Sex Differences in Neurovascular Control: Implications for Obstructive Sleep Apnea.

Patients with obstructive sleep apnea (OSA) have a heightened risk of developing cardiovascular diseases, namely hypertension. While seminal evidence indicates a causal role for sympathetic nerve activity in the hypertensive phenotype commonly observed in patients with OSA, no studies have investigated potential sex differences in the sympathetic regulation of blood pressure in this population. Supporting this exploration are large-scale observational data, as well as controlled interventional studies in healthy adults, indicating that sleep disruption increases blood pressure to a greater extent in females relative to males. Furthermore, females with severe OSA demonstrate a more pronounced hypoxic burden (i.e., disease severity) during rapid eye movement sleep when sympathetic nerve activity is greatest. These findings would suggest that females are at greater risk for the hemodynamic consequences of OSA and related sleep disruption. Accordingly, the purpose of this review is three-fold: (1) to review the literature linking sympathetic nerve activity to hypertension in OSA, (2) to highlight recent experimental data supporting the hypothesis of sex differences in the regulation of sympathetic nerve activity in OSA, and (3) to discuss the potential sex differences in peripheral adrenergic signaling that may contribute to, or offset, cardiovascular risk in patients with OSA.

Blood pressure and muscle sympathetic nerve activity are associated with trait anxiety in humans.

Chronic anxiety is prevalent and associated with an increased risk of cardiovascular disease. Prior studies that have reported a relationship between muscle sympathetic nerve activity (MSNA) and anxiety have focused on participants with anxiety disorders and/or metabolic syndrome. The present study leverages a large cohort of healthy adults devoid of cardiometabolic disorders to examine the hypothesis that trait anxiety severity is positively associated with resting MSNA and blood pressure. Resting blood pressure (BP) (sphygmomanometer and finger plethysmography), MSNA (microneurography), and heart rate (HR; electrocardiogram) were collected in 88 healthy participants (52 males, 36 females, 25 ± 1 yr, 25 ± 1 kg/m2). Multiple linear regression was performed to assess the independent relationship between trait anxiety, MSNA, resting BP, and HR while controlling for age and sex. Trait anxiety was significantly correlated with systolic arterial pressure (SAP; r = 0.251, P = 0.018), diastolic arterial pressure (DAP; r = 0.291, P = 0.006), mean arterial pressure (MAP; r = 0.328, P = 0.002), MSNA burst frequency (BF; r = 0.237, P = 0.026), and MSNA burst incidence (BI; r = 0.225, P = 0.035). When controlling for the effects of age and sex, trait anxiety was independently associated with SAP (ß = 0.206, P = 0.028), DAP (ß = 0.317, P = 0.002), MAP (ß = 0.325, P = 0.001), MSNA BF (ß = 0.227, P = 0.030), and MSNA BI (ß = 0.214, P = 0.038). Trait anxiety is associated with increased blood pressure and MSNA, demonstrating an important relationship between anxiety and autonomic blood pressure regulation.NEW & NOTEWORTHY Anxiety is associated with development of cardiovascular disease. Although the sympathetic nervous system is a likely mediator of this relationship, populations with chronic anxiety have shown little, if any, alteration in resting levels of directly recorded muscle sympathetic nerve activity (MSNA). The present study is the first to reveal an independent relationship between trait anxiety, resting blood pressure, and MSNA in a large cohort of healthy males and females devoid of cardiometabolic comorbidities.

Effects of alcohol on sleep and nocturnal heart rate: Relationships to intoxication and morning-after effects.

