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.

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.

Physiological Mechanisms of Dietary Salt Sensing in the Brain, Kidney, and Gastrointestinal Tract.

Excess dietary salt (NaCl) intake is strongly correlated with cardiovascular disease and is a major contributing factor to the pathogenesis of hypertension. NaCl-sensitive hypertension is a multisystem disorder that involves renal dysfunction, vascular abnormalities, and neurogenically-mediated increases in peripheral resistance. Despite a major research focus on organ systems and these effector mechanisms causing NaCl-induced increases in arterial blood pressure, relatively less research has been directed at elucidating how NaCl is sensed by various tissues to elicit these downstream effects. The purpose of this review is to discuss how the brain, kidney, and gastrointestinal tract sense NaCl including key cell types, the role of NaCl versus osmolality, and the underlying molecular and electrochemical mechanisms.

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.

Effect of acute handgrip and aerobic exercise on wasted pressure effort and arterial wave reflections in healthy aging.

Aging increases arterial stiffness and wave reflections that augment left ventricular wasted pressure effort (WPE). A single bout of exercise may be effective at acutely reducing WPE via reductions in arterial wave reflections. In young adults (YA) acute aerobic exercise decreases, whereas handgrip increases, wave reflections. Whether acute exercise mitigates or exacerbates WPE and arterial wave reflection in healthy aging warrants further examination. The purpose of this study was to determine if there are age-related differences in WPE and wave reflection during acute handgrip and aerobic exercise. When compared with baseline, WPE increased substantially in older adults (OA) during handgrip (5,219 ± 2,396 vs. 7,019 ± 2,888 mmHg·ms, P < 0.001). When compared with baseline, there was a robust reduction in WPE in OA during moderate-intensity aerobic exercise (5,428 ± 2,084 vs. 3,290 ± 1,537 mmHg·ms, P < 0.001), despite absolute WPE remaining higher in OA compared with YA during moderate-intensity aerobic exercise (OA 3,290 ± 1,537 vs. YA 1,188 ± 962 mmHg·ms, P < 0.001). There was no change in wave reflection timing indexed to ejection duration in OA during handgrip (40 ± 6 vs. 38 ± 4%, P = 0.41) or moderate-intensity aerobic exercise (40 ± 5 vs. 42 ± 8%, P = 0.99). Conversely, there was an earlier return of wave reflection in YA during handgrip (60 ± 11 vs. 52 ± 6%, P < 0.001) and moderate-intensity aerobic exercise (59 ± 7 vs. 51 ± 9%, P < 0.001). Changes in stroke volume were not different between groups during handgrip (P = 0.08) or aerobic exercise (P = 0.47). The greater increase in WPE during handgrip and decrease in WPE during aerobic exercise suggest that aortic hemodynamic responses to acute exercise are exaggerated with healthy aging without affecting stroke volume.NEW & NOTEWORTHY We demonstrated that acute aerobic exercise attenuated, whereas handgrip augmented, left ventricular hemodynamic load from wave reflections more in healthy older (OA) compared with young adults (YA) without altering stroke volume. These findings suggest an exaggerated aortic hemodynamic response to acute exercise perturbations with aging. They also highlight the importance of considering exercise modality when examining aortic hemodynamic responses to acute exercise in older adults.

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.

Impact of angiotensin receptor-neprilysin inhibition on vascular function in heart failure with reduced ejection fraction: A pilot study.

The mechanisms for the benefits of Angiotensin Receptor Neprilysin Inhibition (ARNi) in heart failure patients with reduced ejection fraction (HFrEF) are likely beyond blood pressure reduction. Measures of vascular function such as arterial stiffness and endothelial function are strong prognostic markers of cardiovascular outcomes in HFrEF, yet the impact of ARNi on vascular health remains to be explored. We hypothesized that arterial stiffness and endothelial function would improve after 12 weeks of ARNi in HFrEF. We tested 10 stable HFrEF patients at baseline and following 12 weeks of ARNi [64 ± 9 years, Men/Women: 9/1, left ventricular ejection fraction (EF): 28 ± 6%] as well as 10 stable HFrEF patients that remained on conventional treatment (CON: 60 ± 7 years, Men/Women: 6/4, EF: 31 ± 5%; all p = NS). Arterial stiffness was assessed via carotid-femoral pulse wave velocity (PWV) and endothelial function was assessed via brachial artery flow-mediated dilation (FMD). PWV decreased after 12 weeks of ARNi (9.0 ± 2.1 vs. 7.1 ± 1.2 m/s; p < 0.01) but not in CON (7.0 ± 2.4 vs. 7.5 ± 2.3 m/s; p = 0.35), an effect that remained when controlling for reductions in mean arterial pressure (p < 0.01). FMD increased after 12 weeks of ARNi (2.2 ± 1.9 vs. 5.5 ± 2.1%; p < 0.001) but not in CON (4.8 ± 3.8 vs. 5.4 ± 3.4%; p = 0.34). Baseline PWV (p = 0.06) and FMD (p = 0.07) were not different between groups. These preliminary data suggest that 12 weeks of ARNi therapy may reduce arterial stiffness and improve endothelial function in HFrEF. Thus, the findings from this pilot study suggest that the benefits of ARNi are beyond blood pressure reduction and include improvements in vascular function.

