Post-meal exercise under ecological conditions improves post-prandial glucose levels but not 24-hour glucose control.

We investigated whether post-meal walking (PMW) improved post-prandial glucose and 24h glucose control under free-living conditions among physically inactive young women. METHODS: Young women (Age: 20±1years; percent body fat: 28.2 ± 12%; BMI: 23.8 ± 4.2kg·m-1) completed a randomised crossover study to assess if PMW confers benefit. On the PMW day, women completed three bouts of brisk walks, and on the Control day they were instructed to follow normal habitual activities. Continuous glucose monitors captured post-prandial and 24h glucose, and physical activity monitors tracked physical activity throughout the study. RESULTS: PMW walking increased total daily step count (Control = 9,159 ± 2,962 steps vs. PMW = 14,611±3,891 steps, p<0.001) and activity scores (Control=33.87±1.16 METs·h vs. PMW = 36.11±1.58 METs·h, p < 0.001). PMW led to lower 3h average post-prandial glucose (main effect of condition, p=0.011) and 3h post-prandial area under curve glucose responses (main effect of condition, p = 0.027) compared to the control condition. Post hoc analysis revealed the largest decline occurred after dinner (3h average glucose Control = 7.55±1.21 mmol/L vs. PMW = 6.71 ± 0.80mmol/L, p = 0.039), when insulin sensitivity is typically diminished. Despite improvements in post-prandial glucose control, this did not translate to improvements in 24h glucose control (p > 0.05). CONCLUSION: Physically inactive and metabolically healthy young women, PMW improves post-prandial glucose but not 24h glucose control.

Adjusting for muscle strength and body size attenuates sex differences in the exercise pressor reflex in young adults.

Females typically exhibit lower blood pressure (BP) during exercise than males. However, recent findings indicate that adjusting for maximal strength attenuates sex differences in BP during isometric handgrip (HG) exercise and postexercise ischemia (PEI; metaboreflex isolation). In addition, body size is associated with HG strength but its contribution to sex differences in exercising BP is less appreciated. Therefore, the purpose of this study was to determine whether adjusting for strength and body size would attenuate sex differences in BP during HG and PEI. We obtained beat-to-beat BP in 110 participants (36 females, 74 males) who completed 2 min of isometric HG exercise at 40% of their maximal voluntary contraction followed by 3 min of PEI. In a subset (11 females, 17 males), we collected muscle sympathetic nerve activity (MSNA). Statistical analyses included independent t tests and mixed models (sex × time) with covariate adjustment for 40% HG force, height2, and body surface area. Females exhibited a lower absolute 40% HG force than male participants (Ps < 0.001). Females exhibited lower Δsystolic, Δdiastolic, and Δmean BPs during HG and PEI than males (e.g., PEI, Δsystolic BP, 15 ± 11 vs. 23 ± 14 mmHg; P = 0.004). After covariate adjustment, sex differences in BP responses were attenuated. There were no sex differences in MSNA. In a smaller strength-matched cohort, there was no sex × time interactions for BP responses (e.g., PEI systolic BP, P = 0.539; diastolic BP, P = 0.758). Our data indicate that sex differences in exercising BP responses are attenuated after adjusting for muscle strength and body size.NEW & NOTEWORTHY When compared with young males, females typically exhibit lower blood pressure (BP) during exercise. Adjusting for maximal strength attenuates sex differences in BP during isometric handgrip (HG) exercise and postexercise ischemia (PEI), but the contribution of body size is unknown. Novel findings include adjustments for muscle strength and body size attenuate sex differences in BP reactivity during exercise and PEI, and sex differences in body size contribute to HG strength differences.

Apocynin and Tempol ameliorate dietary sodium-induced declines in cutaneous microvascular function in salt-resistant humans.

