Population aging and widespread sedentary lifestyles have increased the prevalence of chronic non-communicable diseases, many of which are linked to progressive disruptions of cellular homeostasis. Autophagy, a conserved cellular degradation and recycling pathway, plays a central role in maintaining metabolic flexibility, proteostasis, and organ function. However, aging and physical inactivity impair autophagic regulation, thereby contributing to the development of sarcopenia, cardiovascular diseases, metabolic disorders, and neurodegenerative diseases. Physical exercise is a non-pharmacological intervention that can restore autophagic activity and confer systemic health benefits in multiple preclinical and clinical contexts. Increasing evidence indicates that these benefits are mediated not only by local tissue adaptations but also by complex inter-organ communication. Central to this process are exercise-induced bioactive factors, collectively termed exerkines, including myokines, cardiokines, adipokines, hepatokines, osteokines, and circulating miRNAs. Rather than acting independently, exerkines form an integrated signaling network that fine-tunes autophagic flux across multiple tissues. Exerkine-mediated regulation of autophagy involves key pathways such as AMPK/mTOR, FoxO, SIRT1, ULK1, and TFEB, thereby coordinating energy metabolism, mitochondrial quality control, inflammation, and protein turnover in skeletal muscle, heart, liver, adipose tissue, bone, and the central nervous system. This review summarizes current evidence on representative exerkines and their roles in autophagy-dependent inter-organ crosstalk, highlighting the exercise-exerkine-autophagy axis as a promising target for preventing and managing chronic diseases.

Background Alzheimer’s disease (AD) presents a significant challenge to global healthcare systems, with an exacerbation by an aging population. Although the plethora of hypotheses are proposed to elucidate the underlying mechanisms of AD, from amyloid-beta (Aβ) accumulation and Tau protein aggregation to neuroinflammation, a comprehensive understanding of its pathogenesis remains elusive. Recent research has highlighted the critical role of calcium (Ca2+) signaling pathway in the progression of AD, indicating a complex interplay between Ca2+ dysregulation and various pathological processes. Aim of Review This review aims to consolidate the current understanding of the role of Ca2+ signaling dysregulation in AD, thus emphasizing its central role amidst various pathological hypotheses. We aim to evaluate the potential of the Ca2+ signaling hypothesis to unify existing theories of AD pathogenesis and explore its implications for developing innovative therapeutic strategies through targeting Ca2+ dysregulation. Key Scientific Concepts of Review The review focuses on three principal concepts. First, the indispensable role of Ca2+ homeostasis in neuronal function and its disruption in AD. Second, the interaction between Ca2+ signaling dysfunction and established AD hypotheses posited that Ca2+ dysregulation is a unifying pathway. Third, the dual role of Ca2+ in neurodegeneration and neuroprotection, highlighting the nuanced effects of Ca2+ levels on AD pathology.

OBJECTIVES:This study sought to investigate the effect of muscle mass, muscle strength, and physical function on postural balance in Sarcopenia. METHODS:A total of 1026 subjects aged 60-years and older were screened for sarcopenia and assessed using clinical tests including the Romberg's test, Single Leg Standing Test (SLS), Five Times Sit to Stand Test (FTSST), Timed Up & Go Test (TUGT), and Y-Balance Test (YBT). RESULTS:The authors identified distinct predictive patterns: 1) Hand grip strength(muscle strength) emerged as the dominant predictor of static balance performance, while 2) Dynamic balance outcomes were jointly influenced by gait speed (physical function), muscle strength, and age. Notably, dynamic balance demonstrated greater susceptibility to age-related skeletal muscle decline compared to static balance. CONCLUSION:These findings propose clinically actionable pathways: resistance training to target muscle strength deficits for static balance improvement, and combined strength-functional training protocols for dynamic balance rehabilitation in sarcopenia management.