High dietary salt intake increases urinary NGAL excretion and creatinine clearance in healthy young adults.

In rodents and older patients with elevated blood pressure (BP), high dietary sodium increases excretion of biomarkers of kidney injury, but it is unclear whether this effect occurs in healthy young adults. The purpose of this study was to determine whether short-term high dietary salt increases urinary excretion of the kidney injury biomarkers neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) in healthy young adults. Twenty participants participated in a double-blind, placebo-controlled, randomized crossover study. For 10 days each, participants were asked to consume salt (3,900 mg sodium) or placebo capsules. We measured BP during each visit, obtained 24-h urine samples for measurements of electrolytes, NGAL, and KIM-1, and assessed creatinine clearance. Compared with placebo, salt loading increased daily urinary sodium excretion (placebo: 130.3 ± 62.4 mmol/24 h vs. salt: 287.2 ± 72.0 mmol/24 h, P < 0.01). There was no difference in mean arterial BP (placebo: 77 ± 7 mmHg vs. salt: 77 ± 6 mmHg, P = 0.83) between conditions. However, salt loading increased the urinary NGAL excretion rate (placebo: 59.8 ± 44.4 ng/min vs. salt: 80.8 ± 49.5 ng/min, P < 0.01) and increased creatinine clearance (placebo: 110.5 ± 32.9 mL/min vs. salt: 145.0 ± 24.9 mL/min, P < 0.01). Urinary KIM-1 excretion was not different between conditions. In conclusion, in healthy young adults 10 days of dietary salt loading increased creatinine clearance and increased urinary excretion of the kidney injury biomarker marker NGAL but not KIM-1.NEW & NOTEWORTHY In healthy young adults, 10 days of dietary salt loading increased creatinine clearance and increased urinary excretion of the kidney injury biomarker marker neutrophil gelatinase-associated lipocalin despite no change in resting blood pressure.

Dietary sodium and health: How much is too much for those with orthostatic disorders?

High dietary salt (NaCl) increases blood pressure (BP) and can adversely impact multiple target organs including the vasculature, heart, kidneys, brain, autonomic nervous system, skin, eyes, and bone. However, patients with orthostatic disorders are told to increase their NaCl intake to help alleviate symptoms. While there is evidence to support the short-term benefits of increasing NaCl intake in these patients, there are few studies assessing the benefits and side effects of long-term high dietary NaCl. The evidence reviewed suggests that high NaCl can adversely impact multiple target organs, often independent of BP. However, few of these studies have been performed in patients with orthostatic disorders. We conclude that the recommendation to increase dietary NaCl in patients with orthostatic disorders should be done with care, keeping in mind the adverse impact on dietary NaCl in people without orthostatic disorders. Modest, rather than robust, increases in NaCl intake may be sufficient to alleviate symptoms but also minimize any long-term negative effects.

A systematic review and meta-analysis of the effects of aerobic exercise interventions on cardiorespiratory fitness in adults with intellectual disability.

