Development of a prediction equation to estimate lower-limb arterial occlusion pressure with a thigh sphygmomanometer.

INTRODUCTION: Previous investigators have developed prediction equations to estimate arterial occlusion pressure (AOP) for blood flow restriction (BFR) exercise. Most equations have not been validated and are designed for use with expensive cuff systems. Thus, their implementation is limited for practitioners. PURPOSE: To develop and validate an equation to predict AOP in the lower limbs when applying an 18 cm wide thigh sphygmomanometer (SPHYG18cm). METHODS: Healthy adults (n = 143) underwent measures of thigh circumference (TC), skinfold thickness (ST), and estimated muscle cross-sectional area (CSA) along with brachial and femoral systolic (SBP) and diastolic (DBP) blood pressure. Lower-limb AOP was assessed in a seated position at the posterior tibial artery (Doppler ultrasound) using a SPHYG18cm. Hierarchical linear regression models were used to determine predictors of AOP. The best set of predictors was used to construct a prediction equation to estimate AOP. Performance of the equation was evaluated and internally validated using bootstrap resampling. RESULTS: Models containing measures of either TC or thigh composition (ST and CSA) paired with brachial blood pressures explained the most variability in AOP (54%) with brachial SBP accounting for majority of explained variability. A prediction equation including TC, brachial SBP, and age showed good predictability (R2 = 0.54, RMSE = 7.18 mmHg) and excellent calibration. Mean difference between observed and predicted values was 0.0 mmHg and 95% Limits of Agreement were ± 18.35 mmHg. Internal validation revealed small differences between apparent and optimism adjusted performance measures, suggesting good generalizability. CONCLUSION: This prediction equation for use with a SPHYG18cm provided a valid way to estimate lower-limb AOP without expensive equipment.

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 Single-Session Meditation on Aortic Pulsatility and Anxiety in Mildly to Moderately Anxious Adults.

Context: Anxiety is a common mental health concern in the USA that is associated with an increased risk of hypertension, arterial stiffness, and cardiovascular disease. Therapists have used eight-week programs for mindfulness meditation to treat anxiety; however little is known about the psychophysiological effects of a single meditation session. Objective: The study intended to assess the effects of a one-hour, mindfulness-meditation session on anxiety symptomology and cardiovascular function, including aortic pulsatility. Design: The research team performed a prospective, single-group study. Setting: The study took place at Michigan Technological University. Participants: Participants were 14 young adults with an initial Beck Anxiety Inventory (BAI) score of 8 to 26, showing mild to moderate anxiety. Intervention: Participants took part in a single, one-hour, guided, mindfulness-meditation session. Outcome Measures: The research team: (1) administered the BAI during an orientation session and at 60-minutes post intervention, and (2) measured the cardiovascular variables of qualified participants at the orientation, at baseline prior to the intervention, immediately post intervention, and at 60 minutes post intervention, including systolic arterial blood pressure (SAP), diastolic arterial blood pressure (DAP), heart rate (HR), aortic pulse pressure (aPP), aortic pulsatility, aortic augmentation index (AIx) at 75 bpm, carotid-radial pulse wave velocity (crPWV), carotid-femoral pulse wave velocity (cfPWV), and respiratory rate. Results: Participants had a significant decrease in the BAI scores between baseline and 60-minutes post intervention (P = .01) and a significant reduction in aortic pulsatility-aPP x HR-between baseline and immediately post intervention and between baseline and 60-minutes post intervention (both P < .01). Conclusions: Preliminary results suggest that one hour of introductory mindfulness meditation can have both psychological and cardiovascular benefits for anxious individuals.

An experiential learning course for cardiovascular and sleep technology.

Undergraduate programs related to allied health are often pursued by students to prepare for entrance into professional programs, but many students also ask about what types of employment options they may have upon completion of the bachelor's degree. This experiential learning course in cardiovascular and sleep technology was designed to provide opportunities for students to gain hands-on clinical skills that could help them to enter professional programs or to find employment in an allied health field such as cardiopulmonary rehabilitation, cardiovascular technology, or sleep technology. The prerequisites for this course were the completion of two semesters of anatomy and physiology. This course was based on experiential learning and was structured into three modules: clinical exercise physiology, autonomic physiology, and sleep physiology. As part of the course students completed a 4-page scientific report for one designated topic within each of the modules. The two exams in the course were essay based. The design of this course required students to review key topics from anatomy and physiology, to comprehend peer-reviewed manuscripts, to gain hands-on experiences with sophisticated physiological equipment, to work as individuals and in groups, and to become better oral and written communicators. The sleep physiology module included an introduction to electroencephalography (EEG) and a student-led nap study, which may be an effective way to introduce students to sleep medicine. We are hopeful that the summary of this course will be useful to physiology educators as they work to provide the most meaningful experiences to their undergraduates in the health sciences.NEW & NOTEWORTHY Experiential learning in clinical exercise, autonomic regulation, and sleep physiology is an impactful way to train undergraduate biomedical students to enter a variety of careers in healthcare, graduate programs in the health professions, or traditional research graduate programs. A hands-on course such as Cardiovascular and Sleep Technology provides a way, in addition to or independent of original research, to provide clinically relevant training.

