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BACKGROUND The STOP AF First trial recently demonstrated that initial treatment with cryoballoon ablation (CBA) is safe and superior to antiarrhythmic drug (AAD) therapy for preventing atrial arrhythmia recurrence in patients with symptomatic atrial fibrillation (AF). OBJECTIVE The purpose of this study was to evaluate the change in quality of life (QoL) and symptoms after first-line CBA vs AAD therapy. METHODS Patients with symptomatic AF not previously receiving rhythm control therapy were randomized to AAD (class I or III) or CBA (Arctic Front Advance, Medtronic, Mounds View, MN). QoL was evaluated at baseline and at 6 and 12 months by using the Atrial Fibrillation Effect on QualiTy-of-Life (AFEQT) and the European Quality of Life-5 Dimensions questionnaires. A review of AF-associated symptoms was conducted at baseline and at 1, 3, 6, and 12 months. RESULTS In total, 203 subjects received either CBA (n = 104 [51.2%]) or AAD therapy (n = 99 [48.8%]). Improvements in the AFEQT summary and subscale scores were significantly larger with CBA than with AAD therapy at 6 and 12 months (P 5 points) in the AFEQT summary score from baseline to 12 months was observed in 96.0% (100) of patients in the CBA arm vs 72.2% (71) of patients in the AAD arm (P < .001). No significant between-group differences were observed in the change in the European Quality of Life-5 Dimensions index or visual analog scale scores. Overall, 54.4% (57) of the CBA group vs 29.7% (29) of the AAD group reported no AF-specific symptom recurrence after a 90-day blanking period (P = .0005). CONCLUSION First-line CBA vs AAD therapy is associated with larger improvements in AF-specific QoL and a higher rate of symptom resolution.

In healthy humans, fructose-sweetened water consumption increases blood pressure variability (BPV) and decreases spontaneous cardiovagal baroreflex sensitivity (cBRS) and heart rate variability (HRV). However, whether consuming commercially available soft drinks containing high levels of fructose elicits similar responses is unknown. We hypothesized that high-fructose corn syrup (HFCS)-sweetened soft drink consumption increases BPV and decreases cBRS and HRV to a greater extent compared with artificially sweetened (diet) and sucrose-sweetened (sucrose) soft drinks and water. Twelve subjects completed four randomized, double-blinded trials in which they drank 500 mL of water or commercially available soft drinks matched for taste and caffeine content. We continuously measured beat-to-beat blood pressure (photoplethysmography) and R-R interval (ECG) before and 30 min after drink consumption during supine rest for 5 min during spontaneous and paced breathing. BPV was evaluated using standard deviation (SD), average real variability (ARV), and successive variation (SV) methods for systolic and diastolic blood pressure. cBRS was assessed using the sequence method. HRV was evaluated using the root mean square of successive differences (RMSSD) in R-R interval. There were no differences between conditions in the magnitude of change from baseline in SD, ARV, and SV ( P ≥ 0.07). There were greater reductions in cBRS during spontaneous breathing in the HFCS (−3 ± 5 ms/mmHg) and sucrose (−3 ± 5 ms/mmHg) trials compared with the water trial (+1 ± 5 ms/mmHg, P < 0.03). During paced breathing, HFCS evoked greater reductions in RMSSD compared with water (−26 ± 34 vs. +2 ± 26 ms, P < 0.01). These findings suggest that sugar-sweetened soft drink consumption alters cBRS and HRV but not BPV.

Recurring hot head-out water immersion (HOWI) enhances peripheral vascular function and cerebral blood velocity during non-immersion conditions. However, it is unknown if an acute bout of hot HOWI alters cerebrovascular function. Using two experimental studies, we tested the hypotheses that dynamic cerebral autoregulation (dCA) and cerebrovascular reactivity (CVR) are improved during an acute bout of hot (HOT; 39 °C) vs. thermoneutral (TN; 35 °C) HOWI. Eighteen healthy participants (eight females) completed the dCA study, and 14 participants (6 females) completed the CVR study. Both studies consisted of two randomized (TNdCA vs. HOTdCA; TNCVR vs. HOTCVR) 45minute HOWI visits. Middle cerebral artery blood velocity (MCAvmean) was continuously recorded. dCA was assessed using a respiratory impedance device and analyzed via transfer gain and phase in the low-frequency band. CVR was assessed using stepped hypercapnia. Assessments were completed PRE and 30 minutes into HOWI. Values are reported as a change (Δ) from PRE (mean ± SD). There were no differences at PRE for either study. ΔMCAvmean was greater in TNdCA (TNdCA: 4 ± 4 vs. HOTdCA: -3 ± 5 cm/s; P < 0.01) and TNCVR (TNCVR: 5 ± 4 vs. HOTCVR: -1 ± 6 cm/s; P < 0.01) during HOWI. ΔGain was greater in HOTdCA during HOWI (TNdCA: -0.09 ± 0.15 vs. HOTdCA: 0.10 ± 0.17 cm/s/mmHg; P = 0.04). ΔPhase (P > 0.84) and ΔCVR (P > 0.94) were not different between conditions. These data indicate that hot and thermoneutral water immersion do not acutely alter cerebrovascular function in healthy, young adults.