BACKGROUND: Alcohol consumption produces feelings of well-being and stimulation, but also impairs psychomotor performance, disturbs cardiovascular function and sleep, and can disrupt next-day mood and behavior. A deeper understanding of how the acute effects of alcohol relate to its sleep and morning-after effects is needed to minimize harm resulting from its use. This study examined relationships between the effects of a high dose of alcohol on subjective and psychomotor measures, nocturnal heart rate, sleep quality, and morning-after mood and behavior. We hypothesized that alcohol would produce disturbances in cardiovascular and sleep regulation during the night, which would predict morning-after mood and behavioral performance. METHODS: Thirty-one men and women participated in two overnight laboratory visits during which they consumed either alcohol (1.0 g/kg for men, 0.85 g/kg for women) or placebo (randomized, crossover design). They consumed the beverage from 8 to 9 pm, and remained in the laboratory overnight for polysomnographic sleep recording. Subjective and behavioral measures were obtained during consumption and at 7-8 am the morning after. RESULTS: Alcohol increased both negative and positive arousal, urge to drink and sedation, and it impaired performance on behavioral tasks. During sleep, alcohol produced expected tachycardia and detriments in sleep quality including decreased total sleep time, sleep efficiency, and altered sleep architecture. Only modest effects on mood or performance were detected the following morning. The acute sedative-like effects of alcohol were related to increases in N2 sleep, but not to other disruptions in sleep or nocturnal heart rate, and neither sleep impairments nor nocturnal heart rate were related to mood or task performance the morning after. CONCLUSIONS: The effects of alcohol on sleep and nocturnal heart rate were not strongly related to either its acute or morning-after effects. These findings do not provide strong support for the idea that alcohol-induced sleep disruptions underlie morning-after effects.

Sympathetic neural reactivity to the Trier social stress test.

Sympathetic responsiveness to laboratory mental stress is highly variable, making interpretations of its role in stress reactivity challenging. The present study assessed muscle sympathetic nerve activity (MSNA, microneurography) responsiveness to the Trier social stress test (TSST), which employs an anticipatory stress phase, followed by a public speaking and mental arithmetic task. We hypothesized that sympathetic reactivity to the anticipatory phase would offer a more uniform response between individuals due to elimination of confounds (i.e. respiratory changes, muscle movement, etc.) observed during more common stress tasks. Participants included 26 healthy adults (11 men, 15 women, age: 25 ± 6 years, body mass index: 24 ± 3 kg/m2 ). Continuous heart rate (electrocardiogram) and beat-to-beat blood pressure (finger plethysmography) were recorded from all participants, while MSNA recordings were obtained in 20 participants. MSNA burst frequency was significantly reduced during anticipatory stress. During the speech, although burst frequency was unchanged, total MSNA was significantly increased. Changes in diastolic arterial pressure were predictive of changes in MSNA during anticipatory (ß = -0.680, P = 0.001), but not the speech (P = 0.318) or mental maths (P = 0.051) phases. Lastly, sympathetic reactivity to anticipatory stress was predictive of subsequent reactivity to both speech (ß = 0.740, P = 0.0002) and maths (ß = 0.663, P = 0.001). In conclusion, anticipatory social stress may offer a more versatile means of assessing sympathetic reactivity to mental stress in the absence of confounds and appears to predict reactivity to subsequent mental stress paradigms. KEY POINTS: Cardiovascular reactivity to laboratory mental stress is predictive of future health outcomes. However, reactivity of the sympathetic nervous system to mental stress is highly variable. The current study assessed peripheral muscle sympathetic nerve activity in response to the Trier social stress test, a psychosocial stressor that includes anticipatory stress, public speaking and mental arithmetic. Our findings demonstrate that sympathetic neural activity is consistently reduced during anticipatory stress. Conversely, the classically observed inter-individual variability of sympathetic responsiveness was observed during speech and maths tasks. Additionally, sympathetic reactivity to the anticipatory period accurately predicted how an individual would respond to both speech and maths tasks, outlining the utility of anticipatory stress in future research surrounding stress reactivity. Utilization of the Trier social stress test in autonomic physiology may offer an alternative assessment of sympathetic responsiveness to stress with more consistent inter-individual responsiveness and may be a useful tool for further investigation of stress reactivity.

Reliability of heart rate variability during stable and disrupted polysomnographic sleep.

