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Physical Activity: Relationship between Mitochondrial Energetics and Muscle Quality

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biophysics".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 8025

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Special Issue Editor

Prof. Dr. Loredana Capobianco

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Guest Editor

Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce, Italy
Interests: mitochondria; energetic metabolism; mitochondrial carrier; recombinant protein

Special Issue Information

Dear Colleagues,

It is known that physical inactivity is a risk factor that contributes to lifestyle-related diseases, including many causes of “preventable death”. Public health recommendations recognize regular exercise and physical activity as a essential element in the prevention, management, and treatment of numerous chronic conditions, including hypertension, coronary heart disease, obesity, type 2 diabetes mellitus (T2DM), and age-related muscle wasting (sarcopenia). In fact, regular exercise combined with dietary intervention can prove more successful than pharmacological intervention in the treatment and prevention of T2DM or sarcopenia. It is, therefore, important to highlight how life-long endurance/aerobic-type exercise can preserve muscle mass and function with age.

Efficient energy production and overall mitochondrial health are crucial for maintaining skeletal muscle function. Recent data indicate an important link between mitochondrial energetics and the control of muscle mass, suggesting a central role for mitochondrial energetics in regulating muscle mass. For example, mitochondrial oxidative stress has been shown to stimulate muscle protein breakdown by activating lysosome autophagy and proteasome systems and energetic stress, due to reduced ATP production, activating the adenosine monophosphate-activated protein kinase (AMPK)–FoxO3 pathways, leading to increased protein degradation.

Mitochondria are dynamic organelles that regulate cellular functions such as cellular respiration, calcium homeostasis, and reactive oxygen species (ROS) production. The most important role of mitochondria is energy metabolism, which involves the production of adenosine triphosphate (ATP) through oxidative phosphorylation in skeletal muscle mitochondria. The availability of ATP is critical for skeletal muscle contractile activity, both in explosive-power or sprint events lasting for seconds or minutes and in endurance events lasting for hours.

The metabolic and therapeutic effects of regular exercise on lifestyle-related chronic disease are long established, but the molecular bases for the adaptive changes in skeletal muscle mass and metabolic function remain an area of intense research.

Papers related to any aspect of the regulation of skeletal muscle energy metabolism and the adaptations that occur with physical training will be considered for this Special Issue.

Prof. Dr. Loredana Capobianco
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

bioenergetics
mitochondria
skeletal muscle
physical exercise
training
aerobic function

Published Papers (3 papers)

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Research

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16 pages, 2712 KiB

Open AccessArticle

Exercise and Doxorubicin Modify Markers of Iron Overload and Cardiolipin Deficiency in Cardiac Mitochondria

by Ryan N. Montalvo, Franccesco P. Boeno, Imtiaz M. Dowllah, Cesar E. Jacintho Moritz, Branden L. Nguyen, Vivian Doerr, Matthew P. Bomkamp and Ashley J. Smuder

Int. J. Mol. Sci. 2023, 24(9), 7689; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24097689 - 22 Apr 2023

Cited by 3 | Viewed by 1639

Abstract

Doxorubicin (DOX) is a chemotherapeutic agent highly effective at limiting cancer progression. Despite the efficacy of this anticancer drug, the clinical use of DOX is limited due to cardiotoxicity. The cardiac mitochondria are implicated as the primary target of DOX, resulting in inactivation of electron transport system complexes, oxidative stress, and iron overload. However, it is established that the cardiac mitochondrial subpopulations reveal differential responses to DOX exposure, with subsarcolemmal (SS) mitochondria demonstrating redox imbalance and the intermyofibrillar (IMF) mitochondria showing reduced respiration. In this regard, exercise training is an effective intervention to prevent DOX-induced cardiac dysfunction. Although it is clear that exercise confers mitochondrial protection, it is currently unknown if exercise training mitigates DOX cardiac mitochondrial toxicity by promoting beneficial adaptations to both the SS and IMF mitochondria. To test this, SS and IMF mitochondria were isolated from sedentary and exercise-preconditioned female Sprague Dawley rats exposed to acute DOX treatment. Our findings reveal a greater effect of exercise preconditioning on redox balance and iron handling in the SS mitochondria of DOX-treated rats compared to IMF, with rescue of cardiolipin synthase 1 expression in both subpopulations. These results demonstrate that exercise preconditioning improves mitochondrial homeostasis when combined with DOX treatment, and that the SS mitochondria display greater protection compared to the IMF mitochondria. These data provide important insights into the molecular mechanisms that are in part responsible for exercise-induced protection against DOX toxicity. Full article

