Midlife health crisis of former competitive athletes: dissecting their experiences via qualitative study.

Sports participation confers many health benefits yet greatly increases injury risk. Long-term health outcomes in former athletes and transition to life after competitive sports are understudied. Ending a sport may pose physical and psychosocial challenges. The purpose was to determine the lived experiences of former competitive athletes and how their sports participation impacted their long-term health and well-being. Former college varsity athletes participated in semistructured interviews focusing on their experiences, including past and current health, the impact of injuries, activity, exercise, diet and transition to life after competitive sport. Thematic analysis was completed using a collaborative, iterative process. Thirty-one (16 female, 15 male) former college athletes aged 51.3±7.4 years were interviewed. Six themes emerged: (1) lifelong athlete identity; (2) structure, support and challenges of the college athlete experience; (3) a big transition to life beyond competitive sport; (4) impact of competitive sport on long-term health; (5) facilitators and barriers to long-term health after sport and (6) transferable life skills. Continuing sports eased the transition for many but often delayed their postathlete void. Challenges included managing pain and prior injury (eg, If I didn't have my knee injury, I would definitely be more active), reducing energy needs and intake (eg, When I was an athlete, I could eat anything; and unfortunately, that's carried into my regular life), lack of accountability, changed identity and lost resources and social support. Participants suggested a programme, toolkit, mentoring or exit course to facilitate the transition. While former athletes benefit from transferrable life skills and often continue sports and exercise, they face unique challenges such as managing pain and prior injury, staying active, reducing energy intake and changing identity. Future research should develop and evaluate a toolkit, programme and other resources to facilitate life after ending competitive sports under 'normal' conditions (eg, retirement) and after a career-ending injury.

Medical nutrition therapy provided by a dietitian improves outcomes in adults with prehypertension or hypertension: a systematic review and meta-analysis.

BACKGROUND: Hypertension is an important risk factor for cardiovascular disease (CVD). Interventions with dietitians can help modify dietary intake and reduce hypertension risk. OBJECTIVES: We aimed to examine the following research question: In adults with prehypertension or hypertension, what is the effect of medical nutrition therapy (MNT) provided by a dietitian on blood pressure (BP), CVD risk and events, and anthropometrics compared with standard care or no intervention? METHODS: MEDLINE, CINAHL, and Cochrane Central databases were searched for randomized controlled trials (RCTs) published in peer-reviewed journals from 1985-2022. Risk of bias was assessed using version 2 of the Cochrane tool for RCTs. Meta-analyses were conducted using the DerSimonian-Laird random-effects model. Certainty of evidence (COE) was assessed for each outcome using the Grading of Recommendations, Assessment and Evaluation method. RESULTS: Forty articles representing 31 RCTs were included and analyzed. MNT provided by a dietitian may reduce systolic [mean difference (MD): -3.63 mmHg; 95% confidence interval (CI): -4.35, -2.91 mmHg] and diastolic (MD: -2.02 mmHg; 95% CI: -2.56, -1.49 mmHg) BP (P < 0.001) and body weight (MD: -1.84 kg; 95% CI: -2.72, -0.96 kg; P < 0.001) and improve antihypertensive medication usage, relative risk of stroke (MD: 0.34; 95% CI: 0.14, 0.81; P = 0.02), and CVD risk score [standardized mean difference (SMD): -0.20; 95% CI: -0.30, -0.09; P < 0.001] compared with control participants, and COE was moderate. Additionally, MNT may reduce arterial stiffness (SMD: -0.45; 95% CI: -0.71, -0.19; P = 0.008) and waist circumference (SMD: -1.18 cm; 95% CI: -2.00, -0.36; P = 0.04), and COE was low. There was no significant difference in risk of myocardial infarction between groups. Dietitian interventions reduced BP and related cardiovascular outcomes for adults with prehypertension or hypertension. CONCLUSIONS: Dietitians play a critical role in improving cardiometabolic risk factors for adults with elevated BP; thus, improved payment for and access to MNT services has the potential to significantly impact public health. This review was registered at PROSPERO as CRD42022351693.

