Background Regular physical training induces adaptive effects across multiple organ systems,highlighting the existence of inter-organ communication networks.However,the molecular mechanisms underlying both exercise-in...Background Regular physical training induces adaptive effects across multiple organ systems,highlighting the existence of inter-organ communication networks.However,the molecular mechanisms underlying both exercise-induced adaptations and organ-to-organ signaling are not fully characterized.Circulating extracellular vesicles(EVs),including exosomes,carry molecules like microRNAs(miRNAs)that may mediate tissue crosstalk.This study aimed to identify specific exercise training-responsive miRNAs that affect skeletal muscle function.Methods miRNA expression profiles of serum-derived EVs were analyzed in healthy young individuals before and after 3 weeks endurance exercise training.Exercise training-responsive miRNAs were then validated for a functional role in cellular metabolic processes in human myotubes.Results We identified several exercise training-responsive miRNAs within exosome-rich EVs in serum,including miR-136-3p.In human myotubes,miR-136-3p enhanced glucose uptake and targeted the nardilysin convertase(NRDC)gene.Transfection of miR-136-3p or silencing of NRDC induced a shift towards glycolytic metabolism in mitochondria and modulated gene expressions related to myogenesis.Pancreatic islets were identified as a potential source of miR-136-3p based on in silico analysis of gene expression and a molecular analysis of conditioned media from isolated pancreatic islets.Conclusion MiR-136-3p is an endurance training-responsive molecular transducer that modulates glucose metabolism and cellular proliferation in myocytes.Associated with EVs,extracellular miR-136-3p may serve as a molecular messenger to communicate islet–skeletal muscle crosstalk after exercise.Extracellular miR-136-3p may serve as a molecular messenger to communicate islet–skeletal muscle crosstalk.Our results highlight a miRNA-mediated mechanism that participates in inter-organ communication to fine tune the metabolic adaptations to exercise.展开更多
Background:This paper aimed to systematically review the literature regarding the effects of resistance training(RT)performed at longer-muscle length(LML)versus shorter-muscle length(SML)on proxy measurements for long...Background:This paper aimed to systematically review the literature regarding the effects of resistance training(RT)performed at longer-muscle length(LML)versus shorter-muscle length(SML)on proxy measurements for longitudinal hypertrophy.Methods:We included studies that satisfied the following criteria:(1)be a resistance training intervention with a comparison of LML vs SML-RT;(2)assess both fascicle length(FL)and muscle size pre-and post-intervention;(3)involve healthy adults aged≥18 years;(4)be published in an English-language journal,and;(5)have a minimum training intervention duration of 4 weeks.Three databases were searched in February 2024(Google Scholar,PubMed/Medline,Scopus)for relevant articles,alongside'forward'and'backward'citation searching of articles included and additions via authors'personal knowledge.The results of studies were described narratively,compared,and contrasted.Eight studies met the inclusion criteria,totaling a sample size of 120.Results:Our results suggest that both muscle size and fascicle length increases may be greater following LML-RT versus SML-RT,suggesting LML-RT may lead to greater longitudinal hypertrophy than SML-RT.Notably,evidence is largely mixed;no studies to date have attempted to estimate serial sarcomere number changes from LML versus SML-RT,and all but one study used linear extrapolation methods to estimate FL,which has questionable validity.Therefore,the structural adaptations underlying hypertrophy from LML-RT remain undetermined.Conclusion:In conclusion,results suggest that LML-RT may be superior to SML-RT for inducing muscle hypertrophy and,more specifically,longitudinal growth,though evidence is mixed.展开更多
基金supported by grants from the Knut and Alice Wallenberg foundation(P-OB,JRZ,and AK)the Swedish Research Council(JRZ and AK),Centrum för idrottsforskning(AK and JRZ)+7 种基金the NovoNordisk Foundation Metabolic Stress Associated Molecules(MSAM)consortium NNF15SA0018346 and Metabolite-related Inflammation and Disease(MeRIAD)consortium Grant number 0064142(AK)the Swedish Diabetes Foundation(AK and JRZ)the European Foundation for the Study of Diabetes(JRZ and AK)the Region Stockholm(ALF project)(JRZ and KC)the Strategic Research Program in Diabetes at Karolinska Institutet(JRZ and AK)supported by the Strategic Research Programme in Diabetes(SRP Diabetes)for use of the Seahorse flux analyzer.Human islets were made possible through the Juvenile Diabetes Research Foundation(JDRF)award 31-2008-416(European Coordinating Infrastructure for Islet Transplantation(ECIT),Islet for Basic Research program)AK holds a Distinguished Investigator Grant within Endocrinology and Metabolism from the Novo Nordisk Foundation(NNF24OC0088739)JRZ received the 2024 European Association for the Study of Diabetes(ESAD)-Novo Nordisk Foundation Diabetes Prize for Excellence(NNF24SA0092609).
