Migliaccio, Gianna

Somali Americans, originating from East Africa, are a fast-growing minority in the United States. Emerging data suggest Somali individuals exhibit increased cardiovascular (CV) risk compared to non-Hispanic White adults. Previous data from our laboratory demonstrated elevated ambulatory arterial stiffness in Somali Americans, as derived from 24-hour blood pressure monitoring. We sought to confirm these vascular stiffness findings via gold-standard applanation tonometry and examine potential sex differences, given that females of African ancestry are at elevated risk of CV disease (CVD). We therefore examined aortic hemodynamics and carotid-femoral pulse wave velocity in male and female Somali Americans. We hypothesized that female Somali Americans would present with greater aortic wave reflection and arterial stiffness compared to males. We further examined the accuracy of prediction of aortic wave reflection from a predominantly White population, when applied to the Somali American population. We utilized applanation tonometry to quantify arterial stiffness in 24 female (age: 27±10 years, BMI: 27±6 kg/m 2 ) and 19 male (age: 22±6 years, BMI: 27±5 kg/m 2 ) Somali Americans without CVD. Each participant arrived in the laboratory at Mayo Clinic, fasted for at least three hours, and did not consume caffeine or exercise for at least 12 hours prior to testing. After 15 minutes of supine rest, duplicate recordings of aortic blood pressure and augmentation index (AIx) were obtained via pulse wave analysis. Similarly, aortic stiffness was quantified via duplicate carotid-femoral pulse wave velocity recordings. Statistical analysis included independent samples t-tests to test for sex differences in aortic hemodynamics, and paired samples t-tests to determine differences between estimated and obtained AIx (α≤0.05). Aortic systolic arterial pressure (111±11 vs. 108±7 mmHg, p=0.295) was similar between female and male Somali Americans. Aortic diastolic arterial pressure (75±7 vs. 67±7 mmHg, p<0.001) and heart rate (67±9 vs. 57±7 beats/min, p<0.001) were higher in female Somali adults. Similarly, AIx (28±14 vs. 19±12%, p=0.045) and AIx normalized to 75 heart beats/minute (24±13 vs. 10±13%, p=0.001) were higher in female Somali Americans. Carotid-femoral pulse wave velocity (5.4±0.9 vs. 5.5±0.8 m/s, p=0.661) was similar between sexes. Estimated AIx (corrected for sex, age, height, and resting heart rate) was markedly lower than observed AIx in both female (13±7 vs. 28±14%, p<0.001) and male (6±5 vs. 19±12%, p<0.001) Somali Americans. These findings, obtained in young, healthy Somali adults are suggestive of elevated CVD risk, evident at an early age. These data are particularly concerning regarding vascular dysfunction in Somali females and suggest that prediction models for arterial stiffness should factor in race to optimize performance. Future work into mechanisms underlying vascular dysfunction in Somali Americans is warranted. Sleep Number Grant to Mayo Clinic and by NIH R01-HL160619, R01-HL169320, T32-DK007013, K12 AR084222, and AHA 24POST1241616. 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.

