Human adaptation to immobilization: Novel insights of impacts on glucose disposal and fuel utilization
Background Bed rest (BR) reduces whole‐body insulin‐stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about metabolic adaptation from acute to chronic BR nor the mechanisms involved, particularly when volunteers are maintained in energy balance. Methods Healthy...
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| Published in | Journal of cachexia, sarcopenia and muscle Vol. 13; no. 6; pp. 2999 - 3013 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Germany
John Wiley & Sons, Inc
01.12.2022
John Wiley and Sons Inc Wiley |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2190-5991 2190-6009 2190-6009 |
| DOI | 10.1002/jcsm.13075 |
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| Abstract | Background
Bed rest (BR) reduces whole‐body insulin‐stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about metabolic adaptation from acute to chronic BR nor the mechanisms involved, particularly when volunteers are maintained in energy balance.
Methods
Healthy males (n = 10, 24.0 ± 1.3 years), maintained in energy balance, underwent 3‐day BR (acute BR). A second cohort matched for sex and body mass index (n = 20, 34.2 ± 1.8 years) underwent 56‐day BR (chronic BR). A hyperinsulinaemic euglycaemic clamp (60 mU/m2/min) was performed to determine rates of whole‐body insulin‐stimulated GD before and after BR (normalized to lean body mass). Indirect calorimetry was performed before and during steady state of each clamp to calculate rates of whole‐body fuel oxidation. Muscle biopsies were taken to determine muscle glycogen, metabolite and intramyocellular lipid (IMCL) contents, and the expression of 191 mRNA targets before and after BR. Two‐way repeated measures analysis of variance was used to detect differences in endpoint measures.
Results
Acute BR reduced insulin‐mediated GD (Pre 11.5 ± 0.7 vs. Post 9.3 ± 0.6 mg/kg/min, P < 0.001), which was unchanged in magnitude following chronic BR (Pre 10.2 ± 0.4 vs. Post 7.9 ± 0.3 mg/kg/min, P < 0.05). This reduction in GD was paralleled by the elimination of the 35% increase in insulin‐stimulated muscle glycogen storage following both acute and chronic BR. Acute BR had no impact on insulin‐stimulated carbohydrate (CHO; Pre 3.69 ± 0.39 vs. Post 4.34 ± 0.22 mg/kg/min) and lipid (Pre 1.13 ± 0.14 vs. Post 0.59 ± 0.11 mg/kg/min) oxidation, but chronic BR reduced CHO oxidation (Pre 3.34 ± 0.18 vs. Post 2.72 ± 0.13 mg/kg/min, P < 0.05) and blunted the magnitude of insulin‐mediated inhibition of lipid oxidation (Pre 0.60 ± 0.07 vs. Post 0.85 ± 0.06 mg/kg/min, P < 0.05). Neither acute nor chronic BR increased muscle IMCL content. Plentiful mRNA abundance changes were detected following acute BR, which waned following chronic BR and reflected changes in fuel oxidation and muscle glycogen storage at this time point.
Conclusions
Acute BR suppressed insulin‐stimulated GD and storage, but the extent of this suppression increased no further in chronic BR. However, insulin‐mediated inhibition of fat oxidation after chronic BR was less than acute BR and was accompanied by blunted CHO oxidation. The juxtaposition of these responses shows that the regulation of GD and storage can be dissociated from substrate oxidation. Additionally, the shift in substrate oxidation after chronic BR was not explained by IMCL accumulation but reflected by muscle mRNA and pyruvate dehydrogenase kinase 4 protein abundance changes, pointing to lack of muscle contraction per se as the primary signal for muscle adaptation. |
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| AbstractList | Bed rest (BR) reduces whole-body insulin-stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about metabolic adaptation from acute to chronic BR nor the mechanisms involved, particularly when volunteers are maintained in energy balance.
Healthy males (n = 10, 24.0 ± 1.3 years), maintained in energy balance, underwent 3-day BR (acute BR). A second cohort matched for sex and body mass index (n = 20, 34.2 ± 1.8 years) underwent 56-day BR (chronic BR). A hyperinsulinaemic euglycaemic clamp (60 mU/m
/min) was performed to determine rates of whole-body insulin-stimulated GD before and after BR (normalized to lean body mass). Indirect calorimetry was performed before and during steady state of each clamp to calculate rates of whole-body fuel oxidation. Muscle biopsies were taken to determine muscle glycogen, metabolite and intramyocellular lipid (IMCL) contents, and the expression of 191 mRNA targets before and after BR. Two-way repeated measures analysis of variance was used to detect differences in endpoint measures.
