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Skeletal Muscle and Physical Exercise

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 (15 April 2023) | Viewed by 9583

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Guest Editor
Department of Neuroscience Biomedicine and Movement Sciences, University of Verona, Strada Le Grazie 8, I-37134 Verona, Italy
Interests: muscle; aging; imaging; three-dimensional (3D) scanning; body composition; anthropometry; sensory organs; nervous system
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Special Issue Information

Dear Colleagues,

Skeletal muscle is the actuator of body movement and, therefore, it is inextricably linked to physical exercise. Physical exercise is, in turn, a cornerstone of a healthy life, especially in aging. A deeper understanding of the complex relationships between physical exercise in its diverse forms and skeletal muscle structure, metabolism, and performance is required to tailor physical exercise protocols as a function of age, type of activity, and disease.

This Special Issue is aimed at offering an Open Access forum for the presentation of high-quality research from all over the world presenting advances in the mutual crosstalk of muscle and exercise from a molecular and cell biology point of view. While purely clinical papers do not fall within the scope of this Special Issue, basic science and clinically oriented papers reporting on translational research are welcome. Interdisciplinary research using a combination of techniques and/or experimental approaches to highlight the skeletal muscle/physical exercise relationship in health and disease, with a special focus on children and elderly people, metabolism, the application of imaging techniques, -omics approaches, and pathology (insofar it is related to normal structure and function), is encouraged.

Dr. Carlo Zancanaro
Guest Editor

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Keywords

  • skeletal muscle
  • physical exercise
  • cardiac muscle
  • exercise
  • aging
  • sarcopenia
  • metabolomics
  • pathology
  • genetic diseases

Published Papers (4 papers)

