Gut microbiota are differentially correlated with blood pressure status in African American collegiate athletes: A pilot study.

Hypertension (HTN) is common among athletes and the most recent epidemiologic data reports that cardiovascular (CV) sudden death is significantly greater in African Americans (AAs). Gut microbial dysbiosis (a poorly diverse stool microbial profile) has been associated with HTN in sedentary people but microbial characteristics of athletes with HTN are unknown. Our purpose was to differentiate microbiome characteristics associated with BP status in AA collegiate athletes. Thirty AA collegiate athletes were stratified by normal BP (systolic BP (SBP) ≤130 mmHg; n = 15) and HTN (SBP ≥130 mmHg; n = 15). 16S rRNA gene sequencing was performed on stool samples to identify microbes at the genus level. We did not observe any significant differences in alpha diversity, but beta diversity was different between groups. Principal coordinate analysis was significantly different (PERMANOVA, p < 0.05, R = 0.235) between groups. Spearman rank correlations showed a significant (p < 0.05) correlation between systolic BP and abundances for Adlercreutzia (R = 0.64), Coprococcus (R = 0.49), Granulicatella (R = 0.63), and Veillonella (R = 0.41). Gut microbial characteristics were associated with differentially abundant microbial genus' and BP status. These results will direct future studies to define the functions of these microbes associated with BP in athletes.

Salty Subjects: Unpacking Racial Differences in Salt-Sensitive Hypertension.

PURPOSE OF REVIEW: To review underlying mechanisms and environmental factors that may influence racial disparities in the development of salt-sensitive blood pressure. RECENT FINDINGS: Our group and others have observed racial differences in diet and hydration, which may influence salt sensitivity. Dietary salt elicits negative alterations to the gut microbiota and immune system, which may increase hypertension risk, but little is known regarding potential racial differences in these physiological responses. Antioxidant supplementation and exercise offset vascular dysfunction following dietary salt, including in Black adults. Furthermore, recent work proposes the role of racial differences in exposure to social determinants of health, and differences in health behaviors that may influence risk of salt sensitivity. Physiological and environmental factors contribute to the mechanisms that manifest in racial differences in salt-sensitive blood pressure. Using this information, additional work is needed to develop strategies that can attenuate racial disparities in salt-sensitive blood pressure.

Influence of Race and High Laminar Shear Stress on TNFR1 Signaling in Endothelial Cells.

Tumor necrosis factor (TNF) binding to endothelial TNF receptor-I (TNFR-I) facilitates monocyte recruitment and chronic inflammation, leading to the development of atherosclerosis. In vitro data show a heightened inflammatory response and atherogenic potential in endothelial cells (ECs) from African American (AA) donors. High laminar shear stress (HSS) can mitigate some aspects of racial differences in endothelial function at the cellular level. We examined possible racial differences in TNF-induced monocyte adhesion and TNFR1 signaling complex expression/activity, along with the effects of HSS. Tohoku Hospital Pediatrics-1 (THP-1) monocytes were used in a co-culture system with human umbilical vein ECs (HUVECs) from Caucasian American (CA) and AA donors to examine racial differences in monocyte adhesion. An in vitro exercise mimetic model was applied to investigate the potential modulatory effect of HSS. THP-1 adherence to ECs and TNF-induced nuclear factor kappa B (NF-κB) DNA binding were elevated in AA ECs compared to CA ECs, but not significantly. We report no significant racial differences in the expression of the TNFR-I signaling complex. Application of HSS significantly increased the expression and shedding of TNFR-I and the expression of TRAF3, and decreased the expression of TRAF5 in both groups. Our data does not support TNF-induced NF-κB activation as a potential mediator of racial disparity in this model. Other pathways and associated factors activated by the TNFR1 signaling complex are recommended targets for future research.

Race and sex differences in ROS production and SOD activity in HUVECs.