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.

Moving student research forward during the COVID-19 pandemic.

The COVID--19 pandemic has impacted undergraduate and graduate student research. With the uncertainty right now, it is a challenge for faculty to offer clear guidance for how students can proceed with their research and capstone projects. In this brief editorial, we offer suggestions for moving student research forward during the COVID-19 pandemic.

Chronic eccentric arm cycling improves maximum upper-body strength and power.

INTRODUCTION: Eccentric leg cycling (cycle ergometry adapted to impose muscle lengthening contractions) offers an effective exercise for restoring lower-body muscular function, maintaining health, and improving performance in clinical and athletic populations. PURPOSE: We extended this model to the upper body and evaluated the effectiveness of a 7-week eccentric arm cycling (ECCarm) intervention to improve upper-body muscular function. We also explored whether ECCarm would alter arterial function. METHODS: Participants performed ECCarm (n = 9) or concentric arm cycling (CONarm; n = 8) 3×/week while training intensity increased (5-20 min, 60-70% upper-body peak heart rate). Maximum elbow extensor strength, upper-body concentric power, and peripheral and central arterial stiffness were assessed before and after training. RESULTS: During training, heart rates and perceived exertion did not differ between groups (~68% upper-body peak heart rate, ~12 Borg units, both P > 0.05), whereas power during ECCarm was ~2× that for CONarm (122 ± 43 vs. 59 ± 20 W, P < 0.01). Muscle soreness for ECCarm was greater than CONarm (P = 0.02), however, soreness was minimal for both groups (<0.50 cm). Following training, ECCarm exhibited greater changes in elbow extensor strength (16 ± 10 vs. 1 ± 9%, P = 0.01) and upper-body power (6 ± 8 vs. -3 ± 7%, P < 0.01) compared to CONarm. Peripheral and central arterial stiffness did not change for either group (both P > 0.05). CONCLUSION: Upper-body eccentric exercise improved dynamic muscular function while training at low exertion levels. Results occurred with minimal soreness and without compromising arterial function. ECCarm findings parallel eccentric leg cycling findings and indicate that eccentric cycle ergometry offers a robust model for enhancing upper-body muscular function. ECCarm could have applications in rehabilitation and sport training.

Binge Alcohol Consumption Elevates Sympathetic Transduction to Blood Pressure: A Randomized Controlled Trial.

BACKGROUND: Alcohol consumption is associated with cardiovascular disease, and the sympathetic nervous system is a suspected mediator. The present study investigated sympathetic transduction of muscle sympathetic nerve activity to blood pressure at rest and in response to cold pressor test following evening binge alcohol or fluid control, with the hypothesis that sympathetic transduction would be elevated the morning after binge alcohol consumption. METHODS: Using a randomized, fluid-controlled (FC) crossover design, 26 healthy adults (12 male, 14 female, 25±6 years, 27±4 kg/m2) received an evening binge alcohol dose and a FC. All participants underwent next-morning autonomic-cardiovascular testing consisting of muscle sympathetic nerve activity, beat-to-beat blood pressure, and heart rate during a 10-minute rest period and a 2-minute cold pressor test. Sympathetic transduction was assessed at rest and during the cold pressor test in both experimental conditions. RESULTS: Evening alcohol increased heart rate (FC: 60±9 versus alcohol: 64±9 bpm; P=0.010) but did not alter resting mean arterial pressure (FC: 80±6 versus alcohol: 80±7 mm Hg; P=0.857) or muscle sympathetic nerve activity (FC: 18±9 versus alcohol: 20±8 bursts/min; P=0.283). Sympathetic transduction to mean arterial pressure (time×condition; P=0.003), diastolic blood pressure (time×condition; P=0.010), and total vascular conductance (time×condition; P=0.004) was augmented after alcohol at rest. Sympathetic transduction during the cold pressor test was also elevated after evening binge alcohol consumption (P=0.002). CONCLUSIONS: These findings suggest that evening binge alcohol consumption leads to augmented morning-after sympathetic transduction of muscle sympathetic nerve activity to blood pressure, highlighting a new mechanism whereby chronic or excessive alcohol consumption contributes to cardiovascular disease progression via altered end-organ responsiveness to sympathetic neural outflow. REGISTRATION: URL: https://clinicaltrials.gov/study/NCT03567434; Unique identifier: NCT03567434.