Sex influences blood pressure but not blood pressure variability in response to dietary sodium and potassium in salt-resistant adults.

Dietary sodium and potassium have been shown to affect blood pressure (BP) but their influence on BP variability (BPV) is less studied as is the influence of sex. The aim of this study was to compare 24 h BP and short-term BPV in response to varying dietary levels of sodium and potassium in healthy non-obese normotensive salt-resistant adults. We hypothesized that high sodium would increase short-term BP and BPV while the addition of high potassium would counteract this increase. Furthermore, we hypothesized that women would experience greater increases in BPV under high sodium conditions compared to men while potassium would attenuate this response. Thirty-seven participants (17 M/20 W; 27 ± 5 years old; BMI 24.3 ± 3 kg/m2) completed seven days each of the following randomized diets: moderate potassium/low sodium (MK/LS), moderate potassium/high sodium (MK/HS) and high potassium/high sodium (HK/HS). BP and short-term BPV were assessed using 24 h ambulatory BP monitoring starting on day 6. BPV was calculated using the average real variability (ARV) index. Twenty-four hour, daytime, and nighttime systolic BP (SBP) were lower in women compared to men regardless of diet. However, 24 h and daytime SBP were lowered in women on the HK/HS diet compared to the MK/HS diet. There were no significant effects of diet or sex for 24 h, daytime or nighttime SBP ARV. However, men exhibited a higher 24 hDBP ARV than women regardless of diet. In conclusion, a high potassium diet lowered BP under high sodium conditions in women alone while men exhibited higher short-term BPV that was not influenced by diet.

Melatonin supplementation does not alter vascular function or oxidative stress in healthy normotensive adults on a high sodium diet.

High sodium diets (HSD) can cause vascular dysfunction, in part due to increases in reactive oxygen species (ROS). Melatonin reduces ROS in healthy and clinical populations and may improve vascular function. The purpose was to determine the effect of melatonin supplementation on vascular function and ROS during 10 days of a HSD. We hypothesized that melatonin supplementation during a HSD would improve vascular function and decrease ROS levels compared to HSD alone. Twenty-seven participants (13 M/14 W, 26.7 ± 2.9 years, BMI: 23.6 ± 2.0 kg/m2 , BP: 110 ± 9/67 ± 7 mmHg) were randomized to a 10-day HSD (6900 mg sodium/d) supplemented with either 10 mg of melatonin (HSD + MEL) or a placebo (HSD + PL) daily. Brachial artery flow-mediated dilation, a measure of macrovascular function, (HSD + PL: 7.1 ± 3.8%; HSD + MEL: 6.7 ± 3.4%; p = 0.59) and tissue oxygenation index (TSI) reperfusion rate, a measure of microvascular reactivity, (HSD + PL: 0.21 ± 0.06%/s; HSD + MEL: 0.21 ± 0.08%/s; p = 0.97) and TSI area under the curve (HSD + PL: 199899 ± 10,863 a.u.; HSD + MEL: 20315 ± 11,348 a.u.; p = 0.17) were similar at the end of each condition. Neither nitroxide molarity (HSD + PL: 7.8 × 10-5 ± 4.1 × 10-5 mol/L; HSD + MEL: 8.7 × 10-5 ± 5.1 × 10-5 mol/L; p = 0.55) nor free radical number (HSD + PL: 8.0 × 1015 ± 4.4 × 1015 ; HSD + MEL: 9.0 × 1015 ± 4.9 × 1015 ; p = 0.51) were different between conditions. Melatonin supplementation did not alter vascular function or ROS levels while on a HSD in this sample of young healthy normotensive adults.

Long-term function, body composition and cardiometabolic health in midlife former athletes: a scoping review.

