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The purpose of this study was to examine whether gender differences exist for ventilatory threshold (VT), lactate threshold (LT), and Vo2max during on-ice skating in college hockey players. Ten male and 10 female Division III college hockey players performed a graded exercise skating protocol until reaching volitional fatigue. The graded exercise test employed stages that were 80 seconds in duration, with 40 seconds of rest between each stage to obtain blood lactate samples. Ventilatory threshold occurred at a higher percentage of maximal heart rate (HRmax) in women than in men. The women's VT occurred at 77.3% +/- 1.6% HRmax, while the men's VT occurred at 72.6% +/- 2.0% HRmax (p < 0.02). Men and women had similar HRmax values: 191.3 +/- 2.5 b.min and 185.8 +/- 2.5 b.min, respectively. Vo2max was different between genders, with men at 52.7 +/- 1.3 mL.kg.min and women at 40.1 +/- 1.0 mL.kg.min (p < 0.01). In addition, VT was different between genders when measured as a percentage of Vo2max, with men at 52.7% +/- 3.2% and women at 67.3% +/- 4.0% (p < 0.02). In contrast, LT was similar between genders when expressed as a percentage of HRmax or Vo2max. For each gender, LT occurred at a significantly higher percentage of HRmax or Vo2max than VT did. It can be concluded that VT does not accurately predict LT in male or female hockey players. Additionally, competitive female hockey players have a lower Vo2max but a higher VT than their male counterparts. An increased VT may be a compensatory mechanism to offset the smaller Vo2max values measured in female hockey players. On-ice testing is a practical way to address specific aerobic training needs of hockey players. [ABSTRACT FROM AUTHOR]

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/m 2 ) 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., Competing Interests: None.

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 (SPHYG 18cm )., 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 SPHYG 18cm . 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 (R 2  = 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 SPHYG 18cm provided a valid way to estimate lower-limb AOP without expensive equipment., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

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., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Wedig, Durocher, McDaniel and Elmer.)

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/m 2 ). 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.

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.

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.

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.

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., (© Sleep Research Society 2021. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

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.

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.

Background: Central arterial stiffness is a cardiovascular risk factor that can be readily affected through engagement in physical exercise training, with resistance and aerobic exercise having disparate affects. Despite the growing popularity of high-intensity cross-training (HICT), little is currently known about the effects of this mixed modality exercise stimulus on arterial stiffness. Therefore, the purpose of this study was to characterize the arterial stiffness of habitual HICT participants vs. aerobically active and sedentary controls using a cross-sectional design., Methods: A total of 30 participants were recruited: 10 middle-aged long-term participants of HICT (CrossFit) and 20 age, sex, and height matched controls (10 recreationally active, 10 sedentary). Central and peripheral pulse wave velocities were measured for the carotid-femoral and femoral-dorsalis pedis arterial segments. Aerobic fitness (maximal oxygen uptake, VO 2max ) was measured and typical exercise participation rates were self-reported for each group., Results: HICT participants manifested central pulse wave velocity (PWV) (5.3 ± 1.0 m/s, mean ± SD) and VO 2max (43 ± 6 mL/kg/min) values nearly identical to active controls. Both active groups had significantly better values than sedentary controls (7.1 ± 1.0 m/s, p  ≤ 0.001; and 32 ± 7 mL/kg/min, p  = 0.01). No differences were observed in peripheral PWV between groups., Conclusion: Habitual participation in HICT exercise was not associated with increased central nor peripheral arterial stiffness. Long-term HICT participants presented with similar fitness and arterial stiffness as compared with participants who practiced traditional aerobic exercise. Compared to sedentary living, HICT may offer musculoskeletal and cardiovascular health benefits without negatively impacting arterial stiffness.

Physiological stress in wildlife can be a useful indicator of a population's response to environmental factors. By using non-invasive endocrinological techniques, such as fecal sampling, potential confounding factors associated with the stress of capture can be avoided. A potential drawback of fecal sampling, however, is degradation of samples which may produce aberrant measurements of fecal glucocorticoid metabolites. In vertebrates, glucocorticoids, such as corticosterone, become elevated in response to stress. We sought to gauge the reliability of measurement of fecal glucocorticoid metabolites from white-tailed deer ( Odocoileus virginianus ) fecal samples exposed to a temperate winter with substantial snow cover and cold temperatures for up to 90 days, by repeatedly subsampling fecal samples every 10 days and performing a corticosterone enzyme-linked immunosorbent assay (ELISA). Measurements of fecal glucocorticoid metabolites at 10 days were consistent with initial measurements, after which (20 days) they became aberrant following a period of thawing. Consequently, glucocorticoid metabolite levels in feces appear to remain stable under ambient conditions if temperatures remain below freezing at least for 10 days. While it's possible that samples may remain useful beyond this time frame based on previous laboratory studies of samples stored in a freezer, further work is needed to determine how samples weather in situ under extreme cold (e.g. Arctic) or periods of partial thawing.