The comorbidity of sarcopenia and cognitive impairment constitutes a degenerative syndrome that progresses significantly with age. It has emerged as a critical global health challenge, contributing to functional disability, reduced quality of life, and increased pressure on public healthcare systems. This comorbidity is characterized by a synergistic decline in both physical and cognitive capabilities, manifesting as reduced skeletal muscle mass, diminished muscle strength, impaired physical function, and progressive deterioration in cognitive domains such as memory, executive function, and information processing speed. This dual degeneration not only creates a vicious cycle where each condition exacerbates the other but also substantially increases the risk of falls, fractures, hospitalization, and mortality among older adults. Against the backdrop of rapid global population aging, the prevalence of this comorbidity is anticipated to rise further without effective interventions. Consequently, investigating its underlying mechanisms and developing preventive and therapeutic strategies hold substantial clinical and public health significance. Current evidence indicates that the pathogenesis involves multi-system and multi-level pathophysiological processes, with chronic inflammation, mitochondrial dysfunction, and gut microbiota dysbiosis, identified as three core interacting mechanisms. Age-related chronic low-grade inflammation, termed inflammaging, arises from the senescence-associated secretory phenotype (SASP) and persistent immune cell activation. This inflammatory state inhibits the intramuscular IGF-1/Akt/mTOR anabolic pathway through proinflammatory cytokines (e.g., IL-6, TNF-α), while simultaneously activating protein degradation systems including the ubiquitin-proteasome system (UPS) and autophagy-lysosomal pathway (ALP), ultimately leading to accelerated protein breakdown and muscle atrophy. These circulating inflammatory factors can also compromise blood-brain barrier integrity, activate microglia, trigger neuroinflammation, and consequently damage synaptic structures and neuronal function, thereby accelerating cognitive decline in this comorbidity. Mitochondrial dysfunction presents as impaired oxidative phosphorylation efficiency, excessive reactive oxygen species (ROS) production, and dysregulated mitochondrial quality control. This not only results in inadequate cellular energy supply but also enables mitochondrial-derived factors (e.g., extracellular mtDNA) to activate innate immune pathways such as cGAS-STING, propagating stress signals and amplifying tissue damage in both muscle and brain. Additionally, gut microbiota dysbiosis impairs intestinal barrier function, increases lipopolysaccharide (LPS) translocation into circulation, and reduces short-chain fatty acid (SCFA) production. These changes induce systemic inflammation and metabolic disturbances that further impact muscle metabolism and promote pathological protein accumulation in the brain, thereby establishing a gut-brain-muscle axis that exacerbates the progression of this comorbidity. Exerkines represent a class of biologically active signaling molecules—including cytokines, peptides, metabolites, and exosomes—secreted by various tissues in response to exercise. These exerkines mediate systemic adaptations and protective effects through endocrine and paracrine actions on target organs. Key exerkines such as IL-6, irisin, brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), fibroblast growth factor-21 (FGF-21), lactate, and cathepsin B (CTSB) play central roles in coordinately ameliorating the comorbidity of sarcopenia and cognitive impairment. The beneficial effects of these exerkines are mediated through multiple mechanisms including inflammation modulation, energy metabolism remodeling, neuroprotection, and enhanced neuroplasticity. As a non-pharmacological intervention, exercise effectively stimulates the production and release of exerkines, thereby targeting the comorbidity through multiple pathways. Aerobic exercise elevates lactate levels and activates the Sirt1/PGC-1α pathway, improving cerebral metabolism and cognitive function. Resistance training significantly upregulates IGF-1, irisin, and CTSB expression, enhancing muscle anabolism and hippocampal function. Other modalities like high-intensity interval training (HIIT) and traditional practices also help modulate inflammatory status and optimize the neurotrophic environment through the action of various exerkines. Different exercise types work synergistically by engaging distinct signaling pathways and exerkine combinations, collectively alleviating chronic inflammation, correcting mitochondrial dysfunction, and optimizing gut microecology to achieve concurrent musculoskeletal and cognitive protection against this comorbidity. Synthesizing current evidence, this review emphasizes the necessity of transcending a single-organ perspective by recognizing muscle and brain as an integrated functional unit, with exerkines playing a pivotal role in the muscle-brain axis. The field nevertheless faces several challenges: the secretion dynamics of exerkines during aging remain unclear, mechanisms underlying individual differences in exercise response require elucidation, and the compensatory and imbalance characteristics of exercise-induced exerkine networks across disease stages need further characterization. Future research should employ large-sample cohorts and randomized controlled trials integrated with multi-omics technologies to establish personalized exercise interventions based on exerkine profiling for managing this comorbidity. Parallel efforts should focus on developing quantifiable efficacy assessment systems to provide robust theoretical foundation and practical guidance for precise management of the comorbidity of sarcopenia and cognitive impairment and the promotion of healthy aging.

