Obesity is a common metabolic disorder caused by a sedentary lifestyle, and a high-fat and a high-glucose diet in the form of fast foods. High-fat diet-induced obesity is a major cause of diabetes and cardiovascular diseases, whereas exercise and physical activity can ameliorate these disorders. Moreover, exercise and the gut microbiota are known to be interconnected, since exercise can increase the gut microbial diversity and contribute to the beneficial health effects. In this context, we analyzed the effect of diet and exercise on the gut microbiota of mice, by next-generation sequencing of the bacterial V4 region of 16S rRNA. Briefly, mice were divided into four groups: chow-diet (CD), high-fat diet (HFD), high-fat diet + exercise (HFX), and exercise-only (EX). The mice underwent treadmill exercise and diet intervention for 8 weeks, followed by the collection of their feces and DNA extraction for sequencing. The data were analyzed using the QIIME 2 bioinformatics platform and R software to assess their gut microbial composition, richness, and diversity. The Bacteroidetes to Firmicutes ratio was found to be decreased manifold in the HFD and HFX groups compared to the CD and EX groups. The gut microbial richness was comparatively lower in the HFD and HFX groups and higher in the CD and EX groups (ACE, Chao1, and observed OTUs). However, the Shannon alpha diversity index was higher in the HFD and HFX groups than in the CD and EX groups. The beta diversity based on Jaccard, Bray–Curtis, and weighted UniFrac distance metrics was significant among the groups, as measured by PERMANOVA. Paraprevotella, Desulfovibrio, and Lactococcus were the differentially abundant/present genera based on the intervention groups and in addition to these three bacteria, Butyricimonas and Desulfovibrio C21c20 were differentially abundant/present based on diet. Hence, diet significantly contributed to the majority of the changes in the gut microbiota.

Particulate matter (PM) has deleterious consequences not only on the respiratory system but also on essential human organs, such as the heart, blood vessels, kidneys, and liver. However, the effects of PM inhalation on skeletal muscles have yet to be sufficiently elucidated. Female C57BL/6 or mt-Keima transgenic mice were randomly assigned to one of the following four groups: control (CON), PM exposure alone (PM), treadmill exercise (EX), or PM exposure and exercise (PME). Mice in the three-treatment group were subjected to treadmill running (20 m/min, 90 min/day for 1 week) and/or exposure to PM (100 μg/m³). The PM was found to exacerbate oxidative stress and inflammation, both at rest and during exercise, as assessed by the levels of proinflammatory cytokines, manganese-superoxide dismutase activity, and the glutathione/oxidized glutathione ratio. Furthermore, we detected significant increases in the levels of in vivo mitophagy, particularly in the PM group. Compared with the EX group, a significant reduction in the level of mitochondrial DNA was recorded in the PME group. Moreover, PM resulted in a reduction in cytochrome c oxidase activity and an increase in hydrogen peroxide generation. However, exposure to PM had no significant effect on mitochondrial respiration. Collectively, our findings in this study indicate that PM has adverse effects concerning both oxidative stress and inflammatory responses in skeletal muscle and mitochondria, both at rest and during exercise.

Inhalation of ambient particulate matter (PM) can disrupt the gut microbiome, while exercise independently influences the gut microbiome by promoting beneficial bacteria. In this study, we analyzed changes in gut microbial diversity and composition in response to combined interventions of PM exposure and aerobic exercise, extending up to 12 weeks. This investigation was conducted using mice, categorized into five groups: control group (Con), exercise group (EXE), exercise group followed by 3-day exposure to PM (EXE + 3-day PM), particulate matter exposure (PM), and PM exposure with concurrent treadmill exercise (PME). Notably, the PM group exhibited markedly lower alpha diversity and richness compared to the Con group and our analysis of beta diversity revealed significant variations among the intervention groups. Members of the Lachnospiraceae family showed significant enhancement in the exercise intervention groups (EXE and PME) compared to the Con and PM groups. The biomarker Lactobacillus, Coriobacteraceae, and Anaerofustis were enriched in the EXE group, while Desulfovibrionaceae, Mucispirillum schaedleri, Lactococcus and Anaeroplasma were highly enriched in the PM group. Differential abundance analysis revealed that Paraprevotella, Bacteroides, and Blautia were less abundant in the 12-week PM exposure group than in the 3-day PM exposure group. Moreover, both the 3-day and 12-week PM exposure groups exhibited a reduced relative abundance of Bacteroides uniformis, SMB53, and Staphylococcus compared to non-PM exposure groups. These findings will help delineate the possible roles and associations of altered microbiota resulting from the studied interventions, paving the way for future mechanistic research.