(This article belongs to the Special Issue Physical Activity: Relationship between Mitochondrial Energetics and Muscle Quality)

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15 pages, 8894 KiB

Open AccessArticle

Effects of Low-Intensity and Long-Term Aerobic Exercise on the Psoas Muscle of mdx Mice: An Experimental Model of Duchenne Muscular Dystrophy

by Emilly Sigoli, Rosangela Aline Antão, Maria Paula Guerreiro, Tatiana Oliveira Passos de Araújo, Patty Karina dos Santos, Daiane Leite da Roza, Dilson E. Rassier and Anabelle Silva Cornachione

Int. J. Mol. Sci. 2022, 23(9), 4483; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23094483 - 19 Apr 2022

Cited by 4 | Viewed by 2195

Abstract

Duchenne muscular dystrophy (DMD) is a muscle disease characterized by the absence of the protein dystrophin, which causes a loss of sarcolemma integrity, determining recurrent muscle injuries, decrease in muscle function, and progressive degeneration. Currently, there is a need for therapeutic treatments to improve the quality of life of DMD patients. Here, we investigated the effects of a low-intensity aerobic training (37 sessions) on satellite cells, peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1α protein (PGC-1α), and different types of fibers of the psoas muscle from mdx mice (DMD experimental model). Wildtype and mdx mice were randomly divided into sedentary and trained groups (n = 24). Trained animals were subjected to 37 sessions of low-intensity running on a motorized treadmill. Subsequently, the psoas muscle was excised and analyzed by immunofluorescence for dystrophin, satellite cells, myosin heavy chain (MHC), and PGC-1α content. The minimal Feret’s diameters of the fibers were measured, and light microscopy was applied to observe general morphological features of the muscles. The training (37 sessions) improved morphological features in muscles from mdx mice and caused an increase in the number of quiescent/activated satellite cells. It also increased the content of PGC-1α in the mdx group. We concluded that low-intensity aerobic exercise (37 sessions) was able to reverse deleterious changes determined by DMD. Full article

(This article belongs to the Special Issue Physical Activity: Relationship between Mitochondrial Energetics and Muscle Quality)

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Review

Jump to: Research

12 pages, 567 KiB

Open AccessReview

The Effect of Physical Exercise on Cognitive Impairment in Neurodegenerative Disease: From Pathophysiology to Clinical and Rehabilitative Aspects

by Giacomo Farì, Paola Lunetti, Giovanni Pignatelli, Maria Vittoria Raele, Alessandra Cera, Giulia Mintrone, Maurizio Ranieri, Marisa Megna and Loredana Capobianco

Int. J. Mol. Sci. 2021, 22(21), 11632; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111632 - 27 Oct 2021

Cited by 26 | Viewed by 3397

Abstract

Neurodegenerative diseases are a group of pathologies that cause severe disability due to motor and cognitive limitations. In particular, cognitive impairment is a growing health and socioeconomic problem which is still difficult to deal with today. As there are no pharmacologically effective treatments for cognitive deficits, scientific interest is growing regarding the possible impacts of healthy lifestyles on them. In this context, physical activity is gaining more and more evidence as a primary prevention intervention, a nonpharmacological therapy and a rehabilitation tool for improving cognitive functions in neurodegenerative diseases. In this descriptive overview we highlight the neurobiological effects of physical exercise, which is able to promote neuroplasticity and neuroprotection by acting at the cytokine and hormonal level, and the consequent positive clinical effects on patients suffering from cognitive impairment. Full article

(This article belongs to the Special Issue Physical Activity: Relationship between Mitochondrial Energetics and Muscle Quality)

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