Obesity cardiomyopathy (OCM) represents a rapidly growing health concern globally, characterized by metabolic, structural, and functional abnormalities of the heart. Current research has demonstrated that inflammation plays a pivotal role in obesity-induced cardiomyopathy, and that regular exercise can ameliorate lipid disturbances and inflammatory abnormalities effectively. However, the underlying mechanisms are not fully elucidated. We investigated the effects of an 8-week aerobic exercise intervention on myocardial structure, function, and inflammation in HFD-induced obese mice. The results revealed that aerobic exercise alleviated myocardium pyroptosis and inflammation by down-regulating the PI3K/AKT signaling pathway. Furthermore, the inhibition of the PI3K pathway by LY294002, coupled with exercise, attenuated and suppressed HFD-induced myocardial impairments, inflammation, and pyroptosis, with a synergistic effect. Based on these findings, we concluded that eight weeks of aerobic exercise synergizes with the inhibition of PI3K through inflammatory and pyroptosis mechanisms to improve obesity-associated myocardial remodeling and dysfunction. Therefore, long-term regular aerobic exercise represents a potential strategy in the treatment of OCM.

Objective This study aimed to explore the effects of aerobic exercise on cognitive function in aging mice and to elucidate the underlying molecular mechanisms by which aerobic exercise ameliorates cognitive decline through the regulation of gut microbiota-metabolite network. By providing novel insights into the interplay between exercise, gut microbiota, and cognitive health, this research seeks to offer a robust theoretical foundation for developing anti-aging strategies and personalized exercise interventions targeting aging-related cognitive dysfunction. Methods Using naturally aged C57BL/6 mice as the experimental model, this study employed a multi-omics approach combining 16S rRNA sequencing and wide-targeted metabolomics analysis. A total of 18 mice were divided into 3 groups: young control (YC, 4-month-old), old control (OC, 21-month-old), and old+exercise (OE, 21-month-old with 12 weeks of moderate-intensity treadmill training) groups. Behavioral assessments, including the Morris water maze (MWM) test, were conducted to evaluate cognitive function. Histopathological examinations of brain tissue sections provided morphological evidence of neuronal changes. Fecal samples were collected for gut microbiota and metabolite profiling via 16S rRNA sequencing and ultra-performance liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry (UPLC-QTOF-MS). Data were analyzed using a combination of statistical and bioinformatics tools to identify differentially abundant microbial taxa and metabolites and to construct interaction networks between them. Results Behavioral tests revealed that 12 weeks of aerobic exercise significantly improved spatial learning and memory capacity of aged mice, as evidenced by reduced escape latency and increased target area exploration and platform crossings in the MWM. Histopathological analysis demonstrated that exercise mitigated aging-related neuronal damage in the hippocampus, enhancing neuronal density and morphology. 16S rRNA sequencing indicated that exercise increased gut microbiota alpha-diversity and enriched beneficial bacterial genera, including Bifidobacterium, Parabacteroides, and Rikenella. Metabolomics analysis identified 32 differentially regulated metabolites between OC and OE groups, with 94 up-regulated and 30 down-regulated in the OE group when compared with OC group. These metabolites were primarily involved in energy metabolism reprogramming (e. g., L-homocitrulline), antioxidant defense (e. g., L-carnosine), neuroprotection (e. g., lithocholic acid), and DNA repair (e. g., ADP-ribose). Network analysis further revealed strong positive correlations between specific bacteria and metabolites, such as Parabacteroides with ADP-ribose and Bifidobacterium with lithocholic acid, suggesting potential neuroprotective pathways mediated by the gut microbiota-metabolite axis. Conclusion This study provides comprehensive evidence that aerobic exercise elicits cognitive benefits in aging mice by modulating the gut microbiota-metabolite network. These findings highlight three key mechanisms: (1) the proliferation of beneficial gut bacteria enhances metabolic reprogramming to boost DNA repair pathways; (2) elevated neuroinflammationinhibiting factors reduce neurodegenerative changes; and (3) enhanced antioxidant defenses maintain neuronal homeostasis. These results underscore the critical role of the "microbiota-metabolite-brain" axis in mediating the cognitive benefits of aerobic exercise. This study not only advances our understanding of the gut-brain axis in aging but also offers a scientific basis for developing personalized exercise and probiotic-based interventions targeting aging-related cognitive decline. Future research should further validate these mechanisms in non-human primates and human clinical trials to establish the translational potential of exercise-induced gut microbiotametabolite modulation for combating neurodegenerative diseases.

