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.</p

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/night, while 61% received/night. Subjective assessments revealed that 35% had PSQI \u3e5, 28% had ISI scores \u3e7, and 19% had ESS scores \u3e10. Objective TST was not different between sexes (6.7±0.1 vs. 6.7±0.1 hours, p=0.99), but females demonstrated higher SE (87±1 vs. 82±1%, p 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

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

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 (β = 0.206, P = 0.028), DAP (β = 0.317, P = 0.002), MAP (β = 0.325, P = 0.001), MSNA BF (β = 0.227, P = 0.030), and MSNA BI (β = 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

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 two hours) 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 (7 men, 9 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\u3c0.001), 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

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 \u3c2 \u3eh) 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\u27s 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 \u3c 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

Morning Cardiovascular and Sympathetic Reactivity to Cold Pressor Test After Evening Binge Drinking: Sex Differences

Heavy alcohol consumption, including binge drinking, is associated with increased cardiovascular risk There is consistent evidence for increased muscle sympathetic nerve activity (MSNA) after acute alcohol consumption, and recent evidence for augmented sympathetic reactivity the morning after evening binge drinking. Given well documented differences in neural cardiovascular control between men and women, we hypothesized that women would exhibit augmented morning cardiovascular and sympathetic neural reactivity to cold stress following evening binge alcohol consumption. Thirty volunteers (15 women, 15 men; 25±1 years; 27±1 kg/m2 ) participated in the present study. Utilizing a randomized, cross-over design, participants visited the laboratory for fluid control and alcohol sessions separated by ~1 month. The alcohol dose was based upon biological sex and body weight (1 g/kg dose in men and 0.85 g/kg dose in women). Beverage consumption occurred at 8:00pm and 9:00pm to simulate binge alcohol consumption (i.e., 4-5 drink equivalent), with lights out at 11:00pm. An 8-hour sleep opportunity was allotted from 11:00pm to 7:00am for overnight polysomnography (NATUS, Middleton, WI). Following lights on, twenty-two (10 women, 12 men) participants were instrumented for a morning autonomic study with measurements of muscle sympathetic nerve activity (MSNA; microneurography), beat-to-beat blood pressure (finger plethysmography), and heart rate (electrocardiogram). MSNA, blood pressure, and heart rate were measured during a 3-minute baseline, 2-minute cold pressor test (CPT), and 3-minute recovery. MSNA was scored and confirmed by one trained investigator (JR Carter). Statistical analysis included repeated measures ANOVA with condition and time as within subject factors and sex as a between subject factor (α = 0.05). Total sleep time and sleep efficiency were reduced following binge alcohol consumption in both sexes (condition: p \u3c 0.05), but women had more frequent arousals following alcohol consumption (condition × sex: p = 0.008). During CPT, women exhibited an augmented pressor response via mean arterial pressure following evening binge alcohol consumption compared to fluid control, while men did not (condition × time × sex: p = 0.010). MSNA burst frequency was elevated during CPT following evening binge alcohol consumption compared to fluid control (condition × time: p = 0.033), but this was not different between sexes. Heart rate reactivity was not different across conditions (condition × time: p = 0.405) or between sexes (condition × time × sex: p = 0.818). In conclusion, our results indicate that evening binge drinking results in augmented cardiovascular reactivity in women compared to men, but these differences do not appear to be mediated via sympathetic neural reactivity

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

© This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. 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 preadaptation, 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

Candidate genes resulting from the 180-line GWAS on 2.0 μg/g and the 37-line GWAS.

<p>Candidate genes resulting from the 180-line GWAS on 2.0 μg/g and the 37-line GWAS.</p