Introduction: Pre-dive altitude exposure may increase respiratory fatigue and subsequently augment exercise ventilation at depth. This study examined pre-dive altitude exposure and the efficacy of resistance respiratory muscle training (RMT) on respiratory fatigue while diving at altitude. Methods: Ten men (26±5 years; V̇ O2peak: 39.8±3.3 mL• kg-1•min-1) performed three dives; one control (ground level) and two simulated altitude dives (3,658 m) to 17 msw, relative to ground level, before and after four weeks of resistance RMT. Subjects performed pulmonary function testing (e.g., inspiratory [PI] and expiratory [PE] pressure testing) pre- and post-RMT and during dive visits. During each dive, subjects exercised for 18 minutes at 55% V̇ O2peak, and ventilation (V̇ E), breathing frequency (ƒb,), tidal volume (VT) and rating of perceived exertion (RPE) were measured. Results: Pre-dive altitude exposure reduced PI before diving (p=0.03), but had no effect on exercise V̇ E, ƒb, or VT at depth. At the end of the dive in the pre-RMT condition, RPE was lower (p=0.01) compared to control. RMT increased PI and PE (p

Background Western corn rootworm (WCR) pyrethroid resistance has been confirmed in the western US Corn Belt. Toxicological and biochemical studies indicated that multiple mechanisms of resistance might be involved in the resistance trait, such as enhanced metabolism and/or kdr target-site mutation(s) in the voltage-gated sodium channels. To characterize the mechanisms of WCR pyrethroid resistance at the molecular level, pairwise comparisons were made between RNA-Seq data collected from pyrethroid-resistant and -susceptible WCR populations. Gene expression levels and sodium channel sequences were evaluated. Results Seven transcripts exhibited significantly different expression (q ≤ 0.05) when comparing field-collected pyrethroid-resistant (R-Field) and -susceptible (S-Field) WCR populations. Three of the differentially expressed transcripts were P450s overexpressed in R-Field (9.2-26.2-fold). A higher number (99) of differentially expressed transcripts was found when comparing laboratory-derived pyrethroid-resistant (R-Lab) and -susceptible (S-Lab) WCR populations. Eight of the significant transcripts were P450s overexpressed in R-Lab (2.7-39.8-fold). This study did not detect kdr mutations in pyrethroid-resistant WCR populations. Other differentially expressed transcripts that may play a role in WCR pyrethroid resistance are discussed. Conclusion This study revealed that P450-mediated metabolism is likely to be a major mechanism of WCR pyrethroid resistance, which could affect the efficacy of other insecticides sharing similar metabolic pathways. Additionally, results suggested that although laboratory selection of a pyrethroid-resistant WCR population may help to characterize resistance mechanisms, a field-selected population provided rare and perhaps major variants corresponding to the resistance trait.