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 (ECC arm ) intervention to improve upper-body muscular function. We also explored whether ECC arm would alter arterial function., Methods: Participants performed ECC arm (n = 9) or concentric arm cycling (CON arm ; 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 ECC arm was ~2× that for CON arm (122 ± 43 vs. 59 ± 20 W, P < 0.01). Muscle soreness for ECC arm was greater than CON arm (P = 0.02), however, soreness was minimal for both groups (<0.50 cm). Following training, ECC arm 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 CON arm . 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. ECC arm findings parallel eccentric leg cycling findings and indicate that eccentric cycle ergometry offers a robust model for enhancing upper-body muscular function. ECC arm could have applications in rehabilitation and sport training.

Background: Lower body negative pressure (LBNP) decreases middle cerebral artery blood velocity (MCAv) and can induce hypotension. Mental stress increases MCAv, but the MCAv response to combined LBNP and mental stress (COMBO) is unknown. We hypothesized that performing a stressful cognitive challenge (i.e., mental stress) concurrently with LBNP would prevent LBNP-induced reductions of MCAv., Methods: There were 18 subjects (9 men, 9 women; ages 20.1±0.3 yr) who completed 3 randomized 3-min trials: 1) LBNP (-40 mmHg); 2) mental stress (serial subtraction); and 3) COMBO (LBNP+mental stress). All reported values are mean±SE. Mean arterial pressure (MAP), heart rate (HR), forearm blood flow (FBF), and MCAv were measured continuously. Subjects also reported perceived stress following the mental stress and COMBO trials., Results: LBNP decreased MAP (Δ-1.4±0.5 mmHg), MCAv (Δ-2.6±1.1 cm s(-1)) and FBF (Δ-0.8±0.1 units), and increased HR (Δ2.7±1.2 bpm). Mental stress increased MAP (Δ10.1±1.3 mmHg), HR (Δ17.4±2.2 bpm), and FBF (Δ2.4±0.4 units), while MCAv (Δ2.8±1.3 cm s(-1)) tended to increase. COMBO increased MAP (Δ5.3±2.3 mmHg) and HR (Δ21.3±2.6 bpm), and tended to increase FBF (Δ0.5±0.3 units). However, MCAv (Δ-4.6±2.0 cm s(-1)) decreased during COMBO. Decreases in MCAv during COMBO were not statistically different from LBNP-induced decreases (Δ-4.6±2.0 vs. Δ-2.6±1.1 cm s(-1)). Subjective ratings of perceived stress (standard 0 to 4 scale) tended to be higher during COMBO than mental stress (2.9±0.1 vs. 2.5±0.1 units)., Conclusion: Our results suggest that mental stress does not effectively preserve MCAv when combined with central hypovolemia (i.e., LBNP).

