BackgroundReduced microbial diversity in human intestines has been implicated in various conditions such as diabetes, colorectal cancer, and inflammatory bowel disease. The role of physical fitness in the context of human intestinal microbiota is currently not known. We used high-throughput sequencing to analyze fecal microbiota of 39 healthy participants with similar age, BMI, and diets but with varying cardiorespiratory fitness levels. Fecal short-chain fatty acids were analyzed using gas chromatography.ResultsWe showed that peak oxygen uptake (VO2peak), the gold standard measure of cardiorespiratory fitness, can account for more than 20 % of the variation in taxonomic richness, after accounting for all other factors, including diet. While VO2peak did not explain variation in beta diversity, it did play a significant role in explaining variation in the microbiomes’ predicted metagenomic functions, aligning positively with genes related to bacterial chemotaxis, motility, and fatty acid biosynthesis. These predicted functions were supported by measured increases in production of fecal butyrate, a short-chain fatty acid associated with improved gut health, amongst physically fit participants. We also identified increased abundances of key butyrate-producing taxa (Clostridiales, Roseburia, Lachnospiraceae, and Erysipelotrichaceae) amongst these individuals, which likely contributed to the observed increases in butyrate levels.ConclusionsResults from this study show that cardiorespiratory fitness is correlated with increased microbial diversity in healthy humans and that the associated changes are anchored around a set of functional cores rather than specific taxa. The microbial profiles of fit individuals favor the production of butyrate. As increased microbiota diversity and butyrate production is associated with overall host health, our findings warrant the use of exercise prescription as an adjuvant therapy in combating dysbiosis-associated diseases.Electronic supplementary materialThe online version of this article (doi:10.1186/s40168-016-0189-7) contains supplementary material, which is available to authorized users.

Cerebral blood flow (CBF) increases from rest to ∼60% of peak oxygen uptake (VO 2peak ) and thereafter decreases towards baseline due to hyperventilation-induced hypocapnia and subsequent cerebral vasoconstriction. It is unknown what happens to CBF in older adults (OA), who experience a decline in CBF at rest coupled with a blunted ventilatory response during VO 2peak . In 14 OA (71±10 year) and 21 young controls (YA; 23±4 years), we hypothesized that OA would experience less hyperventilationinduced cerebral vasoconstriction and therefore an attenuated reduction in CBF at VO 2peak . Incremental exercise was performed on a cycle ergometer, whilst bilateral middle cerebral artery blood flow velocity (MCA V mean ; transcranial Doppler ultrasound), heart rate (HR; ECG) and end-tidal PCO 2 (P ET CO 2 ) were monitored continuously. Blood pressure (BP) was monitored intermittently. From rest to 50% of VO 2peak , despite greater elevations in BP in OA, the change in MCA V mean was greater in YA compared to OA (28% vs. 15%, respectively; P<0.0005). In the YA, at intensities >70% of VO 2peak , the hyperventilationinduced declines in both P ET CO 2 (14 mmHg (YA) vs. 4 mmHg (OA); P<0.05) and MCA V mean (−21% (YA) vs. −7% (OA); P<0.0005) were greater in YA compared to OA. Our findings show (1), from rest-tomild intensity exercise (50% VO 2peak ), elevations in CBF are reduced in OA and (2) age-related declines in hyperventilation during maximal exercise result in less hypocapnic-induced cerebral vasoconstriction.

Despite marked changes in perfusion pressure with HUT or HDT, our findings indicate that cerebral perfusion is well maintained during acute severe changes in posture.