Acute BR reduced insulin-mediated GD (Pre 11.5 ± 0.7 vs. Post 9.3 ± 0.6 mg/kg/min, P < 0.001), which was unchanged in magnitude following chronic BR (Pre 10.2 ± 0.4 vs. Post 7.9 ± 0.3 mg/kg/min, P < 0.05). This reduction in GD was paralleled by the elimination of the 35% increase in insulin-stimulated muscle glycogen storage following both acute and chronic BR. Acute BR had no impact on insulin-stimulated carbohydrate (CHO; Pre 3.69 ± 0.39 vs. Post 4.34 ± 0.22 mg/kg/min) and lipid (Pre 1.13 ± 0.14 vs. Post 0.59 ± 0.11 mg/kg/min) oxidation, but chronic BR reduced CHO oxidation (Pre 3.34 ± 0.18 vs. Post 2.72 ± 0.13 mg/kg/min, P < 0.05) and blunted the magnitude of insulin-mediated inhibition of lipid oxidation (Pre 0.60 ± 0.07 vs. Post 0.85 ± 0.06 mg/kg/min, P < 0.05). Neither acute nor chronic BR increased muscle IMCL content. Plentiful mRNA abundance changes were detected following acute BR, which waned following chronic BR and reflected changes in fuel oxidation and muscle glycogen storage at this time point.
Acute BR suppressed insulin-stimulated GD and storage, but the extent of this suppression increased no further in chronic BR. However, insulin-mediated inhibition of fat oxidation after chronic BR was less than acute BR and was accompanied by blunted CHO oxidation. The juxtaposition of these responses shows that the regulation of GD and storage can be dissociated from substrate oxidation. Additionally, the shift in substrate oxidation after chronic BR was not explained by IMCL accumulation but reflected by muscle mRNA and pyruvate dehydrogenase kinase 4 protein abundance changes, pointing to lack of muscle contraction per se as the primary signal for muscle adaptation. Bed rest (BR) reduces whole-body insulin-stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about metabolic adaptation from acute to chronic BR nor the mechanisms involved, particularly when volunteers are maintained in energy balance.BACKGROUNDBed rest (BR) reduces whole-body insulin-stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about metabolic adaptation from acute to chronic BR nor the mechanisms involved, particularly when volunteers are maintained in energy balance.Healthy males (n = 10, 24.0 ± 1.3 years), maintained in energy balance, underwent 3-day BR (acute BR). A second cohort matched for sex and body mass index (n = 20, 34.2 ± 1.8 years) underwent 56-day BR (chronic BR). A hyperinsulinaemic euglycaemic clamp (60 mU/m2 /min) was performed to determine rates of whole-body insulin-stimulated GD before and after BR (normalized to lean body mass). Indirect calorimetry was performed before and during steady state of each clamp to calculate rates of whole-body fuel oxidation. Muscle biopsies were taken to determine muscle glycogen, metabolite and intramyocellular lipid (IMCL) contents, and the expression of 191 mRNA targets before and after BR. Two-way repeated measures analysis of variance was used to detect differences in endpoint measures.METHODSHealthy males (n = 10, 24.0 ± 1.3 years), maintained in energy balance, underwent 3-day BR (acute BR). A second cohort matched for sex and body mass index (n = 20, 34.2 ± 1.8 years) underwent 56-day BR (chronic BR). A hyperinsulinaemic euglycaemic clamp (60 mU/m2 /min) was performed to determine rates of whole-body insulin-stimulated GD before and after BR (normalized to lean body mass). Indirect calorimetry was performed before and during steady state of each clamp to calculate rates of whole-body fuel oxidation. Muscle biopsies were taken to determine muscle glycogen, metabolite and intramyocellular lipid (IMCL) contents, and the expression of 191 mRNA targets before and after BR. Two-way repeated measures analysis of variance was used to detect differences in endpoint measures.Acute BR reduced insulin-mediated GD (Pre 11.5 ± 0.7 vs. Post 9.3 ± 0.6 mg/kg/min, P < 0.001), which was unchanged in magnitude following chronic BR (Pre 10.2 ± 0.4 vs. Post 7.9 ± 0.3 mg/kg/min, P < 0.05). This reduction in GD was paralleled by the elimination of the 35% increase in insulin-stimulated muscle glycogen storage following both acute and chronic BR. Acute BR had no impact on insulin-stimulated carbohydrate (CHO; Pre 3.69 ± 0.39 vs. Post 4.34 ± 0.22 mg/kg/min) and lipid (Pre 1.13 ± 0.14 vs. Post 0.59 ± 0.11 mg/kg/min) oxidation, but chronic BR reduced CHO oxidation (Pre 3.34 ± 0.18 vs. Post 2.72 ± 0.13 mg/kg/min, P < 0.05) and blunted the magnitude of insulin-mediated inhibition of lipid oxidation (Pre 0.60 ± 0.07 vs. Post 0.85 ± 0.06 mg/kg/min, P < 0.05). Neither acute nor chronic BR increased muscle IMCL content. Plentiful mRNA abundance changes were detected following acute BR, which waned following chronic BR and reflected changes in fuel oxidation and muscle glycogen storage at this time point.RESULTSAcute BR reduced insulin-mediated GD (Pre 11.5 ± 0.7 vs. Post 9.3 ± 0.6 mg/kg/min, P < 0.001), which was unchanged in magnitude following chronic BR (Pre 10.2 ± 0.4 vs. Post 7.9 ± 0.3 mg/kg/min, P < 0.05). This reduction in GD was paralleled by the elimination of the 35% increase in insulin-stimulated muscle glycogen storage following both acute and chronic BR. Acute BR had no impact on insulin-stimulated carbohydrate (CHO; Pre 3.69 ± 0.39 vs. Post 4.34 ± 0.22 mg/kg/min) and lipid (Pre 1.13 ± 0.14 vs. Post 0.59 ± 0.11 mg/kg/min) oxidation, but chronic BR reduced CHO oxidation (Pre 3.34 ± 0.18 vs. Post 2.72 ± 0.13 mg/kg/min, P < 0.05) and blunted the magnitude of insulin-mediated inhibition of lipid oxidation (Pre 0.60 ± 0.07 vs. Post 0.85 ± 0.06 mg/kg/min, P < 0.05). Neither acute nor chronic BR increased muscle IMCL content. Plentiful mRNA abundance changes were detected following acute BR, which waned following chronic BR and reflected changes in fuel oxidation and muscle glycogen storage at this time point.Acute BR suppressed insulin-stimulated GD and storage, but the extent of this suppression increased no further in chronic BR. However, insulin-mediated inhibition of fat oxidation after chronic BR was less than acute BR and was accompanied by blunted CHO oxidation. The juxtaposition of these responses shows that the regulation of GD and storage can be dissociated from substrate oxidation. Additionally, the shift in substrate oxidation after chronic BR was not explained by IMCL accumulation but reflected by muscle mRNA and pyruvate dehydrogenase kinase 4 protein abundance changes, pointing to lack of muscle contraction per se as the primary signal for muscle adaptation.CONCLUSIONSAcute BR suppressed insulin-stimulated GD and storage, but the extent of this suppression increased no further in chronic BR. However, insulin-mediated inhibition of fat oxidation after chronic BR was less than acute BR and was accompanied by blunted CHO oxidation. The juxtaposition of these responses shows that the regulation of GD and storage can be dissociated from substrate oxidation. Additionally, the shift in substrate oxidation after chronic BR was not explained by IMCL accumulation but reflected by muscle mRNA and pyruvate dehydrogenase kinase 4 protein abundance changes, pointing to lack of muscle contraction per se as the primary signal for muscle adaptation. Background Bed rest (BR) reduces whole‐body insulin‐stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about metabolic adaptation from acute to chronic BR nor the mechanisms involved, particularly when volunteers are maintained in energy balance. Methods Healthy males (n = 10, 24.0 ± 1.3 years), maintained in energy balance, underwent 3‐day BR (acute BR). A second cohort matched for sex and body mass index (n = 20, 34.2 ± 1.8 years) underwent 56‐day BR (chronic BR). A hyperinsulinaemic euglycaemic clamp (60 