Enhancement of motor functional recovery in thoracic spinal cord injury: voluntary wheel running versus forced treadmill exercise

Spinal cord injury necessitates effective rehabilitation strategies, with exercise therapies showing promise in promoting recovery. This study investigated the impact of rehabilitation exercise on functional recovery and morphological changes following thoracic contusive spinal cord injury. After a 7-day recovery period after spinal cord injury, mice were assigned to either a trained group(10 weeks of voluntary running wheel or forced treadmill exercise) or an untrained group. Bi-weekly assessments revealed that the exercise-trained group, particularly the voluntary wheel exercise subgroup, displayed significantly improved locomotor recovery, more plasticity of dopaminergic and serotonin modulation compared with the untrained group. Additionally, exercise interventions led to gait pattern restoration and enhanced transcranial magnetic motor-evoked potentials. Despite consistent injury areas across groups, exercise training promoted terminal innervation of descending axons. In summary, voluntary wheel exercise shows promise for enhancing outcomes after thoracic contusive spinal cord injury, emphasizing the role of exercise modality in promoting recovery and morphological changes in spinal cord injuries. Our findings will influence future strategies for rehabilitation exercises, restoring functional movement after spinal cord injury.

Treadmill exercise in combination with acousto-optic and olfactory stimulation improves cognitive function in APP/PS1 mice through the brain-derived neurotrophic factor-and Cygb-associated signaling pathways

A reduction in adult neurogenesis is associated with behavioral abnormalities in patients with Alzheimer's disease.Consequently,enhancing adult neurogenesis represents a promising therapeutic approach for mitigating disease symptoms and progression.Nonetheless,nonpharmacological interventions aimed at inducing adult neurogenesis are currently limited.Although individual non-pharmacological interventions,such as aerobic exercise,acousto-optic stimulation,and olfactory stimulation,have shown limited capacity to improve neurogenesis and cognitive function in patients with Alzheimer's disease,the therapeutic effect of a strategy that combines these interventions has not been fully explored.In this study,we observed an age-dependent decrease in adult neurogenesis and a concurrent increase in amyloid-beta accumulation in the hippocampus of amyloid precursor protein/presenilin 1 mice aged 2-8 months.Amyloid deposition became evident at 4 months,while neurogenesis declined by 6 months,further deteriorating as the disease progressed.However,following a 4-week multifactor stimulation protocol,which encompassed treadmill running(46 min/d,10 m/min,6 days per week),40 Hz acousto-optic stimulation(1 hour/day,6 days/week),and olfactory stimulation(1 hour/day,6 days/week),we found a significant increase in the number of newborn cells(5'-bromo-2'-deoxyuridine-positive cells),immature neurons(doublecortin-positive cells),newborn immature neurons(5'-bromo-2'-deoxyuridine-positive/doublecortin-positive cells),and newborn astrocytes(5'-bromo-2'-deoxyuridine-positive/glial fibrillary acidic protein-positive cells).Additionally,the amyloid-beta load in the hippocampus decreased.These findings suggest that multifactor stimulation can enhance adult hippocampal neurogenesis and mitigate amyloid-beta neuropathology in amyloid precursor protein/presenilin 1 mice.Furthermore,cognitive abilities were improved,and depressive symptoms were alleviated in amyloid precursor protein/presenilin 1 mice following multifactor stimulation,as evidenced by Morris water maze,novel object recognition,forced swimming test,and tail suspension test results.Notably,the efficacy of multifactor stimulation in consolidating immature neurons persisted for at least 2weeks after treatment cessation.At the molecular level,multifactor stimulation upregulated the expression of neuron-related proteins(NeuN,doublecortin,postsynaptic density protein-95,and synaptophysin),anti-apoptosis-related proteins(Bcl-2 and PARP),and an autophagyassociated protein(LC3B),while decreasing the expression of apoptosis-related proteins(BAX and caspase-9),in the hippocampus of amyloid precursor protein/presenilin 1 mice.These observations might be attributable to both the brain-derived neurotrophic factor-mediated signaling pathway and antioxidant pathways.Furthermore,serum metabolomics analysis indicated that multifactor stimulation regulated differentially expressed metabolites associated with cell apoptosis,oxidative damage,and cognition.Collectively,these findings suggest that multifactor stimulation is a novel non-invasive approach for the prevention and treatment of Alzheimer's disease.