BACKGROUND: Adults with an intellectual disability (ID) have low cardiorespiratory fitness (CRF). Low CRF has been associated with a high risk of cardiovascular disease and all-cause mortality. Participation in regular exercise can help adults with ID increase their CRF. OBJECTIVE: To perform a systematic review and meta-analysis of published, peer-reviewed clinical trials that evaluated the effects of aerobic exercise (AE) interventions on CRF in adults with ID, ages 18-65 years. METHODS: English-language articles were searched up to June 2021 from 11 electronic databases. Data were extracted using an author-developed form. Two independent authors assessed the risk of bias using the Tool for the Assessment of Study Quality and reporting in Exercise (TESTEX). Meta-analysis was performed using the RevMan 5.3. RESULTS: Of the 1870 article titles and abstracts screened, 16 articles were included. The average TESTEX score (out of 15) was 8.1 (SD = 3.5, range 2-14). The pooled effect was statistically significant (SMD = 0.41, 95% CI: 0.19 to 0.63, z = 3.59; p = .000) with moderate heterogeneity (I2 = 35%, p = .000). Both types of intervention produced statistically significant CRF gains, with interventions that combined AE with resistance, balance, and/or flexibility exercises being slightly more effective (SMD = 0.40, 95% CI: 0.11 to 0.70, p = .007) than non-combined interventions (SMD = 0.42, 95% CI: 0.05 to 0.79, p = .02). Heterogeneity was moderate but non-significant for both types of intervention. CONCLUSIONS: The review supports the use of AE interventions in promoting CRF in adults with ID. The interpretation is limited by the quality of evidence and by poorly described and/or executed familiarization and measurement protocols.

Subjective sleep score is associated with central and peripheral blood pressure values in children aged 7-12 years.

Shortened and poor-quality sleep have emerged as non-traditional risk factors for the development of hypertension in adults, and it is likely these relations extend to paediatric populations when evaluating sleep subjectively. Therefore, we aimed to evaluate subjective sleep metrics and their associations with central and peripheral blood pressure (BP) values in children. We hypothesized that poor-quality sleep and short sleep duration would be associated with elevated pressures in healthy children. Subjective sleep habits and sleep duration were evaluated using the Children's Sleep Habits Questionnaire (CSHQ) in 29 children aged 7-12 years (13 male/16 female). A total sleep score was generated by summing subscale scores: a higher score indicates poorer sleep habits. Peripheral BP was measured, and central pressures were estimated using pulse wave analysis. Pearson's r correlations were used to assess relations between total sleep score, sleep duration, and sleep score subscales with BP values. Sleep score was positively associated with central and peripheral systolic pressure (r = 0.43, p = 0.02 and r = 0.41, p = 0.03, respectively), diastolic pressure (r = 0.42, p = 0.02 and r = 0.36, p = 0.05, respectively) and mean arterial pressure (r = 0.40, p = 0.03 and r = 0.36, p = 0.03, respectively). Sleep duration was negatively associated with central and peripheral diastolic pressure (r = -0.40, p = 0.03 and r = -0.41, p = 0.03, respectively). Regarding the CSHQ subscales, daytime sleepiness and parasomnias were consistently positively associated with BP values. These findings support sleep as a primordial prevention target for hypertension and the maintenance of cardiovascular health during childhood. Consideration of a variety of sleep habits using tools such as the CSHQ may provide important insights into early-life cardiovascular risk.

Activation of the Organum Vasculosum of the Lamina Terminalis Produces a Sympathetically Mediated Hypertension.

Neurons in the organum vasculosum of the lamina terminalis (OVLT) sense extracellular NaCl and angiotensin II concentrations to regulate body fluid homeostasis and arterial blood pressure. Lesion of the anteroventral third ventricular region or OVLT attenuates multiple forms of neurogenic hypertension. However, the extent by which OVLT neurons directly regulate sympathetic nerve activity to produce hypertension is not known. Therefore, the present study tested this hypothesis by using a multi-faceted approach including optogenetics, single-unit and multifiber nerve recordings, and chemogenetics. First, optogenetic activation of OVLT neurons in conscious Sprague-Dawley rats (250-400 g) produced frequency-dependent increases in arterial blood pressure and heart rate. These responses were not altered by the vasopressin receptor antagonist (ß-mercapto-ß,ß-cyclopentamethylenepropionyl1,O-me-Tyr2,Arg8)-vasopressin but eliminated by the ganglionic blocker chlorisondamine. Second, optogenetic activation of OVLT neurons significantly elevated renal, splanchnic, and lumbar sympathetic nerve activity. Third, single-unit recordings revealed optogenetic activation of the OVLT significantly increased the discharge of bulbospinal, sympathetic neurons in the rostral ventrolateral medulla. Lastly, chronic chemogenetic activation of OVLT neurons for 7 days significantly increased 24-hour fluid intake and mean arterial blood pressure. When the 24-hour fluid intake was clamped at baseline intakes, chemogenetic activation of OVLT neurons still produced a similar increase in arterial blood pressure. Neurogenic pressor activity assessed by the ganglionic blocker chlorisondamine was greater at 7 days of OVLT activation versus baseline. Collectively, these findings indicate that acute or chronic activation of OVLT neurons produces a sympathetically mediated hypertension.

