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SUMMARY: Both the academic and popular worlds have paid close attention to the link between exercise and cognitive performance. It is increasingly important to understand the numerous mechanisms by which exercise might influence cognitive abilities in view of the continuous societal issues caused by aging populations and the prevalence of disorders associated to cognitive decline. A rising amount of evidence showing a favorable association between physical activity and cognitive well-being serves as the foundation for the justification for studying the effects of exercise on cognitive function and learning ability. The study employed an 8-week treadmill based on exercise on male adults C57BL/6 mice. The exercise group were engaged in 5 sessions a week gradually increasing the intensity of the protocol by 5 % each week. The Mice cognitive assessments were done using Morris Water Maze and Novel Object Recognition tests. The long term-impact on learning ability were further assessed through immmohistochemistry and molecular analysis of the hippocampal and prefrontal cortex tissues of the animals' brain tissues. The findings showed improved spatial learning abilities, recognition memory, and heighted synaptic plasticity indicated by elevated synaptic makers. The study underscores the role of long-term aerobic exercise in augmenting cognitive performance. It not only contributes to the understanding of the interplay between neuroplasticity and cognitive benefits but also the growing body of research on the impact of exercise on cognitive function.
Tanto el mundo académico como el popular han prestado mucha atención al vínculo entre el ejercicio y el rendimiento cognitivo. Es cada vez más importante comprender los numerosos mecanismos por los cuales el ejercicio podría influir en las capacidades cognitivas en vista de los continuos problemas sociales causados por el envejecimiento de la población y la prevalencia de trastornos asociados al deterioro cognitivo. Una cantidad cada vez mayor de evidencia que muestra una asociación favorable entre la actividad física y el bienestar cognitivo sirve como base para justificar el estudio de los efectos del ejercicio sobre la función cognitiva y la capacidad de aprendizaje. El estudio se realizó en ratones machos adultos C57BL/6 utilizándose en los ejercicios una cinta rodante durante 8 semanas. El grupo de ejercicio realizó 5 sesiones por semana aumentando gradualmente la intensidad del protocolo en un 5 % cada semana. Las evaluaciones cognitivas de los ratones se realizaron utilizando las pruebas Morris Water Maze y Novel Object Recognition. El impacto a largo plazo en la capacidad de aprendizaje se evaluó mediante inmunohistoquímica y análisis molecular de los tejidos del hipocampo y la corteza prefrontal de los tejidos cerebrales de los animales. Los hallazgos mostraron mejoras en las habilidades de aprendizaje espacial, la memoria de reconocimiento y una mayor plasticidad sináptica indicada por unos creadores sinápticos elevados. El estudio subraya el papel del ejercicio aeróbico a largo plazo para aumentar el rendimiento cognitivo. No sólo contribuye a la comprensión de la interacción entre la neuroplasticidad y los beneficios cognitivos, sino también al creciente conjunto de investigaciones sobre el impacto del ejercicio en la función cognitiva.
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Active physical exercise can effectively alleviate the pathological process of chronic cerebral ischemia(CCH)and improve learning and memory ability.This paper reviews the possible biological mechanisms of aerobic exercise to delay the pathological process of chronic cerebral ischemia and improve learning and memory.Previous studies have found that aerobic exercise can improve the neuroprotective effect,enhance the plasticity of hippocampal synapses,improve the activity of the upper and lower pathways of hippocampal tissue,and improve learning and memory ability.However,the intervention effect of aerobic exercise on chronic cerebral ischemia should be fully considered at the intervention time,and the intervention effect is also different.
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BACKGROUND:Clinical studies have shown that aerobic exercise is an important supplement to the clinical treatment of patients with pulmonary hypertension,which can alleviate the disease condition,increase exercise tolerance and improve the quality of life.However,it is not clear whether patients at different stages of pulmonary hypertension can benefit equally from exercise training. OBJECTIVE:To compare the intervention effects of early or late aerobic training on right heart failure in rats with pulmonary hypertension and explore its possible mechanism. METHODS:Sixty male Wistar rats were randomly divided into control group,model sedentary group,model early exercise group and model late exercise group,with 15 rats in each group.The model of pulmonary hypertension was established by intraperitoneal injection of monocrotaline(60 mg/kg)in the latter three groups.The model early exercise group was given 8 weeks of treadmill aerobic exercise(60%maximum running speed,60 minutes per day,5 days a week)after modeling,while the model late exercise group was trained for 6 weeks after 2 weeks of modeling.The control and model sedentary groups were fed quietly in the rat cage for 8 weeks.After training,the exercise performance,right ventricular hemodynamics,cardiopulmonary function,cardiopulmonary histopathology,reactive oxygen species level in mitochondria,activity of mitochondrial respiratory chain complex and expressions of myocardial tissue proteins were detected. RESULTS AND CONCLUSION:Compared with the model sedentary group,exercise performance and right ventricular function improved(P<0.05),myocardial collagen content,endothelin-1,tumor necrosis factor-α/interleukin-10 ratio and β-myosin heavy chain/α-myosin heavy chain ratio decreased(P<0.05),vascular endothelial growth factor and sarcoplasmic reticulum calcium-adenosine triphosphate enzyme expression increased(P<0.05),immunofluorescence intensity of mitochondrial reactive oxygen species and the protein expression of 3-nitrotyrosine decreased(P<0.05),the activities of complex I,II,IV and V increased in the model early exercise and model late exercise groups(P<0.05),but there were no significant changes in right ventricular maximum pressure,pulmonary acceleration time and pulmonary artery wall area/total vascular area ratio(P>0.05).Compared with the model late exercise group,the model early exercise group further improved exercise performance and right ventricular function,and downregulated collagen content,brain natriuretic peptide protein expression,tumor necrosis factor-α/interleukin-10 ratio and β-myosin heavy chain/α-myosin heavy chain ratio(P<0.05).To conclude,although pulmonary vascular remodeling and right ventricular overload persist in rats with pulmonary hypertension,exercise training at different stages of the disease has a cardioprotective effect.The mechanism is related to the improvement of cardiac remodeling,neurohormone system imbalance,inflammatory response and mitochondrial oxidative stress.Greater benefit is gained from initiating exercise in the early stage of the disease.