Abstract Introduction Poor sleep quality is bidirectionally associated with cardiovascular and neurocognitive disorders. Preclinical data implicate nitric oxide (NO) in the onset, and maintenance, of sleep. Acute inorganic nitrate supplementation increases NO bioavailability via serial reduction for &gt;12hrs. We tested if objective (Aim 1) or subjective (Aim 2) sleep quality was better following acute, pre-sleep nitrate supplementation relative to a placebo. Methods Seven non-shift working adults (4F/3M, 40±8yrs, 25.8±1.6kg/m2) with no history of sleep, cardiovascular, or neurocognitive disorders completed three overnight polysomnography (PSG) visits with time in bed standardized to 2200-0600hrs. Visit 1 was for acclimation and screening for sleep-disordered breathing. On Visits 2 and 3, participants consumed beetroot juice containing (6.45mmol) or devoid of (0mmol) inorganic nitrate at 2200 using a randomized, cross-over study design. PSG-derived outcomes included slow-wave (SWS) and rapid eye-movement (REM) sleep, sleep efficiency, and wake after sleep onset (WASO). Subjective sleep quality assessments were administered in-laboratory including a 0-10 scale, the Stanford Sleepiness Scale (SSS), and performance with mental arithmetic shortly after awakening. Results No participant demonstrated evidence for sleep-disordered breathing (apnea-hypopnea index = 1.7±0.9events/hr). Total sleep time (TST, 434±17 vs. 412±19min), sleep efficiency (89±3 vs. 85±4%), as well as SWS duration (75±10 vs. 66±9min) and percent of TST (17±2 vs. 16±2%) were higher after nitrate relative to the placebo (p&lt; 0.05 for all). WASO (47±16 vs. 62±19min, p&lt; 0.05) was lower after nitrate versus placebo and no differences were seen in REM sleep duration (131±23 vs. 117±12min, p=0.45) nor percent of TST (30±5 vs. 29±3%, p=0.80). Neither the 0-10 scale (6.7±0.5 vs. 6.8±0.6units, p=0.84), SSS (2.6±0.4 vs. 2.5±0.3units, p=0.68), or arithmetic performance (82±3 vs. 81±5% correct, p=0.85) differed post-nitrate compared to post-placebo. Conclusion These data suggest that acutely increasing nocturnal NO levels via pre-sleep inorganic nitrate supplementation improves objective indices of sleep quality in healthy adults. However, greater amounts of nitrate or prolonged supplementation (weeks) may be needed to improve perceived sleep quality. Support (if any) The National Institutes of Health (K12 AR084222 to JMB, R01s HL160619 and HL65176 to VKS), Sleep Research Society Foundation (CDA 038-JP-23 to JMB), and the American Heart Association (24POST1241616 to IMG).

Increased cognitive hyperarousal is a proposed mechanism associated with clinical poor sleep including insomnia. An objective marker of nocturnal hyperarousal is high frequency electroencephalography during sleep, including increased beta frequency during stage two (N2) sleep. Acute and chronic poor sleep quality are associated with autonomic dysfunction, but little is known regarding the relationship between nocturnal beta frequency intrusion and nocturnal autonomic function. The purpose of this study was to explore the association between beta spectral power during stage two (N2) sleep and nocturnal heart rate variability (HRV) in healthy female and male adults. We hypothesized that heightened beta spectral power during N2 sleep would be associated with reduced nocturnal HRV. Twenty-four participants (12 males, 12 females; age, 25 ± 1 years; BMI 27 ± 1 kg/m2) underwent an 8-hour overnight sleep opportunity with continuous polysomnography and 5-lead electrocardiogram monitoring. Periods of 5 – 10 minutes of stable N2 sleep absent of cortical arousals, respiratory events, and limb movement-associated arousals were identified (one per cycle) for analysis. Periods from the first two cycles of N2 sleep from the full night were selected for analysis. Beta spectral power from the central and frontal regions and nocturnal HRV data were analyzed and averaged across each hemisphere. Time-domain HRV was quantified as the root mean squared of successive differences (RMSSD) and proportion of R-R intervals (RRI) varying by greater than 50 ms (pNN50). An inverse correlation was observed between central beta power and RRI (R= -0.473, p=0.019), pNN50 (R= -0.450, p=0.028), and RMSSD (R= -0.406, p=0.049). This was paralleled by a similar relationship between frontal beta and RRI (R= -0.487, p=0.016) and pNN50 (R= -0.423, p=0.039). Our results indicate a negative association between N2 beta power and nocturnal HRV measures. These findings suggest that nocturnal hyperarousal may be associated with poor cardiac autonomic function and has implications for individuals with insomnia in whom cognitive hyperarousal is frequently reported. Support is provided by the National Institutes of Health (AA-024892, U54GM115371; P20GM103474, 2TL1 TR002318). 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.