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Molecular and Cellular Exercise Physiology in Metabolism

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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: closed (31 August 2022) | Viewed by 54264

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Prof. Dr. Jin-Ho Koh

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Guest Editor

College of Medicine, Yeungnam University, Daegu, Korea
Interests: exercise; mitochondria; metabolism; metabolic disease; aging
Special Issues, Collections and Topics in MDPI journals

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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

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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

Related Special Issue

Molecular and Cellular Exercise Physiology in Metabolism 2.0 in International Journal of Molecular Sciences (3 articles)

Published Papers (11 papers)

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Research

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17 pages, 2719 KiB

Open AccessArticle

Resistance Training Improves Beta Cell Glucose Sensing and Survival in Diabetic Models

by Gabriela Alves Bronczek, Gabriela Moreira Soares, Carine Marmentini, Antonio Carlos Boschero and José Maria Costa-Júnior

Int. J. Mol. Sci. 2022, 23(16), 9427; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23169427 - 21 Aug 2022

Cited by 1 | Viewed by 6562

Abstract

Resistance training increases insulin secretion and beta cell function in healthy mice. Here, we explored the effects of resistance training on beta cell glucose sensing and survival by using in vitro and in vivo diabetic models. A pancreatic beta cell line (INS-1E), incubated with serum from trained mice, displayed increased insulin secretion, which could be linked with increased expression of glucose transporter 2 (GLUT2) and glucokinase (GCK). When cells were exposed to pro-inflammatory cytokines (in vitro type 1 diabetes), trained serum preserved both insulin secretion and GCK expression, reduced expression of proteins related to apoptotic pathways, and also protected cells from cytokine-induced apoptosis. Using 8-week-old C57BL/6 mice, turned diabetic by multiple low doses of streptozotocin, we observed that resistance training increased muscle mass and fat deposition, reduced fasting and fed glycemia, and improved glucose tolerance. These findings may be explained by the increased fasting and fed insulinemia, along with increased beta cell mass and beta cell number per islet, observed in diabetic-trained mice compared to diabetic sedentary mice. In conclusion, we believe that resistance training stimulates the release of humoral factors which can turn beta cells more resistant to harmful conditions and improve their response to a glucose stimulus. Full article

(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism)

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18 pages, 1993 KiB

Open AccessArticle

Localized Heat Therapy Improves Mitochondrial Respiratory Capacity but Not Fatty Acid Oxidation

by Erik D. Marchant, Jamie P. Kaluhiokalani, Taysom E. Wallace, Mohadeseh Ahmadi, Abigail Dorff, Jessica J. Linde, Olivia K. Leach, Robert D. Hyldahl, Jayson R. Gifford and Chad R. Hancock

Int. J. Mol. Sci. 2022, 23(15), 8500; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23158500 - 31 Jul 2022

Cited by 3 | Viewed by 2164

Abstract

AIM: Mild heat stress can improve mitochondrial respiratory capacity in skeletal muscle. However, long-term heat interventions are scarce, and the effects of heat therapy need to be understood in the context of the adaptations which follow the more complex combination of stimuli from exercise training. The purpose of this work was to compare the effects of 6 weeks of localized heat therapy on human skeletal muscle mitochondria to single-leg interval training. METHODS: Thirty-five subjects were assigned to receive sham therapy, short-wave diathermy heat therapy, or single-leg interval exercise training, localized to the quadriceps muscles of the right leg. All interventions took place 3 times per week. Muscle biopsies were performed at baseline, and after 3 and 6 weeks of intervention. Mitochondrial respiratory capacity was assessed on permeabilized muscle fibers via high-resolution respirometry. RESULTS: The primary finding of this work was that heat therapy and exercise training significantly improved mitochondrial respiratory capacity by 24.8 ± 6.2% and 27.9 ± 8.7%, respectively (p < 0.05). Fatty acid oxidation and citrate synthase activity were also increased following exercise training by 29.5 ± 6.8% and 19.0 ± 7.4%, respectively (p < 0.05). However, contrary to our hypothesis, heat therapy did not increase fatty acid oxidation or citrate synthase activity. CONCLUSION: Six weeks of muscle-localized heat therapy significantly improves mitochondrial respiratory capacity, comparable to exercise training. However, unlike exercise, heat does not improve fatty acid oxidation capacity. Full article

(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism)