Black individuals and men are predisposed to an earlier onset and higher prevalence of hypertension, compared with White individuals and women, respectively. Therefore, the influence of race and sex on reactive oxygen species (ROS) production and superoxide dismutase (SOD) activity following induced inflammation was evaluated in female and male human umbilical vein endothelial cells (HUVECs) from Black and White individuals. It was hypothesized that HUVECs from Black individuals and male HUVECs would exhibit greater ROS production and impaired SOD activity. Inflammation was induced in HUVEC cell lines (n = 4/group) using tumor necrosis factor-alpha (TNF-α, 50ng/ml). There were no between group differences in ROS production or SOD activity in HUVECs from Black and White individuals, and HUVECs from Black individuals exhibited similar SOD activity at 24hr compared with 4hr of TNF-α treatment (p>0.05). However, HUVECs from White individuals exhibited significantly greater SOD Activity (p<0.05) at 24hr as compared to 4hr in the control condition but not with TNF-α treatment (p>0.05). Female HUVECs exhibited significantly lower ROS production than male HUVECs in the control condition and following TNF-α induced inflammation (p<0.05). Only female HUVECs exhibited significant increases in SOD activity with increased exposure time to TNF-α induced inflammation (p<0.05). HUVECs from White individuals alone exhibit blunted SOD activity when comparing control and TNF-α conditions. Further, compared to female HUVECs, male HUVECs exhibit a pro-inflammatory state.

The Effect of Race and Shear Stress on CRP-Induced Responses in Endothelial Cells.

BACKGROUND: C-reactive protein (CRP) is an independent biomarker of systemic inflammation and a predictor of future cardiovascular disease (CVD). More than just a pure bystander, CRP directly interacts with endothelial cells to decrease endothelial nitric oxide synthase (eNOS) expression and bioactivity, decrease nitric oxide (NO) production, and increase the release of vasoconstrictors and adhesion molecules. Race is significantly associated with CRP levels and CVD risks. With aerobic exercise, the vessel wall is exposed to chronic high laminar shear stress (HiLSS) that shifts the endothelium phenotype towards an anti-inflammatory, antioxidant, antiapoptotic, and antiproliferative environment. Thus, the purpose of this study was to assess the racial differences concerning the CRP-induced effects in endothelial cells and the potential role of HiLSS in mitigating these differences. METHODS: Human umbilical vein endothelial cells (HUVECs) from four African American (AA) and four Caucasian (CA) donors were cultured and incubated under the following conditions: (1) static control, (2) CRP (10 µg/mL, 24 hours), (3) CRP receptor (FcγRIIB) inhibitor followed by CRP stimulation, (4) HiLSS (20 dyne/cm2, 24 hours), and (5) HiLSS followed by CRP stimulation. RESULTS: AA HUVECs had significantly higher FcγRIIB receptor expression under both basal and CRP incubation conditions. Blocking FcγRIIB receptor significantly attenuated the CRP-induced decrements in eNOS expression only in AA HUVECs. Finally, HiLSS significantly counteracted CRP-induced effects. CONCLUSION: Understanding potential racial differences in endothelial function is important to improve CVD prevention. Our results shed light on FcγRIIB receptor as a potential contributor to racial differences in endothelial function in AA.

Exercise and the Microbiome: Mechanistic Perspectives of the Impact of Exercise on the Gut-Vascular Axis.

Given the participation of the microbiome in human health and disease, understanding the context of host-microbe interactions involved in vascular pathophysiology is now evolving through identifying microbial communities, specific taxa, and metabolic profiling which can be coupled to human health outcomes. Exercise has been used to define mechanisms related to improved vascular health, which may involve the microbiome. Motivated by the clinical significance that both exercise and the gut microbiome have; the objective of our work is to assist in defining the gut-vascular axis while identifying biomarkers of gut microbial health linked to vascular function. In this commentary, we will provide context to the mechanistic perspectives of exercise-induced improvements in gut microbial characteristics coupled to vascular health outcomes and offer insight on necessary future prospective investigations.

Comparative Analysis of Gut Microbiota Following Changes in Training Volume Among Swimmers.

