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The Impact of Nutrition and Exercise Interventions to Modulate Muscle Metabolism in Health and Disease

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (10 January 2023) | Viewed by 7228

Special Issue Editor


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Guest Editor
CRBS, UR3072: Mitochondria, Oxidative Stress and Muscular Protection, University of Strasbourg, 1 rue Eugène Boeckel, 67000 Strasbourg, France
Interests: mitochondria; nutrition; skeletal muscle; ketogenic diet; intermittent fasting; physical exercise
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Special Issue Information

Dear Colleagues,

Physical exercise and nutrition are among the main hygienic and dietary measures that can reduce the risk factors for a large number of pathologies, and for cardiovascular diseases in particular. More and more, the integrative responses to exercise and nutrition are attracting interest, leading to its integration into clinical settings. At the molecular level, these measures are capable of efficiently modulating muscle metabolism by activating a large number of molecular signaling pathways, but some of them are not yet clearly identified. Moreover, studies assessing the impact of combined exercise and dietary interventions are limited and need to be further explored. This Special Issue aims to demonstrate both the clinical interests but also the mechanisms by which physical exercise and diet impact muscle metabolism and improve general homeostasis by impacting almost all organs of the body.

Dr. Joffrey Zoll
Guest Editor

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Keywords

  • skeletal muscle
  • physical exercise
  • diet
  • nutrition
  • metabolic disease
  • molecular pathways

Published Papers (3 papers)