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12 pages, 2451 KiB

Open AccessArticle

Effects of Exercise Training during Advanced Maternal Age on the Cognitive Function of Offspring

by Tae-Woon Kim, Sang-Seo Park and Hye-Sang Park

Int. J. Mol. Sci. 2022, 23(10), 5517; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23105517 - 15 May 2022

Cited by 3 | Viewed by 1745

Abstract

Advanced maternal age (AMA) denotes an age of ≥35 years during the time of delivery. Maternal metabolism affects the offspring’s physical and neurological development as well as their cognitive function. This study aimed to elucidate the effects of exercise training among old female animals on the cognitive function, hippocampal neuroplasticity, mitochondrial function, and apoptosis in the offspring. We found that the offspring of mothers with AMA without exercise training had decreased spatial learning and memory, brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD-95) protein levels, neurogenesis, and mitochondrial function, as well as hippocampal cell death. Contrastingly, offspring of mothers with AMA with exercise training showed improved spatial learning, memory, hippocampal neuroplasticity, and mitochondrial function. These findings indicate that despite the AMA, increasing fitness through exercise significantly contributes to a positive prenatal environment for fetuses. The maternal exercises augmented the hippocampal levels of BDNF, which prevents decreased cognitive function in the offspring of mothers with AMA. Full article

(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism)

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12 pages, 1837 KiB

Open AccessArticle

TLR4-Mediated Inflammatory Responses Regulate Exercise-Induced Molecular Adaptations in Mouse Skeletal Muscle

by Haruna Fujiyoshi, Tatsuro Egawa, Eriko Kurogi, Takumi Yokokawa, Kohei Kido and Tatsuya Hayashi

Int. J. Mol. Sci. 2022, 23(3), 1877; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031877 - 07 Feb 2022

Viewed by 2460

Abstract

Endurance exercise induces various adaptations that yield health benefits; however, the underlying molecular mechanism has not been fully elucidated. Given that it has recently been accepted that inflammatory responses are required for a specific muscle adaptation after exercise, this study investigated whether toll-like receptor (TLR) 4, a pattern recognition receptor that induces proinflammatory cytokines, is responsible for exercise-induced adaptations in mouse skeletal muscle. The TLR4 mutant (TLR4m) and intact TLR4 control mice were each divided into 2 groups (sedentary and voluntary wheel running) and were housed for six weeks. Next, we removed the plantaris muscle and evaluated the expression of cytokines and muscle regulators. Exercise increased cytokine expression in the controls, whereas a smaller increase was observed in the TLR4m mice. Mitochondrial markers and mitochondrial biogenesis inducers, including peroxisome proliferator-activated receptor beta and heat shock protein 72, were increased in the exercised controls, whereas this upregulation was attenuated in the TLR4m mice. In contrast, exercise increased the expression of molecules such as peroxisome proliferator-activated receptor-gamma coactivator 1-alpha and glucose transporter 4 in both the controls and TLR4m mice. Our findings indicate that exercise adaptations such as mitochondrial biogenesis are mediated via TLR4, and that TLR4-mediated inflammatory responses could be involved in the mechanism of adaptation. Full article

(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism)

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18 pages, 2670 KiB

Open AccessArticle

The Effect of Long-Lasting Swimming on Rats Skeletal Muscles Energy Metabolism after Nine Days of Dexamethasone Treatment

by Damian Jozef Flis, Emilia Gabriela Bialobrodzka, Ewa Aleksandra Rodziewicz-Flis, Zbigniew Jost, Andzelika Borkowska, Wieslaw Ziolkowski and Jan Jacek Kaczor

Int. J. Mol. Sci. 2022, 23(2), 748; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23020748 - 11 Jan 2022

Cited by 2 | Viewed by 1846

Abstract

This study investigates the effect of Dexamethasone (Dex) treatment on blood and skeletal muscle metabolites level and skeletal muscle activity of enzymes related to energy metabolism after long-duration swimming. To evaluate whether Dex treatment, swimming, and combining these factors act on analyzed data, rats were randomly divided into four groups: saline treatment non-exercise and exercise and Dex treatment non-exercised and exercised. Animals in both exercised groups underwent long-lasting swimming. The concentration of lipids metabolites, glucose, and lactate were measured in skeletal muscles and blood according to standard colorimetric and fluorimetric methods. Also, activities of enzymes related to aerobic and anaerobic metabolism were measured in skeletal muscles. The results indicated that Dex treatment induced body mass loss and increased lipid metabolites in the rats’ blood but did not alter these changes in skeletal muscles. Interestingly, prolonged swimming applied after 9 days of Dex treatment significantly intensified changes induced by Dex; however, there was no difference in skeletal muscle enzymatic activities. This study shows for the first time the cumulative effect of exercise and Dex on selected elements of lipid metabolism, which seems to be essential for the patient’s health due to the common use of glucocorticoids like Dex. Full article