Exercise can influence gut microbial community structure and diversity; however, the temporal dynamics of this association have rarely been explored. Here we characterized fecal microbiota in response to short term changes in training volume. Fecal samples, body composition, and training logs were collected from Division I NCAA collegiate swimmers during peak training through their in-season taper in 2016 (n=9) and 2017 (n=7), capturing a systematic reduction in training volume near the conclusion of their athletic season. Fecal microbiota were characterized using 16S rRNA V4 amplicon sequencing and multivariate statistical analysis, Spearman rank correlations, and random forest models. Peak training volume, measured as swimming distance, decreased significantly during the study period from 32.6±4.8 km/wk to 11.3±8.1 km/wk (ANOVA, p<0.05); however, body composition showed no significant changes. Coinciding with the decrease in training volume, the microbial community structure showed a significant decrease in overall microbial diversity, a decrease in microbial community structural similarity, and a decrease in the proportion of the bacterial genera Faecalibacterium and Coprococcus. Together these data demonstrate a significant association between short-term changes in training volume and microbial composition and structure in the gut; future research will establish whether these changes are associated with energy balance or nutrient intake.

Ultra-endurance triathlon performance and markers of whole-body and gut-specific inflammation.

PURPOSE: To examine the influence of the Ultraman Florida triathlon (3 days of non-continuous racing; stage 1: 10 km swim and 144.8 km cycle; stage 2: 275.4 km cycle; stage 3: 84.4 km run) on circulating plasma concentrations of whole-body (C-reactive protein (CRP), interleukin (IL)-6 (IL-6), and IL-10 and surrogate gut-specific inflammatory markers (IL-17 and IL-23), and determine whether these variables are associated with performance. METHODS: Eighteen triathletes (N = 18; 15 men, 3 women; age: 37 ± 8 yrs) were evaluated at baseline and post-race for circulating concentrations of CRP, IL-6, IL-10, IL-17, and IL-23. Blood samples were drawn two days prior to stage 1 (1600 h) and one day after stage 3 (1200 h). RESULTS: Plasma CRP significantly increased from baseline (1985.8 ± 5962.3 ng/mL) to post-race (27,013.9 ± 12,888.8 ng/mL, p < 0.001, 13-fold increase). Both plasma IL-6 and IL-10 did not significantly change from baseline to post-race. Baseline and post-race concentrations of IL-17 and IL-23 were below detectable limits. Pearson's correlation between mean finish time and post-race IL-10 revealed a significant positive correlation (r = 0.54, p < 0.05). CONCLUSIONS: Our results suggest that cytokines such as IL-6 and IL-10 involved in the inflammatory response return to near-baseline concentrations rapidly even after ultra-endurance events of extreme duration. The absence of IL-17 and IL-23 may suggest positive gut adaptations from ultra-endurance training. A significant positive correlation between post-race IL-10 concentrations and mean finish time may indicate that a relationship between anti-inflammatory responses and performance exists.

Making cell culture more physiological: a call for a more comprehensive assessment of racial disparities in endothelial cell culture studies.

In the United States, cardiovascular diseases (CVDs) are the leading cause of death and disproportionately affect ethnic and racial minority populations. Black individuals are more likely to develop advanced CVD and microvascular complications resulting in end-organ damage. Endothelial cell dysfunction leads to microvascular and macrovascular dysfunction and is predictive of the development of CVD. Black versus white racial disparities in in vivo and in vitro studies of endothelial cell function are well documented. However, race-related disparities in maternal environment and lifestyle may be a major unconsidered factor in racial differences in endothelial cell culture studies. Further, rates of hypertensive disorders of pregnancy are higher in black versus white women. These pregnancy complications may result in placental dysfunction, including excess production of inflammatory and antiangiogenic molecules that impair endothelial function. Therefore, studies that include other ethnic and racial minorities are needed, in addition to a more thorough characterization of endothelial cell donors and targeted cell culture studies (e.g., genotyping) to generate information that can be translated into effective preventive or treatment strategies for ethnic/racial disparities in CVD.

Firefighting Induces Acute Inflammatory Responses that are not Relieved by Aspirin in Older Firefighters.

