{"title":"Mechanisms of eccentric contraction-induced muscle damage and nutritional supplementations for mitigating it.","authors":"Keita Kanzaki, Daiki Watanabe, Jiayu Shi, Masanobu Wada","doi":"10.1007/s10974-022-09625-1","DOIUrl":"https://doi.org/10.1007/s10974-022-09625-1","url":null,"abstract":"<p><p>Eccentric contraction (ECC) often results in large and long-lasting force deficits accompanied by muscle soreness, primarily due to muscle damage. In this sense, exercises that involve ECC are less desirable. Paradoxically, exercise training that includes a substantial eccentric phase leads to a more powerful activation of the genes responsible for skeletal muscle remodeling (e.g., hypertrophy) than other types of training that emphasize a concentric or isometric phase. Therefore, effective strategies that lessen ECC-induced muscle damage will be of interest and importance to many individuals. The purpose of this brief review is to highlight the published literature on the effects of ECC and/or nutritional supplementations on proteins, lipids, metabolic and ionic changes, and enzyme activities in skeletal muscles subjected to an acute bout of ECC. First, we discuss the potential mechanisms by which ECC causes muscle damage. Previous findings implicate a Ca<sup>2+</sup> overload-oxidative modification pathway as one possible mechanism contributing to muscle damage. Thereafter, the efficacy of two nutritional supplementations, i.e., L-arginine and antioxidant, is discussed because L-arginine and antioxidant would be expected to ameliorate the adverse effects of Ca<sup>2+</sup> overload and oxidative modification, respectively. Of these, L-arginine ingestion before ECC seems likely to be the effective strategy for mitigating ECC-related proteolysis. More studies are needed to establish the effectiveness of antioxidant ingestion. The application of effective strategies against muscle damage may contribute to improvements in health and fitness, muscle function, and sports performance.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"43 3","pages":"147-156"},"PeriodicalIF":2.7,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40519258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jing Jin, Fanyi Li, Caihong Fan, Yu Wu, Chunhui He
{"title":"Elevated mir-145-5p is associated with skeletal muscle dysfunction and triggers apoptotic cell death in C2C12 myotubes.","authors":"Jing Jin, Fanyi Li, Caihong Fan, Yu Wu, Chunhui He","doi":"10.1007/s10974-022-09624-2","DOIUrl":"https://doi.org/10.1007/s10974-022-09624-2","url":null,"abstract":"<p><p>Skeletal muscle dysfunction is a common comorbidity of chronic obstructive pulmonary disease (COPD), and the molecular mechanisms regarding to the pathogenesis of this disease have not been elucidated. In this study, a novel miR-145-5p was significantly upregulated in the serum collected from patients with COPD-associated muscle atrophy, in contrast with the normal participants. Then, we evidenced that silencing of miR-145-5p suppressed cell death and elongated cell survival during cell culture process. Consistently, upregulation of miR-145-5p induced cell apoptosis and restrain cell viability in the C2C12 cells, suggesting that miR-145-5p contributes to cell death. Further experiments evidenced that miR-145-5p decreased the expression levels of phosphorylated PI3K (p-PI3K), Akt (p-Akt) and mTOR (p-mTOR) to inactivate the PI3K/Akt/mTOR pathway, and this pathway was also reactivated by miR-145-5p ablation. Finally, we proved that the protective effects of miR-145-5p ablation were abrogated by co-treating cells with PI3K inhibitor LY294002. Taken together, we concluded that miR-145-5p promoted cell death to facilitate muscle dysfunctions via inactivating the PI3K/Akt/mTOR pathway.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"43 3","pages":"135-145"},"PeriodicalIF":2.7,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40399505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The effect of muscle length on post-tetanic potentiation of C57BL/6 and skMLCK<sup>-/-</sup> mouse EDL muscles.","authors":"Angelos Angelidis, Rene Vandenboom","doi":"10.1007/s10974-022-09620-6","DOIUrl":"https://doi.org/10.1007/s10974-022-09620-6","url":null,"abstract":"<p><p>Post-tetanic potentiation of fast-twitch skeletal muscle is dependent on muscle length, with greater potentiation observed at shorter compared to longer lengths. The structural effects of the primary potentiation mechanism, phosphorylation of the regulatory light chain (RLC) of myosin, are thought to explain this relationship. The purpose