High sodium intakes are a key contributor to cardiovascular disease burden. The Dietary Reference Intakes for sodium recommend all healthy individuals consume below 2,300 mg/d, regardless of energy needs. Newer evidence suggests the relation between sodium and blood pressure varies by energy intake. Whether the relation between sodium and endothelial dysfunction, a precursor to atherosclerosis, varies with energy intake in salt-resistant individuals is unknown. The objective of this secondary analysis was to determine if the magnitude of change in endothelial function on a low sodium diet vs a high sodium diet differs by energy level. We hypothesized that the magnitude of the change in endothelial function from low sodium to high sodium would be larger in individuals consuming fewer kcals. Twenty-three healthy young adults (15W/8M, age 28±6 y, BP 109±11/70±8 mmHg, BMI 24.9±2.8 kg/m 2 ) consumed a low sodium (1100 mg Na/d) and a high sodium (6900 mg Na/d) controlled diet for 10 days each in random order. Diets were customized to meet participants’ calculated energy needs. On day 10, endothelial function was assessed via brachial artery flow-mediated dilation (FMD), and mean difference in FMD from the low to high sodium diet (Δ%FMD) was calculated. Participants were evenly divided into three groups based on energy needs: low (1837±196 kcal/d), moderate (2262±58 kcal/d), and high (2543±215 kcal/d). For all participants, 24h ambulatory mean arterial pressure did not increase by ≥6 mmHg from the low to the high sodium diet, confirming salt resistance. Regardless of energy intake, %FMD was lower on the high sodium vs. low sodium diet (5.4±2.8% vs. 7.6±3.7%, p<0.001). Δ%FMD from the low sodium to high sodium diet was greatest in the low kcal group and smallest in the high kcal group (-2.80±2.6% vs. -2.38±3.2% vs. -1.44±1.9%) though group differences did not reach statistical significance (model p=0.61). The magnitude of change in dietary sodium density (mg Na/kcal, ΔNaDensity) from the low sodium to the high sodium diet was greatest in the low kcal group and smallest in the high kcal group (3.2±0.3 mg/kcal vs. 2.6±0.1 mg/kcal vs. 2.3±0.2, model p<0.001). After controlling for BMI, Δ%FMD was inversely correlated with ΔNaDensity (r=-0.44, p=0.02) such that a greater decline in %FMD is observed with a greater increase in dietary sodium density. Our findings suggest that FMD responses to alterations in sodium intake may vary with energy intake. This highlights the need to examine sodium relative to energy intake in future studies and when developing dietary intake recommendations for mitigating cardiovascular disease risk. AHA/VIVA 23POST1009835; NHLBI R01 HL145055 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Aging is the primary risk factor for Alzheimer’s disease (AD) which is the most common cause of dementia. The risk factors for AD emerge during midlife and are similar to cardiometabolic diseases. Midlife cardiometabolic changes are worsened by poor lifestyle habits, such as consuming a Western Diet (WD), which is partially characterized by high added sugar intake (i.e., all caloric sweeteners added to food during cooking or processing). This study aimed to investigate if short-term consumption of excessive added sugars acutely alters cardiometabolic risk factors and hippocampal-dependent memory function in midlife adults (50-64 years old). We hypothesized that, compared to a low added sugar diet, the high added sugar diet would be detrimental to cardiometabolic and brain health. In a randomized order, 26 participants (10 males / 16 females) were assigned to consume a 10-day high-added sugar (HS: 25% total calories) and low- added sugar (LS: 5% total calories) diet. At the end of each diet, blood was sampled, blood pressure was measured, and memory recall was tested using the Hopkins Verbal Learning Test (HVLT) and the Brief Visuospatial Memory Test (BVMT). Compared to the LS diet, the HS diet significantly increased plasma triglycerides (LS: 91±31; HS: 102±30 mg/dL; p = 0.04) and mean arterial blood pressure (LS: 80±7; HS: 85±9 mmHg; p = 0.002). After the HS diet, total memory recall scores were significantly lower for BVMT: (LS: 26.0±5.2; HS 23.3±5.9 correct responses; p = 0.02) but not the HVLT. Compared to the LS diet, delayed memory recall scores were significantly lower after the HS diet for both tests [(HVLT: (LS: 10.5±1.5; HS 9.9±1.7 correct responses; p = 0.03) and BVMT: (LS: 10.1±1.6; HS 8.8±2.2 correct responses; p = 0.002)]. A short-term (10-day) diet with an excessive amount of added sugars increases cardiometabolic risk factors, whichmay make the brain susceptible to lower memory recall in otherwise healthy midlife adults. This study highlights the importance of diet on cardiometabolic and brain health in midlife adults. Future studies should examine the long-term impact of added sugars on AD risk and explore the underlying mechanisms by which added sugars contribute to cognitive aging.