OBJECTIVE: Sudden cardiac events account for 40% to 50% of firefighter line-of-duty deaths. Inflammatory proteins are strong biomarkers of cardiovascular inflammation. The present study investigated the effects of aspirin supplementation on inflammatory biomarkers following firefighting. METHODS: Using a randomized, placebo-controlled, double-blind crossover design, 24 male firefighters (48.2 ±â€Š5.9 years) were allocated into four conditions: acute (81 mg; single-dose) aspirin and placebo supplementation, and chronic (81 mg; 14 days) aspirin and placebo supplementation. Inflammatory proteins [interleukin (IL)-6, C-reactive protein (CRP), intracellular adhesion molecule (ICAM)-1, P-selectin, matrix metalloproteinase-9 (MMP-9)] and antioxidant potential [total antioxidant capacity (TAC)] were measured pre- and post-structural firefighting drills. RESULTS: Firefighting activities significantly increased IL-6, MMP-9, and P-Selectin; however, no changes in TAC and ICAM-1 were detected. Neither acute nor chronic aspirin supplementation attenuated this inflammatory response. CONCLUSION: Firefighting significantly increases inflammatory biomarkers and neither acute nor chronic low-dose aspirin mitigates this response.

Effect of acute maximal exercise on vasodilatory function and arterial stiffness in African-American and white adults.

INTRODUCTION: African-Americans are at increased risk of cardiovascular disease compared with their white counterparts, potentially due to greater arterial stiffness and reduced vasodilatory capacity. Racial differences also exist in arterial stiffness and blood pressure (BP) following maximal aerobic exercise; African-Americans do not exhibit central post exercise BP reductions. Whether impaired vasodilatory function contributes to the lack of BP response is unknown. PURPOSE: To evaluate vasodilatory function, arterial stiffness, and hemodynamics following a maximal aerobic exercise test in young, healthy African-American and white adults. METHODS: Twenty-seven African-American and 35 white adults completed measures at baseline, 15 and 30 min after a maximal exercise test. Measures included vasodilatory capacity of forearm resistance arteries, central pulse wave velocity (PWV), and carotid artery stiffness (ß). RESULTS: Forearm reactive hyperemia was greater in white but increased similarly following exercise in both groups (P < 0.05). Carotid ß-stiffness increased at 15 and 30 min (P = 0.03) in both groups, but PWV controlled for mean arterial pressure decreased after maximal exercise (P = 0.03). White exhibited reductions in systolic and mean pressure, whereas no changes were seen for African-Americans (interaction effects: P < 0.05). CONCLUSION: African-American and white adults had similar decreases in PWV, increases in ß-stiffness, and increases in vasodilatory function following maximal exercise. African-American adults, however, did not display reductions in BP and had overall lower vasodilatory function in comparison with white adults. Our results suggest African-Americans exhibit similar vasodilatory function changes following aerobic exercise as their white counterparts, and therefore vasodilatory function likely does not explain the lack of BP response in African-Americans.

The Effects of Exercise, Aspirin, and Celecoxib in an Atherogenic Environment.

INTRODUCTION: Optimal vascular function is a hallmark of cardiovascular health. Specifically, the balance of vasoconstricting and vasodilating substances is recognized as a marker of vascular health. One of the greatest challenges to vascular health and vasodilatory balance is tumor necrosis factor alpha (TNFα)-mediated inflammation. Uncovering effective strategies that maintain a vascular environment that is more vasodilatory and antithrombotic in the face of an inflammatory challenge is favorable. PURPOSE: To test the ability of various antithrombotic and provasodilatory treatments, as well as combinations thereof, to prevent unfavorable changes in markers of endothelial dysfunction in human umbilical vein endothelial cells when presented with an inflammatory challenge. METHODS: Human umbilical vein endothelial cells were pretreated with exercise-like levels of laminar shear stress (LSS), aspirin, celecoxib, and their combination before a TNFα challenge. Western blot analysis as well as colorimetric assays were used to determine levels of endothelial nitric oxide synthase (eNOS) and prostacyclin (6-keto PGF1α)/thromboxane (TXB2) metabolite ratio, respectively. RESULTS: Neither aspirin nor celecoxib were effective in preventing TNFα-induced reduction in eNOS. Further, aspirin was unable to maintain baseline levels of prostacyclin/thromboxane ratio in the face of the inflammatory challenge. Laminar shear stress, aspirin/LSS combination, and celecoxib/LSS combination were all able to prevent TNFα-induced alterations in eNOS levels and prostacyclin/thromboxane ratio. CONCLUSIONS: Effective strategies to maintain a healthy endothelium, and therefore resistance vessel health, need to include exercise-levels of shear stress to be effective.