Exercise preconditioning alleviates ischemia-induced memory deficits by increasing circulating adiponectin

Cerebral ischemia is a major health risk that requires preventive approaches in addition to drug therapy.Physical exercise enhances neurogenesis and synaptogenesis,and has been widely used for functional rehabilitation after stroke.In this study,we determined whether exercise training before disease onset can alleviate the severity of cerebral ischemia.We also examined the role of exercise-induced circulating factors in these effects.Adult mice were subjected to 14 days of treadmill exercise training before surgery for middle cerebral artery occlusion.We found that this exercise pre-conditioning strategy effectively attenuated brain infarct area,inhibited gliogenesis,protected synaptic proteins,and improved novel object and spatial memory function.Further analysis showed that circulating adiponectin plays a critical role in these preventive effects of exercise.Agonist activation of adiponectin receptors by Adipo Ron mimicked the effects of exercise,while inhibiting receptor activation abolished the exercise effects.In summary,our results suggest a crucial role of circulating adiponectin in the effects of exercise pre-conditioning in protecting against cerebral ischemia and supporting the health benefits of exercise.

Impacts of Nutlin-3a and exercise on murine double minute 2-enriched glioma treatment

Recent research has demonstrated the impact of physical activity on the prognosis of glioma patients,with evidence suggesting exercise may reduce mortality risks and aid neural regeneration.The role of the small ubiquitin-like modifier(SUMO)protein,especially post-exercise,in cancer progression,is gaining attention,as are the potential anti-cancer effects of SUMOylation.We used machine learning to create the exercise and SUMO-related gene signature(ESLRS).This signature shows how physical activity might help improve the outlook for low-grade glioma and other cancers.We demonstrated the prognostic and immunotherapeutic significance of ESLRS markers,specifically highlighting how murine double minute 2(MDM2),a component of the ESLRS,can be targeted by nutlin-3.This underscores the intricate relationship between natural compounds such as nutlin-3 and immune regulation.Using comprehensive CRISPR screening,we validated the effects of specific ESLRS genes on low-grade glioma progression.We also revealed insights into the effectiveness of Nutlin-3a as a potent MDM2 inhibitor through molecular docking and dynamic simulation.Nutlin-3a inhibited glioma cell proliferation and activated the p53 pathway.Its efficacy decreased with MDM2 overexpression,and this was reversed by Nutlin-3a or exercise.Experiments using a low-grade glioma mouse model highlighted the effect of physical activity on oxidative stress and molecular pathway regulation.Notably,both physical exercise and Nutlin-3a administration improved physical function in mice bearing tumors derived from MDM2-overexpressing cells.These results suggest the potential for Nutlin-3a,an MDM2 inhibitor,with physical exercise as a therapeutic approach for glioma management.Our research also supports the use of natural products for therapy and sheds light on the interaction of exercise,natural products,and immune regulation in cancer treatment.

The effects of exercise interventions on brain-derived neurotrophic factor levels in children and adolescents:a meta-analysis

Brain-derived neurotrophic factor is a crucial neurotrophic factor that plays a significant role in brain health. Although the vast majority of meta-analyses have confirmed that exercise interventions can increase brain-derived neurotrophic factor levels in children and adolescents, the effects of specific types of exercise on brain-derived neurotrophic factor levels are still controversial. To address this issue, we used meta-analytic methods to quantitatively evaluate, analyze, and integrate relevant studies. Our goals were to formulate general conclusions regarding the use of exercise interventions, explore the physiological mechanisms by which exercise improves brain health and cognitive ability in children and adolescents, and provide a reliable foundation for follow-up research. We used the Pub Med, Web of Science, Science Direct, Springer, Wiley Online Library, Weipu, Wanfang, and China National Knowledge Infrastructure databases to search for randomized controlled trials examining the influences of exercise interventions on brain-derived neurotrophic factor levels in children and adolescents. The extracted data were analyzed using Review Manager 5.3. According to the inclusion criteria, we assessed randomized controlled trials in which the samples were mainly children and adolescents, and the outcome indicators were measured before and after the intervention. We excluded animal experiments, studies that lacked a control group, and those that did not report quantitative results. The mean difference(MD;before versus after intervention) was used to evaluate the effect of exercise on brain-derived neurotrophic factor levels in children and adolescents. Overall, 531 participants(60 children and 471 adolescents, 10.9–16.1 years) were included from 13 randomized controlled trials. Heterogeneity was evaluated using the Q statistic and I^(2) test provided by Review Manager software. The meta-analysis showed that there was no heterogeneity among the studies(P = 0.67, I^(2) = 0.00%). The combined effect of the interventions was significant(MD = 2.88, 95% CI: 1.53–4.22, P < 0.0001), indicating that the brain-derived neurotrophic factor levels of the children and adolescents in the exercise group were significantly higher than those in the control group. In conclusion, different types of exercise interventions significantly increased brain-derived neurotrophic factor levels in children and adolescents. However, because of the small sample size of this meta-analysis, more high-quality research is needed to verify our conclusions. This metaanalysis was registered at PROSPERO(registration ID: CRD42023439408).