Background: Available methods for screening anterior cruciate ligament (ACL) injury risk are effective but limited in application as they generally rely on expensive and time-consuming biomechanical movement analysis. A potentially efficient alternative to biomechanical screening is skilled movement analysis via visual inspection (ie, having experts estimate injury risk factors based on observations of athletes' movements)., Purpose: To develop a brief, valid psychometric assessment of ACL injury risk factor estimation skill: the ACL Injury Risk Estimation Quiz (ACL-IQ)., Study Design: Cohort study (diagnosis); Level of evidence, 3., Methods: A total of 660 individuals participated in various stages of the study, including athletes, physicians, physical therapists, athletic trainers, exercise science researchers/students, and members of the general public in the United States. The ACL-IQ was fully computerized and made available online (www.ACL-IQ.org). Item sampling/reduction, reliability analysis, cross-validation, and convergent/discriminant validity analyses were conducted to refine the efficiency and validity of the assessment., Results: Psychometric optimization techniques identified a short (mean time, 2 min 24 s), robust, 5-item assessment with high reliability (test-retest: r = 0.90) and high test sensitivity (average difference of exercise science professionals vs general population: Cohen d = 2). Exercise science professionals and individuals from the general population scored 74% and 53% correct, respectively. Convergent and discriminant validity was demonstrated. Scores on the ACL-IQ were best predicted by ACL knowledge and specific judgment strategies (ie, cue use) and were largely unrelated to domain-general spatial/decision-making ability, personality, or other demographic variables. Overall, 23% of the total sample (40% of exercise science professionals; 6% of general population) performed better than or equal to the ACL nomogram., Conclusion: This study presents the results of a systematic approach to assess individual differences in ACL injury risk factor estimation skill; the assessment approach is efficient (ie, it can be completed in <3 min) and psychometrically robust. The results provide evidence that some individuals have the ability to visually estimate ACL injury risk factors more accurately than other instrument-based ACL risk estimation methods (ie, ACL nomogram). The ACL-IQ provides the foundation for assessing the efficacy of observational ACL injury risk factor assessment (ie, does simple skilled visual inspection reduce ACL injuries?). The ACL-IQ can also be used to increase our understanding of the perceptual-cognitive mechanisms underlying injury risk assessment expertise, which can be leveraged to accelerate learning and improve performance., (© 2015 The Author(s).)

The midluteal (ML) phase of the ovarian cycle is often sympathoexcitatory compared with the early follicular (EF) phase. We recently reported that 24-h total sleep deprivation (TSD) augmented cardiovascular reactivity in both men and women, but that sex differences existed in resting muscle sympathetic nerve activity (MSNA) responses to TSD. In the present study, we hypothesized increased resting MSNA and augmented cardiovascular reactivity to acute laboratory stressors during the ML phase in sleep-deprived women. Heart rate (HR), mean arterial pressure (MAP), forearm vascular conductance (FVC), and MSNA were measured in 14 eumenorrheic women (age, 20 ± 1 yr) during 10 min supine rest, 5 min mental stress (MS) trial, and 2 min cold pressor test (CPT) trial. Subjects were tested twice after TSD: once during EF phase and once during ML phase (randomized, crossover design). Estradiol (29 ± 2 vs. 63 ± 8 pg/ml, P = 0.001) and progesterone (1.6 ± 0.2 vs. 4.4 ± 0.7 ng/ml, P = 0.002) were elevated during the ML phase. Resting supine MAP (75 ± 2 vs. 72 ± 1 mmHg, P = 0.042) was lower during the ML phase. In contrast, resting supine HR, MSNA, and FVC were not significantly different between EF and ML phases. MAP, HR and FVC reactivity to MS were not statistically different between the EF and ML phases. Similarly, MAP and HR reactivity to CPT were not different between the ovarian phases. Contrary to our original hypothesis, the ML phase was not associated with sympathoexcitation or exaggerated cardiovascular reactivity in sleep-deprived premenopausal women. However, our data reveal elevated resting blood pressure during the EF phase in sleep-deprived women., (Copyright © 2015 the American Physiological Society.)

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.

Exaggerated cardiovascular reactivity to mental stress (MS) and cold pressor test (CPT) has been linked to increased risk of cardiovascular disease. Recent epidemiological studies identify sleep deprivation as an important risk factor for hypertension, yet the relations between sleep deprivation and cardiovascular reactivity remain equivocal. We hypothesized that 24-h total sleep deprivation (TSD) would augment cardiovascular reactivity to MS and CPT and blunt the MS-induced forearm vasodilation. Because the associations between TSD and hypertension appear to be stronger in women, a secondary aim was to probe for sex differences. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were recorded during MS and CPT in 28 young, healthy subjects (14 men and 14 women) after normal sleep (NS) and 24-h TSD (randomized, crossover design). Forearm vascular conductance (FVC) was recorded during MS. MAP, FVC, and MSNA (n = 10) responses to MS were not different between NS and TSD (condition × time, P > 0.05). Likewise, MAP and MSNA (n = 6) responses to CPT were not different between NS and TSD (condition × time, P > 0.05). In contrast, increases in HR during both MS and CPT were augmented after TSD (condition × time, P ≤ 0.05), and these augmented HR responses persisted during both recoveries. When analyzed for sex differences, cardiovascular reactivity to MS and CPT was not different between sexes (condition × time × sex, P > 0.05). We conclude that TSD does not significantly alter MAP, MSNA, or forearm vascular responses to MS and CPT. The augmented tachycardia responses during and after both acute stressors provide new insight regarding the emerging links among sleep deprivation, stress, and cardiovascular risk.