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

PURPOSE: Exercise is associated with altered gut microbial composition, but studies have not investigated whether the gut microbiota and associated metabolites are modulated by exercise training in humans. We explored the impact of 6 wk of endurance exercise on the composition, functional capacity, and metabolic output of the gut microbiota in lean and obese adults with multiple-day dietary controls before outcome variable collection. METHODS: Thirty-two lean (n = 18 [9 female]) and obese (n = 14 [11 female]), previously sedentary subjects participated in 6 wk of supervised, endurance-based exercise training (3 d·wk) that progressed from 30 to 60 min·d and from moderate (60% of HR reserve) to vigorous intensity (75% HR reserve). Subsequently, participants returned to a sedentary lifestyle activity for a 6-wk washout period. Fecal samples were collected before and after 6 wk of exercise, as well as after the sedentary washout period, with 3-d dietary controls in place before each collection. RESULTS: ß-diversity analysis revealed that exercise-induced alterations of the gut microbiota were dependent on obesity status. Exercise increased fecal concentrations of short-chain fatty acids in lean, but not obese, participants. Exercise-induced shifts in metabolic output of the microbiota paralleled changes in bacterial genes and taxa capable of short-chain fatty acid production. Lastly, exercise-induced changes in the microbiota were largely reversed once exercise training ceased. CONCLUSION: 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.

Short-term regular aerobic exercise reduces oxidative stress produced by acute in the adipose microvasculature.

High blood pressure has been shown to elicit impaired dilation in the vasculature. The purpose of this investigation was to elucidate the mechanisms through which high pressure may elicit vascular dysfunction and determine the mechanisms through which regular aerobic exercise protects arteries against high pressure. Male C57BL/6J mice were subjected to 2 wk of voluntary running (~6 km/day) for comparison with sedentary controls. Hindlimb adipose resistance arteries were dissected from mice for measurements of flow-induced dilation (FID; with or without high intraluminal pressure exposure) or protein expression of NADPH oxidase II (NOX II) and superoxide dismutase (SOD). Microvascular endothelial cells were subjected to high physiological laminar shear stress (20 dyn/cm2) or static condition and treated with ANG II + pharmacological inhibitors. Cells were analyzed for the detection of ROS or collected for Western blot determination of NOX II and SOD. Resistance arteries from exercised mice demonstrated preserved FID after high pressure exposure, whereas FID was impaired in control mouse arteries. Inhibition of ANG II or NOX II restored impaired FID in control mouse arteries. High pressure increased superoxide levels in control mouse arteries but not in exercise mouse arteries, which exhibited greater ability to convert superoxide to H2O2 Arteries from exercised mice exhibited less NOX II protein expression, more SOD isoform expression, and less sensitivity to ANG II. Endothelial cells subjected to laminar shear stress exhibited less NOX II subunit expression. In conclusion, aerobic exercise prevents high pressure-induced vascular dysfunction through an improved redox environment in the adipose microvasculature.NEW & NOTEWORTHY We describe potential mechanisms contributing to aerobic exercise-conferred protection against high intravascular pressure. Subcutaneous adipose microvessels from exercise mice express less NADPH oxidase (NOX) II and more superoxide dismutase (SOD) and demonstrate less sensitivity to ANG II. In microvascular endothelial cells, shear stress reduced NOX II but did not influence SOD expression.

Effect of acute aerobic exercise and histamine receptor blockade on arterial stiffness in African Americans and Caucasians.

African Americans (AA) exhibit exaggerated central blood pressure (BP) and arterial stiffness measured by pulse wave velocity (PWV) in response to an acute bout of maximal exercise compared with Caucasians (CA). However, whether potential racial differences exist in central BP, elastic, or muscular arterial distensibility after submaximal aerobic exercise remains unknown. Histamine receptor activation mediates sustained postexercise hyperemia in CA but the effect on arterial stiffness is unknown. This study sought to determine the effects of an acute bout of aerobic exercise on central BP and arterial stiffness and the role of histamine receptors, in AA and CA. Forty-nine (22 AA, 27 CA) young and healthy subjects completed the study. Subjects were randomly assigned to take either histamine receptor antagonist or control placebo. Central blood BP and arterial stiffness measurements were obtained at baseline, and at 30, 60, and 90 min after 45 min of moderate treadmill exercise. AA exhibited greater central diastolic BP, elevated brachial PWV, and local carotid arterial stiffness after an acute bout of submaximal exercise compared with CA, which may contribute to their higher risk of cardiovascular disease. Unexpectedly, histamine receptor blockade did not affect central BP or PWV in AA or CA after exercise, but it may play a role in mediating local carotid arterial stiffness. Furthermore, histamine may mediate postexercise carotid arterial dilation in CA but not in AA. These observations provide evidence that young and healthy AA exhibit an exaggerated hemodynamic response to exercise and attenuated vasodilator response compared with CA.NEW & NOTEWORTHY African Americans are at greater risk for developing cardiovascular disease than Caucasians. We are the first to show that young and healthy African Americans exhibit greater central blood pressure, elevated brachial stiffness, and local carotid arterial stiffness following an acute bout of submaximal exercise compared with Caucasians, which may contribute to their higher risk of cardiovascular disease. Furthermore, African Americans exhibit attenuated vasodilator response compared with Caucasians.