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BACKGROUND:Exercise as a viable non-pharmacological treatment has the potential to reverse skeletal muscle aging that deteriorates with age.The role of autophagy in the skeletal muscle aging process is indispensable.During skeletal muscle aging,Atg genes involved in regulating autophagy regulate the autophagic process in either a facilitative or inhibitory manner to improve the physiological morphology of skeletal muscle.However the specific molecular mechanisms of autophagy in the exercise regulation of skeletal muscle aging remain puzzling. OBJECTIVE:To search for general patterns of the effects of autophagic mechanisms on skeletal muscle aging during exercise through a review of articles in this field. METHODS:(1)CNKI and Web of Science were searched,reviewed,and screened for relevant literature using the keywords of"Atg genes(proteins),autophagy,exercise,and skeletal muscle aging"to lay the theoretical foundation for the full-text analysis.(2)The comparative analysis method was used to compare the similarities and differences among the included documents to provide reasonable theoretical support for the arguments.By the further comparative analysis of the literature,the relationship between relevant indicators was clarified,to provide the ideas for the full-text analysis. RESULTS AND CONCLUSION:Atg family-mediated autophagy is indispensable for delaying skeletal muscle aging.Atg genes involved in regulating autophagy regulate the autophagic process in either a facilitative or inhibitory manner to improve the physiological morphology and function of skeletal muscle.Different exercise patterns,such as age,time,or intensity at initiation,may have heterogeneous effects on the expression of autophagy-related proteins,but long-term aerobic exercise regulates Atg-related proteins,induces skeletal muscle autophagy,and delays the loss of muscle mass.
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BACKGROUND:Obesity and its relevant chronic inflammation are important risk factors for inducing type 2 diabetes.This inflammatory response will further involve skeletal muscle,leading to an increase in catabolic and autophagic fluxes in skeletal muscle.Aerobic exercise is the mainstream mode of exercise in the prevention and treatment of type 2 diabetes,and may also has a certain protective effect on skeletal muscle. OBJECTIVE:To explore the effects and regulatory mechanisms of aerobic exercise on glucolipid metabolism,skeletal muscle inflammation and autophagy in type 2 diabetic rats. METHODS:Animal models of type 2 diabetes were established in rats by 8-week high-fat feeding combined with streptozotocin injection,and the experimental rats were then divided into normal control group,normal exercise group,diabetic control group and diabetic exercise group.The exercise group performed 4 weeks of aerobic exercise(16 m/min,60 min/d,5 d/wk).The levels of blood glucose,high-density lipoprotein,low-density lipoprotein and triglyceride in serum were measured by an automated biochemical analyzer.Serum insulin level was determined using enzyme-linked immunosorbent assay and the insulin resistance index and area under the glucose metabolism curve were calculated.The levels of interleukin 6 and tumor necrosis factor α in skeletal muscle were measured by enzyme-linked immunosorbent assay after 4 weeks of aerobic exercise,and the expression levels of forkhead box protein O3(FoxO3),LC3 and p62 in skeletal muscle were measured by western blot assay. RESULTS AND CONCLUSION:The area under the glucose tolerance curve and insulin resistance index both increased significantly in type 2 diabetic rats(P<0.001,P=0.025),and aerobic exercise significantly reduced the area under the glucose tolerance curve and insulin resistance index in the normal exercise group(P<0.001,P=0.038)and diabetic exercise group(P<0.001,P=0.004).Serum high-density lipoprotein significantly decreased(P=0.030),and low-density lipoprotein and triglyceride(P=0.027,P=0.014)levels significantly increased in the diabetic control group compared with the normal control group.Aerobic exercise significantly reduced triglyceride and low-density lipoprotein levels in the normal exercise group(P=0.019,P=0.008)as well as triglyceride levels in the diabetic exercise group(P=0.022).Both interleukin-6 and tumor necrosis factor α levels were significantly increased in the skeletal muscle of type 2 diabetic rats compared with the normal control group(P<0.001,P=0.007),and aerobic exercise significantly reduced tumor necrosis factor α levels in the diabetic exercise group(P=0.017).The LC3-Ⅱ/LC3-I was significantly increased in the skeletal muscle of type 2 diabetic rats compared with the normal control group.Aerobic exercise significantly increased the LC3-Ⅱ/LC3-I in the normal exercise group(P<0.001)and decreased the LC3-Ⅱ/LC3-I,FoxO3 and p62 protein expression levels in the diabetic exercise group(P=0.026,P=0.050,P=0.048).To conclusion,type 2 diabetes model established by high-fat feeding combined with streptozotocin injection has obvious glycolipid metabolism disorder,and leads to inflammatory response and excessive activation of autophagy in skeletal muscle.Aerobic exercise can improve glycolipid metabolism,reduce local inflammation in skeletal muscle and inhibit autophagy,and finally play a protective role in skeletal muscle.