The effect of squat depth on multiarticular muscle activation in collegiate cross-country runners.

The squat is a closed-chain lower body exercise commonly performed by many athletes. Muscle activity has been examined during partial and parallel squats in male weightlifters, but not in male and female runners. Therefore, this study measured muscle activity with surface electromyography (EMG) during partial and parallel squats in 20 Division I collegiate cross-country runners (10 males and 10 females) in a randomized crossover design. We hypothesized the parallel squat would increase extensor muscle activitation (i.e. hamstrings and erector spinae). Furthermore, we sought to determine if changes in muscle activity were different between males and females. Participants performed 6 repetitions using their 10 repetition maximum loads for each condition during EMG testing. EMG was performed on the right rectus femoris, biceps femoris, lumbar erector spinae, and lateral head of the gastrocnemius. Rectus femoris activity (0.18 ± 0.01 vs. 0.14 ± 0.01 mV) and erector spinae activity (0.16 ± 0.01 vs. 0.13 ± 0.01 mV) were significantly higher (p < 0.05) during the parallel squat than during the partial squat condition. This increase in muscle activity may be attributed to greater ranges of motion at the hip and knee joints. Biceps femoris and gastrocnemius activity were similar between conditions. No significant differences existed between males and females (squat condition × gender; p > 0.05). During preliminary isokinetic testing, both male and female runners demonstrated deficient hamstrings-to-quadriceps ratios, which would not likely improve by performing parallel squats based on our EMG findings. Despite the reduced load of the parallel squat, rectus femoris and erector spinae activity were elevated. Thus, parallel squats may help runners to train muscles vital for uphill running and correct posture, while preventing injury by using lighter weights through a larger range of motion.

Blood flow restriction as a potential therapy to restore physical function following COVID-19 infection.

Accumulating evidence indicates that some COVID-19 survivors display reduced muscle mass, muscle strength, and aerobic capacity, which contribute to impairments in physical function that can persist for months after the acute phase of illness. Accordingly, strategies to restore muscle mass, muscle strength, and aerobic capacity following infection are critical to mitigate the long-term consequences of COVID-19. Blood flow restriction (BFR), which involves the application of mechanical compression to the limbs, presents a promising therapy that could be utilized throughout different phases of COVID-19 illness. Specifically, we hypothesize that: 1) use of passive BFR modalities can mitigate losses of muscle mass and muscle strength that occur during acute infection and 2) exercise with BFR can serve as an effective alternative to high-intensity exercise without BFR for regaining muscle mass, muscle strength, and aerobic capacity during convalescence. The various applications of BFR may also serve as a targeted therapy to address the underlying pathophysiology of COVID-19 and provide benefits to the musculoskeletal system as well as other organ systems affected by the disease. Consequently, we present a theoretical framework with which BFR could be implemented throughout the progression from acute illness to outpatient rehabilitation with the goal of improving short- and long-term outcomes in COVID-19 survivors. We envision that this paper will encourage discussion and consideration among researchers and clinicians of the potential therapeutic benefits of BFR to treat not only COVID-19 but similar pathologies and cases of acute critical illness.

Sympathetic neural responses to 24-hour sleep deprivation in humans: sex differences.

Sleep deprivation has been linked to hypertension, and recent evidence suggests that associations between short sleep duration and hypertension are stronger in women. In the present study we hypothesized that 24 h of total sleep deprivation (TSD) would elicit an augmented pressor and sympathetic neural response in women compared with men. Resting heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) were measured in 30 healthy subjects (age, 22 ± 1; 15 men and 15 women). Relations between spontaneous fluctuations of diastolic arterial pressure and MSNA were used to assess sympathetic baroreflex function. Subjects were studied twice, once after normal sleep and once after TSD (randomized, crossover design). TSD elicited similar increases in systolic, diastolic, and mean BP in men and women (time, P < 0.05; time × sex, P > 0.05). TSD reduced MSNA in men (25 ± 2 to 16 ± 3 bursts/100 heart beats; P = 0.02), but not women. TSD did not alter spontaneous sympathetic or cardiovagal baroreflex sensitivities in either sex. However, TSD shifted the spontaneous sympathetic baroreflex operating point downward and rightward in men only. TSD reduced testosterone in men, and these changes were correlated to changes in resting MSNA (r = 0.59; P = 0.04). Resting HR, respiratory rate, and estradiol were not altered by TSD in either sex. In conclusion, TSD-induced hypertension occurs in both sexes, but only men demonstrate altered resting MSNA. The sex differences in MSNA are associated with sex differences in sympathetic baroreflex function (i.e., operating point) and testosterone. These findings may help explain why associations between sleep deprivation and hypertension appear to be sex dependent.