While sports medicine has traditionally focused on recovering from injury and returning athletes to sport safely after injury, there is a growing interest in the long-term health of athletes. The purpose of this scoping review was to (1) summarise the literature (methodologies and findings) on physical function, body composition and cardiometabolic health in midlife (age 40-65 years) former competitive athletes compared with non-athlete controls, (2) identify areas for future study in long-term health in athletes and (3) determine outcomes that could be evaluated in a future systematic review(s). We searched PubMed, CINAHL, Web of Science and SPORTDiscus for studies published between 2000 and 2022 evaluating former athletes and controls on physical function, body composition and/or cardiometabolic measures using MeSH terms. We identified 20 articles that met our criteria. Outcomes varied considerably across studies, most of which were cross-sectional and evaluated only males. Limited data suggest that former endurance athletes have leaner body compositions, higher aerobic capacity and better cardiometabolic indicators than controls; former athletes who maintain higher physical activity (ie, self-reported exercise) are healthier than those who do not; and former team sport athletes, who have higher injury prevalence, may have poorer functional performance than controls who were recreationally active in college. Studies rarely evaluated functional performance, did not control for prior injury or diet and seldom assessed current physical activity levels. Future research should include females and evaluate sex differences, control for prior sports-related injury(ies), quantify physical activity, use standardised outcome measures including performance-based functional assessments and incorporate longitudinal designs.

Melatonin supplementation reduces nighttime blood pressure but does not affect blood pressure reactivity in normotensive adults on a high-sodium diet.

High-sodium diets (HSDs) can cause exaggerated increases in blood pressure (BP) during physiological perturbations that cause sympathetic activation, which is related to cardiovascular risk. Melatonin supplementation has been shown to play a role in BP regulation. Our aim was to examine the effects of melatonin taken during an HSD on 24-h BP and BP reactivity during isometric handgrip (IHG) exercise, postexercise ischemia (PEI), and the cold pressor test (CPT). Twenty-two participants (11 men/11 women, 26.5 ± 3.1 yr, BMI: 24.1 ± 1.8 kg/m2, BP: 111 ± 9/67 ± 7 mmHg) were randomized to a 10-day HSD (6,900 mg sodium/day) that was supplemented with either 10 mg/day of melatonin (HSD + MEL) or placebo (HSD + PL). Twenty-four-hour ambulatory BP monitoring was assessed starting on day 9. Mean arterial pressure (MAP) was quantified during the last 30 s of IHG at 40% of maximal voluntary contraction and CPT, and during 3 min of PEI. Melatonin did not change 24-h MAP (HSD + PL: 83 ± 6 mmHg; HSD + MEL: 82 ± 5 mmHg; P = 0.23) but decreased nighttime peripheral (HSD + PL: 105 ± 10 mmHg; HSD + MEL: 100 ± 10 mmHg; P = 0.01) and central systolic BP (HSD + PL: 97 ± 9 mmHg; HSD + MEL: 93 ± 8 mmHg; P = 0.04) on the HSD compared with the HSD + PL. The absolute and percent change in MAP during IHG was not different between conditions (all P > 0.05). In conclusion, melatonin supplementation did not alter BP reactivity to the perturbations tested on an HSD but may be beneficial in lowering BP in young healthy normotensive adults.NEW & NOTEWORTHY BP reactivity was assessed during isometric handgrip (IHG) exercise, postexercise ischemia (PEI), and the cold pressor test (CPT) after 10 days of a high-sodium diet with and without melatonin supplementation. Melatonin did not alter BP reactivity in healthy normotensive men and women. However, melatonin did decrease nighttime peripheral and central systolic BP, suggesting it may be beneficial in lowering BP even in those with a normal BP.

Inverse salt sensitivity in normotensive adults: role of demographic factors.