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BACKGROUND:Exercise improves Alzheimer's disease,dementia,and age-related cognitive abilities.A potential mediator between exercise and these health benefits may be adult hippocampal neurogenesis.Therefore,it is of great significance to explore whether and how exercise affects the adult hippocampal neurogenesis process in Alzheimer's disease mice. OBJECTIVE:To observe the effect of aerobic exercise on adult hippocampal neurogenesis of Alzheimer's disease mice,and to explore whether aerobic exercise can promote their adult hippocampal neurogenesis. METHODS:Three-month-old wild-type(C57BL/6Jnju)and APP/PS1 double transgenic Alzheimer's disease mice were randomly divided into four groups:wild control group,wild exercise group,Alzheimer's disease control group and Alzheimer's disease exercise group,with 20 mice in each group.The control group did not do exercise,and the exercise group did aerobic exercise for 5 months.After exercise intervention,real-time PCR,immunofluorescence and western blot assay were used to detect the expression levels of DCX,Ki67,βIII-tubulin and NeuN in the hippocampal tissue of mice in each group. RESULTS AND CONCLUSION:The expressions of DCX,βIII-tubulin and NeuN in the hippocampal dentate gyrus in the Alzheimer's disease control group were significantly lower than those in the wild control group(P<0.05).The expressions of DCX,Ki67,βIII-tubulin and NeuN were significantly higher in the hippocampal dentate gyrus in the Alzheimer's disease exercise group than those in the Alzheimer's disease control group(P<0.05).It is indicated that long-term aerobic exercise intervention can strengthen the proliferation,migration and differentiation of neurons during adult hippocampal neurogenesis and significantly increase the number of neuronal precursor cells and new neurons in Alzheimer's disease mice.
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BACKGROUND:Type 2 diabetes is often accompanied by renal dysfunction.Increasing studies have shown that exercise can alleviate metabolic disorders and renal dysfunction in diabetic patients.However,the specific mechanism underlying the renal protective effect of exercise in patients with type 2 diabetes is rarely reported. OBJECTIVE:To investigate whether aerobic exercise can improve renal function in type 2 diabetic rats by inhibiting transforming growth factor β1/Notch1 pathway. METHODS:Male Sprague-Dawley rats were randomly divided into normal control group and diabetes model group.After successful modeling,they were randomly divided into diabetes control group and diabetes exercise group.Rats in the diabetes exercise group were subjected to an 8-week aerobic exercise.Samples were collected after exercise,and the relevant indexes of glucose and lipid metabolism and renal function were detected by automatic biochemical analyzer and ELISA.The microscopic structure of renal cortex was observed by electron microscope.ELISA and RT-PCR were used to detect the expression of related proteins and genes in rat kidney tissue. RESULTS AND CONCLUSION:Compared with the normal control group,fasting blood glucose,total cholesterol,and triglyceride levels and insulin resistance index were significantly increased in the diabetic control group(P＜0.05).Aerobic exercise could significantly reduce fasting blood glucose and triglyceride levels(P＜0.05).Compared with the normal control group,the diabetic control group had significantly increased contents of urinary microalbumin,serum urea nitrogen and serum creatinine(P＜0.01),thickened renal basement membrane,mesangial matrix hyperplasia,accompanied by a certain degree of foot process fusion,and obvious lesion of the kidney.Aerobic exercise could significantly down-regulate the overexpressions of urinary microalbumin,serum urea nitrogen and serum creatinine in type 2 diabetic rats(P＜0.01),and significantly improve the pathological changes of the kidney in diabetic rats.Compared with the normal control group,the protein and gene expression levels of transforming growth factor β1,Notch1,Jagged1 and Hes1 in rat kidney tissue were significantly increased in the diabetic control group(P＜0.01).Aerobic exercise had a highly significant inhibitory effect on the overexpression of transforming growth factor β1,Notch1 and Jagged1 proteins and genes(P＜0.01)and also significantly inhibited the overexpression of Hes1 protein(P＜0.05).In conclusion,aerobic exercise can protect renal function and delay the pathological progression of the kidney in diabetic rats,which may be achieved by inhibiting the overexpression of transforming growth factor β1/Notch1 signaling pathway.
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BACKGROUND:Patients with Alzheimer's disease mainly show cognitive and memory dysfunctions.Aerobic exercise can inhibit endoplasmic reticulum stress and improve cognitive function of the patients.However,whether aerobic exercise can inhibit endoplasmic reticulum stress dependent neuroinflammation is still unclear. OBJECTIVE:To explore the effect of aerobic exercise on neuroinflammation and cognitive impairment in a mouse model of Alzheimer's disease. METHODS:Fifty C57BL/6J wild-type male mouse mice were randomly divided into wild-type control and wild-type exercise groups,while another 50 APP/PS1 double transgenic male mice were randomly divided into Alzheimer's disease group and Alzheimer's disease exercise group,with 25 mice in each group.Mice in the wild-type exercise and Alzheimer's disease exercise groups received aerobic exercise training(treadmill training,45 min/d,12 m/min,5 d/wk,8 weeks in total).Mice in the wild-type control and Alzheimer's disease groups were placed on the quiet running platform.Morris water maze test was used to detect the cognitive ability of mice.Hematoxylin-eosin staining and Nissl staining were used to detect hippocampal tissue damage in mice.Thioflavin-S staining was used to detect β-amyloid content in hippocampal tissue.Immunohistochemistry was used to detect β-amyloid and p-Tau levels in hippocampal tissue.Immunofluorescence staining was used to detect the number of positive cells for neuroinflammation-related factors in hippocampal tissue.Western blot was used to detect p-IRE1,IRE1,p-PERK,PERK,ATF6,GRP78,Bip,Caspase-12,Iba-1,and GFAP protein levels. RESULTS AND CONCLUSION:Compared with the wild-type control group,escape latency was increased,the number of times they reached the previous platform and the time they stayed on the platform were decreased,β-amyloid and Tau levels,p-IRE1/IRE1,p-PERK/PERK,ATF6,GRP78,Bip,Caspase-12,Iba-1,and GFAP protein levels,Iba-1+,Iba-1+TNF-α+,Iba-1+IL-6+,Iba-1+IL-1β+,GFAP+,GFAP+TNF-α+,GFAP+IL-6+,GFAP+IL-1β+ positive cells in hippocampal tissue were increased,and Iba-1+IL-4+,Iba-1+IL-10+,GFAP+IL-4+,GFAP+IL-10+ positive cells were decreased in the Alzheimer's disease group(P＜0.05).Compared with Alzheimer's disease group,escape latency was decreased,the number of times they reached the previous platform and the time they stayed on the platform were increased,β-amyloid and Tau levels,p-IRE1/IRE1,p-PERK/PERK,ATF6,GRP78,Bip,Caspase-12,Iba-1,GFAP protein levels,Iba-1+,Iba-1+TNF-α+,Iba-1+IL-6+,Iba-1+IL-1β+,GFAP+,GFAP+TNF-α+,GFAP+IL-6+,and GFAP+IL-1β+ positive cells in hippocampal tissue were decreased,and Iba-1+IL-4+,Iba-1+IL-10+,GFAP+IL-4+,GFAP+IL-10+ positive cells were increased in the Alzheimer's disease exercise group(P＜0.05).To conclude,aerobic exercise can reduce cognitive impairment in Alzheimer's disease mice by inhibiting endoplasmic reticulum stress and neuroinflammation in hippocampal tissue.