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Research

14 pages, 3588 KiB  
Article
Melatonin and Exercise Counteract Sarcopenic Obesity through Preservation of Satellite Cell Function
by Sakulrat Mankhong, Sujin Kim, Sohee Moon, Jae-Seon Lee, Eun-Jeong Cho, Hyo-Bum Kwak, Dong-Ho Park, Ji-Kan Ryu and Ju-Hee Kang
Int. J. Mol. Sci. 2023, 24(7), 6097; https://doi.org/10.3390/ijms24076097 - 23 Mar 2023
Cited by 4 | Viewed by 2241
Abstract
Sarcopenic obesity (SO) is characterized by atrophic skeletal muscle impairment (sarcopenia) and obesity, which is associated with adverse outcomes of morbidity and mortality in elderly people. We investigated the effects of melatonin and exercise training on SO in 32-week-old senescence-accelerated mouse-prone-8 (SAMP8) mice [...] Read more.
Sarcopenic obesity (SO) is characterized by atrophic skeletal muscle impairment (sarcopenia) and obesity, which is associated with adverse outcomes of morbidity and mortality in elderly people. We investigated the effects of melatonin and exercise training on SO in 32-week-old senescence-accelerated mouse-prone-8 (SAMP8) mice fed a normal diet or a high-fat diet for 16 weeks. Melatonin, exercise, or melatonin and exercise for 8 weeks displayed reductions in the SO-induced impairment of skeletal muscle function and atrophy. Specifically, a decrease in mitochondrial calcium retention capacity in skeletal muscles observed in the HFD-con group was attenuated in melatonin and/or exercise intervention groups. More importantly, HFD-con mice displayed a lower number of Pax7+ satellite cells (SCs) and higher expression of p16ink than P8ND mice, which were attenuated by melatonin and/or exercise interventions. The cellular senescence in SC-derived primary myoblasts from HFD-con mice was significantly attenuated in myoblasts from the melatonin and/or exercise groups, which was reproduced in a senescence model of H2O2-treated C2C12 myoblasts. Our results suggest that melatonin and exercise training attenuate SO-induced skeletal muscle dysfunction, at least in part, through preserving the SC pool by inhibiting cellular senescence and attenuating mitochondrial dysfunction. Full article
(This article belongs to the Special Issue Skeletal Muscle and Physical Exercise)
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17 pages, 5588 KiB  
Article
Effects of Adjunct Antifibrotic Treatment within a Regenerative Rehabilitation Paradigm for Volumetric Muscle Loss
by Jessica M. Motherwell, Connor P. Dolan, Sergey S. Kanovka, Jorge B. Edwards, Sarah R. Franco, Naveena B. Janakiram, Michael S. Valerio, Stephen M. Goldman and Christopher L. Dearth
Int. J. Mol. Sci. 2023, 24(4), 3564; https://doi.org/10.3390/ijms24043564 - 10 Feb 2023
Cited by 2 | Viewed by 1443
Abstract
The use of a rehabilitation approach that promotes regeneration has the potential to improve the efficacy of pro-regenerative therapies and maximize functional outcomes in the treatment of volumetric muscle loss (VML). An adjunct antifibrotic treatment could further enhance functional gains by reducing fibrotic [...] Read more.
The use of a rehabilitation approach that promotes regeneration has the potential to improve the efficacy of pro-regenerative therapies and maximize functional outcomes in the treatment of volumetric muscle loss (VML). An adjunct antifibrotic treatment could further enhance functional gains by reducing fibrotic scarring. This study aimed to evaluate the potential synergistic effects of losartan, an antifibrotic pharmaceutical, paired with a voluntary wheel running rehabilitation strategy to enhance a minced muscle graft (MMG) pro-regenerative therapy in a rodent model of VML. The animals were randomly assigned into four groups: (1) antifibrotic with rehabilitation, (2) antifibrotic without rehabilitation, (3) vehicle treatment with rehabilitation, and (4) vehicle treatment without rehabilitation. At 56 days, the neuromuscular function was assessed, and muscles were collected for histological and molecular analysis. Surprisingly, we found that the losartan treatment decreased muscle function in MMG-treated VML injuries by 56 days, while the voluntary wheel running elicited no effect. Histologic and molecular analysis revealed that losartan treatment did not reduce fibrosis. These findings suggest that losartan treatment as an adjunct therapy to a regenerative rehabilitation strategy negatively impacts muscular function and fails to promote myogenesis following VML injury. There still remains a clinical need to develop a regenerative rehabilitation treatment strategy for traumatic skeletal muscle injuries. Future studies should consider optimizing the timing and duration of adjunct antifibrotic treatments to maximize functional outcomes in VML injuries. Full article
(This article belongs to the Special Issue Skeletal Muscle and Physical Exercise)
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23 pages, 8702 KiB  
Article
Skeletal Muscles of Sedentary and Physically Active Aged People Have Distinctive Genic Extrachromosomal Circular DNA Profiles
by Daniela Gerovska and Marcos J. Araúzo-Bravo
Int. J. Mol. Sci. 2023, 24(3), 2736; https://doi.org/10.3390/ijms24032736 - 1 Feb 2023
Cited by 6 | Viewed by 2404
Abstract
To bring new extrachromosomal circular DNA (eccDNA) enrichment technologies closer to the clinic, specifically for screening, early diagnosis, and monitoring of diseases or lifestyle conditions, it is paramount to identify the differential pattern of the genic eccDNA signal between two states. Current studies [...] Read more.
