - physiology ; Internal Medicine ; Male ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Metabolism ; Mitochondria ; Mitochondria - metabolism ; Muscle, Skeletal - physiology ; Oxidative phosphorylation ; Oxygen consumption ; Phosphorylation ; Respiration ; Sarcopenia ; Skeletal muscle ; Translocase</subject><ispartof>Diabetologia, 2017-08, Vol.60 (8), p.1491-1501</ispartof><rights>Springer-Verlag Berlin Heidelberg 2017</rights><rights>Diabetologia is a copyright of Springer, 2017.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-6edbc473eac89644f0b7b44a2ab442cdf10800c78f0553a844a77d1632f5bdb13</citedby><cites>FETCH-LOGICAL-c449t-6edbc473eac89644f0b7b44a2ab442cdf10800c78f0553a844a77d1632f5bdb13</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/s00125-017-4298-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00125-017-4298-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,777,781,882,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28500394$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-01613882$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Kenny, Helena C.</creatorcontrib><creatorcontrib>Rudwill, Floriane</creatorcontrib><creatorcontrib>Breen, Laura</creatorcontrib><creatorcontrib>Salanova, Michele</creatorcontrib><creatorcontrib>Blottner, Dieter</creatorcontrib><creatorcontrib>Heise, Tim</creatorcontrib><creatorcontrib>Heer, Martina</creatorcontrib><creatorcontrib>Blanc, Stephane</creatorcontrib><creatorcontrib>O’Gorman, Donal J.</creatorcontrib><title>Bed rest and resistive vibration exercise unveil novel links between skeletal muscle mitochondrial function and insulin resistance</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><addtitle>Diabetologia</addtitle><description>Aims/hypothesis
Physical inactivity has broad implications for human disease including insulin resistance, sarcopenia and obesity. The present study tested the hypothesis that (1) impaired mitochondrial respiration is linked with blunted insulin sensitivity and loss of muscle mass in healthy young men, and (2) resistive vibration exercise (RVE) would mitigate the negative metabolic effects of bed rest.
Methods
Participants (
n
= 9) were maintained in energy balance during 21 days of bed rest with RVE and without (CON) in a crossover study. Mitochondrial respiration was determined by high-resolution respirometry in permeabilised fibre bundles from biopsies of the vastus lateralis. A hyperinsulinaemic–euglycaemic clamp was used to determine insulin sensitivity, and body composition was assessed by dual-energy x-ray absorptiometry (DEXA).
Results
Body mass (−3.2 ± 0.5 kg vs −2.8 ± 0.4 kg for CON and RVE, respectively,
p
< 0.05), fat-free mass (−2.9 ± 0.5 kg vs −2.7 ± 0.5 kg,
p
< 0.05) and peak oxygen consumption (
V
⋅
O
2
peak
) (10–15%,
p
< 0.05) were all reduced following bed rest. Bed rest decreased insulin sensitivity in the CON group (0.04 ± 0.002 mg kgFFM
−1
[pmol l
−1
] min
−1
vs 0.03 ± 0.002 mg kgFFM
−1
[pmol l
−1
] min
−1
for baseline vs post-CON), while RVE mitigated this response (0.04 ± 0.003 mg kgFFM
−1
[pmol l
−1
] min
−1
). Mitochondrial respiration (oxidative phosphorylation and electron transport system capacity) decreased in the CON group but not in the RVE group when expressed relative to tissue weight but not when normalised for citrate synthase activity. LEAK respiration, indicating a decrease in mitochondrial uncoupling, was the only component to remain significantly lower in the CON group after normalisation for citrate synthase. This was accompanied by a significant decrease in adenine nucleotide translocase protein content.
