Diabetes,a leading global chronic disease,poses a significant health threat,with physical inactivity being a major risk factor for its development and progression.This guideline,developed by the Chinese Society of End...Diabetes,a leading global chronic disease,poses a significant health threat,with physical inactivity being a major risk factor for its development and progression.This guideline,developed by the Chinese Society of Endocrinology,synthesizes the latest evidence and expert insights to provide evidence-based recommendations for physical activity and exercise therapy in adults with type 2 diabetes(T2D).It is generally recommended that all adult patients with T2D engage in at least 150—300 min of moderate-intensity aerobic exercise per week,or a minimum of75—150 min of vigorous-intensity exercise,or an equivalent combination of moderate-and vigorous-intensity exercise(with a total exercise volume of at least 450 metabolic equivalent-min per week).For patients with T2D who are capable,moderate over-exercise and a combination of different forms of exercise(aerobic,resistance,flexibility,and/or balance training)are encouraged.The guideline also underscores the necessity of targeting specific subgroups of patients with T2D,including the elderly,individuals with obesity or pre-obesity,cardiovascular disease,hypertension,chronic kidney disease,metabolic dysfunction-associated steatotic liver disease,and/or diabetic foot and its high-risk populations.The guideline provides a scientific basis for clinicians to develop personalized exercise guidance and recommendations,with the goal of improving the disease prognosis of the relevant population.展开更多
Chronic diseases,broadly defined as long-duration conditions that require sustained medical care and/or limit activities of daily living,are a major problem that threatens human health and imposes large social and eco...Chronic diseases,broadly defined as long-duration conditions that require sustained medical care and/or limit activities of daily living,are a major problem that threatens human health and imposes large social and economic burdens.Physical activity has many beneficial effects for human health and is among the most cost-effective ways to prevent and treat chronic diseases.Animal exercise intervention studies are widely used and provide valuable scientific evidence about the cellular and molecular mechanisms underlying the effects of exercise training in a variety of chronic disease models.This consensus statement will provide expert opinions and recommendations for the appropriate design and application of animal exercise intervention studies and models in fundamental investigations of prevention and treatment of chronic diseases,especially focusing on cardiovascular and cerebrovascular diseases(coronary artery disease and stroke),metabolic diseases(obesity and type 2 diabetes mellitus),chronic respiratory diseases(chronic obstructive pulmonary disease),and neurological diseases(Alzheimer's disease).This statement highlights various exercise models(as determined by frequency,intensity,time,and type of exercise intervention)utilized for each disease.Additionally,it includes a list of functional,structural,biochemical,and disease-specific evaluation metrics of exercise effects,followed by outlined recommendations for the exercise study design and evaluations for the mentioned chronic diseases.This consensus aimed to offer practical recommendations for better design and conduct of fundamental research in animal exercise intervention studies to improve our understanding of the effects of exercise on chronic diseases,and to further develop physical exercise or exercise-mimetic interventions for disease prevention and treatment.展开更多
Purpose:The aim of this study was to investigate the potential of dynamic resistance exercise to generate skeletal muscle-derived follistatin like-1(FSTL1),which may induce cardioprotection in rats following myocardia...Purpose:The aim of this study was to investigate the potential of dynamic resistance exercise to generate skeletal muscle-derived follistatin like-1(FSTL1),which may induce cardioprotection in rats following myocardial infarction(MI)by inducing angiogenesis.Methods:Male,adult Sprague-Dawley rats were randomly divided into 5 groups(n=12 in each group):sham group(S),sedentary MI group(MI),MI+resistance exercise group(MR),MI+adeno-associated virus(AAV)-FSTL1 injection group(MA),and MI+AAV-FSTL1 injection+resistance exercise group(MAR).The AAV-FSTL1 vector was prepared by molecular biology methods and injected into the