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BACKGROUND:Aging is associated with increased susceptibility to cardiovascular disease,and mitochondrial dysfunction plays a key role in the pathogenesis of cardiovascular disease.Regular physical activity is beneficial to cardiovascular health and can prevent and treat chronic heart disease.However,the specific mechanism of mitochondria in the protective effect of exercise on the aging heart has not yet been clarified. OBJECTIVE:To explore the effect of aerobic exercise on cardiac pathological remodeling in aging rats and to investigate the possible mechanism of mitochondrial quality control system. METHODS:Sixty Wistar rats were randomly divided into young sedentary group(6 months old),old sedentary group(20 months old)and old exercise group(20 months old)with 20 rats in each group.Rats in the young sedentary and old sedentary groups were fed in cages for 12 weeks,while those in the old exercise group underwent moderate-intensity aerobic treadmill exercise(60%of the maximal running speed,slope 0°,60 minute per day,5 days per week)for 12 weeks.After the experiment,the heart was extracted for relevant indicator tests. RESULTS AND CONCLUSION:Cardiac morphology and myocardial histopathology:compared with the young sedentary group,the rats in the old sedentary group presented with concentric cardiac hypertrophy,myocardial fibrosis,myocardial cell apoptosis and loss,and cardiac diastolic dysfunction(P＜0.05);compared with the old sedentary group,animals in the old exercise group showed reduced myocardial fibrosis and apoptosis rates,increased cell numbers,improved cardiac function(P＜0.05),and a transition in cardiac phenotype from pathological to physiological hypertrophy.Mitochondrial function:compared with the young sedentary group,the generation rate of mitochondrial hydrogen peroxide increased(P＜0.05),respiration rate and respiratory control ratio of state 3 and state 4 decreased(P＜0.05),activities of respiratory chain complexes Ⅰ,Ⅱ and Ⅳ decreased(P＜0.05),mitochondrial calcium retention capacity decreased(P＜0.05),and mitochondrial permeability transition pore opening increased(P＜0.05)in the old sedentary group.Compared with the old sedentary group,all of the above indicators were significantly improved in the old exercise group(P＜0.05).Mitochondrial quality control:compared with the young sedentary group,mitochondrial biogenesis decreased(P＜0.05),mitophagy activity increased(P＜0.05),mitochondrial fusion reduced(P＜0.05),and fission raised(P＜0.05)in the old sedentary group;compared with the old sedentary group,mitochondrial biogenesis and mitophagy activity increased(P＜0.05),mitochondrial fusion raised(P＜0.05)and fission decreased(P＜0.05)in the old exercise group.To conclude,regular aerobic exercises exert cardioprotective effects in aging rats by regulating the mitochondrial quality control system,thus reversing pathological cardiac remodeling and improving cardiac function.
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BACKGROUND:β-amyloid protein and Tau protein have adverse effects on the cognitive function of Alzheimer's disease patients,and Notch1 and Caspase-3 can regulate the expression of β-amyloid protein and Tau protein.It is not clear whether Notch1 and Caspase-3 mediate the process of aerobic exercise to improve the cognitive ability of Alzheimer's disease patients.At present,there is a lack of studies on the effect of long-term aerobic exercise on the expression of Notch1 and Caspase-3 in the hippocampus of Alzheimer's disease mice. OBJECTIVE:To observe the expression of Notch1 and Caspase-3 in the hippocampus of Alzheimer's disease mice undergoing long-term aerobic exercise and to investigate the effects of Notch1 and Caspase-3 in Alzheimer's disease mice. METHODS:Wild type and APP/PS1 double-transgenic Alzheimer's disease mice aged 3 months were randomly divided into four groups:wild control group,wild exercise group,Alzheimer's disease control group and Alzheimer's disease exercise group,with 20 mice in each group.Mice in the control groups were not subjected to exercise,while those in the exercise groups received aerobic exercise intervention for 5 months.After the exercise intervention,Morris water maze was used to detect the spatial learning and memory ability of mice.Real-time PCR,immunofluorescence and western blot were used to detect the expressions of Aβ1-42,Tau,Notch1 and Caspase-3 in the hippocampal tissues of mice in each group. RESULTS AND CONCLUSION:The spatial learning and memory ability of Alzheimer's mice was significantly worse than that of wild-type mice(P＜0.05).The spatial learning and memory ability of mice in the exercise groups were significantly better than that in the corresponding control groups(P＜0.05).The expressions of Aβ1-42,Tau,Notch1 and Caspase-3 in the hippocampus were significantly higher in the Alzheimer's disease control group than the wild control group(P＜0.05)and were significantly lower in the Alzheimer's disease exercise group than the Alzheimer's disease control group(P＜0.05).To conclude,long-term aerobic exercise can improve the spatial learning and memory ability of Alzheimer's disease mice,which may be related to the decreased expression of Notch1,Caspase-3,Aβ1-42 and Tau protein in the hippocampus of Alzheimer's disease mice.