Therapeutic potential of exercise-hormone irisin in Alzheimer's disease

Irisin is a myokine that is generated by cleavage of the membrane protein fibronectin type Ⅲ domain-containing protein 5(FNDC5) in response to physical exercise. Studies reveal that irisin/FNDC5 has neuroprotective functions against Alzheimer's disease, the most common form of dementia in the elderly, by improving cognitive function and reducing amyloid-β and tau pathologies as well as neuroinflammation in cell culture or animal models of Alzheimer's disease. Although current and ongoing studies on irisin/FNDC5 show promising results, further mechanistic studies are required to clarify its potential as a meaningful therapeutic target for alleviating Alzheimer's disease. We recently found that irisin treatment reduces amyloid-β pathology by increasing the activity/levels of amyloid-β-degrading enzyme neprilysin secreted from astrocytes. Herein, we present an overview of irisin/FNDC5's protective roles and mechanisms against Alzheimer's disease.

Additive neurorestorative effects of exercise and docosahexaenoic acid intake in a mouse model of Parkinson’s disease

There is a need to develop interventions to slow or reverse the degeneration of dopamine neurons in Parkinson’s disease after diagnosis.Given that preclinical and clinical studies suggest benefits of dietary n-3 polyunsaturated fatty acids,such as docosahexaenoic acid,and exercise in Parkinson’s disease,we investigated whether both could synergistically interact to induce recovery of the dopaminergic pathway.First,mice received a unilateral stereotactic injection of 6-hydroxydopamine into the striatum to establish an animal model of nigrostriatal denervation.Four weeks after lesion,animals were fed a docosahexaenoic acid-enriched or a control diet for the next 8 weeks.During this period,the animals had access to a running wheel,which they could use or not.Docosahexaenoic acid treatment,voluntary exercise,or the combination of both had no effect on(i)distance traveled in the open field test,(ii)the percentage of contraversive rotations in the apomorphine-induction test or(iii)the number of tyrosine-hydroxylase-positive cells in the substantia nigra pars compacta.However,the docosahexaenoic acid diet increased the number of tyrosine-hydroxylase-positive terminals and induced a rise in dopamine concentrations in the lesioned striatum.Compared to docosahexaenoic acid treatment or exercise alone,the combination of docosahexaenoic acid and exercise(i)improved forelimb balance in the stepping test,(ii)decreased the striatal DOPAC/dopamine ratio and(iii)led to increased dopamine transporter levels in the lesioned striatum.The present results suggest that the combination of exercise and docosahexaenoic acid may act synergistically in the striatum of mice with a unilateral lesion of the dopaminergic system and provide support for clinical trials combining nutrition and physical exercise in the treatment of Parkinson’s disease.

Getting physical with medical education:Exercise based virtual anatomy review classes for medical students

The benefits of regular physical activity are well known.Yet,few studies have examined the effectiveness of integrating physical activity(PA)into curricula within a post-secondary setting.To investigate the incorporation of PA into medical curriculum,we developed a series of optional exercise-based review sessions designed to reinforce musculoskeletal(MSK)anatomy course material.These synchronous sessions were co-taught by a group fitness instructor and an anatomy instructor.The fitness instructor would lead students through both strength and yoga style exercises,while the anatomy instructor asked questions about relevant anatomical structures related to course material previously covered.After the sessions,participants were asked to evaluate the classes on their self-reported exam preparedness in improving MSK anatomy knowledge,PA levels,and mental wellbeing.Thirty participants completed surveys;a majority agreed that the classes increased understanding of MSK concepts(90.0%)and activity levels(97.7%).Many(70.0%)felt that the classes helped reduce stress.The majority of respondents(90.0%)agreed that the classes contributed to increased feelings of social connectedness.Overall,medical students saw benefit in PA based interventions to supplement MSK course concepts.Along with increasing activity levels and promoting health behaviours,integrating PA into medical curriculum may improve comprehension of learning material,alleviate stress and foster social connectivity among medical students.

Regulator of G protein signaling 6 mediates exercise-induced recovery of hippocampal neurogenesis,learning,and memory in a mouse model of Alzheimer’s disease

