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The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment
Chronic sleep loss is a potent catabolic stressor, increasing the risk of metabolic dysfunction and loss of muscle mass and function. To provide mechanistic insight into these clinical outcomes, we sought to determine if acute sleep deprivation blunts skeletal muscle protein synthesis and promotes a...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7785053/ https://www.ncbi.nlm.nih.gov/pubmed/33400856 http://dx.doi.org/10.14814/phy2.14660 |
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author | Lamon, Séverine Morabito, Aimee Arentson‐Lantz, Emily Knowles, Olivia Vincent, Grace Elizabeth Condo, Dominique Alexander, Sarah Elizabeth Garnham, Andrew Paddon‐Jones, Douglas Aisbett, Brad |
author_facet | Lamon, Séverine Morabito, Aimee Arentson‐Lantz, Emily Knowles, Olivia Vincent, Grace Elizabeth Condo, Dominique Alexander, Sarah Elizabeth Garnham, Andrew Paddon‐Jones, Douglas Aisbett, Brad |
author_sort | Lamon, Séverine |
collection | PubMed |
description | Chronic sleep loss is a potent catabolic stressor, increasing the risk of metabolic dysfunction and loss of muscle mass and function. To provide mechanistic insight into these clinical outcomes, we sought to determine if acute sleep deprivation blunts skeletal muscle protein synthesis and promotes a catabolic environment. Healthy young adults (N = 13; seven male, six female) were subjected to one night of total sleep deprivation (DEP) and normal sleep (CON) in a randomized cross‐over design. Anabolic and catabolic hormonal profiles were assessed across the following day. Postprandial muscle protein fractional synthesis rate (FSR) was assessed between 13:00 and 15:00 and gene markers of muscle protein degradation were assessed at 13:00. Acute sleep deprivation reduced muscle protein synthesis by 18% (CON: 0.072 ± 0.015% vs. DEP: 0.059 ± 0.014%·h(‐1), p = .040). In addition, sleep deprivation increased plasma cortisol by 21% (p = .030) and decreased plasma testosterone by 24% (p = .029). No difference was found in the markers of protein degradation. A single night of total sleep deprivation is sufficient to induce anabolic resistance and a procatabolic environment. These acute changes may represent mechanistic precursors driving the metabolic dysfunction and body composition changes associated with chronic sleep deprivation. |
format | Online Article Text |
id | pubmed-7785053 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-77850532021-01-08 The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment Lamon, Séverine Morabito, Aimee Arentson‐Lantz, Emily Knowles, Olivia Vincent, Grace Elizabeth Condo, Dominique Alexander, Sarah Elizabeth Garnham, Andrew Paddon‐Jones, Douglas Aisbett, Brad Physiol Rep Original Research Chronic sleep loss is a potent catabolic stressor, increasing the risk of metabolic dysfunction and loss of muscle mass and function. To provide mechanistic insight into these clinical outcomes, we sought to determine if acute sleep deprivation blunts skeletal muscle protein synthesis and promotes a catabolic environment. Healthy young adults (N = 13; seven male, six female) were subjected to one night of total sleep deprivation (DEP) and normal sleep (CON) in a randomized cross‐over design. Anabolic and catabolic hormonal profiles were assessed across the following day. Postprandial muscle protein fractional synthesis rate (FSR) was assessed between 13:00 and 15:00 and gene markers of muscle protein degradation were assessed at 13:00. Acute sleep deprivation reduced muscle protein synthesis by 18% (CON: 0.072 ± 0.015% vs. DEP: 0.059 ± 0.014%·h(‐1), p = .040). In addition, sleep deprivation increased plasma cortisol by 21% (p = .030) and decreased plasma testosterone by 24% (p = .029). No difference was found in the markers of protein degradation. A single night of total sleep deprivation is sufficient to induce anabolic resistance and a procatabolic environment. These acute changes may represent mechanistic precursors driving the metabolic dysfunction and body composition changes associated with chronic sleep deprivation. John Wiley and Sons Inc. 2021-01-05 /pmc/articles/PMC7785053/ /pubmed/33400856 http://dx.doi.org/10.14814/phy2.14660 Text en © 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society 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. |
spellingShingle | Original Research Lamon, Séverine Morabito, Aimee Arentson‐Lantz, Emily Knowles, Olivia Vincent, Grace Elizabeth Condo, Dominique Alexander, Sarah Elizabeth Garnham, Andrew Paddon‐Jones, Douglas Aisbett, Brad The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment |
title | The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment |
title_full | The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment |
title_fullStr | The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment |
title_full_unstemmed | The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment |
title_short | The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment |
title_sort | effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7785053/ https://www.ncbi.nlm.nih.gov/pubmed/33400856 http://dx.doi.org/10.14814/phy2.14660 |
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