Post-Exercise Arterial Stiffness Responses Are Similar After Acute Eccentric and Concentric Arm Cycling.

Upper-body resistance exercise effectively increases muscular strength, but may concomitantly increase arterial stiffness. Eccentric exercise can lead to muscle soreness and arterial stiffness in untrained participants. However, it is unclear if upper-body eccentric exercise could reduce arterial stiffness in a single session for participants that have undergone progressive training. Our purpose was to compare acute responses to upper-body eccentric (novel, ECCarm) and concentric (traditional, CONarm) steady state arm cycling. We hypothesized that arm arterial stiffness would be reduced after both ECCarm and CONarm. Twenty-two young healthy individuals performed either ECCarm (n = 11) or CONarm (n = 11) at ~70% of peak heart rate for 20 min after a training period. Heart rate, central pulse wave velocity (cPWV), and peripheral pulse wave velocity (pPWV; i.e., arm arterial stiffness) were assessed before, 10 min, and 30 min after exercise. Heart rate was not elevated at 10 min post ECCarm, but was elevated at 10- and 30-min post CONarm (p < 0.01). After exercise, pPWV was decreased at 10 min post for both ECCarm (7.1 ± 0.3 vs. 6.5 ± 0.2 m/s) and CONarm (7.0 ± 0.2 vs. 6.5 ± 0.2 m/s; p < 0.05), while both groups returned to baseline values 30 min post. cPWV did not change in either group. Our results indicate that acute ECCarm provides a high-force, low energy cost form of resistance exercise that acutely reduces arm arterial stiffness. The reduction in pPWV and rapid heart rate recovery suggests that ECCarm is a safe form of exercise for overall and cardiovascular health.

Influence of acute alcohol ingestion on sympathetic neural responses to orthostatic stress in humans.

Acute alcohol consumption is reported to decrease mean arterial pressure (MAP) during orthostatic challenge, a response that may contribute to alcohol-mediated syncope. Muscle sympathetic nerve activity (MSNA) increases during orthostatic stress to help maintain MAP, yet the effects of alcohol on MSNA responses during orthostatic stress have not been determined. We hypothesized that alcohol ingestion would blunt arterial blood pressure and MSNA responses to lower body negative pressure (LBNP). MAP, MSNA, and heart rate (HR) were recorded during progressive LBNP (-5, -10, -15, -20, -30, and -40 mmHg; 3 min/stage) in 30 subjects (age 24 ± 1 yr). After an initial progressive LBNP (pretreatment), subjects consumed either alcohol (0.8 g ethanol/kg body mass; n = 15) or placebo (n = 15), and progressive LBNP was repeated (posttreatment). Alcohol increased resting HR (59 ± 2 to 65 ± 2 beats/min, P < 0.05), MSNA (13 ± 3 to 19 ± 4 bursts/min, P < 0.05), and MSNA burst latency (1,313 ± 16 to 1,350 ± 17 ms, P < 0.05) compared with placebo (group × treatment interactions, P < 0.05). During progressive LBNP, a pronounced decrease in MAP was observed after alcohol but not placebo (group × time × treatment, P < 0.05). In contrast, MSNA and HR increased during all LBNP protocols, but there were no differences between trials or groups. However, alcohol altered MSNA burst latency response to progressive LBNP. In conclusion, the lack of MSNA adjustment to a larger drop in arterial blood pressure during progressive LBNP, coupled with altered sympathetic burst latency responses, suggests that alcohol blunts MSNA responses to orthostatic stress.

Attenuation of sympathetic baroreflex sensitivity during the onset of acute mental stress in humans.