Hippocampal neuronal loss causes cognitive dysfunction in Alzheimer’s disease.Adult hippocampal neurogenesis is reduced in patients with Alzheimer’s disease.Exercise stimulates adult hippocampal neurogenesis in rodents and improves memory and slows cognitive decline in patients with Alzheimer’s disease.However,the molecular pathways for exercise-induced adult hippocampal neurogenesis and improved cognition in Alzheimer’s disease are poorly understood.Recently,regulator of G protein signaling 6(RGS6)was identified as the mediator of voluntary running-induced adult hippocampal neurogenesis in mice.Here,we generated novel RGS6fl/fl;APP_(SWE) mice and used retroviral approaches to examine the impact of RGS6 deletion from dentate gyrus neuronal progenitor cells on voluntary running-induced adult hippocampal neurogenesis and cognition in an amyloid-based Alzheimer’s disease mouse model.We found that voluntary running in APP_(SWE) mice restored their hippocampal cognitive impairments to that of control mice.This cognitive rescue was abolished by RGS6 deletion in dentate gyrus neuronal progenitor cells,which also abolished running-mediated increases in adult hippocampal neurogenesis.Adult hippocampal neurogenesis was reduced in sedentary APP_(SWE) mice versus control mice,with basal adult hippocampal neurogenesis reduced by RGS6 deletion in dentate gyrus neural precursor cells.RGS6 was expressed in neurons within the dentate gyrus of patients with Alzheimer’s disease with significant loss of these RGS6-expressing neurons.Thus,RGS6 mediated voluntary running-induced rescue of impaired cognition and adult hippocampal neurogenesis in APP_(SWE) mice,identifying RGS6 in dentate gyrus neural precursor cells as a possible therapeutic target in Alzheimer’s disease.

运动是良医(Exercise is Medicine):运动促进健康的新理念——王正珍教授学术访谈录

面对科技进步、社会发展带来的生活方式转型与体力活动不足的现实困境,王正珍教授从医体结合有利于促进全民健身的视角入手,畅谈了体力活动与健康的关联、静坐少动与慢性疾病的关系、运动是良医(Exercise is Medicine)的理念、以及流行病学对体育科研的方法学启示等方面的内容,其相关论点对今后运动人体学科发展及体力活动与健康促进领域研究具有指导价值。

运动时间生物学(Exercise Chronobiology)浅谈

运动时间生物学是研究在体育运动影响下人体时间结构的本质、特点以及机能变化与时间变量的函数关系(规律)的一门新兴分枝学科。本文拟较系统地阐述运动时间生物学的概念、性质、任务以及与其它学科的关系;概述运动时间生物学在国内外的研究状况;初步展望运动时间生物学的发展前景。

运动员的肠道菌群特征

背景:了解运动员肠道菌群的特征及影响因素有助于确定相关运动项目的最佳肠道微生物组成,寻求提高运动表现和恢复的有效途径,并为个性化营养方案提供独特视角。目的:总结运动员的肠道菌群特征,从运动训练和饮食摄入两方面阐述影响运动员肠道菌群特征的重要因素。方法:检索PubMed、ScienceDirect、中国知网、万方和维普数据库2004-2024年发表的文献,英文检索词为“microbiota,microbiome,athlete,exercise,training,diet,nutrition,dietary fiber,protein,ketogenic,fat”,中文检索词为“肠道菌群,肠道微生物,运动员,训练,比赛,饮食,营养”。排除研究质量较差及内容不相关的文献后,最终纳入65篇文献进行综述分析。结果与结论:①与普通人群相比,精英运动员的肠道菌群以α多样性增加、厚壁菌门/拟杆菌门比值升高、健康有益菌丰度增加、有助于运动表现的功能途径富集为主要特征;②项目类型和训练负荷与运动员肠道菌群物种结构及功能表达密切相关;③由代谢物介导的宿主与肠道微生物间的双向交流,是运动影响肠道菌群的重要机制;④阶段训练通常能够引发肠道微生物群产生适应性变化,并且菌群在结构或功能上的改变具有持续效应;⑤宏量营养素的种类、数量及组合形式能够显著影响肠道菌群结构和功能,并与运动训练发挥协同叠加或削弱抵消的作用;⑥未来应持续加强对运动员肠道菌群的相关探索,明确因果关系,建立运动训练干预新靶点。

