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Skeletal muscle metabolic gene response to carbohydrate feeding during exercise in the heat

BACKGROUND: Heat stress down-regulates mitochondrial function, while carbohydrate supplementation attenuates the exercise induced stimulation of mitochondrial biogenesis in humans. The effects of exogenous carbohydrate during exercise in the heat on metabolic mRNA have not been investigated in human...

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Autores principales: Dumke, Charles L, Slivka, Dustin R, Cuddy, John S, Hailes, Walter S, Ruby, Brent C
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3848455/
https://www.ncbi.nlm.nih.gov/pubmed/24034227
http://dx.doi.org/10.1186/1550-2783-10-40
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author Dumke, Charles L
Slivka, Dustin R
Cuddy, John S
Hailes, Walter S
Ruby, Brent C
author_facet Dumke, Charles L
Slivka, Dustin R
Cuddy, John S
Hailes, Walter S
Ruby, Brent C
author_sort Dumke, Charles L
collection PubMed
description BACKGROUND: Heat stress down-regulates mitochondrial function, while carbohydrate supplementation attenuates the exercise induced stimulation of mitochondrial biogenesis in humans. The effects of exogenous carbohydrate during exercise in the heat on metabolic mRNA have not been investigated in humans. The purpose of this study was to determine the impact of exercise with and without carbohydrate supplementation on skeletal muscle metabolic response in the heat. METHODS: Eight recreationally active males (4.05 ± 0.2 L(.)min(-1)) completed 2 trials which included 1 hr of cycling at 70% workload max and 3 hr recovery in a hot environment. Both trials were conducted in a climate controlled environmental chamber (38°C and 40% RH). The trials differed by the consumption of either a 6% carbohydrate (CHO) containing beverage (8 ml(.)kg(-1.)hr(-1)) or placebo (P) during exercise in random order. Muscle biopsies were obtained from the vastus lateralis before exercise, immediately post-exercise and at the end of the 3 hr recovery period. Muscle was analyzed for muscle glycogen and mRNA related to metabolic and mitochondrial development (MFN2, PGC-1α, GLUT4, UCP3). Expired gases were measured to determine whole body substrate use during exercise. RESULTS: Carbohydrate oxidation and muscle glycogen utilization did not differ between trials, whereas fat oxidation was elevated during exercise in P. Exercise caused an increase in PGC-1α, and GLUT4 (P < 0.05) independent of exogenous carbohydrate provision. Carbohydrate consumption attenuated the mRNA response in UCP3 (P < 0.05). CONCLUSIONS: This study indicates that the provision of exogenous carbohydrate attenuates the stimulation of mRNA expression of UCP3 following exercise in the heat.
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spelling pubmed-38484552013-12-04 Skeletal muscle metabolic gene response to carbohydrate feeding during exercise in the heat Dumke, Charles L Slivka, Dustin R Cuddy, John S Hailes, Walter S Ruby, Brent C J Int Soc Sports Nutr Research Article BACKGROUND: Heat stress down-regulates mitochondrial function, while carbohydrate supplementation attenuates the exercise induced stimulation of mitochondrial biogenesis in humans. The effects of exogenous carbohydrate during exercise in the heat on metabolic mRNA have not been investigated in humans. The purpose of this study was to determine the impact of exercise with and without carbohydrate supplementation on skeletal muscle metabolic response in the heat. METHODS: Eight recreationally active males (4.05 ± 0.2 L(.)min(-1)) completed 2 trials which included 1 hr of cycling at 70% workload max and 3 hr recovery in a hot environment. Both trials were conducted in a climate controlled environmental chamber (38°C and 40% RH). The trials differed by the consumption of either a 6% carbohydrate (CHO) containing beverage (8 ml(.)kg(-1.)hr(-1)) or placebo (P) during exercise in random order. Muscle biopsies were obtained from the vastus lateralis before exercise, immediately post-exercise and at the end of the 3 hr recovery period. Muscle was analyzed for muscle glycogen and mRNA related to metabolic and mitochondrial development (MFN2, PGC-1α, GLUT4, UCP3). Expired gases were measured to determine whole body substrate use during exercise. RESULTS: Carbohydrate oxidation and muscle glycogen utilization did not differ between trials, whereas fat oxidation was elevated during exercise in P. Exercise caused an increase in PGC-1α, and GLUT4 (P < 0.05) independent of exogenous carbohydrate provision. Carbohydrate consumption attenuated the mRNA response in UCP3 (P < 0.05). CONCLUSIONS: This study indicates that the provision of exogenous carbohydrate attenuates the stimulation of mRNA expression of UCP3 following exercise in the heat. BioMed Central 2013-09-13 /pmc/articles/PMC3848455/ /pubmed/24034227 http://dx.doi.org/10.1186/1550-2783-10-40 Text en Copyright © 2013 Dumke et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Dumke, Charles L
Slivka, Dustin R
Cuddy, John S
Hailes, Walter S
Ruby, Brent C
Skeletal muscle metabolic gene response to carbohydrate feeding during exercise in the heat
title Skeletal muscle metabolic gene response to carbohydrate feeding during exercise in the heat
title_full Skeletal muscle metabolic gene response to carbohydrate feeding during exercise in the heat
title_fullStr Skeletal muscle metabolic gene response to carbohydrate feeding during exercise in the heat
title_full_unstemmed Skeletal muscle metabolic gene response to carbohydrate feeding during exercise in the heat
title_short Skeletal muscle metabolic gene response to carbohydrate feeding during exercise in the heat
title_sort skeletal muscle metabolic gene response to carbohydrate feeding during exercise in the heat
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3848455/
https://www.ncbi.nlm.nih.gov/pubmed/24034227
http://dx.doi.org/10.1186/1550-2783-10-40
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