Diastolic dysfunction is a major cardiac dysfunction, and an important predisposing factor is age. Although exercise training is often used for the prevention and treatment of cardiovascular disease nowadays, little is currently known about whether exercise interventions associated with the slowing of cardiac aging are related to mtp‐related pathways. In the present study, the UAS/Tub‐Gal4 system was used to knockdown whole‐body mtp expression levels in Drosophila, which underwent 2 weeks of endurance training. By conducting different assays and quantifying different indicators, we sought to investigate the relationship between mtp, exercise, and age‐related diastolic dysfunction. We found that (1) Drosophila in the mtp^RNAi youth group exhibited age‐related diastolic dysfunction and had a significantly shorter mean lifespan. (2) Endurance exercise could improve diastolic dysfunction and prolong lifespan in aged Drosophila. (3) Endurance exercise could increase the expression levels of apolpp and Acox3, and decrease the levels of TC, LDL‐C, and TG in the aged group. In summary, aging causes age‐associated diastolic dysfunction in Drosophila, and systemic knockdown of mtp causes premature age‐associated diastolic dysfunction in young Drosophila. Besides, endurance exercise improves age‐related diastolic dysfunction and prolongs lifespan.

This study investigates the rising trends, sociological drivers, health benefits, and the interaction of night running and night cycling with urban green spaces. Findings indicate that night running and night cycling are mainly driven by increased health awareness, changes in work patterns, social media promotion, and urban economic development. Physiologically, night running and cycling enhance cardiovascular function, alleviate stress, and improve sleep. However, air pollution, inadequate infrastructure, and safety concerns limit the sustainability of these activities. Urban green spaces play a crucial role in promoting nocturnal exercise, with improvements in lighting, safety, and recreational areas due to the growing demand for night fitness. Governments are encouraged to enhance infrastructure and optimize green space planning to foster healthier urban environments.

Alzheimer’s disease (AD) is a progressive and debilitating neurodegenerative disorder for which existing pharmacotherapies are inadequate to arrest pathological progression, highlighting the imperative to identify safe and effective nonpharmacological interventions. Exercise, as a multi‐target therapeutic modality, has been shown to reverse multiple facets of AD‐related neuropathology through diverse mechanisms. In this systematic review, we synthesize evidence on the effects of voluntary running, structured swimming, and modulation of the gut microbiota in transgenic murine models of AD. Exercise was found to ameliorate AD pathology by modulating amyloid precursor protein (APP) processing and β‐amyloid (Aβ) production/clearance, restoring mitochondrial integrity and function, attenuating neuroinflammatory responses, enhancing synaptic plasticity, and upregulating neurotrophic factors. Moreover, exercise reshapes the intestinal microbiome and thereby modulates the gut–brain axis, further promoting neuroimmune homeostasis and cognitive resilience. Through RNA sequencing data analysis, key genes such as Tlr4, Cdc42, and F13a1 were identified, which may play significant roles in neuroimmune regulation and cognitive protection. By integrating multi‐omics evidence, we propose a coordinated “exercise–microbiota–brain” mechanistic framework that offers theoretical support for personalized, exercise‐based therapeutic strategies and translational applications in AD. We also emphasize the necessity of future studies combining exercise with complementary interventions to accelerate the clinical translation of multimodal therapeutic approaches.

Cardiovascular disease (CVD) places a heavy burden on older patients and the global healthcare system. A large body of evidence suggests that exercise training is essential in preventing and treating cardiovascular disease, but the underlying mechanisms are not well understood. Here, we used the Drosophila melanogaster animal model to study the effects of early-life exercise training (ELET) on the aging heart and lifespan. We found in flies that age-induced arrhythmias are conserved across different genetic backgrounds. The fat body is the primary source of circulating lipoproteins in flies. Inhibition of fat body apoLpp (the flies apoB homolog) demonstrated that low expression of apoLpp reduced the development of arrhythmias in aged flies but did not affect average lifespan. At the same time, ELET can also reduce the expression of apoLpp mRNA in aged flies and have a protective effect on the heart, which is similar to the inhibition of apoLpp mRNA. Although treatment of apoLppRNAi and ELET alone had no significant effect on lifespan, the combination of apoLppRNAi and ELET extended the average lifespan of flies. Therefore, we conclude that apoLppRNAi and ELET are sufficient to resist age-induced arrhythmias, which may be related to the decreased expression of apoLpp mRNA, and that apoLppRNAi and ELET have a combined effect on prolonging the average lifespan.

Objective: Overweight and obesity are major global health issues. Traditional interventions have limited efficacy, while pharmacological treatments are hindered by side effects and weight rebound. This study evaluates the effects of combined exercise and medication on body composition and metabolic health in overweight/obese adults, using network pharmacology to explore potential synergistic mechanisms. Methods: A systematic search of PubMed, EMBASE, Scopus, Web of Science, Medline, and Cochrane up to October 2025 identified 18 randomized controlled trials with 5,620 participants. Meta-analysis was performed using RevMan 5.4 and Stata 14. Outcomes included weight, BMI, body fat percentage, and metabolic markers. Network pharmacology was conducted using liraglutide and orlistat to identify shared targets and perform enrichment analysis. Results: Combined exercise and medication significantly reduced weight (MD = − 2.49, 95% CI: − 3.83, − 1.14), BMI (MD = − 0.79, 95% CI: − 1.25, − 0.34), and body fat percentage (MD = − 1.97, 95% CI: − 3.76, − 0.18) compared to exercise alone. The combined intervention also significantly reduced systolic and diastolic blood pressure and triglycerides. However, compared to medication alone, it showed only reductions in weight and BMI, with no significant improvements in lean body mass, HDL, LDL, or fasting glucose. Network pharmacology revealed 109 obesity-related targets, including IL1B, STAT3, and SIRT1, involved in inflammation, lipid metabolism, and energy regulation. GO/KEGG analysis showed enrichment in fatty acid metabolism and AMPK signaling pathways. These pathways were highly consistent with metabolic adaptations induced by exercise, suggesting potential synergistic effects between exercise and medication in metabolic regulation. Conclusion: Combined exercise and medication significantly enhance weight loss in overweight/obese adults. Network pharmacology suggests that the IL1B-STAT3 inflammatory axis and SIRT1/CD36 lipid metabolism network may be central to the mechanisms. Future studies should explore the long-term efficacy and mechanistic specificity of different drug-exercise combinations.