游泳运动对大鼠创伤性关节挛缩的影响及机制

背景:早期运动是预防创伤性关节挛缩的主要方式,也是近期研究热点。游泳运动借助水的特殊物理特性,可能是潜在有益的干预方式。目的:观察游泳运动对大鼠关节挛缩发展的影响,探究游泳运动预防关节挛缩的相关机制。方法:24只SD大鼠随机分为空白对照组(n=8)和关节挛缩造模组(n=16),手术制备膝关节挛缩模型后,再随机分为手术对照组(n=8)和游泳干预组(n=8)。游泳干预组在术后第2周开始游泳干预,共干预5周。在术后第6周,测试各组大鼠体质量、术侧膝关节活动度、股四头肌直径,计算直径-体质量指数;苏木精-伊红染色观察膝关节囊和股四头肌病理变化;Masson染色观察关节囊胶原纤维化改变;免疫组化检测膝关节囊中转化生长因子β1和Ⅰ型胶原蛋白表达;Western blot检测股四头肌中MuRF1蛋白的表达。结果与结论:①与空白对照组比较,手术对照组和游泳干预组大鼠膝关节活动度下降,总伸膝受限角度和关节源性伸膝受限角度均明显增加(P<0.01),股四头肌直径下降(P<0.01),关节囊出现明显纤维化表现,股四头肌萎缩,手术对照组直径-体质量指数降低(P<0.01);与手术对照组比较,游泳干预组大鼠膝关节活动度和股四头肌直径明显增加(P<0.01),关节囊纤维化病变和股四头肌萎缩明显改善;②与空白对照组比较,手术对照组和游泳干预组大鼠关节囊中胶原纤维含量、转化生长因子β1和Ⅰ型胶原蛋白表达均增加(P<0.01);与手术对照组比较,游泳干预组大鼠关节囊中胶原纤维含量、转化生长因子β1和Ⅰ型胶原蛋白表达均降低(P<0.01);③与空白对照组比较,手术对照组和游泳干预组大鼠股四头肌中MuRF1蛋白表达增加(P<0.05);与手术对照组比较,游泳干预组大鼠股四头肌中MuRF1蛋白表达降低(P<0.05)。结果表明:早期游泳干预能够降低创伤性挛缩大鼠关节囊中转化生长因子β1和Ⅰ型胶原蛋白表达,降低股四头肌中MuRF1蛋白表达,提高关节活动度和股四头肌直径,抑制关节挛缩的发展。

8周运动预适应增强脂肪干细胞治疗心肌梗死大鼠的效果

背景:干细胞移植是心肌梗死的崭新疗法,然而梗死区域极其恶劣的微环境造成干细胞存活率低下并导致远期疗效甚微。运动预适应是一种通过运动诱导机体产生内源性保护效应的方式,可作为心脏康复预防与治疗的新策略。目的:评估运动预适应是否能够增强大鼠心肌梗死后脂肪干细胞移植的心脏保护效应,探讨血管生成在其中的作用机制。方法:6周龄雄性SD大鼠随机分为对照组、造模组、干细胞组以及干细胞运动组。利用冠状动脉闭塞术制作急性心肌梗死模型,对照组同期行假手术;干细胞运动组于造模前进行8周有氧运动,造模后30 min进行脂肪干细胞移植;干细胞组仅进行脂肪干细胞移植。干细胞移植后1 d和7 d,利用免疫印迹法测定心肌总Akt(t-Akt)、磷酸化Akt(p-Akt)、血管内皮生长因子(VEGF)、总内皮型一氧化氮合酶(t-eNOS)和磷酸化内皮型一氧化氮合酶(p-eNOS)蛋白表达量,计算p-Akt/t-Akt和p-eNOS/t-eNOS比值;4周后利用彩色多普勒超声诊断系统检测心脏结构与功能以及心肌血流量,TTC染色法检测心肌梗死面积,Masson染色法检测心肌间质胶原沉积,免疫荧光染色法测定心肌毛细血管密度,TUNEL染色法评估心肌细胞凋亡。结果与结论:(1)干细胞移植后4周:与对照组比较,造模组左心室缩短分数、左心室射血分数、心肌毛细血管密度和心肌血流量下降(P<0.05),心肌梗死面积、胶原容积分数和细胞凋亡增加(P<0.05);与造模组比较,干细胞组上述指标(除左心室缩短分数和左心室射血分数外)得到改善(P<0.05);与干细胞组比较,干细胞运动组以上各参数进一步改善(P<0.05)。(2)干细胞移植后1 d:与对照组比较,造模组t-Akt、p-Akt、VEGF、t-eNOS、p-eNOS蛋白表达量以及p-Akt/t-Akt、p-eNOS/t-eNOS比值均无显著性变化(P>0.05);与造模组比较,干细胞组上述指标均无显著性变化(P>0.05),干细胞运动组磷酸化p-Akt蛋白表达量以及p-Akt/t-Akt比值上调(P<0.05)。(3)干细胞移植后7 d:与对照组比较,造模组p-Akt、VEGF、p-eNOS蛋白表达量以及p-Akt/t-Akt、p-eNOS/t-eNOS比值下降(P<0.05);与造模组比较,干细胞组各参数均无显著性变化(P>0.05),干细胞运动组p-Akt、VEGF、p-eNOS蛋白表达量以及p-Akt/t-Akt、p-eNOS/t-eNOS比值升高(P<0.05)。结果表明:运动预适应可增强脂肪干细胞对心肌梗死大鼠心脏重塑的治疗效果,其机制与促进心肌血管生成并增加血流灌注有关。