Heart rate variability (HRV) is commonly used within sleep and cardiovascular research, yet HRV reliability across various sleep stages remains equivocal. The present study examined the reliability of frequency- and time-domain HRV within stage-2 (N2), slow-wave (SWS), and rapid-eye-movement (REM) sleep during both stable and disrupted sleep. We hypothesized that high-frequency (HF) HRV would be reliable in all three sleep stages, low-frequency (LF) HRV would be reliable during N2 and SWS, and that disrupted sleep via spontaneous cortical arousals would decrease HRV reliability. Twenty-seven participants (11 men, 16 women, 26 ± 1 yr) were equipped with laboratory polysomnography for 1 night. Both frequency- and time-domain HRV were analyzed in two 5- to 10-min blocks during multiple stable and disrupted sleep cycles across N2, SWS, and REM sleep. HF HRV was highly correlated across stable N2 (r = 0.839, P < 0.001), SWS (r = 0.765, P < 0.001), and REM (r = 0.881, P < 0.001). LF HRV was moderate-to-highly correlated during stable cycles of N2 sleep (r = 0.694, P < 0.001), SWS, (r = 0.765, P < 0.001), and REM (r = 0.699, P < 0.001) sleep. When stable sleep was compared with disrupted sleep, both time- and frequency-domain HRV were reliable (α > 0.90, P < 0.05) in N2, SWS, and REM, except for LF HRV during SWS (α = 0.62, P = 0.089). In conclusion, time- and frequency-domain HRV demonstrated reliability across stable N2, SWS, and REM sleep, and remained reliable during disrupted sleep. These findings support the use of HRV during sleep as a tool for assessing cardiovascular health and risk stratification.NEW & NOTEWORTHY Heart rate variability (HRV) is a commonly employed indirect estimate of cardiac autonomic activity during sleep with limited reliability studies. Nocturnal frequency-domain HRV was reliable across differing stable sleep cycles of stage-2 (N2), slow-wave (SWS), and rapid-eye-movement (REM) sleep. Moreover, frequency- and time-domain HRV were reliable during stable and disturbed sleep, except SWS low-frequency HRV. Our finding supports nocturnal HRV as a potential tool for cardiovascular risk stratification.

Sympathetic neural responses to sleep disorders and insufficiencies.

Short sleep duration and poor sleep quality are associated with cardiovascular risk, and sympathetic nervous system (SNS) dysfunction appears to be a key contributor. The present review will characterize sympathetic function across several sleep disorders and insufficiencies in humans, including sleep deprivation, insomnia, narcolepsy, and obstructive sleep apnea (OSA). We will focus on direct assessments of sympathetic activation, e.g., plasma norepinephrine and muscle sympathetic nerve activity, but include heart rate variability (HRV) when direct assessments are lacking. The review also highlights sex as a key biological variable. Experimental models of total sleep deprivation and sleep restriction are converging to support several epidemiological studies reporting an association between short sleep duration and hypertension, especially in women. A systemic increase of SNS activity via plasma norepinephrine is present with insomnia and has also been confirmed with direct, regionally specific evidence from microneurographic studies. Narcolepsy is characterized by autonomic dysfunction via both HRV and microneurographic studies but with opposing conclusions regarding SNS activation. Robust sympathoexcitation is well documented in OSA and is related to baroreflex and chemoreflex dysfunction. Treatment of OSA with continuous positive airway pressure results in sympathoinhibition. In summary, sleep disorders and insufficiencies are often characterized by sympathoexcitation and/or sympathetic/baroreflex dysfunction, with several studies suggesting women may be at heightened risk.

Blunted heart rate recovery to spontaneous nocturnal arousals in short-sleeping adults.

Chronic insufficient sleep is a common occurrence around the world and results in numerous physiological detriments and consequences, including cardiovascular complications. The purpose of the present study was to assess the relationship between habitual total sleep time (TST) measured objectively via at-home actigraphy and heart rate (HR) reactivity to nocturnal cortical arousals. We hypothesized that short habitual TST would be associated with exaggerated cardiac reactivity to nocturnal cortical arousals. Participants included 35 healthy individuals [20 men, 15 women, age: 24 ± 1 yr, body mass index (BMI): 27 ± 1 kg/m2], and were split using a median analysis into short-sleeping (SS; n = 17) and normal-sleeping (NS; n = 18) adults based on a minimum of 7 days of at-home actigraphy testing. All participants underwent a full overnight laboratory polysomnography (PSG) testing session, including continuous HR (electrocardiogram, ECG) sampling. HR reactivities to all spontaneous cortical arousals were assessed for 30 cardiac cycles following the onset of the arousal in all participants. Baseline HR was not significantly different between groups (P > 0.05). Spontaneous nocturnal arousal elicited an augmented HR response in the SS group, specifically during the recovery period [F(5.261,163.08) = 3.058, P = 0.01, ηp2 = 0.09]. There were no significant differences in HR reactivity between sexes [F(3.818,118.368) = 1.191, P = 0.318]. These findings offer evidence of nocturnal cardiovascular dysregulation in habitual short sleepers, independent from any diagnosed sleep disorders.NEW & NOTEWORTHY Short habitual sleep is associated with poor cardiovascular outcomes, but mechanisms remain equivocal. The present study used objectively measured habitual sleep via wrist actigraphy, and reports that habitual short sleepers have augmented heart rate recovery responses to spontaneous arousals as determined by gold-standard polysomnography. There were no reported sex differences. The augmented heart rate recovery to spontaneous cortical arousals may be an important mechanism contributing to the associations between insufficient sleep and cardiovascular risk.

