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Antioxidants
Special Issues
Mitochondrial Function, Oxidative Stress and Inflammation in Skeletal Muscle
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Mitochondrial Function, Oxidative Stress and Inflammation in Skeletal Muscle

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 27247

Special Issue Editor

Dr. Bernard Geny

E-Mail Website
Guest Editor
1. Team 3072 “Mitochondria, Oxidative Stress and Muscle Protection”, Translational Medicine Federation of Strasbourg (FMTS), Faculty of Medicine, University of Strasbourg, 11 Rue Humann, 67000 Strasbourg, France
2. Physiology and Functional Exploration Service, University Hospital of Strasbourg, 1 Place de l’Hôpital, 67091 Strasbourg, France
Interests: antioxidants; oxidative stress; mitochondria; skeletal muscles
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Skeletal muscles represent about 40% of our body mass and are indispensable, being involved not only in mobility, but also in major functions, through the release of myokines. Skeletal muscle dysfunctions are frequent and characterize many acute and chronic conditions, determining both the quality of life and prognosis of patients. Although mitochondrial dysfunction, oxidative stress, and inflammation are key factors of muscle pathology, their interactions still have to be investigated both in healthy and diseased situations, in order to improve performance in athletes or for therapeutic approaches in patients.

This Special Issue will publish original research papers and reviews aiming to investigate the molecular, cellular, and systemic mechanisms by which reactive oxygen species and inflammation interact to modulate muscle function, with an emphasis on the beneficial signaling effect of low level oxidative stress and inflammation on muscle performance or exercise recovery, associated or not with improved mitochondrial biogenesis and dynamics. Additionally, studies on the implication of skeletal muscle mitochondrial dysfunction, oxidative stress, and inflammation in acute or chronic diseases such as inflammatory myopathies, peripheral arterial diseases, shock, or major systemic diseases, at experimental or clinical levels, are welcome. Furthermore, new therapeutic avenues, potentially adapted to muscle metabolic phenotypes, and ranging from ischemic and pharmacologic conditioning, including antioxidant therapy, to damage associated pattern modulation and mitochondrial transplantation, could be shared with researchers and clinicians.

Dr. Bernard Geny
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

  • Oxidative stress
  • reactive oxygen species
  • antioxidant
  • mitochondria
  • oxidative capacity
  • inflammation
  • muscle
  • metabolic phenotype
  • health
  • disease

Published Papers (5 papers)