mU/m2/min) was performed to determine rates of whole‐body insulin‐stimulated GD before and after BR (normalized to lean body mass). Indirect calorimetry was performed before and during steady state of each clamp to calculate rates of whole‐body fuel oxidation. Muscle biopsies were taken to determine muscle glycogen, metabolite and intramyocellular lipid (IMCL) contents, and the expression of 191 mRNA targets before and after BR. Two‐way repeated measures analysis of variance was used to detect differences in endpoint measures. Results Acute BR reduced insulin‐mediated GD (Pre 11.5 ± 0.7 vs. Post 9.3 ± 0.6 mg/kg/min, P < 0.001), which was unchanged in magnitude following chronic BR (Pre 10.2 ± 0.4 vs. Post 7.9 ± 0.3 mg/kg/min, P < 0.05). This reduction in GD was paralleled by the elimination of the 35% increase in insulin‐stimulated muscle glycogen storage following both acute and chronic BR. Acute BR had no impact on insulin‐stimulated carbohydrate (CHO; Pre 3.69 ± 0.39 vs. Post 4.34 ± 0.22 mg/kg/min) and lipid (Pre 1.13 ± 0.14 vs. Post 0.59 ± 0.11 mg/kg/min) oxidation, but chronic BR reduced CHO oxidation (Pre 3.34 ± 0.18 vs. Post 2.72 ± 0.13 mg/kg/min, P < 0.05) and blunted the magnitude of insulin‐mediated inhibition of lipid oxidation (Pre 0.60 ± 0.07 vs. Post 0.85 ± 0.06 mg/kg/min, P < 0.05). Neither acute nor chronic BR increased muscle IMCL content. Plentiful mRNA abundance changes were detected following acute BR, which waned following chronic BR and reflected changes in fuel oxidation and muscle glycogen storage at this time point. Conclusions Acute BR suppressed insulin‐stimulated GD and storage, but the extent of this suppression increased no further in chronic BR. However, insulin‐mediated inhibition of fat oxidation after chronic BR was less than acute BR and was accompanied by blunted CHO oxidation. The juxtaposition of these responses shows that the regulation of GD and storage can be dissociated from substrate oxidation. Additionally, the shift in substrate oxidation after chronic BR was not explained by IMCL accumulation but reflected by muscle mRNA and pyruvate dehydrogenase kinase 4 protein abundance changes, pointing to lack of muscle contraction per se as the primary signal for muscle adaptation. Background Bed rest (BR) reduces whole‐body insulin‐stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about metabolic adaptation from acute to chronic BR nor the mechanisms involved, particularly when volunteers are maintained in energy balance. Methods Healthy males (n = 10, 24.0 ± 1.3 years), maintained in energy balance, underwent 3‐day BR (acute BR). A second cohort matched for sex and body mass index (n = 20, 34.2 ± 1.8 years) underwent 56‐day BR (chronic BR). A hyperinsulinaemic euglycaemic clamp (60 mU/m2/min) was performed to determine rates of whole‐body insulin‐stimulated GD before and after BR (normalized to lean body mass). Indirect calorimetry was performed before and during steady state of each clamp to calculate rates of whole‐body fuel oxidation. Muscle biopsies were taken to determine muscle glycogen, metabolite and intramyocellular lipid (IMCL) contents, and the expression of 191 mRNA targets before and after BR. Two‐way repeated measures analysis of variance was used to detect differences in endpoint measures. Results Acute BR reduced insulin‐mediated GD (Pre 11.5 ± 0.7 vs. Post 9.3 ± 0.6 mg/kg/min, P < 0.001), which was unchanged in magnitude following chronic BR (Pre 10.2 ± 0.4 vs. Post 7.9 ± 0.3 mg/kg/min, P < 0.05). This reduction in GD was paralleled by the elimination of the 35% increase in insulin‐stimulated muscle glycogen storage following both acute and chronic BR. Acute BR had no impact on insulin‐stimulated carbohydrate (CHO; Pre 3.69 ± 0.39 vs. Post 4.34 ± 0.22 mg/kg/min) and lipid (Pre 1.13 ± 0.14 vs. Post 0.59 ± 0.11 mg/kg/min) oxidation, but