It has previously been shown that high dietary salt impairs vascular function independent of changes in blood pressure. Rodent studies suggest that NADPH-derived reactive oxygen species mediate the deleterious effect of high salt on the vasculature, and here we translate these findings to humans. Twenty-nine healthy adults (34 ± 2 yr) participated in a controlled feeding study. Participants completed 7 days of a low-sodium diet (LS; 20 mmol sodium/day) and 7 days of a high-sodium diet (HS; 300 mmol sodium/day) in random order. All participants were salt resistant, defined as a ≤5-mmHg change in 24-h mean BP determined while on the LS and HS diets. Laser Doppler flowmetry was used to assess cutaneous vasodilation in response to local heating (42°C) during local delivery of Ringer's (n = 29), 20 mM ascorbic acid (AA; n = 29), 10 µM Tempol (n = 22), and 100 µM apocynin (n = 22). Additionally, endothelial cells were obtained in a subset of participants from an antecubital vein and stained for nitrotyrosine (n = 14). Cutaneous vasodilation was attenuated by the HS diet compared with LS [LS 93.0 ± 2.2 vs. HS 86.8 ± 2.0 percentage of maximal cutaneous vascular conductance (%CVCmax); P < 0.05] and was restored by AA during the HS diet (AA 90.7 ± 1.2 %CVCmax; P < 0.05 vs. HS). Cutaneous vasodilation was also restored with the local infusion of both apocynin (P < 0.01) and Tempol (P < 0.05) on the HS diet. Nitrotyrosine expression was increased on the HS diet compared with LS (P < 0.05). These findings provide direct evidence of dietary sodium-induced endothelial cell oxidative stress and suggest that NADPH-derived reactive oxygen species contribute to sodium-induced declines in microvascular function. NEW & NOTEWORTHY High-sodium diets have deleterious effects on vascular function, likely mediating, in part, the increased cardiovascular risk associated with a high sodium intake. Local infusion of apocynin and Tempol improved microvascular function in salt-resistant adults on a high-salt diet, providing evidence that reactive oxygen species contribute to impairments in microvascular function from high salt. This study provides insight into the blood pressure-independent mechanisms by which dietary sodium impairs vascular function. Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/dietary-sodium-oxidative-stress-and-microvascular-function/ .

Relation between resting sympathetic outflow and vasoconstrictor responses to sympathetic nerve bursts: sex differences in healthy young adults.

Previous studies have demonstrated an inverse relation between resting muscle sympathetic nerve activity (MSNA) and vasoconstrictor responsiveness (i.e., sympathetic transduction), such that those with high resting MSNA have low vascular responsiveness, and vice versa. The purpose of this investigation was to determine whether biological sex influences the balance between resting MSNA and beat-to-beat sympathetic transduction. We measured blood pressure (BP) and MSNA during supine rest in 54 healthy young adults (27 females: 23 ± 4 yr, 107 ± 8/63 ± 8 mmHg; 27 males: 25 ± 3 yr, 115 ± 11/64 ± 7 mmHg; means ± SD). We quantified beat-to-beat fluctuations in mean arterial pressure (MAP, mmHg) and limb vascular conductance (LVC, %) for 10 cardiac cycles after each MSNA burst using signal averaging, an index of sympathetic vascular transduction. In females, there was no correlation between resting MSNA (burst incidence; burst/100 heartbeats) and peak ΔMAP (r = -0.10, P = 0.62) or peak ΔLVC (r = -0.12, P = 0.63). In males, MSNA was related to peak ΔMAP (r = -0.50, P = 0.01) and peak ΔLVC (r = 0.49, P = 0.03); those with higher resting MSNA had blunted increases in MAP and reductions in LVC in response to a burst of MSNA. In a sub-analysis, we performed a median split between high- versus low-MSNA status on ΔMAP and ΔLVC within each sex and found that only males demonstrated a significant difference in ΔMAP and ΔLVC between high- versus low-MSNA groups. These findings support an inverse relation between resting MSNA and sympathetic vascular transduction in males only and advance our understanding on the influence of biological sex on sympathetic nervous system-mediated alterations in beat-to-beat BP regulation.

The influence of acute elevations in plasma osmolality and serum sodium on sympathetic outflow and blood pressure responses to exercise.