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.

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.

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.

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.

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.

Neurovascular responses to mental stress have been linked to several cardiovascular diseases, including hypertension. Mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), and forearm vascular responses to mental stress are well documented in normotensive (NT) subjects, but responses in prehypertensive (PHT) subjects remain unclear. We tested the hypothesis that PHT would elicit a more dramatic increase of MAP during mental stress via augmented MSNA and blunted forearm vascular conductance (FVC). We examined 17 PHT (systolic 120-139 and/or diastolic 80-89 mmHg; 22 ± 1 yr) and 18 NT (systolic < 120 and diastolic < 80 mmHg; 23 ± 2 yr) subjects. Heart rate, MAP, MSNA, FVC, and calf vascular conductance were measured during 5 min of baseline and 5 min of mental stress (mental arithmetic). Mental stress increased MAP and FVC in both groups, but the increases in MAP were augmented (Δ 10 ± 1 vs. Δ14 ± 1 mmHg; P < 0.05), and the increases in FVC were blunted (Δ95 ± 14 vs. Δ37 ± 8%; P < 0.001) in PHT subjects. Mental stress elicited similar increases in MSNA (Δ7 ± 2 vs. Δ6 ± 2 bursts/min), heart rate (Δ21 ± 3 vs. Δ18 ± 3 beats/min), and calf vascular conductance (Δ29 ± 10 vs. Δ19 ± 5%) in NT and PHT subjects, respectively. In conclusion, mental stress elicits an augmented pressor response in PHT subjects. This augmentation appears to be associated with altered forearm vascular, but not MSNA, responses to mental stress.

The purpose of this study was to compare lactate thresholds (LT) and maximal aerobic capacities (VO(2 max) during sport-specific skating (on ice) and cycle ergometry (off ice) in collegiate hockey players. We hypothesized that VO(2 max) and LT would be higher on ice. We also sought to determine if on-ice and off-ice VO(2 max) values were correlated. Twelve collegiate hockey players performed both graded exercise protocols in randomized order to fatigue. Both protocols included 80 s of work during each stage, followed by 40 s of rest to allow for blood lactate sampling. VO(2 max) was significantly higher on ice (46.9 +/- 1.0 mL*kg(-1)*min(-1)) than off ice (43.6 +/- 0.9 mL*kg(-1)*min(-1); p < 0.05). Maximal heart rate (HR(max)) was also higher on ice (192.2 +/- 1.8 beats*min(-1)) than off ice (186.0 +/- 1.5 beats*min(-1); p < 0.01). LT was drastically higher on ice than off ice as a percentage of VO(2 max) (85.9% +/- 1.9% vs. 69.7% +/- 1.3%; p < 0.01) and HR(max) (90.1% +/- 1.3% vs. 79.4% +/- 1.6%; p < 0.01). Finally, no correlation existed between VO(2 max) values off ice and on ice (r = -0.002; p = 0.99). Our results indicate that off-ice VO(2 max) and LT are not adequate predictors of on-ice VO(2 max) and LT in collegiate hockey players. These findings challenge the use of cycle ergometry to assess aerobic capacity at events such as the National Hockey League Entry Draft combine. We suggest that hockey players be tested in a sport-specific manner, regardless of whether those tests are performed on ice or off ice.

Neural and cardiovascular responses to mental stress and acute 6 degrees head-down tilt (HDT) were examined separately and combined. We hypothesized sympathoexcitation during mental stress, sympathoinhibition during HDT, and an additive neural interaction during combined mental stress and HDT. Muscle sympathetic nerve activity (MSNA), mean arterial pressure (MAP), and heart rate (HR) were recorded in 16 healthy subjects (8 men, 8 women) in the supine position during three randomized trials: 1) mental stress (via mental arithmetic), 2) HDT, and 3) combined mental stress and HDT. Mental stress significantly increased MSNA (7+/-1 to 12+/-2 bursts/min; P<0.01), MAP (91+/-2 to 103+/-2 mmHg; P<0.01), and HR (70+/-3 to 82+/-3 beats/min; P<0.01). HDT did not change MSNA or HR, but MAP was reduced (91+/-2 to 89+/-3 mmHg; P<0.05). Combined mental stress and HDT significantly increased MSNA (7+/-1 to 10+/-1 bursts/min; P<0.01), MAP (88+/-3 to 99+/-3 mmHg; P<0.01), and HR (70+/-3 to 82+/-3 beats/min; P<0.01). Increases in MSNA and HR during the combination trial were not different from the sum of the individual trials. However, the increase in MAP during the combination trial was significantly greater than the sum of the individual trials (change of 11+/-1 vs. 9+/-1 mmHg; P<0.05). We conclude that the interaction for MSNA and HR are additive during combined mental stress and HDT but that MAP responses are slightly augmented during the combined trial. These findings demonstrate that sympathetic neural responses to mental stress are unaltered by simulated microgravity.