High sodium diets blunt vascular function when compared to low sodium diets, providing evidence that the vasculature is an early contributor to the increased cardiovascular disease (CVD) risk associated with high sodium intake. In contrast, increased aerobic capacity is associated with decreased CVD risk. It is unclear whether the effects of dietary sodium on pulsatile arterial load are influenced by aerobic capacity. Therefore, we tested the hypothesis that the effects of short-term sodium loading on measures of pulsatile arterial load are inversely associated with aerobic capacity (VO 2 peak). Thirty-one healthy young adults were studied (17M / 14F; 25 ± 4 yr; 24.1 ± 3.0 kg/m 2 ; 112 ± 11 / 68 ± 13 mmHg). VO 2 peak was determined via cardiopulmonary exercise testing on a cycle ergometer and expressed as percent of predicted peak VO 2 (Hansen/Wasserman equation) to account for the influence of sex, age, and body size. Participants consumed capsules containing either table salt (~3.4 g of sodium/day) or a placebo for 10 days in a randomized cross-over design. Participants were instructed to maintain their usual diet throughout the study. Urine was collected for 24 hrs prior to each visit and sodium excretion was used as an index of daily sodium intake. Pulsatile arterial load was assessed at rest on day 11 of both sodium and placebo conditions via pressure-flow analyses using time-aligned left ventricular outflow waveforms (echocardiography) and aortic pressure waveforms derived via radial artery applanation tonometry and a generalized transfer function. The primary arterial hemodynamic variables of interest were reflected wave amplitude (Pb), reflected wave transit time (RWTT), and wasted pressure effort (WPE). Aortic pressure waveform morphology was used to determine augmentation index (AIx), a surrogate marker of wave reflection. Mean VO 2 peak was 39.2 ± 12.0 ml/kg/min and 101 ± 30% of equation predicted peak VO 2 (range: 64 to 191%). Total 24 hr urinary sodium excretion was higher following sodium compared to placebo (310 ± 94 vs. 170 ± 68 mmol/24 hr, p<0.001). Sodium increased AIx (6 ± 14 vs. 2 ± 15%, P=0.02), but did not change Pb (P=0.71) or RWTT (P=0.98). WPE was also not different between conditions (sodium: 2158 ± 768, placebo: 2052 ± 906 mmHg·ms, P=0.41). Percent of predicted peak VO 2 was not associated with ΔAIx (r=-0.09, P=0.63), ΔPb (r=0.04, P=0.83), ΔRWTT (r=0.08, P=0.70), or ΔWPE (r=-0.20, P=0.31).Contrary to our hypothesis, sodium loading-induced changes in pulsatile arterial load were not associated with aerobic capacity. There was no effect of excess sodium intake on Pb, RWTT, or WPE. However, our sample habitually consumed a high sodium diet as shown by the high urinary sodium excretion during the placebo condition. Future studies should include a low sodium condition to ensure that any potential negative effects of high sodium are not masked by the habitual sodium intake of the participants. Supported by NIH 5R01HL104106 and 5P20GM113125; AHA 20POST35080171 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

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.

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.