Mental stress consistently induces a pressor response that is often accompanied by a paradoxical increase of muscle sympathetic nerve activity (MSNA). The purpose of the present study was to evaluate sympathetic baroreflex sensitivity (BRS) by examining the relations between spontaneous fluctuations of diastolic arterial pressure (DAP) and MSNA. We hypothesized that sympathetic BRS would be attenuated during mental stress. DAP and MSNA were recorded during 5 min of supine baseline, 5 min of mental stress, and 5 min of recovery in 32 young healthy adults. Burst incidence and area were determined for each cardiac cycle and placed into 3-mmHg DAP bins; the slopes between DAP and MSNA provided an index of sympathetic BRS. Correlations between DAP and MSNA were strong (> 0.5) during baseline in 31 of 32 subjects, but we evaluated the change in slope only for those subjects maintaining a strong correlation during mental stress (16 subjects). During baseline, the relation between DAP and MSNA was negative when expressed as either burst incidence [slope = -1.95 ± 0.18 bursts·(100 beats)⁻¹)·mmHg⁻¹; r = -0.86 ± 0.03] or total MSNA [slope = -438 ± 91 units·(beat)⁻¹ mmHg⁻¹; r = -0.76 ± 0.06]. During mental stress, the slope between burst incidence and DAP was significantly reduced [slope = -1.14 ± 0.12 bursts·(100 beats)⁻¹·mmHg⁻¹; r = -0.72 ± 0.03; P < 0.01], indicating attenuation of sympathetic BRS. A more detailed analysis revealed an attenuation of sympathetic BRS during the first 2 min of mental stress (P < 0.01) but no change during the final 3 min of mental stress (P = 0.25). The present study demonstrates that acute mental stress attenuates sympathetic BRS, which may partially contribute to sympathoexcitation during the mental stress-pressor response. However, this attenuation appears to be isolated to the onset of mental stress. Moreover, variable MSNA responses to mental stress do not appear to be directly related to sympathetic BRS.

Social technology restriction alters state-anxiety but not autonomic activity in humans.

Social technology is extensively used by young adults throughout the world, and it has been suggested that interrupting access to this technology induces anxiety. However, the influence of social technology restriction on anxiety and autonomic activity in young adults has not been formally examined. Therefore, we hypothesized that restriction of social technology would increase state-anxiety and alter neural cardiovascular regulation of arterial blood pressure. Twenty-one college students (age 18-23 yr) were examined during two consecutive weeks in which social technology use was normal or restricted (randomized crossover design). Mean arterial pressure (MAP), heart rate, and muscle sympathetic nerve activity (MSNA) were measured at rest and during several classic autonomic stressors, including isometric handgrip, postexercise muscle ischemia, cold pressor test, and mental stress. Tertile analysis revealed that restriction of social technology was associated with increases (12 ± 2 au; range 5 to 21; n = 7), decreases (-6 ± 2 au; range -2 to -11; n = 6), or no change (0 ± 0 au; range -1 to 3; n = 8) in state-anxiety. Social technology restriction did not alter MAP (74 ± 1 vs. 73 ± 1 mmHg), heart rate (62 ± 2 vs. 61 ± 2 beats/min), or MSNA (9 ± 1 vs. 9 ± 1 bursts/min) at rest, and it did not alter neural or cardiovascular responses to acute stressors. In conclusion, social technology restriction appears to have an interindividual influence on anxiety, but not autonomic activity. It remains unclear how repeated bouts, or chronic restriction of social technology, influence long-term psychological and cardiovascular health.

Kinetic analysis of several variations of push-ups.

Push-ups are a common and practical exercise that is used to enhance fitness, including upper body strength or endurance. The kinetic characteristics of push-ups and its variations are yet to be quantified. Kinetic quantification is necessary to accurately evaluate the training load, and thus the nature of the training stimulus, for these exercise variations. This study assessed the peak vertical ground reaction forces (GRFs) of push-up variations including the regular push-up and those performed with flexed knee, feet elevated on a 30.48-cm box, and a 60.96-cm box, and hands elevated on a 30.48-cm box and a 60.96-cm box. Twenty-three recreationally fit individuals (14 men, 9 women) performed each of the 6 push-up variations in a randomized order. Peak GRF and peak GRF expressed as a coefficient of subject body mass were obtained with a force platform. Push-ups with the feet elevated produced a higher GRF than all other push-up variations (p ≤ 0.05). Push-ups with hands elevated and push-ups from the flexed knee position produced a lower GRF than all other push-up variations (p ≤ 0.05). No gender differences in response to these push-up variations were found (p > 0.05). Additionally, subject height was not related to the GRF for any of the push-up conditions (p > 0.05) other than the condition where hands were elevated on a 60.96-cm box (p ≤ 0.05; r = 0.63). These data can be used to progress the intensity of push-ups in a program and to quantify the training load as a percentage of body mass.

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.