BACKGROUND: Salt sensitivity and inverse salt sensitivity [ISS; a reduction in blood pressure (BP) on a high sodium diet] are each associated with increased incidence of hypertension. The purpose of this analysis was to determine the prevalence of ISS in normotensive adults and whether ISS is associated with any demographic characteristic(s). METHODS: Healthy normotensive, nonobese adults [ n  = 84; 43 women; age = 37 ±â€Š13 years; baseline mean arterial pressure (MAP) = 89 ±â€Š8 mmHg] participated in a controlled feeding study, consuming 7-day low-sodium (20 mmol sodium/day) and high-sodium (300 mmol sodium/day) diets. Twenty-four-hour ambulatory BP was assessed on the last day of each diet. ISS was defined as a reduction in 24-h MAP more than 5 mmHg, salt sensitivity as an increase in MAP more than 5 mmHg and salt resistance as a change in MAP between -5 and 5 mmHg from low sodium to high sodium. RESULTS: Using this cutoff, 10.7% were ISS, 76.2% salt resistant, and 13.1% salt sensitive. Prevalence of ISS was similar between sexes and age groups ( P  > 0.05). However, ISS was more prevalent in those with normal BMI (15.8% ISS) compared with those with overweight BMI (0% ISS; P  < 0.01). Interestingly, classification of participants using a salt sensitivity index (ΔMAP/Δ urinary sodium excretion) categorized 21.4% as ISS, 48.8% salt resistant, and 29.8% salt sensitive. CONCLUSION: Overall, we found that the prevalence of ISS was 10.7% (5 mmHg cutoff) or 21.4% (salt sensitivity index), and that ISS was associated with lower BMI. These results highlight the importance of future work to understand the mechanisms of ISS and to standardize salt sensitivity assessment.

Nutrition Interactions With Exercise Training on Endothelial Function.

Exercise is advised to improve overall cardiovascular health and endothelial function. However, the role of nutrition on this exercise-induced endothelial adaptation is not clear. Here, we hypothesize that nutrients interact with exercise to influence endothelial function and chronic disease risk.

Greater adherence to healthy dietary patterns is associated with lower diastolic blood pressure and augmentation index in healthy, young adults.

More than two-thirds of cardiovascular disease (CVD) deaths worldwide are attributable to dietary factors. Blood pressure variability (BPV), endothelial dysfunction, and arterial stiffness are important CVD risk factors. Although studies show a link between consuming a healthy diet and lower BPV and stiffness and improved endothelial function, research in young, healthy adults is scarce. We hypothesized that, in young, healthy adults, diet quality would be inversely associated with BPV and arterial stiffness and positively associated with endothelial function. This cross-sectional study included 56 healthy young adults (34 women/22 men, age 26.7 ± 0.8 years, body mass index 23.4 ± 0.4 kg/m2, blood pressure [BP] 113/69 mmHg). Three-day diet records were used to calculate two Dietary Approaches to Stop Hypertension (DASH) diet scores, the alternative Mediterranean Diet (aMED) score, and the Healthy Eating Index-2015 (HEI-2015) based on the 2015-2020 Dietary Guidelines for Americans. Twenty-four-hour ambulatory BP data were used to calculate average real variability of systolic and diastolic BP. Endothelial function was assessed by flow-mediated dilation, and arterial stiffness was assessed by pulse wave velocity and augmentation index (AIx). Overall, the HEI-2015 was inversely associated with 24-hour diastolic BP (DBP) and daytime DBP, and the aMED score was inversely associated with AIx. In our exploratory analyses, the Fung DASH score was inversely associated with 24-hour DBP and daytime DBP in women, but not men. These findings suggest that consuming a diet that aligns with the DASH diet, the Mediterranean diet, and/or the 2015-2020 Dietary Guidelines for Americans is associated with cardiovascular benefits in healthy, young adults.

Arterial Stiffness and Endothelial Function are Comparable in Young Healthy Vegetarians and Omnivores.