PURPOSE: Exercise–microbiome research is expanding rapidly, but methodological heterogeneity and technical limitations still hinder reproducibility and mechanistic interpretation. This review provides a comprehensive methodological roadmap to overcome these barriers.METHODS: We conducted a structured literature search in PubMed, Web of Science, and Scopus for records published between 1998 and 2025 using predefined combinations of exercise and gut-microbiome terms. After deduplication, titles/abstracts and full texts were screened according to prespecified criteria, yielding 99 eligible studies on aerobic and resistance/anaerobic exercise and gut microbiota. Evidence is critically appraised across standard short-read 16S rRNA protocols, shotgun metagenomics, and emerging long-read sequencing, as well as metatranscriptomics, metabolomics, and associated bioinformatics pipelines. A PRISMA-style flow diagram summarizes the study-selection process.RESULTS: Exercise across diverse modalities reshapes gut microbial diversity and community structure, frequently enriching taxa such as Akkermansia muciniphila and Veillonella and enhancing production of short-chain fatty acids (SCFAs). SCFAs strengthen the intestinal barrier, activate anti-inflammatory pathways, and supply energy substrates for colonocytes and exercising muscle. Long-read sequencing now enables species- and strain-level resolution beyond short V-region amplicons, while inclusion of the gut mycobiome and virome expands ecological scope. Multi-omics designs integrating metagenomics, metatranscriptomics, and metabolomics connect microbial composition with functional outputs and host metabolic adaptations.CONCLUSIONS: The future of exercise–microbiome science lies not in enlarging static catalogs of responsive microorganisms but in constructing individual-level predictive models. Integrating long-read sequencing and multi-omics with standardized training metadata will enable precision exercise prescriptions and microbiome-targeted interventions, including tailored probiotics, synbiotics, and nutrition strategies. Adoption of these advanced methodologies can accelerate mechanistic insight and promote translation of exercise– microbiome research into athletic performance optimization and clinical practice.

PURPOSE: A correlation exists between a healthy physiological state and the diversity of the gut microbiome. Menopause-induced deterioration of whole-body metabolism negatively contributes to microbial diversity. The combined effect of acetic acid supplementation and exercise on the gut microbiome remains unknown. This study aimed to investigate 1) whether menopause negatively influences gut microbial diversity, including Firmicutes abundance, and 2) whether the combined treatment of acetic acid supplementation and exercise rescues microbial dysbiosis, and which specific bacteria are related to this rescue effect.METHODS: The 15-week study used 8-week-old female C57BL/6J wild-type mice (n=40), which were randomly assigned to sham (SHM), ovariectomy (OVX), ovariectomy with exercise (OVXE), ovariectomy with acetic acid (OVXA), or ovariectomy with exercise and acetic acid (OVXAE) groups. Gut microbial diversity and abundance were assessed using next-generation sequencing (NGS).RESULTS: Firmicutes were more abundant in the OVX group than in the SHM group. However, OVXA partially protected against the OVX-induced increase in Firmicutes (SHM, 50.6%; OVX, 57.2%; OVXE, 52.0%; OVXA, 50.6%; and OVXAE, 56.5%). In terms of microbial diversity, the acetic acid-supplemented groups (OVXA and OVXAE) showed greater microbial diversity than the SHM and OVX groups (p<.05). The phylogenetic cladogram analysis showed that the OVXA and OVXAE groups had lower levels of UCG009 and Akkermansia (p<.05) than the OVX group.CONCLUSIONS: Ovariectomy increased the relative abundance of Firmicutes. Acetic acid supplementation partially attenuated the increased proportion of Firmicutes in ovariectomized mice. Notably, this study found that acetic acid supplementation showed a significant beneficial effect on microbial diversity in ovariectomized mice, independent of exercise intervention. Future research should explore the potential role of UCG009 in protecting against menopause-related metabolic dysfunction.

Background: Estrogen deficiency following human menopause or rodent ovariectomy (OVX) induces adverse alterations in body composition and metabolic function. This study investigated the combined effects of acetic acid supplementation and voluntary exercise on metabolic health and skeletal muscle mitochondrial function using an OVX mouse model. Methods: Forty female C57BL/6J mice (8 weeks old) were randomly assigned to 5 groups: sham (SHM), ovariectomized control (OVX), OVX with exercise (OVX-E), OVX with acetic acid (OVX-A), and OVX with both interventions (OVX-AE). Following a 1-week recovery from OVX, a 13-week intervention was initiated: 5% sodium acetate-supplemented chow and/or voluntary wheel running. Body composition, glucose tolerance, total energy expenditure, skeletal muscle mitochondrial function, and the contents of AMPKα, PGC-1α, and carbonyl protein were assessed. Results: OVX impaired whole-body metabolism and skeletal muscle mitochondrial function, specifically in the gastrocnemius muscle. While the exercise alone failed to mitigate the OVX-induced mitochondrial dysfunction, the combined treatment of exercise and acetic acid supplementation significantly rescued from the OVX-induced mitochondrial dysfunction. Conclusions: OVX resulted in detrimental changes in whole-body metabolism, but voluntary exercise and/or acetic acid supplementation had no rescuing effects on those parameters. In gastrocnemius muscle, acetic acid supplementation during exercise enhanced mitochondrial function in OVX mice.