(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism)

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15 pages, 16419 KiB

Open AccessArticle

Paternal Exercise Improves the Metabolic Health of Offspring via Epigenetic Modulation of the Germline

by José Maria Costa-Júnior, Sandra Mara Ferreira, Mirian Ayumi Kurauti, Diana L. Bernstein, Elena G. Ruano, Vasumathi Kameswaran, Jonathan Schug, Ricardo Freitas-Dias, Claudio C. Zoppi, Antonio C. Boschero, Camila A. M. de Oliveira, Gustavo J. Santos, Everardo M. Carneiro and Klaus H. Kaestner

Int. J. Mol. Sci. 2022, 23(1), 1; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010001 - 21 Dec 2021

Cited by 13 | Viewed by 4229

Abstract

Background/Aims: Epigenetic regulation is considered the main molecular mechanism underlying the developmental origin of health and disease’s (DOHAD) hypothesis. Previous studies that have investigated the role of paternal exercise on the metabolic health of the offspring did not control for the amount and intensity of the training or possible effects of adaptation to exercise and produced conflicting results regarding the benefits of parental exercise to the next generation. We employed a precisely regulated exercise regimen to study the transgenerational inheritance of improved metabolic health. Methods: We subjected male mice to a well-controlled exercise -training program to investigate the effects of paternal exercise on glucose tolerance and insulin sensitivity in their adult progeny. To investigate the molecular mechanisms of epigenetic inheritance, we determined chromatin markers in the skeletal muscle of the offspring and the paternal sperm. Results: Offspring of trained male mice exhibited improved glucose homeostasis and insulin sensitivity. Paternal exercise modulated the DNA methylation profile of PI3Kca and the imprinted H19/Igf2 locus at specific differentially methylated regions (DMRs) in the skeletal muscle of the offspring, which affected their gene expression. Remarkably, a similar DNA methylation profile at the PI3Kca, H19, and Igf2 genes was present in the progenitor sperm indicating that exercise-induced epigenetic changes that occurred during germ cell development contributed to transgenerational transmission. Conclusion: Paternal exercise might be considered as a strategy that could promote metabolic health in the offspring as the benefits can be inherited transgenerationally. Full article

(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism)

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16 pages, 5859 KiB

Open AccessArticle

Exercise Training Alleviates Cardiac Fibrosis through Increasing Fibroblast Growth Factor 21 and Regulating TGF-β1-Smad2/3-MMP2/9 Signaling in Mice with Myocardial Infarction

by Yixuan Ma, Yixin Kuang, Wenyan Bo, Qiaoqin Liang, Wenfei Zhu, Mengxin Cai and Zhenjun Tian

Int. J. Mol. Sci. 2021, 22(22), 12341; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222212341 - 15 Nov 2021

Cited by 42 | Viewed by 4015

Abstract

Exercise training has been reported to alleviate cardiac fibrosis and ameliorate heart dysfunction after myocardial infarction (MI), but the molecular mechanism is still not fully clarified. Fibroblast growth factor 21 (FGF21) exerts a protective effect on the infarcted heart. This study investigates whether exercise training could increase FGF21 protein expression and regulate the transforming growth factor-β1 (TGF-β1)-Smad2/3-MMP2/9 signaling pathway to alleviate cardiac fibrosis following MI. Male wild type (WT) C57BL/6J mice and Fgf21 knockout (Fgf21 KO) mice were used to establish the MI model and subjected to five weeks of different types of exercise training. Both aerobic exercise training (AET) and resistance exercise training (RET) significantly alleviated cardiac dysfunction and fibrosis, up-regulated FGF21 protein expression, inhibited the activation of TGF-β1-Smad2/3-MMP2/9 signaling pathway and collagen production, and meanwhile, enhanced antioxidant capacity and reduced cell apoptosis in the infarcted heart. In contrast, knockout of Fgf21 weakened the cardioprotective effects of AET after MI. In vitro, cardiac fibroblasts (CFs) were isolated from neonatal mice hearts and treated with H₂O₂ (100 μM, 6 h). Recombinant human FGF21 (rhFGF21, 100 ng/mL, 15 h) and/or 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR, 1 mM, 15 h) inhibited H₂O₂-induced activation of the TGF-β1-Smad2/3-MMP2/9 signaling pathway, promoted CFs apoptosis and reduced collagen production. In conclusion, exercise training increases FGF21 protein expression, inactivates the TGF-β1-Smad2/3-MMP2/9 signaling pathway, alleviates cardiac fibrosis, oxidative stress, and cell apoptosis, and finally improves cardiac function in mice with MI. FGF21 plays an important role in the anti-fibrosis effect of exercise training. Full article