Evening binge alcohol disrupts cardiovagal tone and baroreflex function during polysomnographic sleep.

STUDY OBJECTIVES: Binge alcohol consumption is associated with increased cardiovascular risk. The effects of evening binge alcohol consumption (i.e. 4-5 beverages within 2 h) on the vagal components of HRV and cardiovagal baroreflex sensitivity (cvBRS) during sleep remain largely equivocal. The present study examined the effects of evening binge alcohol consumption on nocturnal cardiac vagal tone and baroreflex sensitivity during stage N2, slow wave (SWS), and rapid eye movement (REM) sleep. We hypothesized that evening binge drinking would reduce HRV and cvBRS in each sleep stage. METHODS: Following a familiarization night within the laboratory, twenty-three participants were examined following a night of binge alcohol consumption and a fluid control (randomized, crossover design). A quality nocturnal beat-to-beat blood pressure signal was obtained in both conditions in 16 participants (seven men, nine women; 25 ± 1 years). RESULTS: Binge drinking reduced both the high frequency (HF) and time-domain components (i.e. pNN50 and RMSSD) of HRV in stage N2 sleep, SWS, and REM. In addition, cvBRS up-up (vagal activation) was reduced following binge alcohol consumption in stage N2 (21 ± 3 vs. 15 ± 3 ms/mmHg, p = 0.035) and REM (15[11-28] vs. 11[9-18] ms/mmHg, p = 0.009). Binge alcohol consumption reduced cvBRS down-down (vagal withdrawal) in stage N2 (23 ± 2 vs. 14 ± 2 ms/mmHg, p < 0.001), SWS (20[14-30] vs. 14[9-17] ms/mmHg, p = 0.022), and REM (14[11-24] vs. 10[7-15] ms/mmHg, p = 0.006). CONCLUSIONS: Evening binge alcohol consumption disrupts cardiac vagal tone and baroreflex function during nearly all sleep stages. These findings provide mechanistic insight into the potential role of binge drinking and alcohol abuse on cardiovascular risk. CLINICAL TRIALS DETAILS: Alcohol and Neural Cardiovascular Control in Binge Drinkers, www.clinicaltrials.gov/ct2/show/NCT03567434, NCT03567434.

Effect of evening blue light blocking glasses on subjective and objective sleep in healthy adults: A randomized control trial.

OBJECTIVES: Evening blue light has been shown to suppress melatonin, which can negatively impact sleep quality. The impact of evening blue light blocking (BLB) interventions on sleep remains ambiguous due to lack of randomized control trials. The present study tests the hypothesis that BLB glasses improve subjective and objective sleep in a population of healthy adults. DESIGN: Two-week, randomized, controlled, crossover design. SETTING: At-home testing of individuals in Michigan and Montana. PARTICIPANTS: Twenty healthy adults (11 men, 9 women, age: 32 ± 12, body mass index: 28 ± 4 kg/m2). INTERVENTION: Following a 1-week run-in baseline (ie, no glasses), participants were randomized to 1-week of BLB or control (ie, clear lens) glasses. Upon finishing the 1-week intervention, participants crossed over to the opposite condition. In both conditions, glasses were worn for 7 consecutive days from 6 PM until bedtime. MEASUREMENTS: Objective sleep parameters were obtained using wrist actigraphy. Subjective sleep measures were assessed using sleep diaries. Karolinska Sleep Diaries were used to assess perceived sleep quality. RESULTS: BLB reduced subjective sleep onset (21 ± 28 vs 24 ± 21 minute, P = .033) and awakenings (1.6 ± 1.0 vs 2.2 ± 1.0 awakenings, P = .019) compared to the control condition. In contrast, objective measures of sleep were not significantly impacted. In fact, our primary outcome variable of total sleep time (TST) tended to be paradoxically shorter in the BLB condition for both subjective (468 ± 45 vs 480 ± 48 minute, P = .066) and objective (433 ± 40 vs 449 ± 39 minute, P = .075) TST. CONCLUSIONS: Blue light blocking glasses did not improve objective measures of sleep time or quality in healthy adults.