INTRODUCTION:Hypoxia-induced hyperventilation is an effect of acute altitude exposure, which may lead to respiratory muscle fatigue and secondary locomotor muscle fatigue. The purpose of this study was to determine if resistive and/or endurance respiratory muscle training (RRMT and ERMT, respectively) vs. placebo respiratory muscle training (PRMT) improve cycling performance at altitude.METHODS:There were 24 subjects who were assigned to PRMT (N8), RRMT (N8), or ERMT (N8). Subjects cycled to exhaustion in a hypobaric chamber decompressed to 3657 m (12,000 ft) at an intensity of 55% sea level maximal oxygen consumption (Vo2max) before and after respiratory muscle training (RMT). Additionally, subjects completed a Vo2max, pulmonary function, and respiratory endurance test (RET) before and after RMT. All RMT protocols consisted of three 30-min training sessions per week for 4 wk.RESULTS:The RRMT group increased maximum inspiratory (PImax) and expiratory (PEmax) mouth pressure after RMT (PImax: 117.7 11.6 vs. 162.6 20.0; PEmax: 164.0 33.2 vs. 216.5 44.1 cmH2O). The ERMT group increased RET after RMT (5.2 5.2 vs.18.6 16.9 min). RMT did not improve Vo2maxin any group. Both RRMT and ERMT groups increased cycling time to exhaustion (RRMT: 35.9 17.2 vs. 45.6 22.2 min and ERMT: 33.8 9.6 vs. 42.9 27.0 min).CONCLUSION:Despite different improvements in pulmonary function, 4 wk of RRMT and ERMT both improved cycle time to exhaustion at altitude.Wheelock CE, Hess HW, Johnson BD, Schlader ZJ, Clemency BM, St. James E, Hostler D.Endurance and resistance respiratory muscle training and aerobic exercise performance in hypobaric hypoxia. Aerosp Med Hum Perform. 2020; 91(10):776784.

Hyperoxia reduces the ventilatory response to hypercapnia by suppressing carotid body (CB) activation. This effect may contribute to CO(2) retention during underwater diving due to the high arterial O(2) content associated with hyperbaria. We tested the hypothesis that CB chemosensitivity to hypercapnia and hypoxia is attenuated during hyperbaria. Ten subjects completed two, 4-h dry dives at 1.6 atmosphere absolute (ATA) breathing either 21% O(2) (Air) or 100% O(2) (100% O(2)). CB chemosensitivity was assessed using brief hypercapnic ventilatory response ([Formula: see text]) and hypoxic ventilatory response ([Formula: see text]) tests predive, 75 and 155 min into the dives, and 15 and 55 min postdive. End-tidal CO(2) pressure increased during the dive at 75 and 155 min [Air: +9 (SD 4) mmHg and +8 (SD 4) mmHg versus 100% O(2): +6 (SD 4) mmHg and +5 (SD 3) mmHg; all P < 0.01] and was higher while breathing Air (P < 0.01). [Formula: see text] was unchanged during the dive (P = 0.73) and was not different between conditions (P = 0.47). However, [Formula: see text] was attenuated from predive during the dive at 155 min breathing Air [−0.035 (SD 0.037) L·min·mmHg(−1); P = 0.02] and at both time points while breathing 100% O(2) [−0.035 (SD 0.052) L·min·mmHg(−1) and −0.034 (SD 0.064) L·min·mmHg(−1); P = 0.02 and P = 0.02, respectively]. These data indicate that the CB chemoreceptors do not appear to contribute to CO(2) retention in hyperbaria. NEW & NOTEWORTHY We demonstrate that carotid body chemosensitivity to brief exposures of hypercapnia was unchanged during a 4-h dive in a dry hyperbaric chamber at 1.6 ATA regardless of breathing gas condition [i.e., air (21% O(2)) versus 100% oxygen]. Therefore, it appears that an attenuation of carotid body chemosensitivity to hypercapnia does not contribute to CO(2) retention in hyperbaria.

Military and civilian emergency situations often involve prolonged exposures to warm and very humid environments. We tested the hypothesis that increases in core temperature and body fluid losses during prolonged exposure to warm and very humid environments are dependent on dry bulb temperature. On three occasions, 15 healthy males (23 ± 3 yr) sat in 32.1 ± 0.1°C, 33.1 ± 0.2°C, or 35.0 ± 0.1°C and 95 ± 2% relative humidity normobaric environments for 8 h. Core temperature (telemetry pill) and percent change in body weight, an index of changes in total body water occurring secondary to sweat loss, were measured every hour. Linear regression models were fit to core temperature (over the final 4 h) and percent changes in body weight (over the entire 8 h) for each subject. These equations were used to predict core temperature and percent changes in body weight for up to 24 h. At the end of the 8-h exposure, core temperature was higher in 35°C (38.2 ± 0.4°C, P < 0.01) compared with 32°C (37.2 ± 0.2°C) and 33°C (37.5 ± 0.2°C). At this time, percent changes in body weight were greater in 35°C (−1.9 ± 0.5%) compared with 32°C (−1.4 ± 0.3%, P < 0.01) but not 33°C (−1.6 ± 0.6%, P = 0.17). At 24 h, predicted core temperature was higher in 35°C (39.2 ± 1.4°C, P < 0.01) compared with 32°C (37.6 ± 0.9°C) and 33°C (37.5 ± 0.9°C), and predicted percent changes in body weight were greater in 35°C (−6.1 ± 2.4%) compared with 32°C (−4.6 ± 1.5%, P = 0.04) but not 33°C (−5.3 ± 2.0%, P = 0.43). Prolonged exposure to 35°C, but not 32°C or 33°C, dry bulb temperatures and high humidity is uncompensable heat stress, which exacerbates body fluid losses.