anterior tibialis muscle.The MI model was established by ligation of the left anterior descending coronary artery.Rats in the MR and MAR groups underwent 4 weeks of dynamic resistance exercise training using a weighted climbing-up ladder.Heart function was evaluated by hemodynamic measures.Collagen volume fraction of myocardium was observed and analyzed by Masson’s staining.Human umbilical vein vessel endothelial cells culture and recombinant human FSTL1 protein or transforming growth factor-b receptor 1(TGFbR1)inhibitor treatment were used to elucidate the molecular signaling mechanism of FSTL1.Angiogenesis,cell proliferation,and disco interacting protein 2 homolog A(DIP2A)location were observed by immunofluorescence staining.The expression of FSTL1,DIP2A,and the activation of signaling pathways were detected by Western blotting.Angiogenesis of endothelial cells was observed by tubule experiment.One-way analysis of variance and Student’s t test were used for statistical analysis.Results:Resistance exercise stimulated the secretion of skeletal muscle FSTL1,which promoted myocardial angiogenesis,inhibited pathological remodeling,and protected cardiac function in MI rats.Exercise facilitated skeletal muscle FSTL1 to play a role in protecting the heart.Exogenous FSTL1 promoted the human umbilical vein vessel endothelial cells proliferation and up-regulated the expression of DIP2A,while TGFbR1 inhibitor intervention down-regulated the phosphorylation level of Smad2/3 and the expression of vascular endothelial growth factor-A,which was not conducive to angiogenesis.FSTL1 bound to the receptor,DIP2A,to regulate angiogenesis mainly through the Smad2/3 signaling pathway.FSTL1-DIP2A directly activated Smad2/3 and was not affected by TGFbR1.Conclusion:Dynamic resistance exercise stimulates the expression of skeletal muscle-derived FSTL1,which could supplement the insufficiency of cardiac FSTL1 and promote cardiac rehabilitation through the DIP2A-Smad2/3 signaling pathway in MI rats.展开更多
Sarcopenia is a progressive systemic skeletal muscle disease induced by various physiological and pathological factors,including aging,malnutrition,denervation,and cardiovascular diseases,manifesting as the decline of...Sarcopenia is a progressive systemic skeletal muscle disease induced by various physiological and pathological factors,including aging,malnutrition,denervation,and cardiovascular diseases,manifesting as the decline of skeletal muscle mass and function.Both exercise and nutrition produce beneficial effects on skeletal muscle growth and are viewed as feasible strategies to prevent sarcopenia.Mechanisms involve regulating blood flow,oxidative stress,inflammation,apoptosis,protein synthesis and degradation,and satellite cell activation through exerkines and gut microbiomes.In this review,we summarized and discussed the latest progress and future development of the above mechanisms for providing a theoretical basis and ideas for the prevention and treatment of sarcopenia.展开更多
Exercise training(ET)has been reported to reduce oxidative stress and endoplasmic reticulum(ER)stress in the heart following myocardial infarction(MI).Thioredoxin 1(Trx1)plays a protective role in the infarcted heart....Exercise training(ET)has been reported to reduce oxidative stress and endoplasmic reticulum(ER)stress in the heart following myocardial infarction(MI).Thioredoxin 1(Trx1)plays a protective role in the infarcted heart.However,whether Trx1 regulates ER stress of the infarcted heart and participates in ET-induced cardiac protective effects are still not well known.In this work,H9c2 cells were treated with hydrogen peroxide(H2O2)and recombinant human Trx1 protein(TXN),meanwhile,adult male C57B6L mice were used to establish the MI model,and subjected to a six-week aerobic exercise training(AET)with or without the injection of Trx1 inhibitor,PX-12.Results showed that H2O2significantly increased reactive oxygen species(ROS)level and the expression of TXNIP,CHOP and cleaved caspase12,induced cell apoptosis;TXN intervention reduced ROS level and the expression of CHOP and cleaved caspase12,and inhibited cell apoptosis in H2O2-treated H9c2 cells.Furthermore,AET up-regulated endogenous Trx1 protein expression and down-regulated TXNIP expression,restored ROS level and the expression of ER stress-related proteins,inhibited cell apoptosis as well as improved cardiac fibrosis and heart function in mice after MI.PX-12 partly inhibited the AET-induced beneficial effects in the infarcted heart.This study demonstrates that Trx1 attenuates ER stress-induced cell apoptosis,and AET reduces MI-induced ROS overproduction,ER stress and cell apoptosis partly through up-regulating of Trx1 expression in mice with MI.展开更多
Severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)mainly caused pneumonia and pulmonary fibrosis through upper respiratory tract infection,which resulted in acute respiratory distress syndrome(ARDS)and multio...Severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)mainly caused pneumonia and pulmonary fibrosis through upper respiratory tract infection,which resulted in acute respiratory distress syndrome(ARDS)and multiorgan damage of cardiovascular,nervous,digestive,and genitourinary systems.Although the virus test turned negative after the patient recovered,the damage to multiorgan caused by SARS-CoV-2 may irreversible.Therefore,the health status of the recovered patients has gradually become the focus of people's attention.Whether coronavirus disease 2019(COVID-19)patients can receive exercise rehabilitation training after discharge?and what's the basis?We try to analyze and answer these questions,will provide some ideas about the patients to develop a reasonable and effective exercise rehabilitation program.展开更多
Purpose The aim of this study was to investigate whether skeletal muscle-derived follistatin-like 1(FSTL1)reaches the heart and exerts the angiogenetic function in rats suffering myocardial infarctions(MI)after exerci...Purpose The aim of this study was to investigate whether skeletal muscle-derived follistatin-like 1(FSTL1)reaches the heart and exerts the angiogenetic function in rats suffering myocardial infarctions(MI)after exercise intervention.Methods Forty-eight male adult Sprague-Dawley rats were randomly divided into four groups.MI was provoked by ligation of left anterior descending coronary artery.MI rats underwent adeno-associated virus injection of FST1 in tibialis anterior muscle and 4 weeks of resistance exercise via a tail-suspended incremental weight-climbing method(0-75%body weight,daily load increased by 10%;1 h/day,5 day/w).Heart function was evaluated by hemodynamics including LVSP,LVEDP and±dP/dt max;the cross-sectional area of muscle cells and myocardium fibrosis were analyzed by DiI and Masson’s stain-ing,respectively;the FSTL1 expression,endothelial cell proliferation and angiogenesis were visualized by immunofluores-cence staining;and protein expression was quantified by Western blotting.Results Resistance exercise reverted MI-induced skeletal muscle atrophy,increased muscle FSTL1 expression and stimulated skeletal muscle derived FSTL1 entering into the MI heart via blood circulation.The overexpression of skeletal muscle FSTL1 improved myocardial endothelial cell proliferation,increased small vessel density in the fibrotic border,inhibited myocardial fibrosis and improved heart function in the MI rats after the exercise intervention.Meanwhile,DIP2A-PI3K-Akt-mTOR,Erk1/2 and TGFβ-Smad2/3 pathways were activated in the myocardium.Conclusion Resistance exercise stimulates skeletal muscle derived FSTL1 to reach the myocardium which makes a positive contribution to cardioprotection in MI rat.展开更多
摘要Diabetes,a leading global chronic disease,poses a significant health threat,with physical inactivity being a major risk factor for its development and progression.This guideline,developed by the Chinese Society of Endocrinology,synthesizes the latest evidence and expert insights to provide evidence-based recommendations for physical activity and exercise therapy in adults with type 2 diabetes(T2D).It is generally recommended that all adult patients with T2D engage in at least 150—300 min of moderate-intensity aerobic exercise per week,or a minimum of75—150 min of vigorous-intensity exercise,or an equivalent combination of moderate-and vigorous-intensity exercise(with a total exercise volume of at least 450 metabolic equivalent-min per week).For patients with T2D who are capable,moderate over-exercise and a combination of different forms of exercise(aerobic,resistance,flexibility,and/or balance training)are encouraged.The guideline also underscores the necessity of targeting specific subgroups of patients with T2D,including the elderly,individuals with obesity or pre-obesity,cardiovascular disease,hypertension,chronic kidney disease,metabolic dysfunction-associated steatotic liver disease,and/or diabetic foot and its high-risk populations.The guideline provides a scientific basis for clinicians to develop personalized exercise guidance and recommendations,with the goal of improving the disease prognosis of the relevant population.