The autophagy-lysosome pathway is the major route for protein and organelle clearance, and the functional status of autophagy plays an important role in the performance of skeletal muscle. The functional impairment of autophagy can cause atrophy and contractile dysfunction of skeletal muscle. Exercise can induce autophagy or regulate the functional status of autophagy to promote an increase in muscle mass for the prevention and treatment of muscular atrophy. However, the role and factors of autophagy in this process remain unclear. Meanwhile, the skeletal muscle-specific autophagy-related gene 6 (Atg6/Beclin1) conditioned knockout (BECN1cKO) mice revealed the accumulation of swollen and vacuolated mitochondria, disorganization of sarcomeres with irregular shapes, and the aggregation of centralized nuclei in the skeletal muscle, as well as the atrophy of skeletal muscle. In contrast, compared with the mice with normal functional status of autophagy, resistance exercise further exacerbated skeletal muscle atrophy in the BECN1cKO mice, suggesting a determinant role of autophagy in combating muscle atrophy as a result of exercise intervention.

Obesity, caused by excessive energy, leads to body weight gain and various diseases, including cognitive impairment. Current studies suggest that diet restriction such as optimal fasting and regular exercise are crucial for improving cognitive capacity. However, further exploration is needed to understand the specific mechanisms of high fat diet(HFD)-induced cognitive decline in obesity. In the present study, 4-month-old mice were subjected to HFD feeding for 18 weeks, followed by aerobic exercise and high-intensity intermittent exercise, regular diet feeding, and intermittent fasting for 8 weeks, and then used to evaluate cognitive capacity, inflammation, compromised insulin signaling pathway, and apoptosis in hippocampal tissue, as well as AMPK/SIRT1 and TLR4 signal pathways. Obese mice revealed impaired cognitive capacity as compared with mice fed with regular diets. In contrast, aerobic exercise, high-intensity intermittent exercise, regular diet, and intermittent fasting could inhibit apoptosis caused by inflammation-mediated compromised insulin signaling pathway in hippocampal tissues through activating the AMPK/SIRT1 signal pathway and suppressing the TLR4 signal pathway, thereby rescuing the cognitive impairment of obese mice. Therefore, diet restriction and exercise interventions may play a positive role in reverting obesity-induced cognitive impairment.

Introduction Exercise has been recognized to improve cognitive performance by optimizing gut flora and up-regulating exerkine irisin. Objective Although exercise-induced irisin is beneficial to cognitive improvement, whether this benefit is achieved by optimizing gut microbiota and metabolites is not fully explored. Methods After aerobic exercise and exogenous irisin interventions for 12 weeks, the 16S rRNA and metabolites in feces of 21-month-old mice were analyzed. Meanwhile, the differential miRNAs and mRNAs in hippocampal tissues were screened by high-throughput sequencing. Relevant mRNAs and proteins were evaluated by RT-PCR, Western blot, and immunofluorescence. Results Compared with the young control mice, irisin levels and cognitive capacity of aged mice revealed a significant reduction, while aerobic exercise and intraperitoneal injection of exogenous irisin reversed aging-induced cognitive impairment. Similarly, 147 up-regulated and 173 down-regulated metabolites were detected in aged mice, while 64 and 45 up-regulated and 225 and 187 down-regulated metabolites were detected in aged mice with exercise and irisin interventions, respectively. Moreover, during hippocampal miRNA and mRNA sequencing analysis, 9 differential gut flora and 35 differential genes were identified to be correlated with the inflammatory signaling mediated by the TLR4/MyD88 signal pathway. Conclusion Aging-induced cognitive impairment is due to insulin resistance induced by TLR4/MyD88 signaling activation in hippocampal tissues mediated by gut microbiota and metabolite changes. Myokine irisin may be an important mediator in optimizing gut microbiota and metabolism for an improved understanding of mitigated aging process upon exercise interventions.

