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Role of prior feeding status in mediating the effects of exercise on blood glucose kinetics
Changes in blood glucose concentrations are underpinned by blood glucose kinetics (endogenous and exogenous glucose appearance rates and glucose disappearance rates). Exercise potently alters blood glucose kinetics and can thereby be used as a tool to control blood glucose concentration. However, mo...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Physiological Society
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10635662/ https://www.ncbi.nlm.nih.gov/pubmed/37642241 http://dx.doi.org/10.1152/ajpcell.00271.2023 |
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author | Moreno-Cabañas, Alfonso Gonzalez, Javier T. |
author_facet | Moreno-Cabañas, Alfonso Gonzalez, Javier T. |
author_sort | Moreno-Cabañas, Alfonso |
collection | PubMed |
description | Changes in blood glucose concentrations are underpinned by blood glucose kinetics (endogenous and exogenous glucose appearance rates and glucose disappearance rates). Exercise potently alters blood glucose kinetics and can thereby be used as a tool to control blood glucose concentration. However, most studies of exercise-induced changes in glucose kinetics are conducted in a fasted state, and therefore less is known about the effects of exercise on glucose kinetics when exercise is conducted in a postprandial state. Emerging evidence suggests that food intake prior to exercise can increase postprandial blood glucose flux compared with when meals are consumed after exercise, whereby both glucose appearance rates and disappearance rates are increased. The mechanisms underlying the mediating effect of exercise conducted in the fed versus the fasted state are yet to be fully elucidated. Current evidence demonstrates that exercise in the postprandial state increased glucose appearance rates due to both increased exogenous and endogenous appearance and may be due to changes in splanchnic blood flow, intestinal permeability, and/or hepatic glucose extraction. On the other hand, increased glucose disappearance rates after exercise in the fed state have been shown to be associated with increased intramuscular AMPK signaling via a mismatch between carbohydrate utilization and delivery. Due to differences in blood glucose kinetics and other physiological differences, studies conducted in the fasted state cannot be immediately translated to the fed state. Therefore, conducting studies in the fed state could improve the external validity of data pertaining to glucose kinetics and intramuscular signaling in response to nutrition and exercise. |
format | Online Article Text |
id | pubmed-10635662 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | American Physiological Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-106356622023-11-15 Role of prior feeding status in mediating the effects of exercise on blood glucose kinetics Moreno-Cabañas, Alfonso Gonzalez, Javier T. Am J Physiol Cell Physiol Review Changes in blood glucose concentrations are underpinned by blood glucose kinetics (endogenous and exogenous glucose appearance rates and glucose disappearance rates). Exercise potently alters blood glucose kinetics and can thereby be used as a tool to control blood glucose concentration. However, most studies of exercise-induced changes in glucose kinetics are conducted in a fasted state, and therefore less is known about the effects of exercise on glucose kinetics when exercise is conducted in a postprandial state. Emerging evidence suggests that food intake prior to exercise can increase postprandial blood glucose flux compared with when meals are consumed after exercise, whereby both glucose appearance rates and disappearance rates are increased. The mechanisms underlying the mediating effect of exercise conducted in the fed versus the fasted state are yet to be fully elucidated. Current evidence demonstrates that exercise in the postprandial state increased glucose appearance rates due to both increased exogenous and endogenous appearance and may be due to changes in splanchnic blood flow, intestinal permeability, and/or hepatic glucose extraction. On the other hand, increased glucose disappearance rates after exercise in the fed state have been shown to be associated with increased intramuscular AMPK signaling via a mismatch between carbohydrate utilization and delivery. Due to differences in blood glucose kinetics and other physiological differences, studies conducted in the fasted state cannot be immediately translated to the fed state. Therefore, conducting studies in the fed state could improve the external validity of data pertaining to glucose kinetics and intramuscular signaling in response to nutrition and exercise. American Physiological Society 2023-10-01 2023-08-29 /pmc/articles/PMC10635662/ /pubmed/37642241 http://dx.doi.org/10.1152/ajpcell.00271.2023 Text en Copyright © 2023 The Authors. https://creativecommons.org/licenses/by/4.0/Licensed under Creative Commons Attribution CC-BY 4.0 (https://creativecommons.org/licenses/by/4.0/) . Published by the American Physiological Society. |
spellingShingle | Review Moreno-Cabañas, Alfonso Gonzalez, Javier T. Role of prior feeding status in mediating the effects of exercise on blood glucose kinetics |
title | Role of prior feeding status in mediating the effects of exercise on blood glucose kinetics |
title_full | Role of prior feeding status in mediating the effects of exercise on blood glucose kinetics |
title_fullStr | Role of prior feeding status in mediating the effects of exercise on blood glucose kinetics |
title_full_unstemmed | Role of prior feeding status in mediating the effects of exercise on blood glucose kinetics |
title_short | Role of prior feeding status in mediating the effects of exercise on blood glucose kinetics |
title_sort | role of prior feeding status in mediating the effects of exercise on blood glucose kinetics |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10635662/ https://www.ncbi.nlm.nih.gov/pubmed/37642241 http://dx.doi.org/10.1152/ajpcell.00271.2023 |
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