of these experiments was to determine whether the length-dependence of potentiation would be attenuated in the absence of RLC phosphorylation. To this end, we compared isometric twitch potentiation of mouse extensor digitorum longus (EDL) muscles with (wildtype, WT) and without (skeletal myosin light chain kinase knockout, skMLCK<sup>-/-</sup>) phosphorylation. Force was measured at five muscle lengths (0.90 L<sub>o</sub>, 0.95 L<sub>o</sub>, L<sub>o</sub>, 1.05 L<sub>o</sub>, 1.10 L<sub>o</sub>, where L<sub>o</sub> refers to optimal length) prior to and following a tetanic train. In accordance with prior findings, potentiation was dependent on muscle length, with greater values observed at short (e.g., 44.3 ± 4.6% for WT, 33.5 ± 6.2% for skMLCK<sup>-/-</sup>, at 0.90 L<sub>o</sub>) compared to long lengths (e.g., 16.9 ± 1.3% for WT, 9.1 ± 1.8% for skMLCK<sup>-/-</sup>, at 1.10 L<sub>o</sub>) in both genotypes. WT muscles displayed greater potentiation compared to their skMLCK<sup>-/-</sup> counterparts across lengths (e.g., 16.9 ± 1.6% vs 7.3 ± 1.5% at L<sub>o</sub>). However, the relationship between potentiation and muscle length was not different between genotypes. Thus, the alternative mechanisms of potentiation, present in the skMLCK<sup>-/-</sup> EDL, display a length-dependence of post-tetanic potentiation similar to RLC phosphorylation-dominant potentiation. Additional mechanisms may be required to explain the length-dependence of potentiation.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"43 3","pages":"99-111"},"PeriodicalIF":2.7,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40411079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cory W Baumann, Christopher P Ingalls, Dawn A Lowe
{"title":"Mechanisms of weakness in Mdx muscle following in vivo eccentric contractions.","authors":"Cory W Baumann, Christopher P Ingalls, Dawn A Lowe","doi":"10.1007/s10974-022-09617-1","DOIUrl":"10.1007/s10974-022-09617-1","url":null,"abstract":"<p><p>Skeletal muscle of the dystrophin-deficient mdx mouse is hypersensitive to eccentric (ECC) contraction-induced strength loss due to plasmalemmal electrical dysfunction. Despite plasmalemmal inexcitability being a logical mechanism responsible for weakness, it remains unclear if processes up- and/or down-stream remain functionally intact in injured mdx muscle. The purpose of this study was to analyze additional processes necessary for excitation-contraction coupling that are potentially disrupted by ECC contractions. Anterior crural muscles (tibialis anterior, extensor digitorum longus [EDL], and extensor hallucis muscles) of wildtype (WT) and mdx mice were injured in vivo with 50 ECC contractions and torque was measured immediately before and after the contraction bout. Following the in vivo assessment, EDL ex vivo isometric and caffeine forces were analyzed. In vivo isometric torque and ex vivo force in WT muscle were reduced 38 and 30% (p < 0.001), while caffeine force was also reduced (p = 0.021), albeit to a lesser degree (9%). In contrast, in vivo isometric torque, ex vivo isometric force and ex vivo caffeine-induced force were all reduced 56-67% (p < 0.001) in mdx muscle and did not differ from one another (p = 0.114). Disproportional reductions in isometric strength and caffeine-induced force confirm that ECC contractions uncoupled the plasmalemma from the ryanodine receptors (RyRs) in WT muscle. In mdx muscle, the proportional reductions in isometric strength and caffeine-induced force following ECC contractions reveal that dysfunction occurs at and/or distal to the RyRs immediately post-injury. Thus, weakness in injured mdx muscle cannot be isolated to one mechanism, rather several steps of muscle contraction are disrupted.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"43 2","pages":"63-72"},"PeriodicalIF":1.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9728427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Geyse Gomes, Kayo Moreira Bagri, Ivone de Andrade Rosa, Arnon Dias Jurberg, Claudia Mermelstein, Manoel Luis Costa