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Research

12 pages, 4035 KiB  
Article
A Combination of Acetate, Propionate, and Butyrate Increases Glucose Uptake in C2C12 Myotubes
by Britt M. J. Otten, Mireille M. J. P. E. Sthijns and Freddy J. Troost
Nutrients 2023, 15(4), 946; https://doi.org/10.3390/nu15040946 - 14 Feb 2023
Cited by 3 | Viewed by 2294
Abstract
Background: Dietary fibers are subjected to saccharolytic fermentation by the gut microbiota, leading to the production of short chain fatty acids (SCFAs). SCFAs act as signaling molecules to different cells in the human body including skeletal muscle cells. The ability of SCFAs to [...] Read more.
Background: Dietary fibers are subjected to saccharolytic fermentation by the gut microbiota, leading to the production of short chain fatty acids (SCFAs). SCFAs act as signaling molecules to different cells in the human body including skeletal muscle cells. The ability of SCFAs to induce multiple signaling pathways, involving nuclear erythroid 2-related factor 2 (Nrf2), may contribute to the redox balance, and thereby may be involved in glucose homeostasis. The aim of this study is to investigate whether SCFAs increase glucose uptake by upregulating the endogenous antioxidant glutathione (GSH) in C2C12 myotubes. Methods: C2C12 myotubes were exposed to 1, 5, or 20 mM of single (acetate, propionate, or butyrate) or mixtures of SCFAs for 24 h. Cytotoxicity, glucose uptake, and intracellular GSH levels were measured. Results: 20 mM of mixture but not separate SCFAs induced cytotoxicity. Exposure to a mixture of SCFAs at 5 mM increased glucose uptake in myotubes, while 20 mM of propionate, butyrate, and mixtures decreased glucose uptake. Exposure to single SCFAs increased GSH levels in myotubes; however, SCFAs did not prevent the menadione-induced decrease in glucose uptake in myotubes. Conclusions: The effect of SCFAs on modulating glucose uptake in myotubes is not associated with the effect on endogenous GSH levels. Full article
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12 pages, 1789 KiB  
Article
Protective Role of Chronic Exercise Training in Modulating the Impact of Hyperglycemia on Vascular Sensitivity to Ischemia-Reperfusion
by Antoine Grandperrin, Mathilde Bourgoin, Sandrine Gayrard, Doria Boulghobra, Guillaume Walther, Cyril Reboul and Grégory Meyer
Nutrients 2023, 15(1), 212; https://doi.org/10.3390/nu15010212 - 1 Jan 2023
Viewed by 1736
Abstract
Hyperglycemia (HG) is associated with increased mortality and morbidity in acute ischemic events. Regardless of the tissue or organs involved, the vascular endothelium is a key target of ischemia-reperfusion (I/R) injury severity. Among endothelium-protective strategies, exercise has been widely described as useful. However, [...] Read more.
Hyperglycemia (HG) is associated with increased mortality and morbidity in acute ischemic events. Regardless of the tissue or organs involved, the vascular endothelium is a key target of ischemia-reperfusion (I/R) injury severity. Among endothelium-protective strategies, exercise has been widely described as useful. However, whether this strategy is able to impact the deleterious effect of HG on endothelial function during I/R has never been challenged. For this, 48 male Wistar rats were randomized into 4 groups: sedentary (Sed) or exercised (Ex, 45 min/day, 5 days/week for 5 weeks) rats, treated (hyperglycemic, HG) or not (normoglycemic, NG) with streptozotocin (40 mg/kg, 48 h before procedure). Vascular I/R (120/15 min) was performed by clamping the femoral artery. Arterial and downstream muscular perfusions were assessed using laser speckle contrast imaging. Vascular endothelial function was assessed in vivo 15 min after reperfusion. HG was responsible for impairment of reperfusion blood flow as well as endothelial function. Interestingly exercise was able to prevent those impairments in the HG group. In agreement with the previous results, HG increased reactive oxygen species production and decreased nitric oxide bioavailability whereas exercise training normalized these parameters. It, therefore, appears that exercise may be an effective prevention strategy against the exacerbation of vascular and muscular damage by hyperglycemia during I/R. Full article
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14 pages, 3825 KiB  
Article
Octanoic Acid-Enrichment Diet Improves Endurance Capacity and Reprograms Mitochondrial Biogenesis in Skeletal Muscle of Mice
by Anouk Charlot, Lucas Morel, Anthony Bringolf, Isabelle Georg, Anne-Laure Charles, Fabienne Goupilleau, Bernard Geny and Joffrey Zoll
Nutrients 2022, 14(13), 2721; https://doi.org/10.3390/nu14132721 - 29 Jun 2022
Cited by 3 | Viewed by 2551
Abstract
Background: Medium Chain Fatty Acids (MCFAs) are a dietary supplement that exhibit interesting properties, due to their smaller molecular size. The acute consumption of MCFAs is expected to enhance exercise performance. However, the short-term effects of MCFAs on endurance performance remains poorly understood. [...] Read more.
Background: Medium Chain Fatty Acids (MCFAs) are a dietary supplement that exhibit interesting properties, due to their smaller molecular size. The acute consumption of MCFAs is expected to enhance exercise performance. However, the short-term effects of MCFAs on endurance performance remains poorly understood. The aim of our study is to evaluate the octanoic acid (C8)-rich diet effect on endurance capacity, and to explore their molecular and cellular effects. Methods: C57BL/6J mice were fed with a chow diet (Control group) or an octanoic acid-rich diet (C8 diet) for 6 weeks. Spontaneous activity, submaximal and maximal exercise tests were carried out to characterize the exercise capacities of the mice. Beta-oxidation and mitochondrial biogenesis pathways were explored in skeletal muscle by RT-qPCR, Western Blot (Quadriceps) and histochemical staining (Gastrocnemius). Results: Mice fed with a C8-rich diet presented a higher spontaneous activity (p < 0.05) and endurance capacities (p < 0.05) than the control, but no effect on maximal effort was observed. They also presented changes in the skeletal muscle metabolic phenotype, with a higher number of the oxidative fibers, rich in mitochondria. At the molecular level, the C8-diet induced an AMPK activation (p < 0.05), associated with a significant increase in PGC1a and CS gene expression and protein levels. Conclusion: Our study provided evidence that C8-enrichment as a food supplementation improves endurance capacities and activates mitochondrial biogenesis pathways leading to higher skeletal muscle oxidative capacities. Full article
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