To bring new extrachromosomal circular DNA (eccDNA) enrichment technologies closer to the clinic, specifically for screening, early diagnosis, and monitoring of diseases or lifestyle conditions, it is paramount to identify the differential pattern of the genic eccDNA signal between two states. Current studies using short-read sequenced purified eccDNA data are based on absolute numbers of unique eccDNAs per sample or per gene, length distributions, or standard methods for RNA-seq differential analysis. Previous analyses of RNA-seq data found significant transcriptomics difference between sedentary and active life style skeletal muscle (SkM) in young people but very few in old. The first attempt using circulomics data from SkM and blood of aged lifelong sedentary and physically active males found no difference at eccDNA level. To improve the capability of finding differences between circulomics data groups, we designed a computational method to identify Differentially Produced per Gene Circles (DPpGCs) from short-read sequenced purified eccDNA data based on the circular junction, split-read signal, of the eccDNA, and implemented it into a software tool DifCir in Matlab. We employed DifCir to find to the distinctive features of the influence of the physical activity or inactivity in the aged SkM that would have remained undetected by transcriptomics methods. We mapped the data from tissue from SkM and blood from two groups of aged lifelong sedentary and physically active males using Circle_finder and subsequent merging and filtering, to find the number and length distribution of the unique eccDNA. Next, we used DifCir to find up-DPpGCs in the SkM of the sedentary and active groups. We assessed the functional enrichment of the DPpGCs using Disease Gene Network and Gene Set Enrichment Analysis. To find genes that produce eccDNA in a group without comparison with another group, we introduced a method to find Common PpGCs (CPpGCs) and used it to find CPpGCs in the SkM of the sedentary and active group. Finally, we found the eccDNA that carries whole genes. We discovered that the eccDNA in the SkM of the sedentary group is not statistically different from that of physically active aged men in terms of number and length distribution of eccDNA. In contrast, with DifCir we found distinctive gene-associated eccDNA fingerprints. We identified statistically significant up-DPpGCs in the two groups, with the top up-DPpGCs shed by the genes AGBL4, RNF213, DNAH7, MED13, and WWTR1 in the sedentary group, and ZBTB7C, TBCD, ITPR2, and DDX11-AS1 in the active group. The up-DPpGCs in both groups carry mostly gene fragments rather than whole genes. Though the subtle transcriptomics difference, we found RYR1 to be both transcriptionally up-regulated and up-DPpGCs gene in sedentary SkM. DifCir emphasizes the high sensitivity of the circulome compared to the transcriptome to detect the molecular fingerprints of exercise in aged SkM. It allows efficient identification of gene hotspots that excise more eccDNA in a health state or disease compared to a control condition. Full article
(This article belongs to the Special Issue Skeletal Muscle and Physical Exercise)
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16 pages, 2424 KiB  
Article
Endurance Training Increases the Running Performance of Untrained Men without Changing the Mitochondrial Volume Density in the Gastrocnemius Muscle
by Jerzy A. Zoladz, Joanna Majerczak, Lukasz Galganski, Marcin Grandys, Justyna Zapart-Bukowska, Piotr Kuczek, Leszek Kołodziejski, Lucyna Walkowicz, Dorota Szymoniak-Chochół, Wincenty Kilarski and Wieslawa Jarmuszkiewicz
Int. J. Mol. Sci. 2022, 23(18), 10843; https://doi.org/10.3390/ijms231810843 - 16 Sep 2022
Cited by 4 | Viewed by 2786
Abstract
The activity and quantity of mitochondrial proteins and the mitochondrial volume density (MitoVD) are higher in trained muscles; however, the underlying mechanisms remain unclear. Our goal was to determine if 20 weeks’ endurance training simultaneously increases running performance, the amount and [...] Read more.
The activity and quantity of mitochondrial proteins and the mitochondrial volume density (MitoVD) are higher in trained muscles; however, the underlying mechanisms remain unclear. Our goal was to determine if 20 weeks’ endurance training simultaneously increases running performance, the amount and activity of mitochondrial proteins, and MitoVD in the gastrocnemius muscle in humans. Eight healthy, untrained young men completed a 20-week moderate-intensity running training program. The training increased the mean speed of a 1500 m run by 14.0% (p = 0.008) and the running speed at 85% of maximal heart rate by 9.6% (p = 0.008). In the gastrocnemius muscle, training significantly increased mitochondrial dynamics markers, i.e., peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) by 23%, mitochondrial transcription factor A (TFAM) by 29%, optic artrophy-1 (OPA1) by 31% and mitochondrial fission factor (MFF) by 44%, and voltage-dependent anion channel 1 (VDAC1) by 30%. Furthermore, training increased the amount and maximal activity of citrate synthase (CS) by 10% and 65%, respectively, and the amount and maximal activity of cytochrome c oxidase (COX) by 57% and 42%, respectively, but had no effect on the total MitoVD in the gastrocnemius muscle. We concluded that not MitoVD per se, but mitochondrial COX activity (reflecting oxidative phosphorylation activity), should be regarded as a biomarker of muscle adaptation to endurance training in beginner runners. Full article
(This article belongs to the Special Issue Skeletal Muscle and Physical Exercise)
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