不同强度运动抑制糖尿病大鼠肾脏PI3K/AKT/mTOR信号通路改善自噬的比较

背景:2型糖尿病损害肾功能。研究表明运动干预可以保护肾脏;鸢尾素可以通过抑制磷脂酰肌醇3-激酶/蛋白激酶B/雷帕霉素靶蛋白信号通路恢复自噬,保护糖尿病肾病患者的肾功能。目的:探讨运动能否通过抑制肾脏磷脂酰肌醇3-激酶/蛋白激酶B/雷帕霉素靶蛋白信号通路过度激活来恢复自噬,改善肾损伤,以及分析不同方式运动产生影响的差异。方法:将6周龄的SD大鼠随机分为空白对照组(正常大鼠)和糖尿病组,其中糖尿病组大鼠经过高脂高糖喂养加腹腔注射低剂量1%链脲佐菌素(30 mg/kg)建立2型糖尿病模型。造模成功后再将糖尿病组大鼠随机分成糖尿病模型组、中强度持续运动组和高强度间歇运动组。两个运动组大鼠分别进行8周不同强度运动干预。取材后采用葡萄糖氧化酶法检测大鼠空腹血糖,使用试剂盒检测糖化血红蛋白水平,Elisa法检测血清胰岛素浓度,计算胰岛素抵抗指数,RT-PCR检测肾组织磷脂酰肌醇3-激酶、蛋白激酶B、雷帕霉素靶蛋白、Beclin-1、podocin、nephrin的基因表达量,Western Blot检测肾组织雷帕霉素靶蛋白及自噬标记蛋白LC3-1、LC3-2、Beclin-1的蛋白表达量。结果与结论:①2型糖尿病大鼠空腹血糖和糖化血红蛋白水平极显著性升高,胰岛素抵抗水平显著上升,胰岛素水平显著下降;两种运动均能使2型糖尿病大鼠空腹血糖和糖化血红蛋白水平极显著下降,胰岛素抵抗水平显著下降,胰岛素水平显著上升;与中强度持续运动组相比,高强度间歇运动组胰岛素水平显著上升。②2型糖尿病大鼠podocin、nephrin基因表达量显著降低;两种不同形式运动均能显著提高其表达;与高强度间歇运动组相比,中等强度持续性运动组足细胞相关蛋白基因表达有进一步上升趋势,但无显著性差异。③2型糖尿病大鼠肾组织磷脂酰肌醇3-激酶、蛋白激酶B、mTORC1的mRNA及蛋白的表达量显著增加,自噬标志蛋白Beclin-1、LC3-2表达量以及LC3-2/LC3-1显著降低;两种不同形式运动均能使肾组织磷脂酰肌醇3-激酶、蛋白激酶B、mTORC1的mRNA及雷帕霉素靶蛋白蛋白的表达量显著降低,自噬标志蛋白Beclin-1、LC3-2以及LC3-2/LC3-1显著升高;与中等强度持续性运动组相比,高强度间歇运动的磷脂酰肌醇3-激酶、蛋白激酶B、mTORC1的mRNA及雷帕霉素靶蛋白的蛋白表达量有进一步下降的趋势,Beclin-1、LC3-2以及LC3-2/LC3-1有进一步升高的趋势,但仅Beclin-1有显著性差异。④结果说明2型糖尿病肾脏足细胞损伤,自噬受到抑制,与磷脂酰肌醇3-激酶/蛋白激酶B/mTORC1信号通路被异常激活密切相关。高强度间歇运动和中等强度持续性运动可以保护糖尿病肾脏,减少足细胞损伤,促进自噬恢复,这可能与运动抑制磷脂酰肌醇3-激酶/蛋白激酶B/雷帕霉素靶蛋白信号通路过度激活有关。与中等强度持续性运动相比,高强度间歇运动恢复自噬的效果呈更优趋势,但足细胞蛋白表达稍有下降。