BACKGROUND:The related functions of skeletal muscle and brain decrease significantly with age, and muscle-brain-related diseases are primarily associated with each other. Exercise can promote the secretion of myokines in skeletal muscle, showing a beneficial effect on the function of both, reflecting muscle-brain crosstalk. However, the key mechanism of action of exercise-regulated myokines in muscle-brain diseases remains unclear. SUMMARY:This review is intended to sort out and explore the key mechanism of the effect of exercise regulatory myokines on muscle-brain diseases through summarizing the relevant literature on the level of motor regulatory myokines in recent years and pay special attention to the impact of exercise type, intensity, and duration on myokine expression levels. KEY MESSAGES:The mechanism by which exercise regulates myokine levels in muscle-brain diseases is explained, and an effective exercise prescription for myokine expression that is more suitable for the elderly based on relevant literature is proposed. This work may hold certain value for subsequent exercise treatment of chronic diseases in the elderly and for further research on muscle-brain crosstalk.

Exercise-derived exosomes have been identified as novel players in mediating cell-to-cell communication in the beneficial effects of improving cardiovascular disease (CVD). This review aimed to systematically investigate exosomes as delivery tools for the benefits of exercise in the prevention and treatment of CVD and summarize these outcomes with an overview of their therapeutic implications. Among the 1417 articles obtained in nine database searches (PubMed, EBSCO, Embase, Web of Science, CENTRAL, Ovid, Science Direct, Scopus, and Wiley), 12 articles were included based on eligibility criteria. The results indicate that exercise increases the release of exosomes, increasing exosomal markers (TSG101, CD63, and CD81) and exosome-carried miRNAs (miR-125b-5p, miR-122-5p, miR-342-5p, miR-126, miR-130a, miR-138-5p, and miR-455). These miRNAs mainly regulate the expression of MAPK, NF-kB, VEGF, and Caspase to protect the cardiovascular system. Moreover, the outcome indicators of myocardial apoptosis and myocardial infarction volume are significantly reduced following exercise-induced exosome release, and angiogenesis, microvessel density and left ventricular ejection fraction are significantly increased, as well as alleviating myocardial fibrosis following exercise-induced exosome release. Collectively, these results further confirm that exercise-derived exosomes have a beneficial role in potentially preventing and treating CVD and support the use of exercise-derived exosomes in clinical settings.

Alzheimer's disease (AD) is a chronic neurodegenerative disease, with the characteristics of neurofibrillary tangle (NFT) and senile plaque (SP) formation. Although great progresses have been made in clinical trials based on relevant hypotheses, these studies are also accompanied by the emergence of toxic and side effects, and it is an urgent task to explore the underlying mechanisms for the benefits to prevent and treat AD. Herein, based on animal experiments and a few clinical trials, neuroinflammation in AD is characterized by long-term activation of pro-inflammatory microglia and the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasomes. Damaged signals from the periphery and within the brain continuously activate microglia, thus resulting in a constant source of inflammatory responses. The long-term chronic inflammatory response also exacerbates endoplasmic reticulum oxidative stress in microglia, which triggers microglia-dependent immune responses, ultimately leading to the occurrence and deterioration of AD. In this review, we systematically summarized and sorted out that exercise ameliorates AD by directly and indirectly regulating immune response of the central nervous system and promoting hippocampal neurogenesis to provide a new direction for exploring the neuroinflammation activity in AD.

The application of multi-tasking (MT), especially dual-tasking (DT), in frail older adults is currently gaining attention. The aim was to review the application of the MT mode on cognition and lower limb function in frail older adults, including the MT test and MT training. By searching five electronic databases, Scopus, PubMed, PEDro, Web of Science and the Chinese electronic database, a total of 18 studies were finally included in this study, with 7 articles on MT testing and 11 articles on MT training. The results of the study showed that the current testing and training of MT is mainly based on the DT mode, with a wide variety of test types and protocols, as well as a variety of outcomes. The included studies suggested that DT can be used as a test to assess cognitive and lower limb function in the frail population and that an MT (DT) training program with an intervention period of ≥3 months or a duration of ≥60 min per session could improve cognitive and lower limb function in the frail population, thereby reducing the risk of falls. Further research is required to explore the effects of different types of MT and task prioritization in frail older adults.