chronic BR reduced CHO oxidation (Pre 3.34 ± 0.18 vs. Post 2.72 ± 0.13 mg/kg/min, P < 0.05) and blunted the magnitude of insulin‐mediated inhibition of lipid oxidation (Pre 0.60 ± 0.07 vs. Post 0.85 ± 0.06 mg/kg/min, P < 0.05). Neither acute nor chronic BR increased muscle IMCL content. Plentiful mRNA abundance changes were detected following acute BR, which waned following chronic BR and reflected changes in fuel oxidation and muscle glycogen storage at this time point. Conclusions Acute BR suppressed insulin‐stimulated GD and storage, but the extent of this suppression increased no further in chronic BR. However, insulin‐mediated inhibition of fat oxidation after chronic BR was less than acute BR and was accompanied by blunted CHO oxidation. The juxtaposition of these responses shows that the regulation of GD and storage can be dissociated from substrate oxidation. Additionally, the shift in substrate oxidation after chronic BR was not explained by IMCL accumulation but reflected by muscle mRNA and pyruvate dehydrogenase kinase 4 protein abundance changes, pointing to lack of muscle contraction per se as the primary signal for muscle adaptation. Abstract Background Bed rest (BR) reduces whole‐body insulin‐stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about metabolic adaptation from acute to chronic BR nor the mechanisms involved, particularly when volunteers are maintained in energy balance. Methods Healthy males (n = 10, 24.0 ± 1.3 years), maintained in energy balance, underwent 3‐day BR (acute BR). A second cohort matched for sex and body mass index (n = 20, 34.2 ± 1.8 years) underwent 56‐day BR (chronic BR). A hyperinsulinaemic euglycaemic clamp (60 mU/m2/min) was performed to determine rates of whole‐body insulin‐stimulated GD before and after BR (normalized to lean body mass). Indirect calorimetry was performed before and during steady state of each clamp to calculate rates of whole‐body fuel oxidation. Muscle biopsies were taken to determine muscle glycogen, metabolite and intramyocellular lipid (IMCL) contents, and the expression of 191 mRNA targets before and after BR. Two‐way repeated measures analysis of variance was used to detect differences in endpoint measures. Results Acute BR reduced insulin‐mediated GD (Pre 11.5 ± 0.7 vs. Post 9.3 ± 0.6 mg/kg/min, P < 0.001), which was unchanged in magnitude following chronic BR (Pre 10.2 ± 0.4 vs. Post 7.9 ± 0.3 mg/kg/min, P < 0.05). This reduction in GD was paralleled by the elimination of the 35% increase in insulin‐stimulated muscle glycogen storage following both acute and chronic BR. Acute BR had no impact on insulin‐stimulated carbohydrate (CHO; Pre 3.69 ± 0.39 vs. Post 4.34 ± 0.22 mg/kg/min) and lipid (Pre 1.13 ± 0.14 vs. Post 0.59 ± 0.11 mg/kg/min) oxidation, but chronic BR reduced CHO oxidation (Pre 3.34 ± 0.18 vs. Post 2.72 ± 0.13 mg/kg/min, P < 0.05) and blunted the magnitude of insulin‐mediated inhibition of lipid oxidation (Pre 0.60 ± 0.07 vs. Post 0.85 ± 0.06 mg/kg/min, P < 0.05). Neither acute nor chronic BR increased muscle IMCL content. Plentiful mRNA abundance changes were detected following acute BR, which waned following chronic BR and reflected changes in fuel oxidation and muscle glycogen storage at this time point. Conclusions Acute BR suppressed insulin‐stimulated GD and storage, but the extent of this suppression increased no further in chronic BR. However, insulin‐mediated inhibition of fat oxidation after chronic BR was less than acute BR and was accompanied by blunted CHO oxidation. The juxtaposition of these responses shows that the regulation of GD and storage can be dissociated from substrate oxidation. Additionally, the shift in substrate oxidation after chronic BR was not explained by IMCL accumulation but reflected by muscle mRNA and pyruvate dehydrogenase kinase 4 protein abundance changes, pointing to lack of muscle contraction per se as the primary signal for muscle adaptation. |