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BACKGROUND:Sarcopenia is an age-related degenerative syndrome,and the relationship between mitochondrial autophagy and exercise in preventing and treating sarcopenia has been demonstrated.However,there is a lack of comprehensive reviews detailing the specific receptor proteins and signaling pathways involved in the role of exercise in sarcopenia prevention and treatment. OBJECTIVE:To comprehensively introduce the specific receptor proteins and signaling pathways related to mitochondrial autophagy and their role in the prevention and treatment of sarcopenia through exercise. METHODS:A literature search was conducted between February 1,2023,and April 1,2023,covering literature from database inception to April 2023.Databases included the Web of Science,PubMed,China National Knowledge Infrastructure(CNKI),WanFang Data,and VIP.Keywords used for the search included sarcopenia,muscle wasting,aging,elderly,mitochondria,mitochondrial function,proteins,pathways,and others.After strict inclusion and exclusion criteria,76 articles were ultimately included. RESULTS AND CONCLUSION:Sarcopenia is a disease characterized by a decline in muscle mass and function with age,and its pathogenesis involves neuro-muscular functional decline,chronic inflammation,acid-base imbalance,and mitochondrial dysfunction.Mitochondrial autophagy is an important process for clearing damaged mitochondria in cells,in which receptor proteins and signaling pathways are involved in the regulation of mitochondrial autophagy.Exercise can promote the occurrence of mitochondrial autophagy by regulating the activity of these receptor proteins and signaling pathways,thereby playing an important role in the prevention and treatment of sarcopenia.Exercise can induce mitochondrial autophagy in sarcopenia by upregulating AMPK,phosphorylating ULK1,and reducing mitochondrial energy,enhancing the expression of mitochondrial autophagy-related proteins associated with AMBRA1,and regulating the PINK1/Parkin pathway,to improve mitochondrial dysfunction caused by sarcopenia.In addition,exercise can activate the mTOR pathway to promote muscle growth and increase glucose uptake,thereby preventing and treating sarcopenia.Future studies are needed to further investigate the specific mechanisms and regulatory pathways of mitochondrial autophagy-related receptor proteins and signaling pathways in the prevention and treatment of sarcopenia by exercise,and to conduct more clinical trials in humans,thereby to promote further development in this field.
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BACKGROUND:Parkinson's disease is a neurodegenerative disease,and its pathogenesis involves mitochondrial dysfunction.Exercise has a potential ameliorative effect on mitochondrial dysfunction related to Parkinson's disease,but there is no comprehensive review and in-depth analysis in this field. OBJECTIVE:To comprehensively review and analyze mitochondrial dysfunction related to Parkinson's disease and the potential ameliorative effect of exercise,thereby providing new ideas and methods for the treatment and prevention of Parkinson's disease. METHODS:We searched the Web of Science,PubMed,CNKI,WanFang,and VIP databases with the keywords of"mitochondria,mitochondrial function,mitochondrial disease,mitochondrial dysfunction,Parkinson's disease,Parkinson,exercise,physical activity,exercise training,exercise therapy,mitochondrial impairment,mitochondrial damage,mitochondrial defects"in Chinese and"mitochondria,Parkinson's disease,Parkinson disease,physical exercise,exercise,physical activity,mitochondrial dysfunction,mitochondrial damage,mitochondrial impairment,athletic training,exercise training,rehabilitation"in English.A total of 89 articles were included for review and analysis. RESLUTS AND CONCLUSION:Parkinson's disease is closely related to mitochondrial dysfunction,including mitochondrial biogenesis inhibition,reduced autophagy,increased apoptosis,abnormal elevation of Ca2+ concentration,and increased oxidative stress in Parkinson's disease patients.Exercise has a positive effect on mitochondrial dysfunction related to Parkinson's disease,by promoting mitochondrial biogenesisand autophagy,regulating mitochondrial morphology,altering the plasticity of the mitochondrial respiratory chain,and reducing oxidative stress,thus helping to improve the development and progression of Parkinson's disease.However,the detailed mechanism between mitochondrial dysfunction and the ameliorative effect of exercise is still not fully understood,and future clinical studies can be conducted to validate the results of animal models and gain insights into the benefits and mechanisms of exercise in patients with Parkinson's disease.
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BACKGROUND:Abnormal Notch1 signaling pathway is mostly found in the brain of Alzheimer's disease patients,but the role of these signaling pathways in the pathogenesis of Alzheimer's disease has not been fully clarified.Long-term aerobic exercise can alter the expression of Notch1 by affecting the methylation rate of factors related to the Notch1 signaling pathway.However,it is not clear whether aerobic exercise affects hippocampal nerve cell proliferation and histopathological features of Alzheimer's disease mice through the Notch1 signaling pathway. OBJECTIVE:To observe the effects of aerobic exercise on the proliferation and histopathological features of hippocampal nerve cells in Alzheimer's disease mice after DAPT inhibited the Notch1 signaling pathway. METHODS:APP/PS1 double transgenic Alzheimer's disease mice aged 3 months were randomly divided into four groups:control group,exercise control group,inhibitor group,and exercise inhibitor group,with 20 mice in each group.The control group was fed naturally,and the exercise group received aerobic exercise intervention.Both natural feeding and exercise intervention lasted for 20 weeks.The mice were injected with solvent or Notch1 inhibitor at week 18.After 20 weeks,the brain tissue was collected,and Aβ1-42,Tau,Ki67,and Notch1 expression levels were detected by real-time PCR,immunofluorescence,and western blot assay. RESULTS AND CONCLUSION:Compared with the control group,the expressions of Ki67 and Notch1 in the dentate gyrus region of the hippocampus were significantly decreased in the inhibitor group(P<0.05),but there were no significant differences in Aβ1-42 and Tau.The expression of Ki67 in the dentate gyrus region of the hippocampus in the exercise control group was significantly higher than that in the control group,while the expressions of Aβ1-42,Tau,and Notch1 were significantly lower than those in the control group(P<0.05).The expressions of Aβ1-42,Tau,Ki67,and Notch1 in the dentate gyrus region of the hippocampus of the exercise inhibitor group were not significantly different from those of the inhibitor group.In conclusion,the Notch1 signaling pathway may mediate exercise to improve the proliferation and histopathological features of hippocampal nerve cells in Alzheimer's disease mice.