Elevated plasma osmolality (pOsm) has been shown to increase resting sympathetic nerve activity in animals and humans. The present study tested the hypothesis that increases in pOsm and serum sodium (sNa+) concentration would exaggerate muscle sympathetic nerve activity (MSNA) and blood pressure (BP) responses to handgrip (HG) exercise and postexercise ischemia (PEI). BP and MSNA were measured during HG followed by PEI before and after a 23-min hypertonic saline infusion (HSI-3% NaCl). Eighteen participants (age 23 ± 1 yr; BMI 24 ± 1 kg/m2) completed the protocol; pOsm and sNa+ increased from pre- to post-HSI (285 ± 1 to 291 ± 1 mosmol/kg H2O; 138.2 ± 0.3 to 141.3 ± 0.4 mM; P < 0.05 for both). Resting mean BP (90 ± 2 vs. 92 ± 1 mmHg) and MSNA (11 ± 2 vs. 15 ± 2 bursts/min) were increased pre- to post-HSI ( P < 0.05 for both). Mean BP responses to HG (106 ± 2 vs. 111 ± 2 mmHg, P < 0.05) and PEI (102 ± 2 vs. 107 ± 2 mmHg, P < 0.05) were higher post-HSI. Similarly, MSNA during HG (20 ± 2 vs. 29 ± 2 bursts/min, P < 0.05) and PEI (19 ± 2 vs. 24 ± 3 bursts/min, P < 0.05) were greater post-HSI. In addition, the change in MSNA was greater post-HSI during HG (Δ9 ± 2 vs. Δ13 ± 3 bursts/min, P < 0.05). A second set of participants ( n = 13, age 23 ± 1 yr; BMI 24 ± 1 kg/m2) completed a time control (TC) protocol consisting of quiet rest instead of an infusion. The TC condition yielded no change in resting sNa+, pOsm, mean BP, or MSNA (all P > 0.05); responses to HG and PEI were not different pre- to post-quiet rest ( P > 0.05). In summary, acutely increasing pOsm and sNa+ exaggerates BP and MSNA responses during HG exercise and PEI. NEW & NOTEWORTHY Elevated plasma osmolality has been shown to increase resting sympathetic activity and blood pressure. This study provides evidence that acute elevations in plasma osmolality and serum sodium exaggerated muscle sympathetic nerve activity and blood pressure responses during exercise pressor reflex activation in healthy young adults.

Alterations in dietary sodium intake affect cardiovagal baroreflex sensitivity.

High dietary sodium intake has been linked to alterations in neurally mediated cardiovascular function, but the effects of high sodium on cardiovagal baroreflex sensitivity (cBRS) in healthy adults are unknown. The purpose of this study was to determine whether high dietary sodium alters cBRS and heart rate variability (HRV) and whether acute intravenous sodium loading similarly alters cBRS and HRV. High dietary sodium (300 mmol/day, 7 days) was compared with low dietary sodium (20 mmol/day, 7 days; randomized) in 14 participants (38 ± 4 yr old, 23 ± 1 kg/m2 body mass index, 7 women). Acute sodium loading was achieved via a 23-min intravenous hypertonic saline infusion (HSI) in 14 participants (22 ± 1 yr old, 23 ± 1 kg/m2 body mass index, 7 women). During both protocols, participants were supine for 5 min during measurement of beat-to-beat blood pressure (photoplethysmography) and R-R interval (ECG). cBRS was evaluated using the sequence method. Root mean square of successive differences in R-R interval (RMSSD) was used as an index of HRV. Serum sodium (137.4 ± 0.7 vs. 139.9 ± 0.5 meq/l, P < 0.05), plasma osmolality (285 ± 1 vs. 289 ± 1 mosmol/kgH2O, P < 0.05), cBRS (18 ± 2 vs. 26 ± 3 ms/mmHg, P < 0.05), and RMSSD (62 ± 6 vs. 79 ± 10 ms, P < 0.05) were increased following high-sodium diet intake compared with low-sodium diet intake. HSI increased serum sodium (138.1 ± 0.4 vs. 141.1 ± 0.5 meq/l, P < 0.05) and plasma osmolality (286 ± 1 vs. 290 ± 1 mosmol/kgH2O, P < 0.05) but did not change cBRS (26 ± 5 vs. 25 ± 3 ms/mmHg, P = 0.73) and RMSSD (63 ± 9 vs. 63 ± 8 ms, P = 0.99). These data suggest that alterations in dietary sodium intake alter cBRS and HRV but that acute intravenous sodium loading does not alter these indexes of autonomic cardiovascular regulation.

Peripheral venous distension elicits a blood pressure raising reflex in young and middle-aged adults.