Aging, not age-associated inflammation, determines blood pressure and endothelial responses to acute inflammation.

BACKGROUND: Aging is characterized by a state of chronic, low-grade inflammation that impairs vascular function. Acute inflammation causes additional decrements in vascular function, but these responses are not uniform in older compared with younger adults. We sought to determine if older adults with low levels of baseline inflammation respond to acute inflammation in a manner similar to younger adults. We hypothesized age-related differences in the vascular responses to acute inflammation, but that older adults with low baseline inflammation would respond similarly to younger adults. METHOD: Inflammation was induced with an influenza vaccine in 96 participants [older = 67 total, 38 with baseline C-reactive protein (CRP) > 1.5 mg/l and 29 with CRP < 1.5 mg/l; younger = 29]; serum inflammatory markers IL-6 and CRP, blood pressure and flow-mediated dilation (FMD) were measured 24 and 48 h later. RESULTS: Younger adults increased IL-6 and CRP more than the collective older adult group and increased pulse pressure, whereas older adults decreased SBP and reduced pulse pressure. The entire cohort decreased FMD from 11.3 ±â€Š0.8 to 8.3 ±â€Š0.7 to 8.7 ±â€Š0.7% in younger and from 5.8 ±â€Š0.3 to 5.0 ±â€Š0.4 to 4.7 ±â€Š0.4% in older adults, P less than 0.05 for main effect. Older adult groups with differing baseline CRP had the same IL-6, blood pressure, and FMD response to acute inflammation, P less than 0.05 for all interactions, but the low-CRP group increased CRP at 24 and 48 h (from 0.5 ±â€Š0.1 to 1.4 ±â€Š0.2 to 1.7 ±â€Š0.3 mg/l), whereas the high-CRP group did not (from 4.8 ±â€Š0.5 to 5.4 ±â€Š0.5 to 5.4 ±â€Š0.6 mg/l), P less than 0.001 for interaction. CONCLUSION: Aging, not age-related chronic, low-grade inflammation, determines the vascular responses to acute inflammation.

Differential Post-Exercise Blood Pressure Responses between Blacks and Caucasians.

Post-exercise hypotension (PEH) is widely observed in Caucasians (CA) and is associated with histamine receptors 1- and 2- (H1R and H2R) mediated post-exercise vasodilation. However, it appears that blacks (BL) may not exhibit PEH following aerobic exercise. Hence, this study sought to determine the extent to which BL develop PEH, and the contribution of histamine receptors to PEH (or lack thereof) in this population. Forty-nine (22 BL, 27 CA) young and healthy subjects completed the study. Subjects were randomly assigned to take either a combined H1R and H2R antagonist (fexofenadine and ranitidine) or a control placebo. Supine blood pressure (BP), cardiac output and peripheral vascular resistance measurements were obtained at baseline, as well as at 30 min, 60 min and 90 min after 45 min of treadmill exercise at 70% heart rate reserve. Exercise increased diastolic BP in young BL but not in CA. Post-exercise diastolic BP was also elevated in BL after exercise with histamine receptor blockade. Moreover, H1R and H2R blockade elicited differential responses in stroke volume between BL and CA at rest, and the difference remained following exercise. Our findings show differential BP responses following exercise in BL and CA, and a potential role of histamine receptors in mediating basal and post-exercise stroke volume in BL. The heightened BP and vascular responses to exercise stimulus is consistent with the greater CVD risk in BL.

