Woods, Jeffrey A.

Introduction The gut microbiota is intricately connected with host health and is known to influence gene expression across multiple organ systems. Both animal and human longitudinal studies have demonstrated that exercise has independent effects on the composition and functionality of the gut microbiota. Previous studies performed by our group have also shown that transplant of an “exercised” microbiota into germ‐free mice confers enhanced protection against colitis compared to transplant of a “sedentary” microbiota. In this study, we assessed how an “exercised” microbiota transplant impacts global gene expression in gut, brain, and muscle tissue compared to a “sedentary” microbiota transplant. Methods Donor mice received access to a running wheel (n=10) or remained without access (n=9) for six weeks prior to euthanasia. Donor cecal contents were pooled by activity group and transplanted into two separate groups of recipient germ‐free mice (n=16 for each group). After five weeks of gut microbial colonization, recipient mice were sacrificed, and tissues were collected. Total RNA was isolated from the distal colon, soleus muscle, and hippocampus. Four representative mice were chosen from each group for whole transcriptome analysis (RNAseq) of these tissues. Anticipated Results We hypothesize that mice that received an “exercised” microbiome will have different global gene expression profiles than those that received a “sedentary” microbiome. We predict that genes related to immune function, cellular metabolism, and gut barrier function may be particularly affected by transplant of the “exercised” microbiome. Support or Funding Information This work supported by a grant from the Mayo Clinic‐University of Illinois Alliance for Technology‐based Healthcare. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

Introduction Heart rate variability (HRV), blood pressure variability (BPV) and baroreflex sensitivity (BRS), measures of autonomic nervous system function, are associated with cardiovascular (CV) outcome. African Americans (AA) have an increased prevalence of CV disorders in comparison to Caucasians (C). Purpose To determine race specific responses in BPV, BRS and HRV before and after maximal exercise. Methods 37 AA and 37 C (24 years) underwent maximal exercise on a cycle ergometer. BPV, BRS and HRV measurements were assessed using finger plethysmography before and after exercise. Data were log transformed and pre‐and post‐max test values were compared by race. Results Acute exercise significantly decreased BRS, LF‐HRV and HF‐HRV and significantly increased LF/HF‐HRV in both AA and C. With exercise, C significantly decreased measures of BRS and HRV more compared to AA; BRS‐SAPRRI transfer mean (C: 2.65±.54 to 1.09±.81 versus AA: 2.70±.40 to 1.70±.92), BRS‐down down (C: 3.21±.55 to 1.74±.49 versus AA: 3.28±1.0 to 2.2±.71), HRV‐LF (C: 6.39±.86 to 3.68±1.42 versus AA: 6.37±1.24 to 5.18±2.14) and HRV‐HF (C: 7.38±1.23 to 3.53±1.73 versus AA: 7.51±1.09 to 5.38±2.16). Conclusion C exhibited increased vagal withdrawal and greater reductions in BRS compared to AA in response to acute exercise. The impact of these racial differences in autonomic control on CV risk needs further investigation.

Many factors are involved in weight gain and metabolic disturbances associated with obesity. The gut microbiota has been of particular interest in recent years, since both human and animal studies have increased our understanding of the delicate symbiosis between the trillions of microbes that reside in the GI tract and the host. It has been suggested that disruption of this mutual tolerance may play a significant role in modulating host physiology during obesity. Environmental influences such as diet, exercise, and early life exposures can significantly impact the composition of the microbiota, and this dysbiosis can in turn lead to increased host adiposity via a number of different mechanisms. The ability of the microbiota to regulate host fat deposition, metabolism, and immune function makes it an attractive target for achieving sustained weight loss.

We have previously shown that voluntary wheel running (VWR) attenuates, whereas forced treadmill running (FTR) exacerbates, intestinal inflammation and clinical outcomes in a mouse model of colitis. As the gut microbiome is implicated in colitis, we hypothesized that VWR and FTR would differentially affect the gut microbiome. Mice (9-10/treatment) were randomly assigned to VWR, FTR, or sedentary home cage control (SED) for 6 wk. VWR were given running wheel access, whereas FTR ran on a treadmill for 40 min/day at 8–12 m/min, 5% grade. Forty-eight hours after the last exercise session, DNA was isolated from the fecal pellets and cecal contents, and the conserved bacterial 16S rRNA gene was amplified and sequenced using the Illumina Miseq platform. Permutational multivariate analysis of variance based on weighted UniFrac distance matrix revealed different bacterial clusters between feces and cecal contents in all groups ( P < 0.01). Interestingly, the community structures of the three treatment groups clustered separately from each other in both gut regions ( P < 0.05). Contrary to our hypothesis, the α-diversity metric, Chao1, indicated that VWR led to reduced bacterial richness compared with FTR or SED ( P < 0.05). Taxonomic evaluation revealed that both VWR and FTR altered many individual bacterial taxa. Of particular interest, Turicibacter spp., which has been strongly associated with immune function and bowel disease, was significantly lower in VWR vs. SED/FTR. These data indicate that VWR and FTR differentially alter the intestinal microbiome of mice. These effects were observed in both the feces and cecum despite vastly different community structures between each intestinal region.

New Findings What is the central question of this study? The aim of the study was to evaluate the effect of acute induced systemic inflammation on endothelial function, wave reflection and arterial function in older adults. What is the main finding and its importance? Acute inflammation induced by influenza vaccination did not affect endothelial function in older adults. These findings have never been shown in older adults, and they emphasize the importance of vascular function during systemic arterial inflammation. Acute inflammation reduces flow‐mediated vasodilatation and increases arterial stiffness in young healthy individuals. However, this response has not been studied in older adults. The aim of this study, therefore, was to evaluate the effect of acute induced systemic inflammation on endothelial function and wave reflection in older adults. Furthermore, an acute bout of moderate‐intensity aerobic exercise can be anti‐inflammatory. Taken together, we tested the hypothesis that acute moderate‐intensity endurance exercise, immediately preceding induced inflammation, would be protective against the negative effects of acute systemic inflammation on vascular function. Fifty‐nine healthy volunteers between 55 and 75 years of age were randomized to an exercise or a control group. Both groups received a vaccine (induced inflammation) and sham (saline) injection in a counterbalanced crossover design. Inflammatory markers, endothelial function (flow‐mediated vasodilatation) and measures of wave reflection and arterial stiffness were evaluated at baseline and at 24 and 48 h after injections. There were no significant differences in endothelial function and arterial stiffness between the exercise and control group after induced inflammation. The groups were then analysed together, and we found significant differences in the inflammatory markers 24 and 48 h after induction of acute inflammation compared with sham injection. However, flow‐mediated vasodilatation, augmentation index normalized for heart rate (AIx75) and β‐stiffness did not change significantly. Our results suggest that acute inflammation induced by influenza vaccination did not affect endothelial function in older adults.