Distension of peripheral veins in humans elicits a pressor and sympathoexcitatory response that is mediated through group III/IV skeletal muscle afferents. There is some evidence that autonomic reflexes mediated by these sensory fibers are blunted with increasing age, yet to date the venous distension reflex has only been studied in young adults. Therefore, we tested the hypothesis that the venous distension reflex would be attenuated in middle-aged compared with young adults. Nineteen young (14 men/5 women, 25 ± 1 yr) and 13 middle-aged (9 men/4 women, 50 ± 2 yr) healthy normotensive participants underwent venous distension via saline infusion through a retrograde intravenous catheter in an antecubital vein during limb occlusion. Beat-by-beat blood pressure, muscle sympathetic nerve activity (MSNA), and model flow-derived cardiac output (Q), and total peripheral resistance (TPR) were recorded throughout the trial. Mean arterial pressure (MAP) increased during the venous distension in both young (baseline 83 ± 2, peak 94 ± 3 mmHg; P < 0.05) and middle-aged adults (baseline 88 ± 2, peak 103 ± 3 mmHg; P < 0.05). MSNA also increased in both groups [young: baseline 886 ± 143, peak 1,961 ± 242 arbitrary units (AU)/min; middle-aged: baseline 1,164 ± 225, peak 2,515 ± 404 AU/min; both P < 0.05]. TPR (P < 0.001), but not Q (P = 0.76), increased during the trial. However, the observed increases in blood pressure, MSNA, and TPR were similar between young and middle-aged adults. Additionally, no correlation was found between age and the response to venous distension (all P > 0.05). These findings suggest that peripheral venous distension elicits a pressor and sympathetic response in middle-aged adults similar to the response observed in young adults.

The Relationship between Sleep Duration and Metabolic Syndrome Severity Scores in Emerging Adults.

BACKGROUND: Research suggests sleep duration can influence metabolic systems including glucose homeostasis, blood pressure, hormone regulation, nervous system activity, and total energy expenditure (TEE), all of which are related to cardiometabolic disease risk, even in young adults. The purpose of this study was to examine the relationship between sleep duration and metabolic syndrome severity scores (MSSS) in a sample of emerging adults (18-24 y/o). METHODS: Data were collected between 2012 and 2021 from the College Health and Nutrition Assessment Survey, an ongoing, cross-sectional study conducted at a midsized northeastern university. Anthropometric, biochemical, and clinical measures were obtained following an overnight fast and used to assess the prevalence of metabolic syndrome (MetS). MetS severity scores (MSSS) were calculated using race- and sex-specific formulas. Sleep duration was calculated from the difference in self-reported bedtime and wake time acquired through an online survey. ANCOVA was used to examine the relationship between sleep duration and MetS severity score while adjusting for covariates (age, sex, BMI, physical activity level, smoking status, alcohol consumption, and academic major). RESULTS: In the final sample (n = 3816), MetS (≥3 criteria) was present in 3.3% of students, while 15.4% of students presented with ≥2 MetS criteria. Mean MSSS was -0.65 ± 0.56, and the reported sleep duration was 8.2 ± 1.3 h/day. MSSS was higher among low sleepers (<7 h/day) and long sleepers (>9 h/day) compared to the reference sleepers (7-8 h/day) (-0.61 ± 0.02 and -0.63 ± 0.01 vs. -0.7 ± 0.02, respectively, p < 0.01). CONCLUSIONS: Our findings suggest short (<7 h/day) and long (>9 h/day) sleep durations raise the risk of MetS in a sample of emerging adults. Further research is needed to elucidate the impact of improving sleep habits on future disease risk.

Impact of a family history of hypertension and physical activity on left ventricular mass.

BACKGROUND: A positive family history of hypertension (FHH) (+FHH) is associated with elevated left ventricular mass (LVM). Regular physical activity (PA) may eliminate differences in LVM between +FHH and negative family history of hypertension (-FHH) adults. The aim of this study was to determine if a +FHH is associated with a greater LVM compared to a -FHH group within a sample of young, mostly active healthy adults with and without statistically controlling for PA. METHODS: Healthy young (18-32 y) participants self-reported FHH status and habitual moderate and vigorous PA frequency. Participants then underwent an echocardiogram. RESULTS: Of the 61 participants, 32 (M=11, W=21; non-active=8) reported -FHH and the remaining 29 (M=13, W=16; non-active=2) reported a +FHH. Mann-Whitney tests found the +FHH group had greater LVM (-FHH 129.5±41.8, +FHH 155.2±42.6 g, P=0.015) and LVM/body surface area (BSA) (-FHH 73.5±17.4, +FHH 88.4±17.3 g/m2, P=0.004). Separate ANCOVA models accounting for moderate and vigorous PA found that FHH status independently predicted LVM/BSA and PA frequencies were significant modifiers (ANCOVA controlling moderate PA: FHH status P=0.004, partial η2=0.133; moderate PA P=0.020, partial η2=0.089), (ANCOVA controlling vigorous PA: FHH status P=0.004, partial η2=0.132; vigorous PA P=0.007, partial η2=0.117). CONCLUSIONS: This analysis suggests that physically active young adults with a +FHH have elevated LVM compared to their -FHH counterparts. This finding is independent of their habitual moderate and vigorous physical activity frequencies.