目的 对国内 2017-2022 年肌少症领域的研究现状、热点及趋势进行可视化分析.方法 以CNKI数据库为搜索来源,运用CiteSpace5.7.R2软件对2017-2022年肌少症的研究进行可视化分析,探讨相关研究的作者、机构分布状况及对关键词进行可视化分析.结果 纳入1165篇文章,发文量最高的作者是张艳,中南大学湘雅护理学院、安徽医科大学第一附属医院风湿免疫科、南京医科大学附属江宁医院骨科三所机构中心性相对较高,是研究肌少症的重要机构.主要的研究热点是肌少症患病及相关危险因素、肌少症与类风湿关节炎和骨质疏松等共病关系的临床研究、肌少症机制的探究.结论 该领域2017-2022年研究热点主要在肌少症相关危险因素研究上;肌少症合并其他疾病的潜在相关性和机制的研究是该领域研究的趋势.

白细胞介素13(interleukin-13,IL-13)是一种新发现的与运动代谢调控相关的细胞因子.运动可刺激外周组织中的免疫细胞分泌IL-13,进而促进线粒体生物发生,增加脂肪酸氧化,改善葡萄糖代谢,协调蛋白质代谢,并最终提升骨骼肌、心肌、肝脏等组织的代谢灵活性,增强运动代谢适应能力,维持细胞代谢稳态效应.靶向IL-13改善代谢灵活性将为运动治疗代谢疾病提供重要理论参考依据.

随着全球老龄化进程加剧,老年人口剧增,伴随着工作和生活方式的改变,导致体育锻炼减少与生活作息不规律等问题愈发严重.这样的结果显著增加了骨骼肌萎缩的发病率,降低了老年和慢性疾病人群机体健康,影响其生活质量.与此同时,饮食不均衡和运动量降低以及激素水平波动等进一步加剧骨骼肌萎缩的发生,其病理机制主要为慢性炎症加重、线粒体功能障碍、自噬功能状态低下、细胞凋亡增加、肌卫星细胞功能受损以及昼夜节律紊乱等.其中,随着昼夜节律相关研究的深入,骨骼肌作为机体最大的外周生物钟,可通过调控昼夜节律核心基因BMAL1以及CLOCK基因,对骨骼肌纤维结构、线粒体功能、肌肉质量等产生影响.运动锻炼作为改善骨骼肌质量的重要干预策略,还可激活昼夜节律信号通路,调控其相位,进而改善肌肉再生、提高肌肉力量,发挥延缓肌萎缩作用.为此,本文从昼夜节律的角度去阐述其与肌萎缩发生以及潜在运动干预的分子机制,以期为肌萎缩的预防、治疗及康复提供新的靶向思路.

Irisin is an exercise-induced myokine expressed as a bioactive peptide in multiple tissues and organs, and exercise and cold exposure are the major inducers for its secretion. Irisin presents a decreasing trend with the extension of age and is also closely associated with a wide range of aging-related diseases. Currently, many studies on irisin are being conducted with respect to physiological functions for health promotion, and the prevention, treatment and rehabilitation of chronic diseases, as well as mechanisms associated with improving energy metabolic balance, enhancing cellular homeostasis by optimizing autophagy, promoting mitochondrial quality control, reducing reactive oxygen species (ROS) production, and mitigating inflammatory responses. These diseases include: metabolic diseases (obesity, type 2 diabetes, and bone metabolism); cardiovascular diseases (hypertension, coronary heart disease, cardiomyopathy and stroke); nervous system diseases (Alzheimer's disease, Parkinson's disease, and stroke); and others (cancer and sarcopenia). Although the current studies on irisin are relatively extensive, some studies have produced unexplained experimental results. This article introduces an overview of the generation, secretion, and tissue distribution, of irisin, and its targeting of tissues or organs for the prevention and treatment of above-mentioned chronic diseases is systematically summarized, with discussion of the underlying molecular mechanisms. This study is expected to improve the understanding of irisin, which may be beneficial to identify novel and effective targets for the screening, diagnosis, or therapy of these chronic diseases, or develop promising interventional strategies, effective drug candidates, functional foods, or exercise mimetics.