运动疗法对前交叉韧带重建后康复疗效影响的网状Meta分析

目的:运动干预被认为是前交叉韧带重建后康复的基础。然而,关于何种运动疗法在改善前交叉韧带重建后患者膝关节肌肉力量和功能方面更有效,目前仍未得出明确结论。为此,文章采用网状Meta分析方法,比较运动疗法治疗前交叉韧带重建后的疗效,为选择最佳运动疗法提供循证医学依据。方法:计算机检索PubMed,Web of Science,Embase,The Cochrane Library及EBSCO数据库运动疗法治疗前交叉韧带重建后的随机对照试验,检索时限均从建库至2023-11-20。结局指标包括股四头肌肌力、腘绳肌肌力、膝关节功能评分3个连续性变量。运用EndNote X9.1软件筛选文献。采用Cochrane风险偏倚评估工具对纳入的文献进行质量评价,根据GRADE评分对文章结果的证据强度进行评级,采用Stata 16.0进行网状Meta分析。结果:①共纳入36项随机对照试验,包括1179例前交叉韧带重建后患者,纳入文献整体质量中等;涉及9种运动疗法:等速训练、交叉训练、离心训练、水中康复、血流限制训练、运动控制训练、增强式训练、全身振动训练和综合训练;对照措施为常规康复训练。②网状Meta分析结果显示:与常规康复训练相比,离心训练(SMD=2.08,95%CI:0.56-3.60,P=0.007)对前交叉韧带重建后患者股四头肌肌力的改善效果最佳,其次是综合训练(SMD=1.69,95%CI:0.11-3.27,P=0.249)和全身振动训练(SMD=0.81,95%CI:0.11-1.51,P=0.042);在提升患者腘绳肌肌力方面,综合训练(SMD=2.08,95%CI:0.30-3.86,P=0.022)效果最佳,其次是增强式训练(SMD=1.51,95%CI:0.18-2.84,P=0.026)和等速训练(SMD=1.37,95%CI:0.06-2.67,P=0.039);综合训练(SMD=4.60,95%CI:2.40-6.80,P<0.001)改善膝关节功能评分最有效,其次是离心训练(SMD=1.75,95%CI:0.24-3.25,P=0.023)和水中康复(SMD=1.65,95%CI:0.07-3.24,P=0.041)。结论:低到中等强度的临床证据证实,在改善前交叉韧带重建后患者膝关节肌肉力量和功能方面,综合训练可能是最有效的运动疗法,其次是离心训练、增强式训练、等速训练、全身振动训练、水中康复。未来仍需更多高质量的临床随机对照试验来验证结论的可靠性。

不同类型贴布对慢性踝关节不稳患者行走时踝关节运动学的影响

背景:慢性踝关节不稳患者行走时倾向于过度足内翻,这将增加步行周期支撑相踝关节扭伤的风险。临床医生常使用肌内效贴布或运动贴布进行踝关节贴扎。由于肌内效贴布具有弹性,而运动贴布无法拉伸,因此两者技术应用和生理机制存在差异,进而可能产生不同的康复疗效。目的:对比肌内效贴布和运动贴布干预对慢性踝关节不稳患者步行支撑相足额状面和胫骨水平面运动的影响。方法:40名慢性踝关节不稳患者随机分为肌内效贴布组和运动贴布组,肌内效贴布组从后足内侧向外侧粘贴2条贴布,以产生外翻拉力;运动贴布组采用踝关节闭锁式编篮贴扎。分别于贴扎前后在电动跑台上进行行走测试,利用三维运动分析系统获取受试者足部和胫骨运动学参数。结果与结论:肌内效贴布组贴扎后于支撑相早期足外翻角度增加(P<0.05),但对支撑相晚期足的位置无影响(P>0.05);运动贴布组贴扎后于支撑相晚期胫骨内旋增加(P<0.05),而支撑相早期胫骨位置无明显改变(P>0.05)。结果表明:与运动贴布相比,肌内效贴布能够提供灵活的拉力,有利于步态周期中支撑相早期足外翻,同时不限制支撑相晚期的正常足内翻。因此,肌内效贴布可能是慢性踝关节不稳患者的实用康复疗法,在纠正踝关节异常运动的同时不限制其自然运动。

不同运动模式影响心肌梗死致心力衰竭大鼠骨骼肌重塑的机制

背景:急性心肌梗死可引起心脏重塑和心力衰竭,同时导致骨骼肌病变,影响患者生活质量。运动疗法是心力衰竭患者的重要康复手段,然而最佳运动处方尚未明确。目的:对比不同运动模式(有氧运动、抗阻运动)对急性心肌梗死诱导心力衰竭模型大鼠骨骼肌重塑的影响,探讨其可能的作用机制,为优化运动康复方案提供依据。方法:48只SD大鼠随机分为假手术组、心肌梗死组、有氧运动组和抗阻运动组。利用冠状动脉结扎术进行心力衰竭模型制作,3个月后有氧运动组和抗阻运动组进行12周相应运动模式干预,假手术组和心肌梗死组于鼠笼内安静饲养。实验后,利用递增负荷跑台运动实验和爬梯实验分别测定大鼠最高跑速和最大负重,超声心动图评估心脏结构与功能;分离出心脏,分别行苏木精-伊红染色和天狼星红染色观察心脏重塑情况;分离出腓肠肌,行ATP酶染色观察肌纤维类型和细胞横截面积改变,二氢乙锭法评估活性氧水平,酶联免疫吸附法测定丙二醛含量以及抗氧化酶活性,免疫印迹法测定泛素-蛋白酶体系统蛋白表达量,双重免疫荧光染色检测活化的卫星细胞数(Pax7^(+)/MyoD^(+))。结果与结论:①运动能力:与假手术组比较,心肌梗死组最高跑速和最大负重下降(P<0.05);与心肌梗死组比较,有氧运动组最高跑速以及抗阻运动组最大负重增加(P<0.05)。②心脏重塑:与假手术组比较,心肌梗死组梗死面积、心肌细胞横截面积、心肌胶原含量升高(P<0.05),左心室射血分数和左心室缩短分数下降(P<0.05);与心肌梗死组比较,有氧运动组和抗阻运动组上述各参数均无统计学差异(P>0.05)。③骨骼肌重塑:与假手术组比较,心肌梗死组腓肠肌质量、腓肠肌质量指数、细胞横截面积、超氧化物歧化酶活性、谷胱甘肽过氧化物酶活性、活化的卫星细胞数量下降(P<0.05),活性氧、丙二醛含量以及泛素、MuRF1、MAFbx蛋白表达量上调(P<0.05);与心肌梗死组比较,有氧运动组和抗阻运动组腓肠肌质量指数、超氧化物歧化酶活性、活化的卫星细胞数量增加(P<0.05),活性氧水平以及泛素、MuRF1、MAFbx蛋白表达量降低(P<0.05);与有氧运动组比较,抗阻运动组腓肠肌质量、腓肠肌质量指数、细胞横截面积、活性氧水平、丙二醛含量、活化的卫星细胞数量升高(P<0.05),超氧化物歧化酶活性、谷胱甘肽过氧化物酶活性下调(P<0.05)。结果表明:有氧运动和抗阻运动均可提升心力衰竭大鼠的运动能力,其机制与减轻氧化应激、抑制泛素-蛋白酶体系统活性以及激活卫星细胞进而改善骨骼肌重塑有关。有氧运动对于改善骨骼肌氧化应激作用更佳,而抗阻运动促进骨骼肌再生方面效果更为显著。