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Research

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18 pages, 2922 KiB  
Article
Effects of Cardiovascular, Resistance and Combined Exercise Training on Cardiovascular, Performance and Blood Redox Parameters in Coronary Artery Disease Patients: An 8-Month Training-Detraining Randomized Intervention
by Tryfonas Tofas, Ioannis G. Fatouros, Dimitrios Draganidis, Chariklia K. Deli, Athanasios Chatzinikolaou, Charalambos Tziortzis, George Panayiotou, Yiannis Koutedakis and Athanasios Z. Jamurtas
Antioxidants 2021, 10(3), 409; https://doi.org/10.3390/antiox10030409 - 09 Mar 2021
Cited by 11 | Viewed by 3070
Abstract
It is well-documented that chronic/regular exercise improves the cardiovascular function, decreases oxidative stress and enhances the antioxidant capacity in coronary artery disease (CAD) patients. However, there is insufficient evidence regarding the chronic effects of different types of training and detraining on cardiovascular function [...] Read more.
It is well-documented that chronic/regular exercise improves the cardiovascular function, decreases oxidative stress and enhances the antioxidant capacity in coronary artery disease (CAD) patients. However, there is insufficient evidence regarding the chronic effects of different types of training and detraining on cardiovascular function and the levels of oxidative stress and antioxidant status in these patients. Therefore, the present study aimed at investigating the effects of cardiovascular, resistance and combined exercise training followed by a three-month detraining period, on cardiovascular function, physical performance and blood redox status parameters in CAD patients. Sixty coronary artery disease patients were randomly assigned to either a cardiovascular training (CVT, N = 15), resistance training (RT, N = 11), combined cardiovascular and resistance training (CT, N = 16) or a control (C, N = 15) group. The training groups participated in an 8-month supervised training program (training three days/week) followed by a 3-month detraining period, while the control group participated only in measurements. Body composition, blood pressure, performance-related variables (aerobic capacity (VO2max), muscle strength, flexibility) and blood redox status-related parameters (thiobarbituric acid reactive substances (TBARS), total antioxidant capacity (TAC), reduced glutathione (GSH), oxidized glutathione (GSSG), catalase activity (CAT), protein carbonyls (PC)) were assessed at the beginning of the study, after 4 and 8 months of training as well as following 1, 2 and 3 months of detraining (DT). CVT induced the most remarkable and pronounced alterations in blood pressure (~9% reduction in systolic blood pressure and ~5% in diastolic blood pressure) and redox status since it had a positive effect on all redox-related variables (ranging from 16 to 137%). RT and CT training affected positively some of the assessed (TAC, CAT and PC) redox-related variables. Performance-related variables retained the positive response of the training, whereas most of the redox status parameters, for all training groups, restored near to the pre-exercise values at the end of the DT period. These results indicate that exercise training has a significant effect on redox status of CAD. Three months of detraining is enough to abolish the exercise-induced beneficial effects on redox status, indicating that for a better antioxidant status, exercise must be a lifetime commitment. Full article
(This article belongs to the Special Issue Mitochondrial Function, Oxidative Stress and Inflammation in Skeletal Muscle)
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20 pages, 3105 KiB  
Article
Vitamin C and E Treatment Blunts Sprint Interval Training–Induced Changes in Inflammatory Mediator-, Calcium-, and Mitochondria-Related Signaling in Recreationally Active Elderly Humans
by Victoria L. Wyckelsma, Tomas Venckunas, Marius Brazaitis, Stefano Gastaldello, Audrius Snieckus, Nerijus Eimantas, Neringa Baranauskiene, Andrejus Subocius, Albertas Skurvydas, Mati Pääsuke, Helena Gapeyeva, Priit Kaasik, Reedik Pääsuke, Jaak Jürimäe, Brigitte A. Graf, Bengt Kayser, Nicolas Place, Daniel C. Andersson, Sigitas Kamandulis and Håkan Westerblad
Antioxidants 2020, 9(9), 879; https://doi.org/10.3390/antiox9090879 - 17 Sep 2020
Cited by 21 | Viewed by 4483
Abstract
Sprint interval training (SIT) has emerged as a time-efficient training regimen for young individuals. Here, we studied whether SIT is effective also in elderly individuals and whether the training response was affected by treatment with the antioxidants vitamin C and E. Recreationally active [...] Read more.
Sprint interval training (SIT) has emerged as a time-efficient training regimen for young individuals. Here, we studied whether SIT is effective also in elderly individuals and whether the training response was affected by treatment with the antioxidants vitamin C and E. Recreationally active elderly (mean age 65) men received either vitamin C (1 g/day) and vitamin E (235 mg/day) or placebo. Training consisted of nine SIT sessions (three sessions/week for three weeks of 4-6 repetitions of 30-s all-out cycling sprints) interposed by 4 min rest. Vastus lateralis muscle biopsies were taken before, 1 h after, and 24 h after the first and last SIT sessions. At the end of the three weeks of training, SIT-induced changes in relative mRNA expression of reactive oxygen/nitrogen species (ROS)- and mitochondria-related proteins, inflammatory mediators, and the sarcoplasmic reticulum Ca2+ channel, the ryanodine receptor 1 (RyR1), were blunted in the vitamin treated group. Western blots frequently showed a major (>50%) decrease in the full-length expression of RyR1 24 h after SIT sessions; in the trained state, vitamin treatment seemed to provide protection against this severe RyR1 modification. Power at exhaustion during an incremental cycling test was increased by ~5% at the end of the training period, whereas maximal oxygen uptake remained unchanged; vitamin treatment did not affect these measures. In conclusion, treatment with the antioxidants vitamin C and E blunts SIT-induced cellular signaling in skeletal muscle of elderly individuals, while the present training regimen was too short or too intense for the changes in signaling to be translated into a clear-cut change in physical performance. Full article
(This article belongs to the Special Issue Mitochondrial Function, Oxidative Stress and Inflammation in Skeletal Muscle)
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Review