Vegetarians (VEG) are reported to have lower body weight, blood pressure (BP), and cardiovascular disease (CVD) risk compared with omnivores (OMN), yet the mechanisms remain unclear. A vegetarian diet may protect the vascular endothelium, reducing the risk of atherosclerosis and CVD. This cross-sectional study compared vascular function between OMN and VEG. We hypothesized that VEG would have greater vascular function compared with OMN. Fifty-eight normotensive young healthy adults participated (40 women [W]/18 men [M]; 28 OMN [15W/13M] and 30 VEG [25W/5M]; 26 ± 7 years; BP: 112 ± 11/67 ± 8 mm Hg). Arterial stiffness, assessed by carotid-to-femoral pulse wave velocity (OMN: 5.6 ± 0.8 m/s, VEG: 5.3 ± 0.8 m/s; P = .17) and wave reflection assessed by aortic augmentation index (OMN: 6.9 ± 12.3%, VEG: 8.8 ± 13.5%; P = .57) were not different between groups. However, central pulse pressure (OMN: 32 ± 5; VEG: 29 ± 5 mm Hg; P = .048) and forward wave reflection were greater in omnivores (OMN: 26 ± 3; VEG: 24 ± 3 mm Hg; P = .048). Endothelial-dependent dilation measured by brachial artery flow-mediated dilation was not different between groups (OMN: 6.0 ± 2.9%, VEG: 6.9 ± 3.3%; P = .29). Percent change in femoral blood flow from baseline during passive leg movement, another assessment of nitric oxide-mediated endothelial dilation, was similar between groups (OMN: 203 ± 88 mL/min, VEG: 253 ± 192 mL/min; P = .50). These data suggest that in healthy young adults, normotensive VEG do not have significantly improved vascular function compared with OMN; however, they have a lower central pulse pressure and forward wave amplitude which may lower the risk of future CVD.

An Update to Scientific Decision Making: The Academy of Nutrition and Dietetics' Scientific Integrity Principles.

In 2015, the Council on Research published their vision for scientific decision making, which provided nutrition and dietetics practitioners and practitioners-in-training key information on the Academy of Nutrition and Dietetics' newly developed scientific integrity principles. Given that it has been 7 years since the original publication, it was believed the original six principles should be revisited and updated. From the Subcommittee on Scientific Integrity Principles under the Council on Research, the 2015 principles were evaluated and updated with new literature and best practices for maintaining scientific integrity principles. After this review process, four new/updated principles were approved by the Council on Research. These include: 1) the ethical conduct of research and protection of human subjects, 2) funder's influence on the research question/methodology/education content and conflicts of interest, 3) review of research-related materials, and 4) maintain and promote a culture of scientific integrity. Moreover, it became clear that newer topics, including diversity, equity, and inclusion should be woven throughout the principles. This article presents the newly updated principles and resources related to scientific integrity principles. We envision that this document can be used by the Academy of Nutrition and Dietetics to educate members and serve as a guide to incorporate these principles into all research practices and at all levels of dietetics practice.

Acrolein, an environmental toxicant and its applications to in vivo and in vitro atherosclerosis models: An update.

Cardiovascular disease, the foremost cause of death worldwide, is an overarching disease term that encompasses a number of disorders involving the heart and circulatory system, including atherosclerosis. Atherosclerosis is a primary cause of cardiovascular diseases and is caused by buildup of plaque and narrowing of blood vessels. Epidemiological studies have suggested that environmental pollutants are implicated in atherosclerosis disease progression. Among many environmental pollutants, acrolein (Acr) is an abundant reactive aldehyde and is ubiquitously present in cigarette smoke as well as food products (e.g., overheated oils and wine). Despite its ubiquitous presence and potential impact on the etiology of cardiovascular disease, a limited consensus has been made in regard to Acr exposure conditions to induce atherosclerosis in vivo. This mini-review summarizes in vivo atherosclerosis models using Acr to investigate biochemical and phenotypic changes related to atherosclerosis and in vitro mechanistic studies involving Acr and atherosclerosis.

Ten days of high dietary sodium does not impair cerebral blood flow regulation in healthy adults.

