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Effects of Moderate–Intensity Physical Training on Skeletal Muscle Substrate Transporters and Metabolic Parameters of Ovariectomized Rats

A deficit of estrogen is associated with energy substrate imbalance, raising the risk of metabolic diseases. Physical training (PT) is a potent metabolic regulator through oxidation and storage of substrates transported by GLUT4 and FAT CD36 in skeletal muscle. However, little is known about the eff...

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Autores principales: Pejon, Taciane Maria Melges, Scariot, Pedro Paulo Menezes, Selistre-de-Araujo, Heloísa Sobreiro, Gobatto, Claudio Alexandre, Cornachione, Anabelle Silva, Beck, Wladimir Rafael
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9145860/
https://www.ncbi.nlm.nih.gov/pubmed/35629906
http://dx.doi.org/10.3390/metabo12050402
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author Pejon, Taciane Maria Melges
Scariot, Pedro Paulo Menezes
Selistre-de-Araujo, Heloísa Sobreiro
Gobatto, Claudio Alexandre
Cornachione, Anabelle Silva
Beck, Wladimir Rafael
author_facet Pejon, Taciane Maria Melges
Scariot, Pedro Paulo Menezes
Selistre-de-Araujo, Heloísa Sobreiro
Gobatto, Claudio Alexandre
Cornachione, Anabelle Silva
Beck, Wladimir Rafael
author_sort Pejon, Taciane Maria Melges
collection PubMed
description A deficit of estrogen is associated with energy substrate imbalance, raising the risk of metabolic diseases. Physical training (PT) is a potent metabolic regulator through oxidation and storage of substrates transported by GLUT4 and FAT CD36 in skeletal muscle. However, little is known about the effects of PT on these carriers in an estrogen-deficit scenario. Thus, the aim of this study was to determine the influence of 12 weeks of PT on metabolic variables and GLUT4 and FAT CD36 expression in the skeletal muscle of animals energetically impaired by ovariectomy (OVX). The trained animals swam 30 min/day, 5 days/week, at 80% of the critical load intensity. Spontaneous physical activity was measured biweekly. After training, FAT CD36 and GLUT4 expressions were quantified by immunofluorescence in the soleus, as well as muscular glycogen and triglyceride of the soleus, gluteus maximus and gastrocnemius. OVX significantly reduced FAT CD36, GLUT4 and spontaneous physical activity (p < 0.01), while PT significantly increased FAT CD36, GLUT4 and spontaneous physical activity (p < 0.01). PT increased soleus glycogen, and OVX decreased muscular triglyceride of gluteus maximus. Therefore, OVX can cause energy disarray through reduction in GLUT4 and FAT CD36 and their muscle substrates and PT prevented these metabolic consequences, masking ovarian estrogen’s absence.
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spelling pubmed-91458602022-05-29 Effects of Moderate–Intensity Physical Training on Skeletal Muscle Substrate Transporters and Metabolic Parameters of Ovariectomized Rats Pejon, Taciane Maria Melges Scariot, Pedro Paulo Menezes Selistre-de-Araujo, Heloísa Sobreiro Gobatto, Claudio Alexandre Cornachione, Anabelle Silva Beck, Wladimir Rafael Metabolites Article A deficit of estrogen is associated with energy substrate imbalance, raising the risk of metabolic diseases. Physical training (PT) is a potent metabolic regulator through oxidation and storage of substrates transported by GLUT4 and FAT CD36 in skeletal muscle. However, little is known about the effects of PT on these carriers in an estrogen-deficit scenario. Thus, the aim of this study was to determine the influence of 12 weeks of PT on metabolic variables and GLUT4 and FAT CD36 expression in the skeletal muscle of animals energetically impaired by ovariectomy (OVX). The trained animals swam 30 min/day, 5 days/week, at 80% of the critical load intensity. Spontaneous physical activity was measured biweekly. After training, FAT CD36 and GLUT4 expressions were quantified by immunofluorescence in the soleus, as well as muscular glycogen and triglyceride of the soleus, gluteus maximus and gastrocnemius. OVX significantly reduced FAT CD36, GLUT4 and spontaneous physical activity (p < 0.01), while PT significantly increased FAT CD36, GLUT4 and spontaneous physical activity (p < 0.01). PT increased soleus glycogen, and OVX decreased muscular triglyceride of gluteus maximus. Therefore, OVX can cause energy disarray through reduction in GLUT4 and FAT CD36 and their muscle substrates and PT prevented these metabolic consequences, masking ovarian estrogen’s absence. MDPI 2022-04-29 /pmc/articles/PMC9145860/ /pubmed/35629906 http://dx.doi.org/10.3390/metabo12050402 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Pejon, Taciane Maria Melges
Scariot, Pedro Paulo Menezes
Selistre-de-Araujo, Heloísa Sobreiro
Gobatto, Claudio Alexandre
Cornachione, Anabelle Silva
Beck, Wladimir Rafael
Effects of Moderate–Intensity Physical Training on Skeletal Muscle Substrate Transporters and Metabolic Parameters of Ovariectomized Rats
title Effects of Moderate–Intensity Physical Training on Skeletal Muscle Substrate Transporters and Metabolic Parameters of Ovariectomized Rats
title_full Effects of Moderate–Intensity Physical Training on Skeletal Muscle Substrate Transporters and Metabolic Parameters of Ovariectomized Rats
title_fullStr Effects of Moderate–Intensity Physical Training on Skeletal Muscle Substrate Transporters and Metabolic Parameters of Ovariectomized Rats
title_full_unstemmed Effects of Moderate–Intensity Physical Training on Skeletal Muscle Substrate Transporters and Metabolic Parameters of Ovariectomized Rats
title_short Effects of Moderate–Intensity Physical Training on Skeletal Muscle Substrate Transporters and Metabolic Parameters of Ovariectomized Rats
title_sort effects of moderate–intensity physical training on skeletal muscle substrate transporters and metabolic parameters of ovariectomized rats
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9145860/
https://www.ncbi.nlm.nih.gov/pubmed/35629906
http://dx.doi.org/10.3390/metabo12050402
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