BACKGROUND:A total of 374 million adults worldwide are living with prediabetes, 70% of whom will develop type 2 diabetes mellitus (T2DM) in their lifetime. Medical nutrition therapy (MNT) provided by a dietitian, such as that found in lifestyle interventions, has the potential to improve glycemic control and prevent progression to T2DM.OBJECTIVES:The objective of this systematic review was to examine the effectiveness of MNT provided by a dietitian, compared with standard care, on glycemic, cardiometabolic, and anthropometric outcomes in adults with prediabetes.METHODS:Searches were conducted for randomized controlled trials (RCTs) published between 1995 and 2022 using electronic databases MEDLINE, CINHAL, and Cochrane Central. The risk of bias was assessed using version 2 of the Cochrane risk-of-bias tool for RCTs. Meta-analyses were conducted using a random-effects model. The certainty of evidence was assessed for each outcome using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) method, and a summary of findings table was created using the GRADEpro Guideline Development Tool.RESULTS:Thirteen RCTs were included in the analysis, showcasing a variety of MNT interventions delivered by dietitians. Intervention durations ranged from 3 to 24 mo. Compared with standard care, MNT improved hemoglobin A1c (HbA1c) (mean difference [95% confidence interval]: -0.30% [-0.49, -0.12]) and fasting blood glucose (FBG) (-4.97 mg/dL [-6.24, -3.71]). Statistically significant improvements were found in anthropometrics (weight, body mass index, and waist circumference), cholesterol (total, high-, and low-density lipoproteins), and blood pressure (systolic and diastolic). No significant effect was found on T2DM or triglycerides. The certainty of evidence was moderate for FBG and low for HbA1c and incidence of T2DM.CONCLUSIONS:In adults with prediabetes, MNT was effective in improving glycemic outcomes, anthropometrics, blood pressure, and most lipid levels. However, most studies had a risk of bias because of the randomization process or deviations from intended interventions. MNT plays a key role in improving cardiometabolic risk factors in adults with prediabetes.TRIAL REGISTRATION NUMBER:This study was registered with the registration ID #351421, available from https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=351421.

Short-term, high sodium diets decrease dilation responses in conduit arteries and the microvasculature when compared to low sodium diets (e.g., 7000 vs. 500 mg/day). Supraphysiological antioxidant treatment mitigates these effects supporting a role for oxidative stress in sodium-induced vascular impairments. It is unclear whether these effects are present when high sodium conditions are compared to the sodium level of a typical American diet (~3400 mg/day). Therefore, we tested the hypotheses that sodium added to the habitual diet of young adults would reduce flow mediated dilation (FMD) and post-ischemic reactive hyperemia (RH) and that an acute infusion of the antioxidant ascorbic acid (AA) would attenuate the vascular consequences of excess sodium. Methods: Young adults (6M / 8F; age: 26 ± 4 y; BMI: 23.6 ± 2.5 kg/m2) were studied following 10 days of sodium loading (SL) via table salt-filled capsules (3900 mg sodium/day) and 10 days of placebo capsules in addition to their normal diet, in random order. Total sodium intake was estimated via 24-hour urinary sodium content on day 10. On day 11, brachial artery diameter and blood velocity were continuously measured via duplex ultrasound at baseline and after 5 min of forearm ischemia. FMD, the post-ischemic change in brachial artery diameter relative to baseline diameter, provided an index of conduit artery endothelial function. The total RH in the 2 min following ischemia was measured for an index of microvascular function. Within each condition, testing was performed before (pre-AA) and after (post-AA) a 20 min intravenous infusion of 0.06 g of AA/kg lean body mass. Results: Urinary sodium content was increased by SL compared to the placebo (285 ± 94 vs. 160 ± 75 mmol/24 h, p<0.001) indicating approximate sodium intakes of 6600 and 3700 mg/day, respectively. Mean arterial pressure did not differ across conditions pre-AA (SL: 77 ± 7; placebo: 75 ± 5 mmHg, P=0.40) or post-AA (SL: 79 ± 8; placebo: 76 ± 5 mmHg, P=0.17). Brachial artery FMD was not different across time or condition (SL pre-AA: 8.7 ± 3.6, post-AA: 8.8 ± 4.2% vs. placebo pre-AA: 8.8 ± 3.2, post-AA: 8.1 ± 3.5%, time x condition interaction P=0.48). RH was similar following SL and placebo (condition effect: P=0.38) but was reduced in both conditions post AA (SL: Δ-45 ± 44 ml, P=0.01; placebo: Δ-72 ± 59ml, p<0.001). Conclusion: Contrary to our hypothesis, 10 days of sodium loading did not decrease FMD or post- ischemic RH in young adults compared to their habitual diet. Likewise, acute antioxidant treatment did not augment FMD in either condition and paradoxically decreased total RH independent of sodium intake. These data suggest that a short-term increase in dietary sodium intake in healthy young adults does not elicit oxidative stress-induced reductions in vascular function. NIH 5R01HL104106 and 5P20GM113125; AHA 20POST35080171. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