Morning sympathetic activity after evening binge alcohol consumption.

Binge alcohol consumption elicits acute and robust increases of muscle sympathetic nerve activity (MSNA), yet the impact of evening binge drinking on morning-after MSNA is unknown. The present study examined the effects of evening binge alcohol consumption on polysomnographic sleep and morning-after MSNA. We hypothesized that evening binge drinking (i.e. 4-5 drink equivalent in <2 h) would reduce sleep quality and increase morning-after blood pressure (BP) and MSNA. Following a familiarization night within the sleep laboratory, 22 participants (12 men, 10 women; 25 ± 1 yr) were examined after simulated binge drinking or fluid control (randomized, crossover design). Morning MSNA was successfully recorded across both conditions in 16 participants (8 men, 8 women) during a 10-min baseline and three Valsalva's maneuvers (VM). Binge drinking reduced rapid eye movement (REM) sleep (15 ± 1 vs. 20 ± 1%, P = 0.003), increased stage II sleep (54 ± 1 vs. 51 ± 1%, P = 0.002), and increased total urine output (2.9 ± 0.2 vs. 2.1 ± 0.1 liters, P < 0.001) but did not alter morning-after urine specific gravity. Binge drinking increased morning-after heart rate [65 (54-72) vs. 58 (51-67) beats/min, P = 0.013] but not resting BP or MSNA. Binge drinking elicited greater sympathoexcitation during VM (38 ± 3 vs. 43 ± 3 bursts/min, P = 0.036). Binge drinking augmented heart rate (P = 0.002), systolic BP (P = 0.022), and diastolic BP (P = 0.037) reactivity to VM phase IV and blunted cardiovagal baroreflex sensitivity during VM phases II (P = 0.028) and IV (P = 0.043). In conclusion, evening binge alcohol consumption disrupted REM sleep and morning-after autonomic function. These findings provide new mechanistic insight into the potential role of binge drinking on cardiovascular risk.NEW & NOTEWORTHY Chronic binge alcohol consumption is associated with future cardiovascular disease (CVD) risk in both men and women. In addition, binge alcohol consumption is known to disrupt normal sleep quality during the early morning hours, coinciding with the morning sympathetic surge. In the present study, an evening of binge alcohol consumption increased baseline morning heart rate and cardiovascular reactivity during the Valsalva maneuver (VM) strain. Specifically, muscle sympathetic nerve activity and phase IV hemodynamic responses increased during VM the morning after binge alcohol consumption. The autonomic dysfunction and increased cardiovascular reactivity during VM suggests a contributing mechanism to CVD risk present in individuals who binge drink.

Sex differences in blood pressure responsiveness to spontaneous K-complexes during stage II sleep.

K-complexes are a key marker of nonrapid eye movement sleep, specifically during stages II sleep. Recent evidence suggests the heart rate responses to a K-complexes may differ between men and women. The purpose of this study was to compare beat-to-beat blood pressure responses to K-complexes in men and women. We hypothesized that the pressor response following a spontaneous K-complex would be augmented in men compared with women. Ten men [age: 23 ± 2 yr, body mass index (BMI): 28 ± 4 kg/m2] and ten women (age: 23 ± 5 yr, BMI: 25 ± 4 kg/m2) were equipped with overnight finger plethysmography and standard 10-lead polysomnography. Hemodynamic responses to a spontaneous K-complex during stable stage II sleep were quantified for 10 consecutive cardiac cycles, and measurements included systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and heart rate. K-complex elicited greater pressor responses in men when blood pressures were expressed as SAP (cardiac cycle × sex: P = 0.007) and DAP (cardiac cycle × sex: P = 0.004). Heart rate trended to be different between men and women (cardiac cycle × sex: P = 0.078). These findings suggest a divergent pressor response between men and women following a spontaneous K-complex during normal stage II sleep. These findings could contribute to sex-specific differences in cardiovascular risk that exist between men and women.NEW & NOTEWORTHY K-complexes during stage II sleep have been shown to elicit acute increases in blood pressure and heart rate, but the role of sex (i.e., male vs. female) in this response is unclear. In the present study, we demonstrate that the pressor response following spontaneous K-complexes were augmented in men compared to age-matched women. The augmented blood pressure reactivity to spontaneous K-complexes during stage II sleep in men advance the field of cardiovascular sex differences, with implications for nocturnal blood pressure control.