Sympathetic neural responses to mental stress are well documented but controversial, whereas sympathetic neural responses to emotional stress are unknown. The purpose of this study was to investigate neural and cardiovascular responses to emotional stress evoked by negative pictures and reexamine the relationship between muscle sympathetic nerve activity (MSNA) and perceived stress. Mean arterial pressure (MAP), heart rate (HR), MSNA, and perceived stress levels were recorded in 18 men during three randomized trials: 1) neutral pictures, 2) negative pictures, and 3) mental stress. MAP and HR increased during mental stress (Delta14 +/- 2 mmHg and Delta15 +/- 2 beats/min, P < 0.001) but did not change during viewing of negative or neutral pictures. MSNA did not change during viewing of neutral (Delta1 +/- 1 burst/min, n = 16) or negative (Delta0 +/- 1 burst/min, n = 16) pictures or during mental stress (Delta1 +/- 2 burst/min, n = 13). Perceived stress levels were higher during mental stress (3 +/- 0 arbitrary units) than during viewing negative pictures (2 +/- 0 arbitrary units, P < 0.001). Perceived stress levels were not correlated to changes in MSNA during negative pictures (r = 0.10, P = 0.84) or mental stress (r = 0.36, P = 0.23). In conclusion, our results demonstrate robust increases in MAP and HR during mental stress, but not during emotional stress evoked by negative pictures. Although the influence of mental stress on MSNA remains unresolved, our findings challenge the concept that perceived stress levels modulate MSNA during mental stress.

Positron-emitting 132Cs (t1/2 = 6.47 days) was generated from stable 133CsCl via the 133Cs (p,pn) 132Cs reaction. BALB/c mice, bearing implanted MT296 mammary tumors, were given 4.6 mEq kg-1 of 132CsCl via a single intraperitoneal injection. Postinjection uptake of 132Cs into body regions was monitored in vivo with external detectors. Positron emission from the tumor region was continuously greater than that from the head, the numerical ratio of mean emission intensities being fourfold at 10 min postinjection. Tissues excised from these mice postmortem showed sequence of relative tissue cesium uptake rates to be kidney 1.8, small intestine 1.7, tumor 1.0, skin 0.75, liver 0.75, skeletal muscle 0.4, and brain 0.28. Comparative studies with multiple injections of stable cesium and rubidium showed this sequence to be ion-specific. These observations suggest that positron-emitting isotopes of cesium could provide useful markers for tumors of several tissues.

A comparison was made of ferrous sulfate (Fricke) and ionometric methods for determining the absorbed dose in a phantom irradiated with 4-MV x-rays, 25-MV x-rays, or electron beams having various incident energies between 10 and 32 MeV. Both chemical and ionization instruments were calibrated in a 60Co beam at a point in water where the absorbed dose had been previously determined. The chemical yield measurements were corrected for spatial variations in dose within the volume of the solution and used to obtain a value of the absorbed dose for each of the x-ray and electron beams. The ratios of G-values required for these determinations were taken from ICRU reports 14 and 21. Ionization instrument readings from three types of commercial ionization chambers were used to obtain alternate values of the absorbed dose for each radiation. C lambda and CE values used in determining these ionization values of dose were also taken from the above ICRU reports. For 4-MV x-rays the values of absorbed dose obtained from chemical measurements agreed to within 0.5% with values obtained from ionization measurements; for 25-MV x-rays the chemical values were about 1% higher than the ionization values; for the electron beams the chemical values were 1%-4% below the ionization values. These discrepancies suggest an inconsistency among the recommended G, C lambda, and CE values similar to that which has been noted by other workers.