High sodium (HS) diets can reduce endothelial function (EF) and increase blood pressure (BP) while high potassium (HK) diets are shown to counter this effect. Furthermore, HS diets have also been shown to lead to gut dysbiosis, which is related to increased intestinal permeability (IP). However, the effect of HS diets on IP and whether the addition of HK can attenuate potential HS-induced changes to IP is unknown. Hypotheses: We hypothesized IP would increase on a HS diet and be mitigated by HK and that a higher IP would be related to elevations in BP and lower EF. Methods: Eleven healthy participants (5W/6M, age 32±8 yrs, BMI 23±1, BP 105±6/66±7 mmHg) consumed three 10-day diets of differing sodium and potassium content in randomized order: low sodium (LS)/low potassium (LK) (50mmol/65mmol), HS/LK (300mmol/65mmol), and HS/HK (300mmol/120mmol). On day 9 of each intervention, they collected their urine and wore an ambulatory BP monitor for 24-hr. On day 10, brachial artery flow-mediated dilation (FMD) was measured. Blood was collected and lipopolysaccharide-binding protein (LBP), a biomarker of IP and bacterial translocation, was measured by ELISA. Mixed design ANOVAs assessed sex differences in LBP, FMD, and BPs between diets. Simple linear regressions assessed relations between variables. Results: Twenty-four-hr urinary sodium excretion was higher on both HS diets compared to LS/LK diet (both p<0.01) and 24-hr urinary potassium excretion was higher on HS/HK compared to LS/LK and HS/LK diets (both p<0.01). LBP was different between diets (p<0.01), and there was a significant diet*sex interaction (p=0.02) where men had increased LBP compared to women on the HS/LK and HS/HK diets (both p<0.01). FMD was not different between diets (p=0.13) although men had a lower FMD compared to women after each diet (sex: p<0.01). Twenty-four-hr mean arterial pressure (MAP) was different between diets (p=0.047) as men demonstrated higher 24-hr MAP on the HS/LK diet compared to LS/LK diet (p=0.03) and lower MAP on the HS/HK diet compared to HS/LK diet (p=0.01). LBP was inversely related to FMD (r=-0.82, p<.01) and positively related to MAP (r=0.72, p<.01), 24-hr systolic BP (r=0.66, p=0.03), and 24-hr diastolic BP (r=0.66, p=0.03) on the HS/LK diet for all participants, but not the LS/LK or HS/HK diets. Conclusions: These pilot data suggest that HS diets may increase IP in men, and, in the context of a HS/LK diet, greater IP is associated with lower FMD and higher BP in all participants. NIH R01 HL145055. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Current recommendations for the general population limit sodium intake to 2,300 mg/d, however meeting these recommendations may be challenging for athletes, who have greater energy needs. Athletes with greater energy needs are recommended to consume an additional 300-600 mg/h of sodium during prolonged exercise. This recommendation contrasts with guidelines for non-athletes. While the link between sodium and blood pressure (BP) is well-established, studies suggest sodium density, the ratio of sodium to energy consumed, may better predict BP than absolute sodium intake. To our knowledge, no studies have examined these relations in athletes. Hypothesis: We hypothesized that sodium density would be a better indicator of BP when compared to absolute sodium intake and that young athletes would have a higher total sodium intake without a significantly higher BP. Methods: Cross-sectional data were collected from healthy men and women that were stratified into four groups: young collegiate athletes ([YA], n=88, aged 21 ± 2 y), young non-athletes ([YNA], n=36, aged 21 ± 2 y), midlife former collegiate athletes ([MFA], n=82, aged 51 ± 7 y), and midlife non-former athletes ([MNA] n=25, aged 52 ± 7 y). Energy and nutrient intakes were assessed from 3-day dietary records. Anthropometric and BP measurements were collected. Group differences were assessed using a one-way ANOVA with Tukey post-hoc tests. Associations between absolute sodium and sodium density and BP were assessed using Pearson correlations. Results: YA (4102 ± 1490 mg) had a significantly higher sodium intake when compared to YNA (3305 ± 1072 mg), MFA (3159 ± 1154 mg), and MNA (2955 ± 956 mg) (p<0.05 for all). Systolic