Exercise Alters Gut Microbiota Composition and Function in Lean and Obese Humans

Allen, John; Mailing, Lucy J.; Niemiro, Grace M.; Moore, Rachel; Cook, Marc D.; White, Bryan A.; Holscher, Hannah D.; Woods, Jeffrey A.

doi:10.1249/mss.0000000000001495

Cited by 574 publications

(648 citation statements)

References 42 publications

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“…Each participant provided written informed consent prior to participating in this study. This study was an additional analysis of some participants previously described (Allen et al . 2018).…”

Section: Methodsmentioning

confidence: 99%

Effects of endurance exercise training on inflammatory circulating progenitor cell content in lean and obese adults

Niemiro

Allen

Mailing

et al. 2018

The Journal of Physiology

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Circulating progenitor cells (CPCs) and subpopulations are normally found in the bone marrow, but can migrate to peripheral tissues to participate in local inflammation and/or remodelling. The purpose of this study was to compare the CPC response, particularly the inflammatory-primed haematopoietic stem and progenitor (HSPC) subpopulation, to a 6 week endurance exercise training (EET) intervention between lean and obese adults. Seventeen healthy weight (age: 23.9 ± 5.4 years, body mass index (BMI): 22.0 ± 2.6 kg m ) and 10 obese (age: 29.0 ± 8.0 years, BMI: 33.1 ± 6.0 kg m ) previously sedentary adults participated in an EET. Blood was collected before and after EET for quantification of CPCs and subpopulations via flow cytometry, colony forming unit assays and plasma concentrations of C-X-C motif chemokine 12 (CXCL12), granulocyte-colony stimulating factor (G-CSF), and chemokine (C-C motif) ligand 2 (CCL2). Exercise training reduced the number of circulating HSPCs and adipose tissue-derived mesenchymal stem cells (AT-MSCs). EET increased the colony forming potential of granulocytes and macrophages irrespective of BMI. EET reduced the number of HSPCs expressing the chemokine receptor CCR2 and the pro-inflammatory marker TLR4. EET-induced changes in adipose tissue-derived MSCs and bone marrow-derived MSCs were negatively related to changes in absolute fitness. Our results indicate that EET, regardless of BMI status, decreases CPCs and subpopulations, particularly those primed for contribution to tissue inflammation.

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Section: Methodsmentioning

confidence: 99%

Effects of endurance exercise training on inflammatory circulating progenitor cell content in lean and obese adults

Niemiro

Allen

Mailing

et al. 2018

The Journal of Physiology

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“…For example, HFD in mice altered the diversity of gut bacteria and caused a decrease and increase in some species of Ruminococcaceae and Rikenellaceae , respectively 21. Exercise training affects gut microbiota in a body mass index (BMI)-dependent manner, with Collinsella spp increased in the higher BMI group, Faecalibacterium spp decreased in higher BMI group but increased in the lower BMI group and Lachnospira spp increased in the lower BMI group 20. Bacterial genes outnumber human genes by approximately 100-fold 22.…”

Section: Gut Microbiomementioning

confidence: 99%

Small metabolites, possible big changes: a microbiota-centered view of non-alcoholic fatty liver disease

Chu

Duan

Yang

et al. 2018

Gut

271

209

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The spectrum of non-alcoholic fatty liver disease (NAFLD) ranges from simple hepatic steatosis, commonly associated with obesity, to non-alcoholic steatohepatitis, which can progress to fibrosis, cirrhosis and hepatocellular carcinoma. NAFLD pathophysiology involves environmental, genetic and metabolic factors, as well as changes in the intestinal microbiota and their products. Dysfunction of the intestinal barrier can contribute to NAFLD development and progression. Although there are technical limitations in assessing intestinal permeability in humans and the number of patients in these studies is rather small, fewer than half of the patients have increased intestinal permeability and translocation of bacterial products. Microbe-derived metabolites and the signalling pathways they affect might play more important roles in development of NAFLD. We review the microbial metabolites that contribute to the development of NAFLD, such as trimethylamine, bile acids, short-chain fatty acids and ethanol. We discuss the mechanisms by which metabolites produced by microbes might affect disease progression and/or serve as therapeutic targets or biomarkers for NAFLD.

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“…Emerging research indicates that exercise modulates the gut microbiota to influence cardiac function. Several studies suggest that exercise elevates the ratio of Firmicutes to Bacteroidetes (Petriz, et al , ; Lambert, et al , ) and increases the levels of the bacterial metabolite butyrate (Allen, et al , ). Alterations in the gut microbial structure induced by physical exercise are associated with the prevention of cardiac dysfunction in myocardial infarction mice (Liu, et al , ).…”

Section: Gut Microbiota Interventions For Cvdmentioning

confidence: 99%

The gut microbiota and its interactions with cardiovascular disease

Wang

Feng

et al. 2020

Microbial Biotechnology

128

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Summary The intestine is colonized by a considerable community of microorganisms that cohabits within the host and plays a critical role in maintaining host homeostasis. Recently, accumulating evidence has revealed that the gut microbial ecology plays a pivotal role in the occurrence and development of cardiovascular disease (CVD). Moreover, the effects of imbalances in microbe–host interactions on homeostasis can lead to the progression of CVD. Alterations in the composition of gut flora and disruptions in gut microbial metabolism are implicated in the pathogenesis of CVD. Furthermore, the gut microbiota functions like an endocrine organ that produces bioactive metabolites, including trimethylamine/trimethylamine N‐oxide, short‐chain fatty acids and bile acids, which are also involved in host health and disease via numerous pathways. Thus, the gut microbiota and its metabolic pathways have attracted growing attention as a therapeutic target for CVD treatment. The fundamental purpose of this review was to summarize recent studies that have illustrated the complex interactions between the gut microbiota, their metabolites and the development of common CVD, as well as the effects of gut dysbiosis on CVD risk factors. Moreover, we systematically discuss the normal physiology of gut microbiota and potential therapeutic strategies targeting gut microbiota to prevent and treat CVD.

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Exercise Alters Gut Microbiota Composition and Function in Lean and Obese Humans

Abstract: These findings suggest that exercise training induces compositional and functional changes in the human gut microbiota that are dependent on obesity status, independent of diet and contingent on the sustainment of exercise.

Cited by 574 publications

References 42 publications

Effects of endurance exercise training on inflammatory circulating progenitor cell content in lean and obese adults

Effects of endurance exercise training on inflammatory circulating progenitor cell content in lean and obese adults

Small metabolites, possible big changes: a microbiota-centered view of non-alcoholic fatty liver disease

The gut microbiota and its interactions with cardiovascular disease

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