基金supported by the National Key R&D Program of China Grant(No.2020YFA0803800 to MX,YB,JL,and RW)grants from the National Natural Science Foundation of China(No.82225005 and No.82020108002 to JX+15 种基金No.82170285to YBNo.82400344 to DZNo.82200549 to YQand No.82200321 to QZ)the Science and Technology Commission of Shanghai Municipality(No.23410750100,No.20DZ2255400,and No.21XD1421300 to JXNo.23010500300 to YBNo.24ZR1425200 to DZand No.24ZR1422700 to JL)the Beijing Natural Science Foundation(No.L248019 to MX)the Chinese Academy of Medical Sciences(CAMS)Innovation Fund for Medical Sciences(No.2021-I2M-5-003 to MX)the“Dawn”Program of Shanghai Education Commission(No.19SG34 to JXand No.24SG36 to YB)the Oriental Scholar of Shanghai Universities(No.TP2022057 to YB)the Shanghai Sailing Program(No.21YF1413200 to QZ)the“Chenguang”Program of Shanghai Education Commission(No.22CGA45 to YQ)supported by the American Heart Association(No.23CDA1045944)。
摘要Chronic diseases,broadly defined as long-duration conditions that require sustained medical care and/or limit activities of daily living,are a major problem that threatens human health and imposes large social and economic burdens.Physical activity has many beneficial effects for human health and is among the most cost-effective ways to prevent and treat chronic diseases.Animal exercise intervention studies are widely used and provide valuable scientific evidence about the cellular and molecular mechanisms underlying the effects of exercise training in a variety of chronic disease models.This consensus statement will provide expert opinions and recommendations for the appropriate design and application of animal exercise intervention studies and models in fundamental investigations of prevention and treatment of chronic diseases,especially focusing on cardiovascular and cerebrovascular diseases(coronary artery disease and stroke),metabolic diseases(obesity and type 2 diabetes mellitus),chronic respiratory diseases(chronic obstructive pulmonary disease),and neurological diseases(Alzheimer's disease).This statement highlights various exercise models(as determined by frequency,intensity,time,and type of exercise intervention)utilized for each disease.Additionally,it includes a list of functional,structural,biochemical,and disease-specific evaluation metrics of exercise effects,followed by outlined recommendations for the exercise study design and evaluations for the mentioned chronic diseases.This consensus aimed to offer practical recommendations for better design and conduct of fundamental research in animal exercise intervention studies to improve our understanding of the effects of exercise on chronic diseases,and to further develop physical exercise or exercise-mimetic interventions for disease prevention and treatment.
基金supported this research:The National Natural Science Foundation of China(No.31671240 to ZT,No.31900828 to YX).
摘要Purpose:The aim of this study was to investigate the potential of dynamic resistance exercise to generate skeletal muscle-derived follistatin like-1(FSTL1),which may induce cardioprotection in rats following myocardial infarction(MI)by inducing angiogenesis.Methods:Male,adult Sprague-Dawley rats were randomly divided into 5 groups(n=12 in each group):sham group(S),sedentary MI group(MI),MI+resistance exercise group(MR),MI+adeno-associated virus(AAV)-FSTL1 injection group(MA),and MI+AAV-FSTL1 injection+resistance exercise group(MAR).The AAV-FSTL1 vector was prepared by molecular biology methods and injected into the anterior tibialis muscle.The MI model was established by ligation of the left anterior descending coronary artery.Rats in the MR and MAR groups underwent 4 weeks of dynamic resistance exercise training using a weighted climbing-up ladder.Heart function was evaluated by hemodynamic measures.Collagen volume fraction of myocardium was observed and analyzed by Masson’s staining.Human umbilical vein vessel endothelial cells culture and recombinant human FSTL1 protein or transforming growth factor-b receptor 1(TGFbR1)inhibitor treatment were used to elucidate the molecular signaling mechanism of FSTL1.Angiogenesis,cell proliferation,and disco interacting protein 2 homolog A(DIP2A)location were observed by immunofluorescence staining.The expression of FSTL1,DIP2A,and the activation of signaling pathways were detected by Western blotting.Angiogenesis of endothelial cells was observed by tubule experiment.One-way analysis of variance and Student’s t test were used for statistical analysis.Results:Resistance exercise stimulated the secretion of skeletal muscle FSTL1,which promoted myocardial angiogenesis,inhibited pathological remodeling,and protected cardiac function in MI rats.Exercise facilitated skeletal muscle FSTL1 to play a role in protecting the heart.Exogenous FSTL1 promoted the human umbilical vein vessel endothelial cells proliferation and up-regulated the expression of DIP2A,while TGFbR1 inhibitor intervention down-regulated the phosphorylation level of Smad2/3 and the expression of vascular endothelial growth factor-A,which was not conducive to angiogenesis.FSTL1 bound to the receptor,DIP2A,to regulate angiogenesis mainly through the Smad2/3 signaling pathway.FSTL1-DIP2A directly activated Smad2/3 and was not affected by TGFbR1.Conclusion:Dynamic resistance exercise stimulates the expression of skeletal muscle-derived FSTL1,which could supplement the insufficiency of cardiac FSTL1 and promote cardiac rehabilitation through the DIP2A-Smad2/3 signaling pathway in MI rats.
基金funded by National Natural Science Foundation of China,grant number“32171128”.
摘要Sarcopenia is a progressive systemic skeletal muscle disease induced by various physiological and pathological factors,including aging,malnutrition,denervation,and cardiovascular diseases,manifesting as the decline of skeletal muscle mass and function.Both exercise and nutrition produce beneficial effects on skeletal muscle growth and are viewed as feasible strategies to prevent sarcopenia.Mechanisms involve regulating blood flow,oxidative stress,inflammation,apoptosis,protein synthesis and degradation,and satellite cell activation through exerkines and gut microbiomes.In this review,we summarized and discussed the latest progress and future development of the above mechanisms for providing a theoretical basis and ideas for the prevention and treatment of sarcopenia.