BP (SBP) was higher in MFA (130 ± 17 mmHg; p<0.05) compared to YA (120 ± 13 mmHg) and YNA (116 ± 13 mmHg). Absolute sodium intake and SBP were positively correlated in YA (r=0.26, p=0.02), YNA (r=0.43, p=0.01) and MFA (r=0.26, p=0.02) but not MNA (r=0.04, p=0.84); however, when corrected for energy intake, these correlations were no longer statistically significant for all groups. Conclusion: These data suggest a weak association between absolute sodium intake and BP in YA. However, when corrected for energy intake this association was no longer present. This may not be specific to YA as this association was also seen in YNA and MFA. Our results highlight the importance of examining both absolute sodium intake and sodium density as it relates to BP in populations with increased energy needs. NIH (DP5 OD031833, R01 HL145055, 2UL1TR001436). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Cardiovascular disease (CVD) is influenced by diet quality, such that poor diets generally lead to increased risk. In particular, diets high in sodium have been shown to raise blood pressure (BP) and can lead to arterial stiffening subsequently increasing CVD risk. Current sodium recommendations aimed at lowering CVD risk are given in absolute amounts and do not account for total energy intake. This makes it difficult for individuals with greater energy intakes to meet daily recommended targets. Dietary sodium density (i.e., mg sodium/kcal energy) has been suggested to be a stronger determinant of BP than absolute sodium intake; however, the relation between sodium density and vascular health has yet to be studied in normotensive adults. Our objective was to examine the association between sodium density and ambulatory BP and arterial stiffness in young, healthy, normotensive adults. We hypothesized that sodium density would relate to 24-hour BP and arterial stiffness just as absolute sodium intake does. Sixty-two participants (23M/39W, age 27±6 years, BMI 23.4±2.7 kg/m², BP 112±11/69±9 mmHg) recorded their habitual diet for three days and wore an ambulatory BP monitor to assess 24-hour, daytime, and nighttime BP. Arterial stiffness was assessed by pulse wave velocity (PWV) and wave reflection with augmentation index (AIx). Associations between absolute sodium intake and sodium density with BP and stiffness measures were assessed using bivariate and partial Pearson correlations. On average, participants consumed 2029±547 kcals and 3250±1231 mg sodium. Daytime BP was 118±11/70±7 mmHg and nighttime BP was 106±14/58±9 mmHg. Sodium intake (r=0.31, p=0.03) and sodium density (r=0.35, p=0.01) both correlated with nighttime systolic BP but not nighttime diastolic BP nor daytime or 24-hour systolic or diastolic BP. After controlling for age and sex, both sodium intake (r=0.44, p=0.01) and sodium density (r=0.56, p<0.001) remained significantly associated with nighttime systolic BP. There were no significant correlations between sodium intake or sodium density and PWV or AIx (all p>0.05). These findings indicate sodium density is associated with elevated BP, specifically nighttime systolic BP, in healthy young men and women, suggesting sodium density relates to BP as strongly as absolute sodium intake. Supported by NIH Grant 1R01HL145055 and P20GM113125. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Sports participation confers many benefits across physical and psychosocial domains, yet greatly increases injury risk. Ending a sport may pose additional challenges to physical and psychological wellbeing. PURPOSE: Describe the transitional experiences of former collegiate varsity athletes in midlife. METHODS: Former varsity college athletes from several sports participated in audio recorded, in-person semi-structured interviews lasting about 30 minutes. Interviews focused on their lived experiences including past and current physical and mental health; impact of injuries; activity, exercise, and dietary trajectories; and transition to life after college athletics. Qualitative interviews were electronically transcribed, checked for accuracy, and transferred to Dedoose for thematic analysis using an iterative process. RESULTS: Fifteen former college athletes (mean age 50 ± 7 [range: 42-61] years, 9 Female/6 Male, 10 Caucasian/5 African American) were interviewed. Several themes emerged: 1) athlete identity; 2) college athlete experiences spanning physical and emotional elements; 3) transferrable life skills such as mental fortitude, time management, work ethic, and leadership skills; 4) transition from both college and athletics; 5) post-college health; and 6) facilitators and barriers to post-college physical and psychological health. Continuing sports post college eased the transition for many but often delayed their post athlete void. Challenges included managing pain and prior injury (e.g., “If I didn't have my knee injury, I would definitely be more active”), reducing energy intake (e.g., “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 program, toolkit, mentoring relationships, or mandatory exit course to facilitate the transition. CONCLUSIONS: While former college athletes benefit from many transferrable life skills and often continue engaging in sports and exercise, they face unique challenges transitioning to life after sport. Future research could evaluate various exit courses, programs, and toolkits to facilitate a healthier transition in aging former college athletes. FUNDING: NIH grant DP5-OD031833