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20 pages, 898 KiB  
Review
Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting Due to Disease, Aging, and Prolonged Inactivity
by Hayden W. Hyatt and Scott K. Powers
Antioxidants 2021, 10(4), 588; https://doi.org/10.3390/antiox10040588 - 11 Apr 2021
Cited by 38 | Viewed by 9313
Abstract
Skeletal muscle is the most abundant tissue in the body and is required for numerous vital functions, including breathing and locomotion. Notably, deterioration of skeletal muscle mass is also highly correlated to mortality in patients suffering from chronic diseases (e.g., cancer). Numerous conditions [...] Read more.
Skeletal muscle is the most abundant tissue in the body and is required for numerous vital functions, including breathing and locomotion. Notably, deterioration of skeletal muscle mass is also highly correlated to mortality in patients suffering from chronic diseases (e.g., cancer). Numerous conditions can promote skeletal muscle wasting, including several chronic diseases, cancer chemotherapy, aging, and prolonged inactivity. Although the mechanisms responsible for this loss of muscle mass is multifactorial, mitochondrial dysfunction is predicted to be a major contributor to muscle wasting in various conditions. This systematic review will highlight the biochemical pathways that have been shown to link mitochondrial dysfunction to skeletal muscle wasting. Importantly, we will discuss the experimental evidence that connects mitochondrial dysfunction to muscle wasting in specific diseases (i.e., cancer and sepsis), aging, cancer chemotherapy, and prolonged muscle inactivity (e.g., limb immobilization). Finally, in hopes of stimulating future research, we conclude with a discussion of important future directions for research in the field of muscle wasting. Full article
(This article belongs to the Special Issue Mitochondrial Function, Oxidative Stress and Inflammation in Skeletal Muscle)
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22 pages, 829 KiB  
Review
Mitochondria Homeostasis and Oxidant/Antioxidant Balance in Skeletal Muscle—Do Myokines Play a Role?
by Brian Pak Shing Pang, Wing Suen Chan and Chi Bun Chan
Antioxidants 2021, 10(2), 179; https://doi.org/10.3390/antiox10020179 - 27 Jan 2021
Cited by 17 | Viewed by 4597
Abstract
Mitochondria are the cellular powerhouses that generate adenosine triphosphate (ATP) to substantiate various biochemical activities. Instead of being a static intracellular structure, they are dynamic organelles that perform constant structural and functional remodeling in response to different metabolic stresses. In situations that require [...] Read more.
Mitochondria are the cellular powerhouses that generate adenosine triphosphate (ATP) to substantiate various biochemical activities. Instead of being a static intracellular structure, they are dynamic organelles that perform constant structural and functional remodeling in response to different metabolic stresses. In situations that require a high ATP supply, new mitochondria are assembled (mitochondrial biogenesis) or formed by fusing the existing mitochondria (mitochondrial fusion) to maximize the oxidative capacity. On the other hand, nutrient overload may produce detrimental metabolites such as reactive oxidative species (ROS) that wreck the organelle, leading to the split of damaged mitochondria (mitofission) for clearance (mitophagy). These vital processes are tightly regulated by a sophisticated quality control system involving energy sensing, intracellular membrane interaction, autophagy, and proteasomal degradation to optimize the number of healthy mitochondria. The effective mitochondrial surveillance is particularly important to skeletal muscle fitness because of its large tissue mass as well as its high metabolic activities for supporting the intensive myofiber contractility. Indeed, the failure of the mitochondrial quality control system in skeletal muscle is associated with diseases such as insulin resistance, aging, and muscle wasting. While the mitochondrial dynamics in cells are believed to be intrinsically controlled by the energy content and nutrient availability, other upstream regulators such as hormonal signals from distal organs or factors generated by the muscle itself may also play a critical role. It is now clear that skeletal muscle actively participates in systemic energy homeostasis via producing hundreds of myokines. Acting either as autocrine/paracrine or circulating hormones to crosstalk with other organs, these secretory myokines regulate a large number of physiological activities including insulin sensitivity, fuel utilization, cell differentiation, and appetite behavior. In this article, we will review the mechanism of myokines in mitochondrial quality control and ROS balance, and discuss their translational potential. Full article
(This article belongs to the Special Issue Mitochondrial Function, Oxidative Stress and Inflammation in Skeletal Muscle)
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23 pages, 2386 KiB  
Review
Skeletal Muscle Mitochondrial Dysfunction and Oxidative Stress in Peripheral Arterial Disease: A Unifying Mechanism and Therapeutic Target
by Kyoungrae Kim, Erik M. Anderson, Salvatore T. Scali and Terence E. Ryan
Antioxidants 2020, 9(12), 1304; https://doi.org/10.3390/antiox9121304 - 18 Dec 2020
Cited by 22 | Viewed by 4902
Abstract
Peripheral artery disease (PAD) is caused by atherosclerosis in the lower extremities, which leads to a spectrum of life-altering symptomatology, including claudication, ischemic rest pain, and gangrene requiring limb amputation. Current treatments for PAD are focused primarily on re-establishing blood flow to the [...] Read more.
Peripheral artery disease (PAD) is caused by atherosclerosis in the lower extremities, which leads to a spectrum of life-altering symptomatology, including claudication, ischemic rest pain, and gangrene requiring limb amputation. Current treatments for PAD are focused primarily on re-establishing blood flow to the ischemic tissue, implying that blood flow is the decisive factor that determines whether or not the tissue survives. Unfortunately, failure rates of endovascular and revascularization procedures remain unacceptably high and numerous cell- and gene-based vascular therapies have failed to demonstrate efficacy in clinical trials. The low success of vascular-focused therapies implies that non-vascular tissues, such as skeletal muscle and oxidative stress, may substantially contribute to PAD pathobiology. Clues toward the importance of skeletal muscle in PAD pathobiology stem from clinical observations that muscle function is a strong predictor of mortality. Mitochondrial impairments in muscle have been documented in PAD patients, although its potential role in clinical pathology is incompletely understood. In this review, we discuss the underlying mechanisms causing mitochondrial dysfunction in ischemic skeletal muscle, including causal evidence in rodent studies, and highlight emerging mitochondrial-targeted therapies that have potential to improve PAD outcomes. Particularly, we will analyze literature data on reactive oxygen species production and potential counteracting endogenous and exogenous antioxidants. Full article
(This article belongs to the Special Issue Mitochondrial Function, Oxidative Stress and Inflammation in Skeletal Muscle)
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