Sex differences in self-report anxiety and sleep quality during COVID-19 stay-at-home orders.

BACKGROUND: COVID-19 and home isolation has impacted quality of life, but the perceived impact on anxiety and sleep remains equivocal. The purpose of this study was to assess the impact of COVID-19 and stay-at-home orders on self-report anxiety and sleep quality, with a focus on sex differences. We hypothesized that the COVID-19 pandemic would be associated with increased anxiety and decreased sleep quality, with stronger associations in women. METHODS: One hundred three participants (61 female, 38 ± 1 years) reported perceived changes in anxiety and sleep quality due to stay-at-home orders during the COVID-19 pandemic and were administered the Spielberger State-Trait Anxiety Inventory (STAI), Pittsburgh Sleep Quality Index (PSQI), and Insomnia Severity Index (ISI). Chi-square and T test analyses were utilized to assess sex differences in reported anxiety and sleep. Analysis of covariance was used to compare the associations between reported impact of COVID-19 and anxiety/sleep parameters. RESULTS: Women (80.3%) reported higher prevalence of increased general anxiety due to COVID-19 when compared to men (50%; p = 0.001) and elevated STAI state anxiety compared to men (43 ± 1 vs. 38 ± 1 a.u., p = 0.007). Despite these differences in anxiety, the perceived impact of COVID-19 on PSQI was not different between sexes. However, when stratified by perceived changes in anxiety due to COVID-19, participants with higher anxiety responses to COVID-19 had higher ISI compared to those with no perceived changes in anxiety (9 ± 1 vs. 5 ± 1 a.u., p = 0.003). Additionally, participants who reported reduced sleep quality due to COVID-19 reported higher state anxiety (45 ± 1 a.u.) compared to those that perceived no change (36 ± 2 a.u., p = 0.002) or increased (36 ± 2 a.u., p < 0.001) sleep quality. CONCLUSION: COVID-19 and state-ordered home isolation was associated with higher anxiety and reduced sleep quality, with a stronger association in women with respect to anxiety.

Subjective and objective sleep differ in male and female collegiate athletes.

BACKGROUND/PURPOSE: Despite the importance of sleep for athletic performance, there is a lack of normative sleep data and sex comparisons in collegiate athletes. The primary purpose of our study was to assess the prevalence of insufficient sleep in collegiate athletes, with a secondary aim to compare male and female athletes. PROCEDURES: Participants included 121 collegiate athletes (65 men and 56 women) from six team sports and three individual sports. Subjective assessments of sleep included at-home sleep diary, Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS), and Insomnia Severity Index (ISI). Objective assessments of sleep included three consecutive off-season weekdays of wrist actigraphy to assess total sleep time (TST) and sleep efficiency (SE). MAIN FINDINGS: Actigraphy revealed that 94% of student-athletes received <8 hours of sleep/night, while 61% received <7 hours/night. Subjective assessments revealed that 35% had PSQI >5, 28% had ISI scores >7, and 19% had ESS scores >10. Objective TST was not different between sexes (6.7±0.1 vs. 6.7±0.1 hours, P = .99), but females demonstrated higher SE (87±1 vs. 82±1%, P < .01) and lower WASO (31±2 vs. 38±2 min, P = .02). Male athletes significantly overestimated TST (i.e., subjective minus objective TST) when compared to female athletes (Δ0.7±0.1 vs. Δ0.3±0.1 hours/night; P < .01). PSQI, ISI, and ESS were not different between sexes. CONCLUSIONS: The majority of male and female collegiate athletes received less than age-recommended levels of sleep, and 44% subjectively reported poor sleep quality, mild severity insomnia, and/or excessive daytime sleepiness. Sex differences were observed in male and female collegiate athletes.

Chronic Standing Desk Use and Arterial Stiffness.