| Author | Macdonald, Ian A. Cordon, Sally M. Constantin, Despina Crossland, Hannah Chivaka, Prince K. Shur, Natalie F. Szewczyk, Nate Lobo, Dileep N. Simpson, Elizabeth J. Constantin‐Teodosiu, Dumitru Stephens, Francis B. Narici, Marco Prats, Clara Greenhaff, Paul L. |
| AuthorAffiliation | 3 MRC/Versus Arthritis Centre for Musculoskeletal Ageing Research, Schools of Life Sciences and Medicine University of Nottingham Nottingham UK 4 Sport and Health Sciences The University of Exeter Exeter UK 2 National Institute for Health and Care Research (NIHR) Nottingham Biomedical Research Centre Nottingham University Hospitals NHS Trust and University of Nottingham Nottingham UK 5 Ohio Musculoskeletal and Neurological Institute, Heritage College of Osteopathic Medicine Ohio University Athens OH USA 6 Present address: Department of Biomedical Sciences University of Padua Padua Italy 7 Present address: Core Facility for Integrated Microscopy The University of Copenhagen Copenhagen Denmark 1 Centre for Sport, Exercise and Osteoarthritis Research Versus Arthritis, School of Life Sciences The University of Nottingham Nottingham UK |
| AuthorAffiliation_xml | – name: 1 Centre for Sport, Exercise and Osteoarthritis Research Versus Arthritis, School of Life Sciences The University of Nottingham Nottingham UK – name: 3 MRC/Versus Arthritis Centre for Musculoskeletal Ageing Research, Schools of Life Sciences and Medicine University of Nottingham Nottingham UK – name: 4 Sport and Health Sciences The University of Exeter Exeter UK – name: 6 Present address: Department of Biomedical Sciences University of Padua Padua Italy – name: 7 Present address: Core Facility for Integrated Microscopy The University of Copenhagen Copenhagen Denmark – name: 2 National Institute for Health and Care Research (NIHR) Nottingham Biomedical Research Centre Nottingham University Hospitals NHS Trust and University of Nottingham Nottingham UK – name: 5 Ohio Musculoskeletal and Neurological Institute, Heritage College of Osteopathic Medicine Ohio University Athens OH USA |
| Author_xml | – sequence: 1 givenname: Natalie F. orcidid: 0000-0002-6622-2525 surname: Shur fullname: Shur, Natalie F. organization: Nottingham University Hospitals NHS Trust and University of Nottingham – sequence: 2 givenname: Elizabeth J. surname: Simpson fullname: Simpson, Elizabeth J. organization: University of Nottingham – sequence: 3 givenname: Hannah surname: Crossland fullname: Crossland, Hannah organization: University of Nottingham – sequence: 4 givenname: Prince K. surname: Chivaka fullname: Chivaka, Prince K. organization: The University of Nottingham – sequence: 5 givenname: Despina surname: Constantin fullname: Constantin, Despina organization: University of Nottingham – sequence: 6 givenname: Sally M. surname: Cordon fullname: Cordon, Sally M. organization: University of Nottingham – sequence: 7 givenname: Dumitru surname: Constantin‐Teodosiu fullname: Constantin‐Teodosiu, Dumitru organization: University of Nottingham – sequence: 8 givenname: Francis B. surname: Stephens fullname: Stephens, Francis B. organization: The University of Exeter – sequence: 9 givenname: Dileep N. surname: Lobo fullname: Lobo, Dileep N. organization: University of Nottingham – sequence: 10 givenname: Nate surname: Szewczyk fullname: Szewczyk, Nate organization: Ohio University – sequence: 11 givenname: Marco surname: Narici fullname: Narici, Marco organization: University of Padua – sequence: 12 givenname: Clara surname: Prats fullname: Prats, Clara organization: The University of Copenhagen – sequence: 13 givenname: Ian A. surname: Macdonald fullname: Macdonald, Ian A. organization: University of Nottingham – sequence: 14 givenname: Paul L. surname: Greenhaff fullname: Greenhaff, Paul L. email: paul.greenhaff@nottingham.ac.uk organization: University of Nottingham |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36058634$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1113_EP091590 crossref_primary_10_14814_phy2_70140 crossref_primary_10_1152_physrev_00022_2022 crossref_primary_10_1113_JP284169 crossref_primary_10_1038_s41598_024_57948_5 crossref_primary_10_1042_CS20231197 crossref_primary_10_1038_s41467_023_41990_4 crossref_primary_10_1016_j_clnu_2023_04_028 crossref_primary_10_1210_endrev_bnad032 crossref_primary_10_1016_S2589_7500_23_00084_5 crossref_primary_10_1113_JP287003 crossref_primary_10_1002_jcsm_13431 crossref_primary_10_1111_nbu_12619 |
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| ContentType | Journal Article |
| Copyright | 2022 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders. 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Issue | 6 |
| Keywords | muscle metabolism insulin resistance bed rest fuel oxidation |
| Language | English |
| License | Attribution 2022 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
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| Notes | Ian A. Macdonald and Paul L. Greenhaff are joint senior authors. Natalie F. Shur and Elizabeth J. Simpson are joint first authors. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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| PublicationTitle | Journal of cachexia, sarcopenia and muscle |
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| References | 2012; 61 1990; 51 1984; 40 2014; 116 2010; 53 2006; 91 1991; 16 2010; 59 1974; 33 2000; 49 1990; 79 2017; 60 2017; 1862 2013; 68 2007; 583 2015; 30 1988; 37 2018; 103 2018; 224 1975; 35 2019; 38 2019; 366 2016; 121 2017; 595 2011; 4 2005; 28 1990; 185 2011; 111 2014; 44 1979; 237 2001; 172 2021; 599 2015; 64 2010; 299 2013; 30 1991; 70 2019 2007; 4 2013; 591 2020; 598 2007; 85 2018; 12 2012; 9 e_1_2_8_28_1 e_1_2_8_29_1 e_1_2_8_24_1 e_1_2_8_25_1 e_1_2_8_46_1 e_1_2_8_26_1 e_1_2_8_27_1 e_1_2_8_3_1 e_1_2_8_2_1 e_1_2_8_5_1 e_1_2_8_4_1 e_1_2_8_7_1 e_1_2_8_6_1 e_1_2_8_9_1 e_1_2_8_8_1 e_1_2_8_20_1 e_1_2_8_43_1 e_1_2_8_42_1 e_1_2_8_22_1 e_1_2_8_45_1 e_1_2_8_23_1 e_1_2_8_44_1 e_1_2_8_41_1 e_1_2_8_40_1 e_1_2_8_17_1 e_1_2_8_18_1 e_1_2_8_39_1 e_1_2_8_19_1 e_1_2_8_13_1 e_1_2_8_36_1 e_1_2_8_14_1 e_1_2_8_35_1 e_1_2_8_15_1 e_1_2_8_38_1 e_1_2_8_16_1 e_1_2_8_37_1 Peronnet F (e_1_2_8_21_1) 1991; 16 e_1_2_8_32_1 e_1_2_8_10_1 e_1_2_8_31_1 e_1_2_8_11_1 e_1_2_8_34_1 e_1_2_8_12_1 e_1_2_8_33_1 e_1_2_8_30_1 |
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| Snippet | Background
Bed rest (BR) reduces whole‐body insulin‐stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about metabolic... Bed rest (BR) reduces whole-body insulin-stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about metabolic adaptation... Background Bed rest (BR) reduces whole‐body insulin‐stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about metabolic... Abstract Background Bed rest (BR) reduces whole‐body insulin‐stimulated glucose disposal (GD) and alters muscle fuel metabolism, but little is known about... |
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| SubjectTerms | Aerospace medicine Antioxidants bed rest Biopsy Diabetes Diet Dietary supplements Energy Exercise fuel oxidation Glucose Glucose - metabolism Glycogen - metabolism Humans Insulin Insulin - metabolism insulin resistance Lipids Male Meals Medical screening Metabolism Metabolites muscle metabolism Muscle, Skeletal - metabolism Musculoskeletal system Original Physical fitness Physiology Proteins RNA, Messenger - metabolism |
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| Title | Human adaptation to immobilization: Novel insights of impacts on glucose disposal and fuel utilization |
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