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OBJECTIVE:Exercise intervention is one of the main treatments for fibromyalgia,but there is no consistent conclusion on the choice of different exercise modalities.In this article,a network Meta-analysis was used to comprehensively and quantitatively evaluate the effects of different exercise modalities on fibromyalgia syndrome. METHODS:PubMed,EMbase,Scoups,The Cochrane Library,Web of Science,CNKI,WanFang Database,and China Biomedical Literature Database were searched for relevant literature,with a search timeframe from the establishment of each database to June 2023.The outcome indicators included five continuous variables,including fibromyalgia impact questionnaire-revised(FIQ)scores,visual analogue scale(VAS)scores,quality of life,quality of sleep,and depression.The Cochrane Risk of Bias Assessment Tool was used to evaluate the quality of the included literature.RevMan 5.4 software was used to perform effect sizes,subgroup analyses,and sensitivity analyses of the data.Stata 17 software was used to perform reticulation and network Meta-analysis of the data. RESULTS:A total of 13 articles with 14 randomized controlled trials were finally included.The overall methodological quality of the literature was high.The results of traditional Meta-analysis showed that,compared with the control group,exercise therapy significantly improved the FIQ score[standardized mean difference(SMD)=-0.67,95％confidence interval(CI):-0.83 to-0.50,P<0.01],VAS score(SMD=-0.72,95％CI:-0.90 to-0.54,P<0.01),quality of life(SMD=1.03,95％CI:0.45 to 1.61,P=0.000 5),sleep quality(SMD=-0.62,95％CI:-0.98 to-0.25,P=0.001),and depression(SMD=-0.63,95％CI:-1.09 to-0.18,P=0.007).Network Meta-analysis showed that the probability of optimal intervention effect of exercise modalities on FIQ scores was ranked as:mind-body exercise(86.5)>resistance exercise(70.5)>aerobic exercise(41.7);the probability of optimal intervention effect of exercise modalities on VAS scores was ranked as:resistance exercise(85.3)>mind-body exercise(74.3)>aerobic exercise(34.5). CONCLUSION:Exercise therapy significantly improves FIQ scores,VAS scores,quality of life,sleep quality,and depression in patients with fibromyalgia syndrome.Mind-body exercise and resistance exercise are the most effective exercise modalities to reduce FIQ scores and VAS scores in patients with fibromyalgia syndrome.
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BACKGROUND:Studies have shown that cardiomyocyte apoptosis is closely related to cardiac decompensation and the cardiac aging process.Appropriate exercise can alter heart pump function in patients with heart failure as well as attenuate aging-induced cardiomyocyte apoptosis,hypertrophy,and fibrotic damage. OBJECTIVE:To investigate the effects of long-term aerobic exercise on cardiomyocyte apoptosis and the thioredoxin system in aging rats. METHODS:Thirty-six male Sprague-Dawley rats were selected and divided into three age groups:3-month-old young group,9-month-old middle-aged group,and 18-month-old elderly group,with 12 rats in each group.Within each age group,rats were randomly assigned to sedentary and exercise subgroups(n=6 per group).The sedentary groups did not undergo any exercise intervention.The exercise groups were acclimated to a treadmill environment and subsequently subjected to treadmill exercise for 45 minutes per day,at a speed of 15 m/min,5 days per week for 10 weeks in total.At 24 hours after the final intervention,ELISA was employed to measure serum levels of cardiac troponin I and creatine kinase-MB in rats.TUNEL assay was utilized to detect cardiomyocyte apoptosis,while western blot assay was employed to assess the protein expression of Bax,Bcl-2,Caspase 3,thioredoxin-1,thioredoxin-2,thioredoxin reductase-1,thioredoxin reductase-2,thioredoxin-interacting protein,apoptosis signal-regulating kinase 1,and P38 mitogen-activated protein kinase in rat myocardial tissue. RESULTS AND CONCLUSION:Serum levels of cardiac troponin I and creatine kinase-MB in the elderly sedentary group were significantly higher than those in the young and middle-aged sedentary groups and elderly exercise group(P<0.01).Serum levels of cardiac troponin I and creatine kinase-MB in the elderly sedentary group were significantly higher than those in the young and middle-aged exercise groups and elderly exercise group(P<0.01).Positive apoptotic cells in rat myocardial tissue,along with increased protein expression of Bax and Caspase 3,exhibited an age-related upward trend,while Bcl-2 protein expression showed a declining trend.In comparison with the sedentary groups within each age category,the number of apoptotic cardiomyocytes and the expression of Bax and Caspase 3 proteins were reduced to different degrees,and the expression of Bcl-2 protein was increased to different degrees in the corresponding exercise groups.Compared with the young sedentary group,middle-aged sedentary group and elderly exercise group,elderly sedentary rats showed a significant decrease in the expression of myocardial thioredoxin 1,thioredoxin 2,thioredoxin reductase 1,and thioredoxin reductase 2 proteins(P<0.05,P<0.01).The expression of myocardial thioredoxin 1,thioredoxin 2,and thioredoxin reductase 2 proteins was lower in the elderly exercise group than in the young exercise group(P<0.05,P<0.01),while the expression of thioredoxin reductase 1 and thioredoxin reductase 2 proteins was lower in the elderly exercise group than in the middle-aged exercise group(P<0.01).The protein expression of thioredoxin-interacting protein,apoptosis signal-regulating kinase 1,and P38 mitogen-activated protein kinase in rat myocardium was significantly higher in the elderly sedentary group than the young sedentary group,middle-aged sedentary group and elderly exercise group(P<0.01).The protein expression of thioredoxin-interacting protein,apoptosis signal-regulating kinase 1,and P38 mitogen-activated protein kinase in rat myocardium was significantly higher in the elderly exercise group than the young exercise group and middle-aged exercise group(P<0.01).To conclude,aerobic exercise may enhance the anti-apoptotic effects of thioredoxin by down-regulating the expression of thioredoxin-interacting protein in aging rat hearts,leading to the downregulation of apoptosis signal-regulated kinase 1 and P38 mitogen-activated kinase protein,thereby alleviating myocardial cell apoptosis in aging rat hearts.
