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Special Issue "Molecular and Cellular Exercise Physiology in Metabolism"

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

Deadline for manuscript submissions: 31 December 2021.

Special Issue Editor

Prof. Dr. Jin-Ho Koh
E-Mail Website
Guest Editor
College of Medicine, Yeungnam University, Daegu, Korea
Interests: exercise; mitochondria; metabolism; metabolic disease; aging

Special Issue Information

Dear Colleagues

Exercise is one of the major strategies to protect and improve metabolic disease induced by a sedentary lifestyle, abnormal diet, and aging. People perform various exercise types, leading to numerous molecular and cellular alterations. These changes enhance cellular metabolism and functions in tissues including skeletal muscle, liver, heart, adipose tissue, brain, and others. Exercise also enhances the interplay between cells, tissues, organs, and systems. Numerous molecules are involved in the interaction, and their crosstalk can facilitate metabolic rate and function to support energy in contracting muscle. In addition, regular exercise training leads to molecular and cellular adaptations, which can help to protect and improve health against various diseases. Understanding molecular and cellular mechanisms that are induced by various exercise types can provide more advanced treatment to improve sports performance or health. In addition, the exercise-induced molecular pathway can be targeted to prevent and treat metabolic disease patients who are unable to perform exercise training regularly. We are interested in metabolic molecules, such as PPARβ/δ, PGC-1α, AMPK, and any other molecules that are linked to metabolic function. We are also interested in not only mitochondrial function that is induced by a specific molecule with exercise but also certain metabolites, anti-inflammatory peptides, and RNA species, termed as exerkines, that are released in response to exercise and which could promote healthy systemic energy homeostasis via signaling and interplay between cells, tissues, and organs.

Thus, this Special Issue entitled ‘Molecular and Cellular Exercise Physiology in Metabolism’ will discuss the recent advances in metabolic molecular mechanisms that are induced by exercise to understand exercise physiology and treat a health problem. Topics related to both original and reviewed articles are welcome.

Prof. Dr. Jin-Ho Koh
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 papers will be 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

  • exercise
  • physiology
  • metabolism
  • molecular mechanisms
  • mitochondria
  • exerkine
  • metabolic disease
  • health
  • aging

Published Papers (3 papers)

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Research

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Article
Exercise, but Not Metformin Prevents Loss of Muscle Function Due to Doxorubicin in Mice Using an In Situ Method
Int. J. Mol. Sci. 2021, 22(17), 9163; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179163 - 25 Aug 2021
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Abstract
Though effective in treating various types of cancer, the chemotherapeutic doxorubicin (DOX) is associated with skeletal muscle wasting and fatigue. The purpose of this study was to assess muscle function in situ following DOX administration in mice. Furthermore, pre-treatments with exercise (EX) or [...] Read more.
Though effective in treating various types of cancer, the chemotherapeutic doxorubicin (DOX) is associated with skeletal muscle wasting and fatigue. The purpose of this study was to assess muscle function in situ following DOX administration in mice. Furthermore, pre-treatments with exercise (EX) or metformin (MET) were used in an attempt to preserve muscle function following DOX. Mice were assigned to the following groups: control, DOX, DOX + EX, or DOX + MET, and were given a single injection of DOX (15 mg/kg) or saline 3 days prior to sacrifice. Preceding the DOX injection, DOX + EX mice performed 60 min/day of running for 5 days, while DOX + MET mice received 5 daily oral doses of 500 mg/kg MET. Gastrocnemius–plantaris–soleus complex function was assessed in situ via direct stimulation of the sciatic nerve. DOX treatment increased time to half-relaxation following contractions, indicating impaired recovery (p < 0.05). Interestingly, EX prevented any increase in half-relaxation time, while MET did not. An impaired relaxation rate was associated with a reduction in SERCA1 protein content (p = 0.07) and AMPK phosphorylation (p < 0.05). There were no differences between groups in force production or mitochondrial respiration. These results suggest that EX, but not MET may be an effective strategy for the prevention of muscle fatigue following DOX administration in mice. Full article
(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism)
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Article
Exercise Pills for Drug Addiction: Forced Moderate Endurance Exercise Inhibits Methamphetamine-Induced Hyperactivity through the Striatal Glutamatergic Signaling Pathway in Male Sprague Dawley Rats
Int. J. Mol. Sci. 2021, 22(15), 8203; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158203 - 30 Jul 2021
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Abstract
Physical exercise reduces the extent, duration, and frequency of drug use in drug addicts during the drug initiation phase, as well as during prolonged addiction, withdrawal, and recurrence. However, information about exercise-induced neurobiological changes is limited. This study aimed to investigate the effects [...] Read more.
Physical exercise reduces the extent, duration, and frequency of drug use in drug addicts during the drug initiation phase, as well as during prolonged addiction, withdrawal, and recurrence. However, information about exercise-induced neurobiological changes is limited. This study aimed to investigate the effects of forced moderate endurance exercise training on methamphetamine (METH)-induced behavior and the associated neurobiological changes. Male Sprague Dawley rats were subjected to the administration of METH (1 mg/kg/day, i.p.) and/or forced moderate endurance exercise (treadmill running, 21 m/min, 60 min/day) for 2 weeks. Over the two weeks, endurance exercise training significantly reduced METH-induced hyperactivity. METH and/or exercise treatment increased striatal dopamine (DA) levels, decreased p(Thr308)-Akt expression, and increased p(Tyr216)-GSK-3β expression. However, the phosphorylation levels of Ser9-GSK-3β were significantly increased in the exercise group. METH administration significantly increased the expression of NMDAr1, CaMKK2, MAPKs, and PP1 in the striatum, and exercise treatment significantly decreased the expression of these molecules. Therefore, it is apparent that endurance exercise inhibited the METH-induced hyperactivity due to the decrease in GSK-3β activation by the regulation of the striatal glutamate signaling pathway. Full article
(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism)
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Review

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Review
Sarcopenia: Etiology, Nutritional Approaches, and miRNAs
Int. J. Mol. Sci. 2021, 22(18), 9724; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22189724 - 08 Sep 2021
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Abstract
Sarcopenia, an age-related decline in skeletal muscle mass and function, dramatically affects the quality of life. Although there is a consensus that sarcopenia is a multifactorial syndrome, the etiology and underlying mechanisms are not yet delineated. Moreover, research about nutritional interventions to prevent [...] Read more.
Sarcopenia, an age-related decline in skeletal muscle mass and function, dramatically affects the quality of life. Although there is a consensus that sarcopenia is a multifactorial syndrome, the etiology and underlying mechanisms are not yet delineated. Moreover, research about nutritional interventions to prevent the development of sarcopenia is mainly focused on the amount and quality of protein intake. The impact of several nutrition strategies that consider timing of food intake, anti-inflammatory nutrients, metabolic control, and the role of mitochondrial function on the progression of sarcopenia is not fully understood. This narrative review summarizes the metabolic background of this phenomenon and proposes an integral nutritional approach (including dietary supplements such as creatine monohydrate) to target potential molecular pathways that may affect reduce or ameliorate the adverse effects of sarcopenia. Lastly, miRNAs, in particular those produced by skeletal muscle (MyomiR), might represent a valid tool to evaluate sarcopenia progression as a potential rapid and early biomarker for diagnosis and characterization. Full article
(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism)
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