BACKGROUND: Sedentary activity and sitting for at least 10 hours per day can increase the risk for cardiovascular disease by more than 60%. Use of standing desks may decrease sedentary time and improve cardiovascular health. Acute standing lowers pulse wave velocity (PWV), but chronic effects remain unknown. The purpose of this study was to determine the effect of chronic standing desk use on arterial stiffness versus seated controls. METHODS: A total of 48 adults participated in this study. Twenty-four participants qualified as seated desk users (age 41 [10] y, body mass index 25 [4] kg/m2) and 24 as standing desk users (age 45 [12] y, body mass index 25 [5] kg/m2). Arterial stiffness was assessed as PWV within the aorta, arm, and leg. RESULTS: Carotid-femoral PWV (cfPWV) was not different between seated (6.6 [1.3] m/s) and standing (6.9 [1.3] m/s) groups (P = .47). Similarly, there were no differences in arm or leg PWV between groups (P = .13 and P = .66, respectively). A secondary analysis of traditional factors of age and aerobic fitness revealed significant differences in cfPWV in seated and standing desk participants. Age also significantly influenced cfPWV across conditions. CONCLUSIONS: Standing for >50% of a workday did not affect PWV. Consistent with previous research, fitness and age are important modulators of arterial stiffness.

Sympathetic neural responsiveness to sleep deprivation in older adults: sex differences.

Our laboratory has previously reported that total sleep deprivation (TSD) modifies muscle sympathetic neural activity (MSNA) differently in young men and women. Because postmenopausal women are among the highest risk for hypertension, this study compares MSNA responses with TSD in older men and women. We hypothesized that TSD would alter MSNA in older adults, with greater sympathoexcitation in postmenopausal women. Twenty-seven participants (14 men and 13 women) between the ages of 55 and 75 yr were tested twice, once after 24-h TSD and once after normal sleep (randomized, crossover design). Our primary outcome measure of MSNA (microneurography) was successful across both conditions in 20 participants (10 men and 10 women). Secondary outcome measures included seated blood pressure, heart rate, and fasting plasma testosterone, estradiol, and progesterone. Age (60 ± 1 vs. 61 ± 2 yr) and BMI (27 ± 1 vs. 26 ± 1 kg/m2) were not different between groups. TSD increased systolic blood pressure in both men (124 ± 5 to 130 ± 4 mmHg) and women (107 ± 5 to 116 ± 4 mmHg), but the increases were not different between groups (condition, P = 0.014; condition × sex, P > 0.05). In contrast, TSD elicited divergent MSNA responses in older men and women. Specifically, MSNA burst frequency increased in postmenopausal women (28 ± 3 to 34 ± 3 burst/min), but not older men (38 ± 3 to 35 ± 3 bursts/min; condition × sex, P = 0.032). In conclusion, TSD elicited sympathoexcitation in postmenopausal women but not age-matched men. These findings provide new mechanistic insight into reported links between sleep deprivation and hypertension.NEW & NOTEWORTHY Epidemiological studies report that sleep deprivation is more strongly associated with hypertension in women than in men. In the present study, 24-h total sleep deprivation (TSD) increased blood pressure in postmenopausal women and age-matched men. In contrast, only women demonstrated increases in muscle sympathetic nerve activity after TSD. The sympathoexcitation observed in postmenopausal women suggests a potential contributing mechanism for epidemiological observations and advances our understanding of the complex relations between sleep, sex, and hypertension.

α-amanitin resistance in Drosophila melanogaster: A genome-wide association approach.

We investigated the mechanisms of mushroom toxin resistance in the Drosophila Genetic Reference Panel (DGRP) fly lines, using genome-wide association studies (GWAS). While Drosophila melanogaster avoids mushrooms in nature, some lines are surprisingly resistant to α-amanitin-a toxin found solely in mushrooms. This resistance may represent a pre-adaptation, which might enable this species to invade the mushroom niche in the future. Although our previous microarray study had strongly suggested that pesticide-metabolizing detoxification genes confer α-amanitin resistance in a Taiwanese D. melanogaster line Ama-KTT, none of the traditional detoxification genes were among the top candidate genes resulting from the GWAS in the current study. Instead, we identified Megalin, Tequila, and widerborst as candidate genes underlying the α-amanitin resistance phenotype in the North American DGRP lines, all three of which are connected to the Target of Rapamycin (TOR) pathway. Both widerborst and Tequila are upstream regulators of TOR, and TOR is a key regulator of autophagy and Megalin-mediated endocytosis. We suggest that endocytosis and autophagy of α-amanitin, followed by lysosomal degradation of the toxin, is one of the mechanisms that confer α-amanitin resistance in the DGRP lines.