不同运动方式促进周围神经损伤后的功能恢复

背景:运动作为一种主动康复的方式可以改善周围神经损伤导致的功能障碍,而不同运动方式针对的病变部位及恢复机制不同。目的:综合分析不同运动方式在周围神经损伤功能恢复中的应用及机制。方法:应用计算机检索中国知网、PubMed数据库建库时间至2024年1月期间的相关文献,英文检索词为“peripheral nerves injury,spinal cord,exercise,cerebral cortex,muscle atrophy,mirror therapy,blood flow restriction training”,中文检索词为“周围神经损伤,脊髓,大脑皮质,肌肉萎缩,有氧运动,血流限制,镜像运动”,最终纳入77篇文献进行分析。结果与结论:周围神经损伤后会引起其支配骨骼肌萎缩、相应脊髓节段病变、感觉运动皮质重塑等系统性的病理变化。有氧运动可以加强免疫反应,促进神经胶质细胞极化以及神经生长因子的释放,改善功能障碍。血流限制运动可以调节肌肉生长因子的分泌,促进肌肉生长及增强肌肉力量。镜像运动在激活大脑皮质、减少皮质重塑方面有良好的作用。不同运动方式在周围神经损伤功能恢复中具有潜在的益处,然而目前仍存在一些问题和挑战,例如运动方式的选择、运动强度和频率的控制及机制的详细解析等。

Exercise training mode effects on myokine expression in healthy adults:A systematic review with meta-analysis

Background:The benefits of exercise are well known;however,many of the underlying molecular mechanisms are not fully understood.Skeletal muscle secretes myokines,which mediate muscleorgan crosstalk.Myokines regulate satellite-cell proliferation and migration,inflammatory cascade,insulin secretion,angiogenesis,fatty oxidation,and cancer suppression.To date,the effects of different exercise modes(namely,aerobic and resistance exercise)on myokine response remain to be elucidated.This is crucial considering the clinical implementation of exercise to enhance general health and wellbeing and as a medical treatment.Methods:A systematic search was undertaken in PubMed,MEDLINE,CINAHL,Embase,SPORTDiscus,andWeb of Science in April 2023.Eligible studies examining the effects of a single bout of exercise on interleukin15(IL-15),irisin,secreted protein acidic and rich in cysteine(SPARC),oncostatinM(OSM),and decorin were included.A random-effects meta-analysis was also undertaken to quantify the magnitude of change.Results:Sixty-two studies were included(n=1193).Overall,exercise appeared to induce small to large increases in myokine expression,with effects observed immediately after to 60 min post-exercise,although these were mostly not statistically significant.Both aerobic and resistance exercise resulted in changes in myokine levels,without any significant difference between training modes,and with the magnitude of change differing across myokines.Myokine levels returned to baseline levels within 180 min to 24 h post-exercise.However,owing to potential sources of heterogeneity,most changes were not statistically significant,indicating that precise conclusions cannot be drawn.Conclusion:Knowledge is limited but expanding with respect to the impact of overall and specific effects of exercise on myokine expression at different time points in the systemic circulation.Further research is required to investigate the effects of different exercise modes at multiple time points on myokine response.