High dietary sodium impairs cerebral blood flow regulation in rodents and is associated with increased stroke risk in humans. However, the effects of multiple days of high dietary sodium on cerebral blood flow regulation in humans is unknown. Therefore, the purpose of this study was to determine whether ten days of high dietary sodium impairs cerebral blood flow regulation. Ten participants (3F/7M; age: 30 ± 10 years; blood pressure (BP): 113 ± 8/62 ± 9 mmHg) participated in this randomized, cross-over design study. Participants were placed on 10-day diets that included either low- (1000 mg/d), medium- (2300 mg/d) or high- (7000 mg/d) sodium separated by ≥four weeks. Urinary sodium excretion, beat-to-beat BP (finger photoplethysmography), middle cerebral artery velocity (transcranial Doppler), and end-tidal carbon dioxide (capnography) was measured. Dynamic cerebral autoregulation during a ten-minute baseline was calculated and cerebrovascular reactivity assessed by determining the percent change in middle cerebral artery blood flow velocity to hypercapnia (8% CO2, 21% oxygen, balance nitrogen) and hypocapnia (via mild hyperventilation). Urinary sodium excretion increased in a stepwise manner (ANOVA P = 0.001) from the low, to medium, to high condition. There were no differences in dynamic cerebral autoregulation between conditions. While there was a trend for a difference during cerebrovascular reactivity to hypercapnia (ANOVA P = 0.06), this trend was abolished when calculating cerebrovascular conductance (ANOVA: P = 0.28). There were no differences in cerebrovascular reactivity (ANOVA P = 0.57) or conductance (ANOVA: P = 0.73) during hypocapnia. These data suggest that ten days of a high sodium diet does not impair cerebral blood flow regulation in healthy adults.

Mechanisms of Dietary Sodium-Induced Impairments in Endothelial Function and Potential Countermeasures.

Despite decades of efforts to reduce sodium intake, excess dietary sodium remains commonplace, and contributes to increased cardiovascular morbidity and mortality independent of its effects on blood pressure. An increasing amount of research suggests that high-sodium diets lead to reduced nitric oxide-mediated endothelial function, even in the absence of a change in blood pressure. As endothelial dysfunction is an early step in the progression of cardiovascular diseases, the endothelium presents a target for interventions aimed at reducing the impact of excess dietary sodium. In this review, we briefly define endothelial function and present the literature demonstrating that excess dietary sodium results in impaired endothelial function. We then discuss the mechanisms through which sodium impairs the endothelium, including increased reactive oxygen species, decreased intrinsic antioxidant defenses, endothelial cell stiffening, and damage to the endothelial glycocalyx. Finally, we present selected research findings suggesting that aerobic exercise or increased intake of dietary potassium may counteract the deleterious vascular effects of a high-sodium diet.

A high salt meal does not impair cerebrovascular reactivity in healthy young adults.

A high sodium (Na+ ) meal impairs peripheral vascular function. In rodents, chronic high dietary Na+ impairs cerebral vascular function, and in humans, habitual high dietary Na+ is associated with increased stroke risk. However, the effects of acute high dietary Na+ on the cerebral vasculature in humans are unknown. The purpose of this study was to determine if acute high dietary Na+ impairs cerebrovascular reactivity in healthy adults. Thirty-seven participants (20F/17M; 25 ± 5 years; blood pressure [BP]: 107 ± 9/61 ± 6 mm Hg) participated in this randomized, cross-over study. Participants were given a low Na+ meal (LSM; 138 mg Na+ ) and a high Na+ meal (HSM; 1,495 mg Na+ ) separated by ≥ one week. Serum Na+ , beat-to-beat BP, middle cerebral artery velocity (transcranial Doppler), and end-tidal carbon dioxide (PET CO2 ) were measured pre- (baseline) and 60 min post-prandial. Cerebrovascular reactivity was assessed by determining the percent change in middle cerebral artery velocity to hypercapnia (via 8% CO2 , 21% oxygen, balance nitrogen) and hypocapnia (via mild hyperventilation). Peripheral vascular function was measured using brachial artery flow-mediated dilation (FMD). Changes in serum Na+ were greater following the HSM (HSM: Δ1.6 ± 1.2 mmol/L vs. LSM: Δ0.7 ± 1.2 mmol/L, p < .01). Cerebrovascular reactivity to hypercapnia (meal effect: p = .41) and to hypocapnia (meal effect: p = .65) were not affected by the HSM. Contrary with previous findings, FMD was not reduced following the HSM (meal effect: p = .74). These data suggest that a single high Na+ meal does not acutely impair cerebrovascular reactivity, and suggests that despite prior findings, a single high Na+ meal does not impair peripheral vascular function in healthy adults.