Introduction: Despite recommendations to ingest <2.3 g of sodium/day, Americans consume an average of 3.4 g daily. The mechanisms through which this excess sodium intake may contribute to cardiovascular disease risk are not fully understood. We have demonstrated that a 7-day high sodium diet containing ~7 g/day blunts endothelium-dependent dilation in normotensive, salt resistant individuals. Ample evidence suggests that oxidative stress contributes to the vascular consequences of experimental high sodium diets. However, it is unknown whether chronic consumption of dietary sodium typical of the average American results in oxidative stress-induced reductions in endothelium-dependent dilation. Therefore, we tested the hypothesis that an acute systemic infusion of the antioxidant ascorbic acid (AA) would augment brachial artery flow-mediated dilation (FMD) in normotensive, non-obese young adults who habitually consume ≥3.4 g/day of dietary sodium. Methods: Twenty-nine participants (13M/16F, 28±6 y) were included based on a 3-day diet record screening. After at least 15 min of supine rest, brachial artery diameter and blood velocity were recorded via duplex ultrasound before and for 3 min after a 5-min occlusion of the forearm. A 20-min infusion of 0.06 g of AA/kg fat free mass dissolved in 100 ml normal saline was administered intravenously at a rate of 5 ml/min. Subsequently, a maintenance AA dose of 0.02 g/kg fat free mass was then infused at 2 ml/min while testing was repeated. All recordings were analyzed via edge tracking software with FMD calculated as the peak diameter change relative to baseline diameter and brachial artery shear rate calculated as 4✕velocity/diameter. Results: Habitual sodium intakes at screening averaged 4.5±1.1 g/day while urinary sodium excretion the day prior to the study visit was 136±57 mmol/24 hr. Following AA, time-to-peak dilation of the brachial artery was reduced from 51±14 to 42±9 s (P<0.001). Likewise, shear rate area under the curve (AUC) to peak dilation was also reduced after AA (3.3±1.5 x104 vs. 2.7±1.5 x104 a.u., P=0.001). FMD was unchanged from pre-AA to post-AA (8.6±3.0 vs. 8.0±3.6%, P=0.26). FMD remained similar after covarying for shear AUC (P=0.60). In contrast, indices of microvascular reactivity were reduced from pre-AA to post-AA, including post-occlusion peak blood flow (Δ-48.7±65.7 ml/min, P<0.001) and total reactive hyperemia (Δ-37.4±46.9 ml, P<0.001). Conclusions: These preliminary data indicate that acute systemic antioxidant treatment does not augment brachial artery endothelium-dependent dilation in normotensive, non-obese young adults who consume or exceed the national average daily sodium intake. This finding suggests that oxidative stress does not reduce conduit artery endothelial function in this population. Further investigation is needed to understand our observation of a diminished post-occlusion microvascular response after AA. This work was supported by the National Institutes of Health (5R01HL104106 and 5P20GM113125) and the American Heart Association (20POST35080171). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Chronic consumption of a Western diet (WD), high in added sugars and saturated fat (SFA) and low in fiber, contributes to increased cardiometabolic risk parameters, including elevated serum lipids and uric acid (UA). Additionally, long-term WD consumption is negatively associated with cognitive function and brain health. Reductions in cerebral blood flow (CBF) have been observed following acute dietary added sugar and SFA intake; however, the direct acute effects of a Western-style meal on cerebrovascular function and the underlying mechanisms are not fully understood. The purpose of this study was to determine the effects of a single Western-style meal on serum lipids and UA along with cerebrovascular function in healthy young and middle-aged adults. 