{"title":"Activation of YAP regulates muscle fiber size in a PKC-dependent mechanism during chick in vitro myogenesis.","authors":"Geyse Gomes, Kayo Moreira Bagri, Ivone de Andrade Rosa, Arnon Dias Jurberg, Claudia Mermelstein, Manoel Luis Costa","doi":"10.1007/s10974-021-09608-8","DOIUrl":"https://doi.org/10.1007/s10974-021-09608-8","url":null,"abstract":"<p><p>The formation of skeletal muscle fibers is an intricate process controlled by a multitude of signaling pathways, including Wnt, Shh, and FGF. However, the role of the Hippo pathway during vertebrate myofiber formation has conflicting reports, which we decided to address in chick muscle cultures. We found that the transcriptional regulator Yes-associated protein (YAP) was highly concentrated within the nuclei of myoblasts. As cells differentiate into myotubes, YAP localization shifted to the cell cytoplasm in more mature myotubes. Treatment of cultures with XMU-MP-1 (XMU), a MST1/2 inhibitor, stimulated the nuclear localization of YAP in myoblasts and in myotubes, upregulated myogenin, and promoted myoblast fusion, ultimately resulting in the formation of large and fully striated multinucleated myotubes. The XMU-induced phenotype was blocked by the protein kinase C (PKC) inhibitor calphostin, which raises the possibility that the Hippo pathway controls the growth of skeletal muscle fibers through a PKC-dependent mechanism.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"73-86"},"PeriodicalIF":2.7,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s10974-021-09608-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39325472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tatiana E Koike, Rodrigo A Dell Aquila, Kellana S Silva, Marcelo S Aoki, Elen H Miyabara
{"title":"Glutamine supplementation improves contractile function of regenerating soleus muscles from rats.","authors":"Tatiana E Koike, Rodrigo A Dell Aquila, Kellana S Silva, Marcelo S Aoki, Elen H Miyabara","doi":"10.1007/s10974-022-09615-3","DOIUrl":"https://doi.org/10.1007/s10974-022-09615-3","url":null,"abstract":"<p><p>This study evaluated the effects of glutamine supplementation immediately after freezing injury on morphological and contractile function of regenerating soleus muscles from rats. Young male Wistar rats were subjected to cryolesion of soleus muscles, and immediately after received a daily supplementation of glutamine (1 g/kg/day). The muscles were evaluated on post-injury days 3 and 10. Glutamine-supplemented injured muscles had a lower number of CD11b positive immune cells and higher mRNA levels of IL-4 compared to those from the cryolesioned muscles analyzed on post-injury day 3. The mRNA and protein expression levels of the myogenic transcription factor MyoD were also higher in glutamine-supplemented injured muscles than in injured muscles examined on post-cryolesion day 3. In addition, glutamine-supplemented injured muscles had a higher size of their regenerating myofibers, attenuated decline in maximum tetanic strength and improved fatigue resistance compared to those from injured muscles evaluated on post-cryolesion day 10. No effect was observed in uninjured muscles supplemented with glutamine. Our results suggest that glutamine supplementation improves the resolution of inflammation, as well as the size and functional recovery of regenerating myofibers from soleus muscles by accelerating the up-regulation of IL-4 and MyoD expression. Future non-pharmacological rehabilitation studies are warranted to investigate the effect of glutamine supplementation on the outcome of injured skeletal muscles.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"87-97"},"PeriodicalIF":2.7,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39826269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Virtually \"muscling\" in pandemic: first virtual European Muscle Conference (September 20-22, 2021).","authors":"Maria Jolanta Rędowicz, Wolfgang A Linke","doi":"10.1007/s10974-022-09616-2","DOIUrl":"https://doi.org/10.1007/s10974-022-09616-2","url":null,"abstract":"<p><p>A report on the first virtual European Muscle Conference.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"45-47"},"PeriodicalIF":2.7,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9208351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40071195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kapila Awasthi, Sudha Bhattacharya, A. Bhattacharya
{"title":"Tissue-specific isoform expression of GNE gene in human tissues","authors":"Kapila Awasthi, Sudha Bhattacharya, A. Bhattacharya","doi":"10.1007/s10974-022-09618-0","DOIUrl":"https://doi.org/10.1007/s10974-022-09618-0","url":null,"abstract":"","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"43 1","pages":"49 - 61"},"PeriodicalIF":2.7,"publicationDate":"2022-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45578254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lucas Dantas Maia Forte, Natália de Almeida Rodrigues, André Vitor Cordeiro, Thais de Fante, Laís Angélica de Paula Simino, Adriana de Souza Torsoni, Márcio Alberto Torsoni, Claudio Alexandre Gobatto, Fúlvia Barros Manchado-Gobatto