Associations of Ultra-Processed and Unprocessed/Minimally Processed Food Consumption with Peripheral and Central Hemodynamics, and Arterial Stiffness in Young Healthy Adults.

Consumption of ultra-processed food (UPF) replaces the intake of freshly prepared unprocessed/minimally processed food (MPF) and is positively associated with hypertension and cardiovascular disease (CVD). The objective of this observational study was to investigate the relation between (1) UPF and (2) MPF with peripheral and central blood pressure (BP), wave reflection, and arterial stiffness. Habitual dietary intake, ambulatory BP, augmentation index (AIx), and pulse wave velocity (PWV) were assessed in 40 normotensive young adults (15 M/25 W; 27 ± 1 y; body mass index 23.6 ± 0.5 kg/m2). UPF consumption was positively associated with overall and daytime peripheral systolic BP (B = 0.25, 95% confidence interval (CI) 0.03, 0.46, p = 0.029; B = 0.32, 95% CI 0.09, 0.56, p = 0.008, respectively), daytime diastolic BP (B = 0.18, 95% CI 0.01, 0.36, p = 0.049) and daytime peripheral pulse pressure (PP; B = 0.22, 95% CI 0.03, 0.41, p = 0.027). MPF consumption was inversely associated with daytime peripheral PP (B = -0.27, 95% CI -0.47, -0.07, p = 0.011), overall and daytime central systolic BP (B = -0.27, 95% CI -0.51, -0.02, p = 0.035; B = -0.31, 95% CI -0.58, -0.04, p = 0.024, respectively), and nighttime central PP (B = -0.10, 95% CI -0.19, -0.01, p = 0.042). Both UPF and MPF were not associated with AIx nor PWV. These data suggest avoidance of UPF and consumption of more MPF may reduce CVD risk factors.

Antioxidant cocktail following a high-sodium meal does not affect vascular function in young, healthy adult humans: a randomized controlled crossover trial.

Chronic high sodium intake is a risk factor for cardiovascular disease as it impairs vascular function through an increase in oxidative stress. The objective of this study was to investigate the acute effects of a high-sodium meal (HSM) and antioxidant (AO) cocktail on vascular function. We hypothesized that a HSM would impair endothelial function, and increase arterial stiffness and wave reflection, while ingestion of the AO cocktail would mitigate this response. Healthy adults ingested either an AO cocktail (vitamin C, E, alpha-lipoic acid) or placebo (PLA) followed by a HSM (1500 mg) in a randomized crossover blinded design. Blood pressure (BP), endothelial function (flow-mediated dilation; FMD) and measures of arterial stiffness (pulse wave velocity; PWV) and wave reflection (augmentation index; AIx) were made at baseline and 30, 60, 90, and 120 min after meal consumption. Forty-one participants (20M/21W; 24 ± 1 years; BMI 23.4 ± 0.4 kg/m2) completed the study. Mean BP increased at 120 min relative to 60 min (60 min: 79 ± 1; 120 min: 81 ± 1 mmHg; time effect P = .01) but was not different between treatments (treatment × time interaction P = .32). AIx decreased from baseline (time effect P < .001) but was not different between treatments (treatment × time interaction P = .31). PWV (treatment × time interaction, P = .91) and FMD (treatment × time interaction P = .65) were also not different between treatments. In conclusion, a HSM does not acutely impair vascular function suggesting young healthy adults can withstand the acute impact of sodium on the vasculature and therefore, the AO cocktail is not necessary to mitigate the response.

High dietary sodium augments vascular tone and attenuates low-flow mediated constriction in salt-resistant adults.