文摘Background Regular physical training induces adaptive effects across multiple organ systems,highlighting the existence of inter-organ communication networks.However,the molecular mechanisms underlying both exercise-induced adaptations and organ-to-organ signaling are not fully characterized.Circulating extracellular vesicles(EVs),including exosomes,carry molecules like microRNAs(miRNAs)that may mediate tissue crosstalk.This study aimed to identify specific exercise training-responsive miRNAs that affect skeletal muscle function.Methods miRNA expression profiles of serum-derived EVs were analyzed in healthy young individuals before and after 3 weeks endurance exercise training.Exercise training-responsive miRNAs were then validated for a functional role in cellular metabolic processes in human myotubes.Results We identified several exercise training-responsive miRNAs within exosome-rich EVs in serum,including miR-136-3p.In human myotubes,miR-136-3p enhanced glucose uptake and targeted the nardilysin convertase(NRDC)gene.Transfection of miR-136-3p or silencing of NRDC induced a shift towards glycolytic metabolism in mitochondria and modulated gene expressions related to myogenesis.Pancreatic islets were identified as a potential source of miR-136-3p based on in silico analysis of gene expression and a molecular analysis of conditioned media from isolated pancreatic islets.Conclusion MiR-136-3p is an endurance training-responsive molecular transducer that modulates glucose metabolism and cellular proliferation in myocytes.Associated with EVs,extracellular miR-136-3p may serve as a molecular messenger to communicate islet–skeletal muscle crosstalk after exercise.Extracellular miR-136-3p may serve as a molecular messenger to communicate islet–skeletal muscle crosstalk.Our results highlight a miRNA-mediated mechanism that participates in inter-organ communication to fine tune the metabolic adaptations to exercise.
文摘Background:This paper aimed to systematically review the literature regarding the effects of resistance training(RT)performed at longer-muscle length(LML)versus shorter-muscle length(SML)on proxy measurements for longitudinal hypertrophy.Methods:We included studies that satisfied the following criteria:(1)be a resistance training intervention with a comparison of LML vs SML-RT;(2)assess both fascicle length(FL)and muscle size pre-and post-intervention;(3)involve healthy adults aged≥18 years;(4)be published in an English-language journal,and;(5)have a minimum training intervention duration of 4 weeks.Three databases were searched in February 2024(Google Scholar,PubMed/Medline,Scopus)for relevant articles,alongside'forward'and'backward'citation searching of articles included and additions via authors'personal knowledge.The results of studies were described narratively,compared,and contrasted.Eight studies met the inclusion criteria,totaling a sample size of 120.Results:Our results suggest that both muscle size and fascicle length increases may be greater following LML-RT versus SML-RT,suggesting LML-RT may lead to greater longitudinal hypertrophy than SML-RT.Notably,evidence is largely mixed;no studies to date have attempted to estimate serial sarcomere number changes from LML versus SML-RT,and all but one study used linear extrapolation methods to estimate FL,which has questionable validity.Therefore,the structural adaptations underlying hypertrophy from LML-RT remain undetermined.Conclusion:In conclusion,results suggest that LML-RT may be superior to SML-RT for inducing muscle hypertrophy and,more specifically,longitudinal growth,though evidence is mixed.