Excess adiposity contributes to higher ambulatory central blood pressure and arterial stiffness in physically inactive young adults.

BACKGROUND: It remains unknown if physical inactivity and excess adiposity increases 24-h central blood pressure and arterial stiffness in young adults. This study examined 24-h central blood pressure and indirect measures of arterial stiffness (e.g., central pulse pressure) in physically inactive young adults with and without excess adiposity. METHODS: Body fat and ambulatory 24-h blood pressure were measured in 31 young adults (men: 22±4 years, N.=15; women: 22±5 years, N=16). Multi-frequency bioelectrical impedance measured body fat. Normal adiposity was defined as <20% body fat in men and <32% body fat in women, whereas excess adiposity was defined as ≥20% and ≥32% in men and women, respectively. Ambulatory 24-h central blood pressure was calculated based on brachial blood pressure and volumetric displacement waveforms. RESULTS: By design, the normal adiposity group had a lower body fat percentage (men: 15.5±4.6%; women: 20.8±2.5%) compared to the physically inactive excess adiposity group (men: 29.8±5.4%; women: 34.3±7.5%). Men and women with excess adiposity group had elevated central blood pressure (central systolic, P<0.05 vs. normal adiposity groups). Central pulse pressure was elevated in the excess adiposity group (men: 45±5 mmHg; women: 41±9 mmHg) compared to normal adiposity groups (men: 36±4 mmHg; women: 32±3 mmHg, P<0.05 for both), while other arterial stiffness (augmentation index and ambulatory arterial stiffness index) measures trended toward significance only in men with excess adiposity. CONCLUSIONS: Physically inactive men and women with excess adiposity have increased 24h central blood pressure and pulse pressure compared to physically inactive young adults with normal adiposity.

The effects of a respiratory training mask on steady-state oxygen consumption at rest and during exercise.

No studies have directly measured ventilatory and metabolic responses while wearing a respiratory training mask (RTM) at rest and during exercise. Eleven aerobically fit adults (age: 21 ± 1 years) completed a randomized cross-over study while wearing an RTM or control mask during cycling at 50% Wmax. An RTM was retrofitted with a gas collection tube and set to the manufacturer's "altitude resistance" setting of 6,000 ft (1,800 m). Metabolic gas analysis, ratings of perceived exertion, and oxygen saturation (SpO2) were measured during rest and cycling exercise. The RTM did not affect metabolic, ventilation, and SpO2 at rest compared to the control mask (all, effect of condition: P > 0.05). During exercise, the RTM blunted respiratory rate and minute ventilation (effect of condition: P < 0.05) compared to control. Similar increases in VO2 and VCO2 were observed in both conditions (both, effect of condition: P > 0.05). However, the RTM led to decreased fractional expired O2 and increased fractional expired CO2 (effect of condition: P < 0.05) compared to the control mask. In addition, the RTM decreased SpO2 and increased RPE (both, effect of condition: P < 0.05) during exercise. Despite limited influence on ventilation and metabolism at rest, the RTM reduces ventilation and disrupts gas concentrations during exercise leading to modest hypoxemia.

Central systolic blood pressure and aortic stiffness response to dietary sodium in young and middle-aged adults.