Abstract-Heart transplant recipients are at an increased risk for cerebral hemorrhage and ischemic stroke; yet, the exact mechanism for this derangement remains unclear. We hypothesized that alterations in cerebrovascular regulation is principally involved. To test this hypothesis, we studied cerebral pressure-flow dynamics in 8 clinically stable male heart transplant recipients (62±8 years of age and 9±7 years post transplant, mean±SD), 9 male age-matched controls (63±8 years), and 10 male donor controls (27±5 years). To increase blood pressure variability and improve assessment of the pressure-flow dynamics, subjects performed squat-stand maneuvers at 0.05 and 0.10 Hz. Beat-to-beat blood pressure, middle cerebral artery velocity, and end-tidal carbon dioxide were continuously measured during 5 minutes of seated rest and throughout the squat-stand maneuvers. Cardiac baroreceptor sensitivity gain and cerebral pressure-flow responses were assessed with linear transfer function analysis. Heart transplant recipients had reductions in R-R interval power and baroreceptor sensitivity low frequency gain (P<0.01) compared with both control groups; however, these changes were unrelated to transfer function metrics. Thus, in contrast to our hypothesis, the increased risk of cerebrovascular complication after heart transplantation does not seem to be related to alterations in cerebral pressure-flow dynamics. Future research is, therefore, warranted. (Hypertension. 2014;64:1314-1320.)

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Long‐term heart transplant recipients (HTR) provide a unique opportunity to examine the relationship between the cerebrovascular and cardiovascular systems. We examined the hypothesis that HTR would have cerebral pressure‐flow responses more comparable to control subjects matched to the age of their cerebrovasculature than their donor hearts. Eight male clinically stable HTR (62 ± 8 yrs of age and 9 ± 7 yrs post transplant), 9 male age‐matched controls (AM: 63 ± 8 yrs) and 10 male donor controls (DC: 27 ± 5 yrs), were tested. Each test involved: seated rest (5‐min), and squat‐stand maneuvers at 0.05 and 0.10 Hz. The BRS and pressure‐flow responses were assessed with TFA. BRS TFA revealed that the HTR had reductions in R‐R interval PSD and LF gain (P<0.01) compared to both control groups. There were comparable TFA cerebral pressure‐flow responses for all groups at all frequencies with coherence and phase. The pressure‐flow gain was significantly greater in DC than both AM and HTR at all frequencies (P<0.05). Cerebrovascular resistance (CVR) was negatively correlated with pressure‐flow gain at all frequencies (P<0.05). These results reveal that pressure‐flow coherence and phase are comparable throughout aging, potentially helping HTR compensate for reductions in BRS. Although pressure‐flow gain did decrease in the HTR and AM, it was related to changes in CVR highlighting the need cautiously interpret this metric. Grant Funding Source: Supported by NSERC

Introduction: Atrial fibrillation (AF), a well-defined ischemic stroke (IS) risk factor whose prevalence increases with age, is associated with higher stroke severity. We aimed to evaluate stroke severity and hospital mortality in a nationally representative sample of AF-related IS patients. Methods: We utilized data from the National (Nationwide) Inpatient Sample databases from 2015 - 2018 using ICD-10 diagnostic codes to identify individuals with IS and comorbid AF. The NIHSS was used to characterize stroke severity in a subset of cases after 10/1/2016. Nonparametric statistics and logistic regression analyses were conducted to evaluate associations between AF and hospital death. Results: Of the 382,758 IS cases, 99,566 (26%) had comorbid AF. AF increased linearly with age, reaching at 47% of all hospitalized IS patients 85+ years of age or older (Figure). Higher age, male sex, white race, obesity, and higher median income were associated with comorbid AF, whereas diabetes, hypertension, tobacco use, and hyperlipidemia were associated with reduced odds of comorbid AF. While 5.8% of all IS patients died during hospitalization, mortality was increased nearly two-fold in those with AF (9.0% vs. 4.6%, p<.001). Among in-hospital deaths from IS, comorbid AF increased with age, present in 59% of those 85+ years of age or older (Figure). NIHSS, reported in 21% of patients, was higher in AF patients (mean NIHSS 6 vs. 9, p<.001). High NIHSS was the strongest independent predictor of hospital death. Conclusion: The burden of AF in a nationally representative sample of hospitalized IS patients is substantial, present in nearly 50% of the 85+ age group. AF-related IS is more severe and more likely to be fatal. As our population ages, the prevalence of AF will only increase. Understanding the severity and fatality of AF-related IS will have profound implications for health systems and may better facilitate anticipatory guidance and AF treatment.