Plain language summary
The gut microbiome differs between healthy people and those with metabolic diseases, including metabolic syndrome and type 2 diabetes (T2D) and it is suggested that this association is mediated by endotoxemia, the release of toxins, in particular lipopolysaccharides (LPS), from the gut bacteria. The aim of this study was to investigate the effects of exercise on gut microbiota composition and metabolic endotoxemia in people with prediabetes and T2D. 26 sedentary participants with either prediabetes or T2D took part in either a sprint interval training (SIT) or moderate-intensity continuous training (MICT) three times per week for two weeks. Both training types induced fat loss and improved the gut microbiota, HbA1C (a marker for whole body insulin sensitivity) as well as some markers of systemic and intestinal inflammation, although there were differences in the way the two types of exercise altered the gut bacterial composition. Only SIT improved aerobic capacity. The authors concluded that exercise training improves the gut microbiota and reduces endotoxemia.
INTRODUCTION Intestinal metabolism and microbiota profiles are impaired in obesity and insulin resistance. Moreover, dysbiotic gut microbiota has been suggested to promote systemic low-grade inflammation and insulin resistance through the release of endotoxins particularly lipopolysaccharides. We have previously shown that exercise training improves intestinal metabolism in healthy men. To understand whether changes in intestinal metabolism interact with gut microbiota and its release of inflammatory markers, we studied the effects of sprint interval (SIT) and moderate-intensity continuous training (MICT) on intestinal metabolism and microbiota in subjects with insulin resistance. METHODS Twenty-six, sedentary subjects (prediabetic, n = 9; type 2 diabetes, n = 17; age, 49 [SD, 4] yr; body mass index, 30.5 [SD, 3]) were randomized into SIT or MICT. Intestinal insulin-stimulated glucose uptake (GU) and fatty acid uptake (FAU) from circulation were measured using positron emission tomography. Gut microbiota composition was analyzed by 16S rRNA gene sequencing and serum inflammatory markers with multiplex assays and enzyme-linked immunoassay kit. RESULTS V˙O2peak improved only after SIT (P = 0.01). Both training modes reduced systematic and intestinal inflammatory markers (tumor necrosis factor-α, lipopolysaccharide binding protein) (time P < 0.05). Training modified microbiota profile by increasing Bacteroidetes phylum (time P = 0.03) and decreasing Firmicutes/Bacteroidetes ratio (time P = 0.04). Moreover, there was a decrease in Clostridium genus (time P = 0.04) and Blautia (time P = 0.051). Only MICT decreased jejunal FAU (P = 0.02). Training had no significant effect on intestinal GU. Colonic GU associated positively with Bacteroidetes and inversely with Firmicutes phylum, ratio Firmicutes/Bacteroidetes and Blautia genus. CONCLUSIONS Intestinal substrate uptake associates with gut microbiota composition and whole-body insulin sensitivity. Exercise training improves gut microbiota profiles and reduces endotoxemia.