11 participants [6M/5F, age: 45±14 y (range: 30-64 y); BMI: 26±3 kg/m 2 ; BP: 118±12/74±6 mmHg] were enrolled in this randomized-controlled crossover trial. Participants were randomized to two meals that were similar in total energy (~1280 kcal) and macronutrient content. The experimental WD meal consisted of 61 g added sugars, 26 g SFA (60 g total fat), and 5 g fiber, while the control meal (CM) consisted of 16 g added sugars, 12 g SFA (60 g total fat), and 19 g fiber. Serum lipids and UA were assessed at baseline and 3 hours after consumption of each meal. Cerebrovascular reactivity (CVR) was measured at both timepoints and was assessed as the maximal % change in gray matter CBF during 3-minutes of hypercapnia. CBF was measured using pseudo-continuous arterial spin labeling (PCASL) with a single post-labeling delay and was acquired using a Siemens 3T Prisma MRI scanner. A 2x2 repeated measures ANOVA was used to quantify serum lipids and UA pre- and post-consumption of each meal. An unpaired Mann-Whitney test was used to assess post-meal changes in CVR following the WD meal and CM. Serum triglyceride (Time: p=0.0003; Meal: p=0.57; Interaction: p=0.97) and VLDL-C concentrations (Time: p=0.0005; Meal: p=0.55; Interaction: p=0.81) were higher while HDL-C (Time: p<0.0001; Meal: p=0.17; Interaction: p=0.55) and LDL-C (Time: p=0.0004; Meal: p=0.26; Interaction: p=0.94) were lower after consuming each meal with no main or interaction effect of meal type. Serum UA concentration was reduced following both meals with a greater decrease following the WD meal (Time: p<0.0001; Meal: p=0.35; Interaction: p=0.03). Post-meal % Δ CVR was increased following the WD meal compared to CM [WD (N=10): 1.88 ± 2.86% vs. CM (N=7): -0.31 ± 0.46%; p=0.03]. These results suggest serum UA concentration is reduced and CVR is increased after acute consumption of a WD meal. Future studies should explore the interaction between UA metabolism and cerebrovascular function following an acute WD meal to better understand the mechanism behind the negative association between chronic WD consumption and cognitive function. Grant Support: NIH grants P20GM103653, P20GM113125, K01AG054731 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

PURPOSE: We tested the hypothesis that salt loading (SL) in young adults increases the magnitude of aortic pulse waves and speeds their reflection to the left ventricle (LV). We further hypothesized that these effects of SL are blunted in physically active individuals compared to their inactive counterparts. METHODS: Healthy young adults (10 M/11F, 26 ± 4 y) were studied after 10 days of SL (10 g/day of NaCl capsules) and 10 days of placebo capsules added to their habitual diets in random order. Physical activity was assessed throughout the study via actigraphy. Participants who averaged >30 min/day of moderate to vigorous physical activity (MVPA) were classified as active. LV outflow waveforms were recorded via Doppler echocardiography and aortic pressure waveforms were generated via a transfer function applied to tonometry-acquired radial artery pulse waves. Wave separation analysis was performed to determine the amplitude of forward (Pf) and backward (Pb) pulse waves and reflected wave travel time (RWTT). The portion of the systolic pressure-time integral attributed to reflected waves was defined as LV wasted pressure effort (WPE). RESULTS: Eleven participants were active based on average MVPA (66 ± 37 vs. 20 ± 8 min/day). Similar increases in urinary sodium excretion from placebo to SL occurred in both groups (active: 175 ± 87 to 291 ± 93 mmol/24 h, inactive: 152 ± 60 to 295 ± 143 mmol/24 h condition p < 0.001, group: p = 0.79). Pf was not different across groups (p = 0.40) or condition (p = 0.23). Likewise, Pb did not differ from placebo to SL across groups (active: ∆0 ± 2 mmHg, inactive: ∆2 ± 3 mmHg, p = 0.13) and RWTT was similar across groups (p = 0.81) and conditions (active: ∆-6 ± 17 ms, inactive: ∆-2 ± 12 ms, p = 0.26). No effect of condition (p = 0.36) or group (p = 0.88) was observed for WPE. CONCLUSIONS: In contrast to our hypothesis, these preliminary data suggest that excess salt does not alter aortic pulse wave amplitude or timing in young adults whether or not they exceed 30 min/day of MVPA. Notably, the average urinary sodium excretion at the placebo visit indicates that sodium intakes in this cohort exceed recommendations. Further investigation is needed to determine if habitual sodium intake influences the effects of salt loading on aortic pulse waves. Supported by NIH Grants 5R01HL104106, 5P20GM113125; AHA 20POST35080171

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 x 10-5 +/- 4.1 x 10-5 mol/L; HSD + MEL: 8.7 x 10-5 +/- 5.1 x 10-5 mol/L; p = 0.55) nor free radical number (HSD + PL: 8.0 x 1015 +/- 4.4 x 1015; HSD + MEL: 9.0 x 1015 +/- 4.9 x 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.

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.