{"title":"Effect of acute swimming exercise at different intensities but equal total load over metabolic and molecular responses in swimming rats.","authors":"Lucas Dantas Maia Forte, Natália de Almeida Rodrigues, André Vitor Cordeiro, Thais de Fante, Laís Angélica de Paula Simino, Adriana de Souza Torsoni, Márcio Alberto Torsoni, Claudio Alexandre Gobatto, Fúlvia Barros Manchado-Gobatto","doi":"10.1007/s10974-022-09614-4","DOIUrl":"https://doi.org/10.1007/s10974-022-09614-4","url":null,"abstract":"<p><p>Acute metabolic and molecular response to exercise may vary according to exercise's intensity and duration. However, there is a lack regarding specific tissue alterations after acute exercise with aerobic or anaerobic predominance. The present study investigated the effects of acute exercise performed at different intensities, but with equal total load on molecular and physiological responses in swimming rats. Sixty male rats were divided into a control group and five groups performing an acute bout of swimming exercise at different intensities (80, 90, 100, 110 and 120% of anaerobic threshold [AnT]). The exercise duration of each group was balanced so all groups performed at the same total load. Gene expression (HIF-1α, PGC-1α, MCT1 and MCT4 mRNA), blood biomarkers and tissue glycogen depletion were analyzed after the exercise session. ANOVA One-Way was used to indicate statistical mean differences considering 5% significance level. Blood lactate concentration was the only biomarker sensitive to acute exercise, with a significant increase in rats exercised above AnT intensities (p < 0.000). Glycogen stores of gluteus muscle were significantly reduced in all exercised animals in comparison to control group (p = 0.02). Hepatic tissue presented significant reduction in glycogen in animals exercised above AnT (p = 0.000, as well as reduced HIF-1α mRNA and increased MCT1 mRNA, especially at the highest intensity (p = 0.002). Physiological parameters did not alter amongst groups for most tissues. Our results indicate the hepatic tissue alterations (glycogen stores and gene expressions) in response to different exercise intensities of exercise, even with the total load matched.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":" ","pages":"35-44"},"PeriodicalIF":2.7,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39862964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Electrostatic interaction of loop 1 and backbone of human cardiac myosin regulates the rate of ATP induced actomyosin dissociation.","authors":"Akhil Gargey, Yuri E Nesmelov","doi":"10.1007/s10974-021-09611-z","DOIUrl":"https://doi.org/10.1007/s10974-021-09611-z","url":null,"abstract":"<p><p>Double mutation D208Q:K450L was introduced in the beta isoform of human cardiac myosin to remove the salt bridge D208:K450 connecting loop 1 and the seven-stranded beta sheet within the myosin head. Beta isoform-specific salt bridge D208:K450, restricting the flexibility of loop 1, was previously discovered in molecular dynamics simulations. Earlier it was proposed that loop 1 modulates nucleotide affinity to actomyosin and we hypothesized that the electrostatic interactions between loop 1 and myosin head backbone regulate ATP binding to and ADP dissociation from actomyosin, and therefore, the time of the strong actomyosin binding. To examine the hypothesis we expressed the wild type and mutant of the myosin head construct (1-843 amino acid residues) in differentiated C2C12 cells, and the kinetics of ATP-induced actomyosin dissociation and ADP release were characterized using stopped-flow spectrofluorometry. Both constructs exhibit a fast rate of ATP binding to actomyosin and a slow rate of ADP dissociation, showing that ADP release limits the time of the strongly bound state of actomyosin. We observed a faster rate of ATP-induced actomyosin dissociation with the mutant, compared to the wild type actomyosin. The rate of ADP release from actomyosin remains the same for the mutant and the wild type actomyosin. We conclude that the flexibility of loop 1 is a factor affecting the rate of ATP binding to actomyosin and actomyosin dissociation. The flexibility of loop 1 does not affect the rate of ADP release from human cardiac actomyosin.</p>","PeriodicalId":16422,"journal":{"name":"Journal of Muscle Research and Cell Motility","volume":"43 1","pages":"1-8"},"PeriodicalIF":2.7,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8897261/pdf/nihms-1760630.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10812231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}