Conclusions
/
interpretation
Reductions in muscle mitochondrial respiration occur concomitantly with insulin resistance and loss of muscle mass during bed rest and may play a role in the adaptations to physical inactivity. Significantly, we show that RVE is an effective strategy to partially prevent some of the deleterious metabolic effects of bed rest.</description><subject>Absorptiometry, Photon</subject><subject>Adaptation</subject><subject>Adenine</subject><subject>Adult</subject><subject>Bed Rest</subject><subject>Body composition</subject><subject>Body Composition - physiology</subject><subject>Body mass</subject><subject>Citrate synthase</subject><subject>Cross-Over Studies</subject><subject>Disease resistance</subject><subject>Dual energy X-ray absorptiometry</subject><subject>Electron transport</subject><subject>Energy balance</subject><subject>Energy Metabolism - physiology</subject><subject>Environmental Sciences</subject><subject>Exercise</subject><subject>Fat-free body mass</subject><subject>Glucose Clamp Technique</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Immobilization</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - physiology</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Muscle, Skeletal - physiology</subject><subject>Oxidative phosphorylation</subject><subject>Oxygen consumption</subject><subject>Phosphorylation</subject><subject>Respiration</subject><subject>Sarcopenia</subject><subject>Skeletal muscle</subject><subject>Translocase</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kcFu1TAQRS0Eoo_CB7BBltjAIjB2nNhZlgpopSexAYmd5TgT6tZxip0E6JIvx2leK4TExh7NnLkz9iXkOYM3DEC-TQCMVwUwWQjeqOLmAdkxUfICBFcPyW4tF0zVX4_Ik5QuAaCsRP2YHHFV5bgRO_L7HXY0YpqoCbeBS5NbkC6ujWZyY6D4E6N1CekcFnSehnFBT70LV4m2OP1ADDRdocfJeDrMyXqkg5tGezGGLrqc7Odgb6XWES6kOTcfRplg8Sl51Buf8NnhPiZfPrz_fHpW7D99PD892RdWiGYqauxaK2SJxqqmFqKHVrZCGG7yyW3XM1AAVqoeqqo0Kpek7Fhd8r5qu5aVx-T1pnthvL6ObjDxlx6N02cne73mgNWsVIovK_tqY6_j-H3O36MHlyx6bwKOc9JMNQ3jrKx5Rl_-g16Ocwz5JZo1TEgJlVgF2UbZOKYUsb_fgIFezdSbmXkJqVcz9U3ueXFQntsBu_uOO_cywDcg5VL4hvGv0f9V_QMduaw3</recordid><startdate>20170801</startdate><enddate>20170801</enddate><creator>Kenny, Helena C.</creator><creator>Rudwill, Floriane</creator><creator>Breen, Laura</creator><creator>Salanova, Michele</creator><creator>Blottner, Dieter</creator><creator>Heise, Tim</creator><creator>Heer, Martina</creator><creator>Blanc, Stephane</creator><creator>O’Gorman, Donal J.</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><general>Springer Verlag</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>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>H94</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><scope>1XC</scope></search><sort><creationdate>20170801</creationdate><title>Bed rest and resistive vibration exercise unveil novel links between skeletal muscle mitochondrial function and insulin resistance</title><author>Kenny, Helena C. ; Rudwill, Floriane ; Breen, Laura ; Salanova, Michele ; Blottner, Dieter ; Heise, Tim ; Heer, Martina ; Blanc, Stephane ; O’Gorman, Donal J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-6edbc473eac89644f0b7b44a2ab442cdf10800c78f0553a844a77d1632f5bdb13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Absorptiometry, Photon</topic><topic>Adaptation</topic><topic>Adenine</topic><topic>Adult</topic><topic>Bed Rest</topic><topic>Body composition</topic><topic>Body Composition - physiology</topic><topic>Body mass</topic><topic>Citrate synthase</topic><topic>Cross-Over Studies</topic><topic>Disease resistance</topic><topic>Dual energy X-ray absorptiometry</topic><topic>Electron transport</topic><topic>Energy balance</topic><topic>Energy Metabolism - physiology</topic><topic>Environmental Sciences</topic><topic>Exercise</topic><topic>Fat-free body mass</topic><topic>Glucose Clamp Technique</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Immobilization</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - physiology</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Mitochondria - metabolism</topic><topic>Muscle, Skeletal - physiology</topic><topic>Oxidative phosphorylation</topic><topic>Oxygen consumption</topic><topic>Phosphorylation</topic><topic>Respiration</topic><topic>Sarcopenia</topic><topic>Skeletal muscle</topic><topic>Translocase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kenny, Helena C.</creatorcontrib><creatorcontrib>Rudwill, Floriane</creatorcontrib><creatorcontrib>Breen, Laura</creatorcontrib><creatorcontrib>Salanova, Michele</creatorcontrib><creatorcontrib>Blottner, Dieter</creatorcontrib><creatorcontrib>Heise, Tim</creatorcontrib><creatorcontrib>Heer, Martina</creatorcontrib><creatorcontrib>Blanc, Stephane</creatorcontrib><creatorcontrib>O’Gorman, Donal J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kenny, Helena C.</au><au>Rudwill, Floriane</au><au>Breen, Laura</au><au>Salanova, Michele</au><au>Blottner, Dieter</au><au>Heise, Tim</au><au>Heer, Martina</au><au>Blanc, Stephane</au><au>O’Gorman, Donal J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bed rest and resistive vibration exercise unveil novel links between skeletal muscle mitochondrial function and insulin resistance</atitle><jtitle>Diabetologia</jtitle><stitle>Diabetologia</stitle><addtitle>Diabetologia</addtitle><date>2017-08-01</date><risdate>2017</risdate><volume>60</volume><issue>8</issue><spage>1491</spage><epage>1501</epage><pages>1491-1501</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Aims/hypothesis
Physical inactivity has broad implications for human disease including insulin resistance, sarcopenia and obesity. The present study tested the hypothesis that (1) impaired mitochondrial respiration is linked with blunted insulin sensitivity and loss of muscle mass in healthy young men, and (2) resistive vibration exercise (RVE) would mitigate the negative metabolic effects of bed rest.