(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism)

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17 pages, 3599 KiB

Open AccessArticle

Exercise Intervention Mitigates Pathological Liver Changes in NAFLD Zebrafish by Activating SIRT1/AMPK/NRF2 Signaling

by Yunyi Zou, Zhanglin Chen, Chenchen Sun, Dong Yang, Zuoqiong Zhou, Xiyang Peng, Lan Zheng and Changfa Tang

Int. J. Mol. Sci. 2021, 22(20), 10940; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222010940 - 10 Oct 2021

Cited by 19 | Viewed by 5088

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a common disease that causes serious liver damage. Exercise is recognized as a non-pharmacological tool to improve the pathology of NAFLD. However, the antioxidative effects and mechanisms by which exercise ameliorates NAFLD remain unclear. The present study conducted exercise training on zebrafish during a 12-week high-fat feeding period to study the antioxidant effect of exercise on the liver. We found that swimming exercise decreased lipid accumulation and improved pathological changes in the liver of high-fat diet-fed zebrafish. Moreover, swimming alleviated NOX4-derived reactive oxygen species (ROS) overproduction and reduced methanedicarboxylic aldehyde (MDA) levels. We also examined the anti-apoptotic effects of swimming and found that it increased the expression of antiapoptotic factor bcl2 and decreased the expression of genes associated with apoptosis (caspase3, bax). Mechanistically, swimming intervention activated SIRT1/AMPK signaling-mediated lipid metabolism and inflammation as well as enhanced AKT and NRF2 activation and upregulated downstream antioxidant genes. In summary, exercise attenuates pathological changes in the liver induced by high-fat diets. The underlying mechanisms might be related to NRF2 and mediated by SIRT1/AMPK signaling. Full article

(This article belongs to the Special Issue Molecular and Cellular Exercise Physiology in Metabolism)

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12 pages, 1500 KiB

Open AccessArticle

Exercise, but Not Metformin Prevents Loss of Muscle Function Due to Doxorubicin in Mice Using an In Situ Method

by Amy D. Mackay, Erik D. Marchant, Makensie Louw, David M. Thomson and Chad R. Hancock

Int. J. Mol. Sci. 2021, 22(17), 9163; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179163 - 25 Aug 2021

Cited by 3 | Viewed by 2144

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 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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16 pages, 1817 KiB

Open AccessArticle

Exercise Pills for Drug Addiction: Forced Moderate Endurance Exercise Inhibits Methamphetamine-Induced Hyperactivity through the Striatal Glutamatergic Signaling Pathway in Male Sprague Dawley Rats

by Suryun Jung, Youjeong Kim, Mingyu Kim, Minjae Seo, Suji Kim, Seungju Kim and Sooyeun Lee

Int. J. Mol. Sci. 2021, 22(15), 8203; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158203 - 30 Jul 2021

Cited by 7 | Viewed by 3147

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 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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19 pages, 1398 KiB

Open AccessReview

Sarcopenia: Etiology, Nutritional Approaches, and miRNAs

by Roberto Cannataro, Leandro Carbone, Jorge L. Petro, Erika Cione, Salvador Vargas, Heidy Angulo, Diego A. Forero, Adrián Odriozola-Martínez, Richard B. Kreider and Diego A. Bonilla

Int. J. Mol. Sci. 2021, 22(18), 9724; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22189724 - 08 Sep 2021

Cited by 53 | Viewed by 19011

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 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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