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BACKGROUND:Sarcopenia refers to age-related progressive,systemic muscle mass reduction and/or muscle strength decline or muscle physiological function decline,which is related to the occurrence of a variety of adverse outcomes in older adults.Exercise is considered to be one of the main strategies for combating sarcopenia in older adults,but there is a lack of specific intervention methods of different exercise patterns to intervene in sarcopenia. OBJECTIVE:To elaborate the main influencing factors of sarcopenia and the research progress of different exercise methods to improve sarcopenia in older adults,providing reference and basis for combating sarcopenia in older adults. METHODS:Web of Science,PubMed,CNKI,VIP,WanFang databases were retrieved for relevant literature published from January 2000 to October 2023 using the keywords of"sarcopenia,sport,exercise intervention,resistant training,aerobic exercise,whole body vibration training,mixed training,physical performance,muscle strength,muscle mass"in Chinese and English,respectively.A total of 126 articles were included for review. RESULTS AND CONCLUSION:Resistance exercise is still the most effective way to prevent and treat senile sarcopenia,and the effect of high-intensity resistance exercise is more significant.However,in practical application,we should pay attention to the gradual increase of training load intensity.Aerobic exercise combined with resistance exercise is more effective to improve muscle mass and function in the elderly than a single exercise mode.It is suggested that older adults can carry out the transition of low-intensity aerobic exercise in the early stage and increase resistance exercise individually in the late stage.Whole body vibration training is a new treatment method for the prevention and treatment of senile sarcopenia,but particular attention should be paid to the effects of frequency,amplitude,and duration on patients during practical application.Multicomponent exercise combines different exercise modes,which can give full play to their respective advantages,so as to personalize exercise interventions.
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Objective:To systematically evaluate the effectiveness and feasibility of aerobic exercise intervention in schizophrenia patients.Methods:Randomized controlled trials on exercise interventions for patients with schizophrenia were searched in eight databases from built up to March 2023, including China National Knowledge Infrastructure (CNKI), VIP Database for Chinese Technical Periodicals (VIP), WanFang Data, China Biomedical Literature Database, PubMed, Cochrane Library, EMBASE and Web of Science. The positive and negative symptom scale (PANSS) and its sub-scales were used as primary outcome indicators, and the negative symptom scale (SANS) and body mass index (BMI) were used as secondary indicators, and Meta-analysis was performed using R 4.1.0 and Stata 14.0.Results:Forty-seven studies including 3 139 patients with schizophrenia were included. Results of a network Meta-analysis based on 24 studies showed that aerobic exercise may be the most effective measure for reducing total PANSS scores in patients with schizophrenia. Compared to conventional treatment, combining aerobic exercise intervention improved patients' PANSS total score (MD= -5.09, 95% CI: -5.90~-4.28), SANS (MD= -12.17, 95% CI: -14.25~-10.10), and BMI (MD=-1.59, 95% CI: -1.93~-1.25). Meanwhile, subgroup analysis showed that 2 months of intervention was more appropriate (MD=-6.12, 95% CI: -7.22~-5.02) and the weekly total exercise time for 140-260 min was more appropriate (MD=-8.59, 95% CI: -12.93~-4.25) in terms of total PANSS score. The adherence rates between the trial and control groups showed no significant difference between the aerobic exercise intervention combined with conventional treatment and conventional treatment alone( P>0.05). Conclusion:Aerobic exercise intervention is an effective measure to relieve the symptoms of schizophrenia patients and has good compliance among inpatients.
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Objective:To explore the intervention effect of moderate intensity aerobic exercise on body composition and glycolipid metabolism in obese adults.Methods:This was a self-controlled study, which enrolled 280 obese adults who received weight loss treatment in the Health Management Institute of the Chinese PLA General Hospital from November 2017 to March 2018 and performed a 12-week precise aerobic exercise intervention (40%-60% of heart reserved rate) based on an independently developed aerobic exercise intervention system for chronic diseases. The following requirements also need to be met as effective exercise time of ≥40 minutes every time, total exercise time of ≤100 minutes per day, effective exercise time of ≥200 minutes per week, exercise frequency of ≥4 times per week, and an interval of ≤48 hours between two exercises. During the research, 77 subjects were excluded due to illness, sports injuries, work reasons, etc., and 203 subjects were included in the analysis. These patients were divided into three groups based on weekly exercise duration, including 97 cases in short-term group (weekly exercise time <300 minutes), 63 cases in medium-term group (weekly exercise time of 300-400 minutes), and 43 cases in long-term group (weekly exercise time >400 minutes). Paired t-tests were used to compare the differences in indicators before and after intervention, and covariance analysis was used to compare the differences in indicators among three groups. The intervention effect of moderate intensity aerobic exercise on the body composition and glucose and lipid metabolism in obese adults was analyzed. Results:The resting heart rate, body weight, body mass index, body fat rate, body fat mass, muscle mass, visceral fat area, subcutaneous fat area, fasting insulin, insulin resistance index, total cholesterol, triglycerides, and low-density lipoprotein cholesterol were all decreased significantly in the 203 patients after the intervention [(66.67±9.38) vs (71.48±10.13)/min, (86.02±13.13) vs (90.16±13.93) kg, (30.33±3.08) vs (31.80±3.27) kg/m 2, 35.64%±7.19% vs 37.87%±7.21%, (30.78±8.14) vs (34.30±8.73) kg, (52±10.30) vs (52.74±10.61) kg, (100.82±38.63) vs (119.53±43.08) cm 2, (270.14±74.19) vs (305.24±77.12) cm 2, (12.33±6.92) vs (17.86±14.23) mmol/L, 3.08±2.22 vs 4.52±4.09, (4.42±0.78) vs (4.62±0.89) mmol/L, (1.46±0.82) vs (1.71±1.11) mmol/L, (2.93±0.70) vs (3.08±0.80) mmol/L] (all P<0.05). The reduction degree of indicators including body weight, body mass rate, body fat rate, and body fat mass were all significantly higher in long-term group when compared with those in medium-term and short-term group [(5.56±0.62) vs (3.97±0.51) vs (3.63±0.41) kg, (1.98±0.21) vs (1.39±0.17) vs (1.31±0.14) kg/m 2, 3.38%±0.40% vs 2.27%± 0.33% vs 1.69%±0.27%, (4.90±0.53) vs (3.54±0.43) vs (2.89±0.35) kg]. Besides, patients in long-term group had significantly higher reduction degree of fasting insulin and higher rising degree of high-density lipoprotein cholesterol [(7.38±0.94) vs (4.54±0.62) mmol/L, (0.07±0.02) vs (0.01±0.02) mmol/L] and higher reduction degree of visceral fat area [(28.45±4.53) vs (12.55±3.67) cm 2] than medium-term group (all P<0.05). Conclusions:Moderate intensity aerobic exercise can be an effective intervention for the body composition and glycolipid metabolism in obese adults. If the weekly exercise time is greater than 400 minutes, the potential benefits of improvement may be more evident.