Methods
Participants (
n
= 9) were maintained in energy balance during 21 days of bed rest with RVE and without (CON) in a crossover study. Mitochondrial respiration was determined by high-resolution respirometry in permeabilised fibre bundles from biopsies of the vastus lateralis. A hyperinsulinaemic–euglycaemic clamp was used to determine insulin sensitivity, and body composition was assessed by dual-energy x-ray absorptiometry (DEXA).
Results
Body mass (−3.2 ± 0.5 kg vs −2.8 ± 0.4 kg for CON and RVE, respectively,
p
< 0.05), fat-free mass (−2.9 ± 0.5 kg vs −2.7 ± 0.5 kg,
p
< 0.05) and peak oxygen consumption (
V
⋅
O
2
peak
) (10–15%,
p
< 0.05) were all reduced following bed rest. Bed rest decreased insulin sensitivity in the CON group (0.04 ± 0.002 mg kgFFM
−1
[pmol l
−1
] min
−1
vs 0.03 ± 0.002 mg kgFFM
−1
[pmol l
−1
] min
−1
for baseline vs post-CON), while RVE mitigated this response (0.04 ± 0.003 mg kgFFM
−1
[pmol l
−1
] min
−1
). Mitochondrial respiration (oxidative phosphorylation and electron transport system capacity) decreased in the CON group but not in the RVE group when expressed relative to tissue weight but not when normalised for citrate synthase activity. LEAK respiration, indicating a decrease in mitochondrial uncoupling, was the only component to remain significantly lower in the CON group after normalisation for citrate synthase. This was accompanied by a significant decrease in adenine nucleotide translocase protein content.
Conclusions
/
interpretation
Reductions in muscle mitochondrial respiration occur concomitantly with insulin resistance and loss of muscle mass during bed rest and may play a role in the adaptations to physical inactivity. Significantly, we show that RVE is an effective strategy to partially prevent some of the deleterious metabolic effects of bed rest.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>28500394</pmid><doi>10.1007/s00125-017-4298-z</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Diabetologia, 2017-08, Vol.60 (8), p.1491-1501 |
| issn | 0012-186X 1432-0428 |
| language | eng |
| recordid | cdi_hal_primary_oai_HAL_hal_01613882v1 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Absorptiometry, Photon Adaptation Adenine Adult Bed Rest Body composition Body Composition - physiology Body mass Citrate synthase Cross-Over Studies Disease resistance Dual energy X-ray absorptiometry Electron transport Energy balance Energy Metabolism - physiology Environmental Sciences Exercise Fat-free body mass Glucose Clamp Technique Human Physiology Humans Hypotheses Immobilization Insulin Insulin resistance Insulin Resistance - physiology Internal Medicine Male Medicine Medicine & Public Health Metabolic Diseases Metabolism Mitochondria Mitochondria - metabolism Muscle, Skeletal - physiology Oxidative phosphorylation Oxygen consumption Phosphorylation Respiration Sarcopenia Skeletal muscle Translocase |
| title | Bed rest and resistive vibration exercise unveil novel links between skeletal muscle mitochondrial function and insulin resistance |
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