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Antioxidants
Special Issues
Oxidative Stress and Mitochondrial Function in Exercise and Physical Activity
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Oxidative Stress and Mitochondrial Function in Exercise and Physical Activity

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 1709

Special Issue Editor

Dr. Cláudia Jacques Lagranha

E-Mail Website
Guest Editor
Graduate Program in Neuropsychiatry and Behavioral Sciences, Center for Medical Sciences, Federal University of Pernambuco, Recife 507400-600, Pernambuco, Brazil
Interests: exercise; mitochondrial function; metabolism; oxidative stress; diseases related to inactivity

Special Issue Information

Dear Colleagues,

Several chronic diseases are related to oxidative stress and are highly related to a higher incidence of sedentarism and inactivity. Several groups have postulated that exercise and physical activity represent good strategies for promoting health and fighting chronic diseases including hypertension, heart failure, myocardial infarction, diabetes, anxiety, and depression, among others. Exercise is also an important tool for stimulating several intracellular cascades that culminate in an increase in proteins and active molecules that are capable of interacting with a higher rate of production of reactive oxygen species (ROS). Therefore, the more we can stimulate antioxidant defenses, the lower the probability of inducing oxidative damage in cellular components. It is well known that the main site where ROS are produced is in the mitochondria; therefore, a homeostatic imbalance in the function of this organelle is associated with an increase in ROS and the establishment of oxidative stress. In this Special Issue, we aim to share research focusing on the effects of physical activity, physical exercise, and training to promote health and counterbalance the deleterious effects of ROS production and oxidative damage associated with the mitochondrial dysfunction induced by inappropriate lifestyles (sedentarism, overnutrition, smoking, alcohol consumption, drug abuse, etc.). With this in mind, we welcome studies that have investigated the outcomes of physical activity, sedentary behavior, and physical exercise and training associated with oxidative stress biomarkers (in lipids, proteins, or DNA) in experimental or clinical studies (involving mice, rats, children, adolescents, adults, older adults, or gender differences) in physiological or disease-related conditions. Our objective in this Special Issue of Antioxidants is to highlight the relevance of the expanding efficacy of physical activity and exercise against chronic diseases.

As Guest Editor, I invite you to contribute to the Special Issue on “Oxidative Stress and Mitochondrial Function in Exercise and Physical Activity”. Original research reports and reviews will be published online in Antioxidants.

Dr. Cláudia Jacques Lagranha
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondrial function
  • oxidative stress
  • diseases
  • exercise
  • physical activity

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Published Papers (2 papers)

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Research

13 pages, 4441 KiB  
Article
Mitochondrial Redox Status Regulates Glycogen Metabolism via Glycogen Phosphorylase Activity
by Ikko Sakamoto, Shuichi Shibuya, Hidetoshi Nojiri, Kotaro Takeno, Hiroshi Nishimune, Keisuke Yaku, Takashi Nakagawa, Muneaki Ishijima and Takahiko Shimizu
Antioxidants 2024, 13(11), 1421; https://doi.org/10.3390/antiox13111421 - 20 Nov 2024
Viewed by 278
Abstract
Mitochondria and glycogen are co-distributed in skeletal muscles to regulate the metabolic status. Mitochondria are also redox centers that regulate the muscle function during exercise. However, the pathophysiological relationship between the mitochondrial redox status and glycogen metabolism in the muscle remains unclear. In [...] Read more.
Mitochondria and glycogen are co-distributed in skeletal muscles to regulate the metabolic status. Mitochondria are also redox centers that regulate the muscle function during exercise. However, the pathophysiological relationship between the mitochondrial redox status and glycogen metabolism in the muscle remains unclear. In the present study, we examined the pathological effects of mitochondrial dysfunction induced by mitochondrial superoxide dismutase (SOD2) depletion on glycogen metabolism. We found that muscle glycogen was significantly accumulated in association with motor dysfunction in mice with a muscle-specific SOD2 deficiency. Muscle glycogen phosphorylase (GP-M) activity, which is a key enzyme for glycogen degradation at times when energy is needed (e.g., during exercise), was significantly decreased in the mutant muscle. Moreover, the GP-M activity on normal muscle sections decreased after treatment with paraquat, a superoxide generator. In contrast, treatment with antioxidants reversed the GP-M activity and motor disturbance of the mutant mice, indicating that GP-M activity was reversibly regulated by the redox balance. These results demonstrate that the maintenance of the mitochondrial redox balance regulates glycogen metabolism via GP-M activity. Full article
(This article belongs to the Special Issue Oxidative Stress and Mitochondrial Function in Exercise and Physical Activity)
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19 pages, 5444 KiB  
Article
Metabolomic Profiling Reveals That Exercise Lowers Biomarkers of Cardiac Dysfunction in Rats with Type 2 Diabetes
by Tutu Wang, Miaomiao Ning, Yurou Mo, Xinyu Tian, Yu Fu, Ismail Laher and Shunchang Li
Antioxidants 2024, 13(10), 1167; https://doi.org/10.3390/antiox13101167 - 26 Sep 2024
Viewed by 1005
Abstract
The increasing prevalence of type 2 diabetes mellitus (T2DM) leads to significant global health challenges, including cardiac structural and functional deficits, which in severe cases can progress to heart failure that can further strain healthcare resources. Aerobic exercise can ameliorate cardiac dysfunction in [...] Read more.
The increasing prevalence of type 2 diabetes mellitus (T2DM) leads to significant global health challenges, including cardiac structural and functional deficits, which in severe cases can progress to heart failure that can further strain healthcare resources. Aerobic exercise can ameliorate cardiac dysfunction in individuals with diabetes, although a comprehensive understanding of its underlying mechanisms remains elusive. This study utilizes untargeted metabolomics to reveal aerobic-exercise-activated metabolic biomarkers in the cardiac tissues of Sprague Dawley rats with T2DM. Metabolomics analysis revealed that diabetes altered 1029 myocardial metabolites, while aerobic exercise reversed 208 of these metabolites, of which 112 were upregulated and 96 downregulated. Pathway topology analysis suggested that these metabolites predominantly contributed to purine metabolism and arginine biosynthesis. Furthermore, receiver operating characteristic curve analysis identified 10 potential biomarkers, including xanthine, hypoxanthine, inosine, dGMP, l-glutamic acid, l-arginine, l-tryptophan, (R)-3-hydroxybutyric acid, riboflavin, and glucolepidiin. Finally, data from Pearson correlation analysis indicated that some metabolic biomarkers strongly correlated with cardiac function. Our data suggest that certain metabolic biomarkers play an important role in ameliorating diabetes-related cardiac dysfunction by aerobic exercise. Full article
(This article belongs to the Special Issue Oxidative Stress and Mitochondrial Function in Exercise and Physical Activity)
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