Consistency where it counts: Sleep regularity is associated with circulating white blood cell count in young adults.

BACKGROUND: Sleep irregularity is predictive of poor health outcomes, and particularly those of cardiometabolic origins. The immune system is implicated in the pathogenesis of cardiometabolic diseases, however the relation between sleep regularity and immune cell profile is unclear. METHODS AND RESULTS: Forty-two healthy young adults (20 â€‹± â€‹2 years) completed 14 days of 24-h wrist actigraphy followed by a morning blood sample to evaluate circulating white blood cells (WBC) and subtypes (neutrophils, lymphocytes, monocytes). Sleep regularity was operationalized as the standard deviation (SD) of nightly sleep duration and SD of sleep onset time. Every 60-min increase in sleep duration SD was associated with an estimated 2.7 â€‹± â€‹0.60 x103 â€‹cells/µL (p<0.001) increase in total WBC count, while every 60-min increase in sleep onset SD was associated with an estimated 2.4 â€‹± â€‹0.60 x103 â€‹cells/µL (p<0.001) increase in WBCs. Sleep duration SD was also associated with lymphocyte count (11.5 â€‹± â€‹3.8 â€‹cells/µL per 1-min increase, p<0.01), while sleep onset SD was associated with neutrophil (34.7 â€‹± â€‹9.8 â€‹cells/µL per 1-min increase, p<0.01) and monocyte counts (3.0 â€‹± â€‹0.9 â€‹cells/µL per 1-min increase, p<0.01). Sleep regularity metrics remained significantly associated with WBCs in a series of regressions which adjusted for sex, body mass index, resting blood pressure, mean sleep duration, physical activity, dietary sodium, and alcohol consumption. CONCLUSIONS: Unfavorable associations between irregular sleep patterns and circulating immune cells are apparent in young adulthood. These findings contribute to the growing body of evidence suggesting that consistent sleep schedules are an important dimension of sleep and circadian health and may reduce excess chronic disease risk.

Actigraphy-derived rest--activity rhythms are associated with nocturnal blood pressure in young women.

INTRODUCTION: Misalignment between lifestyle behaviors and endogenous circadian rhythms is associated with elevated nocturnal blood pressure (BP) in experimental studies; however, less is known about free-living (i.e. nonlaboratory) circadian disruption and nocturnal BP. Additionally, sex-specific cardiovascular implications of circadian disruption are unclear. OBJECTIVE: To examine the associations between rest--activity rhythms (RAR), a field-based estimate of circadian disruption, and nocturnal BP characteristics in young men and women. METHODS: Fifty participants (20 ±â€Š1 years; 20 men/30 women) underwent 24-h ambulatory BP monitoring following 14 days of wrist actigraphy. RAR variables of interdaily stability (day-to-day consistency in RAR), intradaily variability (within-day fragmentation of RAR), and relative amplitude (difference between peak vs. trough activity) were derived from actigraphy. Multivariable regression models of mean nocturnal SBP, DBP, and SBP dipping were generated to test main associations with RAR variables, and sex × RAR interactions. Daytime BP, race, BMI, physical activity, sleep duration, alcohol, caffeine, and sodium intake were considered as covariates. RESULTS: In the full sample, no main associations between RAR and nocturnal BP characteristics were found. Sex interacted with RAR such that in women, higher interdaily stability (ß = -5.39, 95% CI = -10.04 to -0.73, P = 0.024) and relative amplitude (ß = -4.78, 95% CI = -9.22 to -0.34, P = 0.036) were both associated with lower nocturnal SBP. Sex-stratified multivariable models of nocturnal BP also revealed associations between interdaily stability and relative amplitude with SBP dipping in women (all P ≤ 0.01). No associations were apparent in men. CONCLUSION: Consistent and high-amplitude RAR are favorably associated with nocturnal BP characteristics in young women.

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.