Background: Exercise is one of the most effective interventions for preventing and treating skeletal muscle aging. Exercise-induced autophagy is widely acknowledged to regulate skeletal muscle mass and delay skeletal muscle aging. However, the mechanisms underlying of the effect of different exercises on autophagy in aging skeletal muscle remain unclear. Methods: A systematic review was performed following an electronic search of SCOPUS, PubMed, Web of Science, ScienceDirect, and Google Scholar and two Chinese electronic databases, CNKI and Wan Fang. All articles published in English and Chinese between January 2010 and January 2022 that quantified autophagy-related proteins in aging skeletal muscle models. Results: The primary outcome was autophagy assessment, indicated by changes in the levels of any autophagy-associated proteins. A total of fifteen studies were included in the final review. Chronic exercise modes mainly comprise aerobic exercise and resistance exercise, and the intervention types include treadmill training, voluntary wheel running, and ladder training. LC3, Atg5-Atg7/9/12, mTOR, Beclin1, Bcl-2, p62, PGC-1 alpha, and other protein levels were quantified, and the results showed that long-term aerobic exercise and resistance exercise could increase the expression of autophagy-related proteins in aging skeletal muscle (p < 0.05). However, there was no significant difference in short term or high-intensity chronic exercise, and different types and intensities of exercise yielded different levels of significance for autophagy-related protein expression. Conclusion: Existing evidence reveals that high-intensity exercise may induce excessive autophagy, while low-intensity exercise for a short period (Intervention duration < 12 weeks, frequency < 3 times/week) may not reach the threshold for exercise-induced autophagy. Precise control of the exercise dose is essential in the long term to maximize the benefits of exercise. Further investigation is warranted to explore the relationship between chronic exercise and different exercise duration and types to substantiate the delaying of skeletal muscle aging by exercise.

With the rapid improvement of social economy and the enhancement of people's health awareness, it is necessary to make an in-depth analysis of the rationality of physical exercise and the physical quality of residents. Hence, this study aims to explore the algorithm optimization of the improved BP model to analyze the effect of exercise intervention on improving public sports effect. K-clustering and Levenberg–Marquardt algorithm were used to construct an improved BP neural network model to determine the sample clustering center, as well as the weight and threshold of the indicators, so as to optimize the analysis algorithm of improving public sports effect. MATLAB simulation shows that under the target error conditions of 0.01, 0.005, 0.001, and 0.0001, the target error rate and iteration times of the improved BP model are better than the standard BP model, and the time consumption is shorter, which can be conducive to more accurately analyzing the changes of improving public sports effect under exercise intervention. Therefore, the improved BP model can effectively solve the problems of data clustering and result error rate adjustment in the process of improving public sports effect analysis and improve the analysis speed and accuracy.

A ketogenic diet, characterized by low calories with high levels of fat, adequate levels of protein, and low levels of carbohydrates, has beneficial effects on body weight control in overweight patients. In the present study, a meta-analysis was conducted to investigate the role of a ketogenic diet in body weight control and glycemic management in overweight patients with type 2 diabetes mellitus (T2DM). In summary, we systematically reviewed articles from the Embase, PubMed, Web of Science and Cochrane Library databases and obtained eight randomized controlled trials for meta-analysis. The results show that a ketogenic diet had significantly beneficial effects on the loss of body weight (SMD, −5.63, p = 0.008), the reduction of waist circumference (SMD, −2.32, p = 0.04), lowering glycated hemoglobin (SMD, −0.38, p = 0.0008) and triglycerides (SMD, −0.36, p = 0.0001), and increasing high-density lipoproteins (SMD, 0.28, p = 0.003). Overall, these results suggest that a ketogenic diet may be an effective dietary intervention for body weight and glycemic control, as well as improved lipid profiles in overweight patients with T2DM. Hence, a ketogenic diet can be recommended for the therapeutic intervention of overweight patients with T2DM.