High dietary sodium intake can lead to hypertension and increased incidence of cardiovascular disease. We sought to determine the effect of short-term dietary sodium loading on central blood pressure and arterial stiffness in young (YG; 22-40 years) and middle-aged (MA; 41-60 years) normotensive adults. YG (n = 49; age: 27 ± 1 years) and MA (n = 36; age: 52 ± 1 years) subjects were randomized, in a cross-over design, to 7 days of low-sodium (LS; 20 mmol/d) or high-sodium (HS; 300 mmol/d) diet. On the last day of each diet, central pressures, forward and reflected wave amplitudes (via radial artery applanation tonometry), and carotid-femoral pulse wave velocity were assessed. Central systolic blood pressure (cSBP) was greater after HS in both YG (LS: 96 ± 1 vs. HS: 99 ± 1 mm Hg; P = .012) and MA (LS: 106 ± 2 vs. HS: 115 ± 3 mm Hg; P < .001). However, the increase in cSBP was greater in MA (YG: 4 ± 1 vs. MA: 9 ± 2; P = .02). In MA subjects, HS elicited greater forward (LS: 25 ± 1 vs. HS: 29 ± 1 mm Hg; P < .001) and reflected (LS: 19 ± 1 vs. HS: 23 ± 1 mm Hg; P < .001) wave amplitudes. Carotid-femoral pulse wave velocity was also greater in MA on HS but after adjustment for mean arterial pressure, the difference was no longer significant. Our data indicate that HS intake leads to a greater increase in cSBP in MA adults, which may be the result of increased forward and reflected wave amplitudes.

Blood pressure responses to dietary sodium: Association with autonomic cardiovascular function in normotensive adults.

Blood pressure responses to dietary sodium vary widely person-to-person. Salt sensitive rodent models display altered autonomic function, a trait thought to contribute to poor cardiovascular health. Thus, we hypothesized that increased salt sensitivity (SS) in normotensive humans would be associated with increased muscle sympathetic nerve activity (MSNA), decreased high frequency heart rate variability (HF-HRV), and decreased baroreflex sensitivity. Healthy normotensive men and women completed 1week of high (300mmol·day-1) and 1week of low (20mmol·day-1) dietary sodium (random order) with 24h mean arterial pressure (MAP) assessed on the last day of each diet to assess SS. Participants returned to the lab under habitual sodium conditions for testing. Forty-two participants are presented in this analysis, 19 of which successful MSNA recordings were obtained (n=42: age 39±2yrs., BMI 24.3±0.5kg·(m2)-1, MAP 83±1mmHg, habitual urine sodium 93±7mmol·24h-1; n=19: MSNA burst frequency 20±2 bursts·min-1). The variables of interest were linearly regressed over the magnitude of SS. Higher SS was associated with increased MSNA (burst frequency: r=0.469, p=0.041), decreased HF-HRV (r=-0.349, p=0.046), and increased LF/HF-HRV (r=0.363, p=0.034). SS was not associated with sympathetic or cardiac baroreflex sensitivity (p>0.05). Multiple regression analysis accounting for age found that age, not SS, independently predicted HF-HRV (age adjusted no longer significant; p=0.369) and LF/HF-HRV (age adjusted p=0.273). These data suggest that age-related salt sensitivity of blood pressure in response to dietary sodium is associated with altered resting autonomic cardiovascular function.

High dietary sodium reduces brachial artery flow-mediated dilation in humans with salt-sensitive and salt-resistant blood pressure.

Recent studies demonstrate that high dietary sodium (HS) impairs endothelial function in those with salt-resistant (SR) blood pressure (BP). The effect of HS on endothelial function in those with salt-sensitive (SS) BP is not currently known. We hypothesized that HS would impair brachial artery flow-mediated dilation (FMD) to a greater extent in SS compared with SR adults. Ten SR (age 42 ± 5 yr, 5 men, 5 women) and 10 SS (age 39 ± 5 yr, 5 men, 5 women) healthy, normotensive participants were enrolled in a controlled feeding study consisting of a run-in diet followed by a 7-day low dietary sodium (LS) (20 mmol/day) and a 7-day HS (300 mmol/day) diet in random order. Brachial artery FMD and 24-h BP were assessed on the last day of each diet. SS BP was individually assessed and defined as a change in 24-h mean arterial pressure (MAP) of >5 mmHg between the LS and HS diets (ΔMAP: SR -0.6 ± 1.2, SS 7.7 ± 0.4 mmHg). Brachial artery FMD was lower in both SS and SR individuals during the HS diet (P < 0.001), and did not differ between groups (P > 0.05) (FMD: SR LS 10.6 ± 1.3%, SR HS 7.2 ± 1.5%, SS LS 12.5 ± 1.7%, SS HS 7.8 ± 1.4%). These data indicate that an HS diet impairs brachial artery FMD to a similar extent in adults with SS BP and SR BP.