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Objective:To explore the effects of aerobic exercise on learning and memory functions, hippocampal synaptic plasticity and the ADPN signaling pathway in diabetic rats.Methods:6-week-old male SD rats were randomly divided into a blank control group(NC group)and a high-fat diet group, and a rat model for diabetes was induced by feeding rats in the high-fat diet group with a high-fat diet combined with intraperitoneal instillation of low-dose streptozotocin(STZ)for 5 weeks.Rats in the high-fat diet group were further divided into a diabetic group(DC group)and a diabetic aerobic exercise group(DM group)after successful establishment of the model.Rats in the DM group were subjected to aerobic exercise for eight weeks and then the Morris water maze test was conducted to assess learning and memory functions, relevant serum markers were measured, Golgi staining was used to examine synaptic changes in the hippocampus, and Western blot was carried out to detect hippocampal protein expression levels of adiponectin(ADPN), AMP-activated protein kinase(AMPK), glucose transporter 4(GLUT4), synaptic plasticity-related protein synaptophysin(SYN)and postsynaptic density protein 95(PSD-95)for rats in each group.Results:Serum FBG and HBA1c in diabetic rats were markedly significantly decreased after 8 weeks of aerobic exercise( P<0.01), and serum ADPN and insulin were significantly increased after 8 weeks of aerobic exercise( P<0.05).When test results from the three groups of rats compared, the F value was 69.248 for FBG, 6.740 for INS, 7.017 for HBA1C and 14.315 for serum ADPN.The results of the water maze test and hippocampal Golgi staining showed that the escape latency of diabetic rats was highly significantly decreased after 8 weeks of aerobic exercise( P<0.01).The platform crossing times, the number of dendritic branches and the dendritic spine density in the hippocampal CA3 region of diabetic rats were significantly increased after 8 weeks of aerobic exercise( P<0.05).When results from the three groups of rats were compared, the F value was 13.934 for escape latency, 5.864 for platform crossing times, 9.307 and 6.734 for the number of dendritic branches and the density of dendritic spine in hippocampal CA3 region.Hippocampal PSD-95, SYN, ADPN, p-AMPK, and GLUT4 protein expression levels of diabetic rats were significantly increased( P<0.05)after 8 weeks of aerobic exercise.When results from the three groups of rats were compared, the F value was 15.137 for SYN, 5.415 for PSD-95, 9.687 for ADPN, 27.761 for GLUT4, and 9.298 for p-AMPK. Conclusions:Eight weeks of aerobic exercise can improve the learning and memory functions of diabetic rats, and the mechanisms may be related to exercise-induced hippocampal ADPN/AMPK/GLUT4 signaling activation in rats, leading to enhanced synaptic plasticity in the hippocampus.
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Objective:To demonstrate any role of iron metabolism in the inhibition by aerobic exercise of myocardial apoptosis in atherosclerotic mice.Methods:Eight-week-old male ApoE -/- gene knockout mice were randomly divided into a control group, a model group and an aerobic exercise group, each of 9. A model of atherosclerosis was induced in the rats of the model and aerobic exercise groups by feeding them a " western" diet for 12 weeks. During that time the aerobic exercise group only was given aerobic exercise training. The control group was fed normal rat chow during that period. Myocardial apoptosis was detected using TUNEL staining, and the expression and localization of ferritin heavy chain 1 (FTH1) and glutathione peroxidase 4 (GPX4) in the myocardium used immunohistochemistry. Western blotting was applied to detect the FTH1 and GPX4 protein levels, and iron deposition in the myocardium was detected using Prussian blue staining. Iron, lipid peroxide malondialdehyde (MDA) and glutathione peroxidase (GSH-PX) in the myocardial tissue were also measured. Results:The TUNEL staining showed significant apoptosis in the model group. In the aerobic exercise group it was significantly less. There was obvious iron deposition in the myocardia of the model group, which was significantly reduced in the aerobic exercise group. The average FTH1 and GPX4 levels in the model group were lower than in the control group, and significantly elevated in the aerobic exercise group.in the aerobic exercise group than in the model group. Iron and MDA levels in the aerobic exercise group were significantly lower, on average, than among the model group, while that of GSH-PX was significantly higher.Conclusions:Aerobic exercise can significantly inhibit cardiomyocyte apoptosis in atherosclerotic mice. The mechanism may be closely related to better iron metabolism, reduced oxidative stress and the inhibition of iron overload.