INTRODUCTION: Low-flow mediated constriction (L-FMC) has emerged as a valuable and complementary measure of flow-mediated dilation (FMD) for assessing endothelial function non-invasively. High dietary sodium has been shown to impair FMD independent of changes in blood pressure (BP), but its effects on L-FMC are unknown. PURPOSE: To test the hypothesis that high dietary sodium would attenuate brachial artery L-FMC in salt-resistant adults. METHODS: Fifteen healthy, normotensive adults (29 ± 6 years) participated in a controlled feeding study. Following a run-in diet, participants completed a 7-day low sodium (LS; 20 mmol sodium/day) and 7-day high sodium (HS; 300 mmol sodium/day) diet in randomized order. On the last day of each diet, 24 h urine was collected and assessments of 24 h ambulatory BP and L-FMC were performed. Salt-resistance was defined as a change in 24 h ambulatory mean arterial pressure (MAP) between the LS and HS diets of ≤ 5 mmHg. Resting vascular tone and L-FMC were calculated from ultrasound-derived arterial diameters. RESULTS: High dietary sodium increased serum sodium and urinary sodium excretion (p < 0.001 for both), but 24 h MAP was unchanged (p = 0.16) by design. High dietary sodium augmented vascular tone (LS: 91 ± 23%, HS: 125 ± 56%, p = 0.01) and attenuated L-FMC (LS: - 0.58 ± 0.99%, HS: 0.17 ± 1.23%, p = 0.008). CONCLUSION: These findings in salt-resistant adults provide additional evidence that dietary sodium has adverse vascular effects independent of changes in BP.

Dietary Potassium Attenuates the Effects of Dietary Sodium on Vascular Function in Salt-Resistant Adults.

The influence of dietary sodium and potassium on blood pressure (BP) has been extensively studied, however their impact on endothelial function, particularly any interactive effects, has received less attention. The purpose of this study was to determine if dietary potassium can offset the deleterious effect of high dietary sodium on endothelial function independent of BP. Thirty-three adults with salt-resistant BP (16 M and 17 F; 27 ± 1 year) completed seven days each of the following diets in a random order: a moderate potassium/low sodium diet (65 mmol potassium/50 mmol sodium; MK/LS), a moderate potassium/high sodium diet (65mmol potassium/300 mmol sodium; MK/HS) and a high potassium/high sodium (120 mmol potassium/300 mmol sodium; HK/HS). On day seven of each diet, 24-h ambulatory BP and a urine collection were performed. Brachial artery flow-mediated dilation (FMD) was measured in response to reactive hyperemia. Between diets, 24-h BP was unchanged confirming salt resistance (p > 0.05). Sodium excretion increased on both HS diets compared to MK/LS (p < 0.05) and potassium excretion was increased on the HK diet compared to MK/LS and MK/HS (p < 0.05) confirming diet compliance. FMD was lower in MK/HS (5.4 ± 0.5%) compared to MK/LS (6.7 ± 0.5%; p < 0.05) and HK/HS (6.4 ± 0.5%), while there was no difference between the MK/LS and HK/HS diets (p > 0.05). These data suggest that dietary potassium provides vascular protection against the deleterious effects of high dietary sodium by restoring conduit artery function.

Sodium, hypertension, and the gut: does the gut microbiota go salty?

Recent evidence suggests that the gut microbiota contributes to the pathogenesis of hypertension (HTN). The gut microbiota is a highly dynamic organ mediating numerous physiological functions, which can be influenced by external factors such as diet. In particular, a major modifiable risk factor for HTN is dietary sodium intake. Sodium consumption in the United States is significantly greater than that recommended by the federal government and organizations such as the American Heart Association. Because of the emerging connection between the gut microbiota and HTN, the interaction between dietary sodium and gut microbiota has sparked interest. High-sodium diets promote local and systemic tissue inflammation and impair intestinal anatomy compared with low sodium intake in both human and animal studies. It is biologically plausible that the gut microbiota mediates the inflammatory response, as it is in constant interaction with the immune system and is necessary for proper maturation of immune cells. Recent rodent data demonstrate that dietary sodium disrupts gut microbial homeostasis as gut microbiota composition shifts with dietary sodium manipulation. In this review, we will focus on gut microbiota activity in HTN and the influence of high dietary sodium intake with an emphasis on the immune system, bacterial metabolites, and the circadian clock.