Exercise and gut immune function: evidence of alterations in colon immune cell homeostasis and microbiome characteristics with exercise training.

There is robust evidence that habitual physical activity is anti-inflammatory and protective against developing chronic inflammatory disease. Much less is known about the effects of habitual moderate exercise in the gut, the compartment that has the greatest immunological responsibility and interactions with the intestinal microbiota. The link between the two has become evident, as recent studies have linked intestinal dysbiosis, or the disproportionate balance of beneficial to pathogenic microbes, with increased inflammatory disease susceptibility. Limited animal and human research findings imply that exercise may have a beneficial role in preventing and ameliorating such diseases by having an effect on gut immune function and, recently, microbiome characteristics. Emerging data from our laboratory show that different forms of exercise training differentially impact the severity of intestinal inflammation during an inflammatory insult (for example, ulcerative colitis) and may be jointly related to gut immune cell homeostasis and microbiota-immune interactions. The evidence we review and present will provide data in support of rigorous investigations concerning the effects of habitual exercise on gut health and disease.

Aerobic Exercise Training and Arterial Changes in African Americans versus Caucasians.

UNLABELLED: African Americans (AA) have increased carotid artery intima-media thickness and decreased vascular function compared with their Caucasian (CA) peers. Aerobic exercise prevents and potentially reverses arterial dysfunction. PURPOSE: The purpose of this study was to examine the effect of 8 wk of moderate- to high-intensity aerobic training in young healthy sedentary AA and CA men and women. METHODS: Sixty-four healthy volunteers (men, 28; women, 36) with mean age 24 yr underwent measures of arterial structure, function, and blood pressure (BP) variables at baseline, after the 4-wk control period, and 8 wk after training. RESULTS: There was a significant increase in VO2peak among both groups after exercise training. Brachial systolic BP decreased significantly after the control period in both groups but not after exercise training. Carotid pulse pressure decreased significantly in both groups after exercise training as compared with that in baseline. There was no change in any of the other BP variables. AA had higher intima-media thickness at baseline and after the control period but it significantly decreased after exercise training compared with that of CA. AA had significantly lower baseline forearm blood flow and reactive hyperemia compared with those of CA, but exercise training had no effect on these variables. There was no significant difference in arterial stiffness (central pulse wave velocity) and wave-reflection (augmentation index) between the two groups at any time point. CONCLUSIONS: This is the first study to show that 8 wk of aerobic exercise training causes significant improvement in the arterial structure in young, healthy AA, making it comparable with the CA and with minimal effects on BP variables.

Sex differences in autonomic function following maximal exercise.

BACKGROUND: Heart rate variability (HRV), blood pressure variability, (BPV) and heart rate recovery (HRR) are measures that provide insight regarding autonomic function. Maximal exercise can affect autonomic function, and it is unknown if there are sex differences in autonomic recovery following exercise. Therefore, the purpose of this study was to determine sex differences in several measures of autonomic function and the response following maximal exercise. METHODS: Seventy-one (31 males and 40 females) healthy, nonsmoking, sedentary normotensive subjects between the ages of 18 and 35 underwent measurements of HRV and BPV at rest and following a maximal exercise bout. HRR was measured at minute one and two following maximal exercise. RESULTS: Males have significantly greater HRR following maximal exercise at both minute one and two; however, the significance between sexes was eliminated when controlling for VO2 peak. Males had significantly higher resting BPV-low-frequency (LF) values compared to females and did not significantly change following exercise, whereas females had significantly increased BPV-LF values following acute maximal exercise. Although males and females exhibited a significant decrease in both HRV-LF and HRV-high frequency (HF) with exercise, females had significantly higher HRV-HF values following exercise. Males had a significantly higher HRV-LF/HF ratio at rest; however, both males and females significantly increased their HRV-LF/HF ratio following exercise. CONCLUSIONS: Pre-menopausal females exhibit a cardioprotective autonomic profile compared to age-matched males due to lower resting sympathetic activity and faster vagal reactivation following maximal exercise. Acute maximal exercise is a sufficient autonomic stressor to demonstrate sex differences in the critical post-exercise recovery period.