基金supported by National Natural Science Foundation of China(Grant No.31701039,31671240)the Fundamental Research Funds for the Central Universities,Shaanxi Normal University(Grant Number GK201803096).
摘要Exercise training(ET)has been reported to reduce oxidative stress and endoplasmic reticulum(ER)stress in the heart following myocardial infarction(MI).Thioredoxin 1(Trx1)plays a protective role in the infarcted heart.However,whether Trx1 regulates ER stress of the infarcted heart and participates in ET-induced cardiac protective effects are still not well known.In this work,H9c2 cells were treated with hydrogen peroxide(H2O2)and recombinant human Trx1 protein(TXN),meanwhile,adult male C57B6L mice were used to establish the MI model,and subjected to a six-week aerobic exercise training(AET)with or without the injection of Trx1 inhibitor,PX-12.Results showed that H2O2significantly increased reactive oxygen species(ROS)level and the expression of TXNIP,CHOP and cleaved caspase12,induced cell apoptosis;TXN intervention reduced ROS level and the expression of CHOP and cleaved caspase12,and inhibited cell apoptosis in H2O2-treated H9c2 cells.Furthermore,AET up-regulated endogenous Trx1 protein expression and down-regulated TXNIP expression,restored ROS level and the expression of ER stress-related proteins,inhibited cell apoptosis as well as improved cardiac fibrosis and heart function in mice after MI.PX-12 partly inhibited the AET-induced beneficial effects in the infarcted heart.This study demonstrates that Trx1 attenuates ER stress-induced cell apoptosis,and AET reduces MI-induced ROS overproduction,ER stress and cell apoptosis partly through up-regulating of Trx1 expression in mice with MI.
基金Fundamental Research Funds for the Central Universities in China grants(GK261002065 to ZT).
摘要Severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)mainly caused pneumonia and pulmonary fibrosis through upper respiratory tract infection,which resulted in acute respiratory distress syndrome(ARDS)and multiorgan damage of cardiovascular,nervous,digestive,and genitourinary systems.Although the virus test turned negative after the patient recovered,the damage to multiorgan caused by SARS-CoV-2 may irreversible.Therefore,the health status of the recovered patients has gradually become the focus of people's attention.Whether coronavirus disease 2019(COVID-19)patients can receive exercise rehabilitation training after discharge?and what's the basis?We try to analyze and answer these questions,will provide some ideas about the patients to develop a reasonable and effective exercise rehabilitation program.
基金supported by National Natural Science Foundation of China(No.31371199).
摘要Purpose The aim of this study was to investigate whether skeletal muscle-derived follistatin-like 1(FSTL1)reaches the heart and exerts the angiogenetic function in rats suffering myocardial infarctions(MI)after exercise intervention.Methods Forty-eight male adult Sprague-Dawley rats were randomly divided into four groups.MI was provoked by ligation of left anterior descending coronary artery.MI rats underwent adeno-associated virus injection of FST1 in tibialis anterior muscle and 4 weeks of resistance exercise via a tail-suspended incremental weight-climbing method(0-75%body weight,daily load increased by 10%;1 h/day,5 day/w).Heart function was evaluated by hemodynamics including LVSP,LVEDP and±dP/dt max;the cross-sectional area of muscle cells and myocardium fibrosis were analyzed by DiI and Masson’s stain-ing,respectively;the FSTL1 expression,endothelial cell proliferation and angiogenesis were visualized by immunofluores-cence staining;and protein expression was quantified by Western blotting.Results Resistance exercise reverted MI-induced skeletal muscle atrophy,increased muscle FSTL1 expression and stimulated skeletal muscle derived FSTL1 entering into the MI heart via blood circulation.The overexpression of skeletal muscle FSTL1 improved myocardial endothelial cell proliferation,increased small vessel density in the fibrotic border,inhibited myocardial fibrosis and improved heart function in the MI rats after the exercise intervention.Meanwhile,DIP2A-PI3K-Akt-mTOR,Erk1/2 and TGFβ-Smad2/3 pathways were activated in the myocardium.Conclusion Resistance exercise stimulates skeletal muscle derived FSTL1 to reach the myocardium which makes a positive contribution to cardioprotection in MI rat.