We first tested the hypothesis that consuming a high-fructose corn syrup (HFCS)-sweetened soft drink augments kidney vasoconstriction to sympathetic stimulation compared with water ( study 1). In a second study, we examined the mechanisms underlying these observations ( study 2). In study 1, 13 healthy adults completed a cold pressor test, a sympathoexcitatory maneuver, before (preconsumption) and 30 min after drinking 500 mL of decarbonated HFCS-sweetened soft drink or water (postconsumption). In study 2, venous blood samples were obtained in 12 healthy adults before and 30 min after consumption of 500 mL water or soft drinks matched for caffeine content and taste, which were either artificially sweetened (Diet trial), sucrose-sweetened (Sucrose trial), or sweetened with HFCS (HFCS trial). In both study 1 and study 2, vascular resistance was calculated as mean arterial pressure divided by blood velocity, which was measured via Doppler ultrasound in renal and segmental arteries. In study 1, HFCS consumption increased vascular resistance in the segmental artery at rest (by 0.5 ± 0.6 mmHg·cm−1·s−1, P = 0.01) and during the cold pressor test (average change: 0.5 ± 1.0 mmHg·cm−1·s−1, main effect: P = 0.05). In study 2, segmental artery vascular resistance increased in the HFCS trial (by 0.8 ± 0.7 mmHg·cm−1·s−1, P = 0.02) but not in the other trials. Increases in serum uric acid were greater in the HFCS trial (0.3 ± 0.4 mg/dL, P ≤ 0.04) compared with the Water and Diet trials, and serum copeptin increased in the HFCS trial (by 0.8 ± 1.0 pmol/L, P = 0.06). These findings indicate that HFCS acutely increases vascular resistance in the kidneys, independent of caffeine content and beverage osmolality, which likely occurs via simultaneous elevations in circulating uric acid and vasopressin.

Profound increases (>15 mmHg) in arterial carbon dioxide (i.e., hypercapnia) reduce renal blood flow. However, a relatively brief and mild hypercapnia can occur in patients with sleep apnea or in those receiving supplemental oxygen therapy during an acute exacerbation of chronic obstructive pulmonary disease. We tested the hypothesis that a brief, mild hypercapnic exposure increases vascular resistance in the renal and segmental arteries. Blood velocity in 14 healthy adults (26 ± 4 yr; 7 women, 7 men) was measured in the renal and segmental arteries with Doppler ultrasound while subjects breathed room air (Air) and while they breathed a 3% CO2, 21% O2, 76% N2 gas mixture for 5 min (CO2). The end-tidal partial pressure of CO2 ([Formula: see text]) was measured via capnography. Mean arterial pressure (MAP) was measured beat to beat via the Penaz method. Vascular resistance in the renal and segmental arteries was calculated as MAP divided by blood velocity. [Formula: see text] increased with CO2 (Air: 45 ± 3, CO2: 48 ± 3 mmHg, P < 0.01), but there were no changes in MAP ( P = 0.77). CO2 decreased blood velocity in the renal (Air: 35.2 ± 8.1, CO2: 32.2 ± 7.3 cm/s, P < 0.01) and segmental (Air: 24.2 ± 5.1, CO2: 21.8 ± 4.2 cm/s, P < 0.01) arteries and increased vascular resistance in the renal (Air: 2.7 ± 0.9, CO2: 3.0 ± 0.9 mmHg·cm−1·s, P < 0.01) and segmental (Air: 3.9 ± 1.0, CO2: 4.4 ± 1.0 mmHg·cm−1·s, P < 0.01) arteries. These data provide evidence that the kidneys are hemodynamically responsive to a mild and acute hypercapnic stimulus in healthy humans.

To optimize study design and data interpretation, there is a need to understand the reliability of Doppler ultrasound-derived measures of blood velocity (BV) measured in the renal and segmental arteries. Thus, this study tested the following two hypotheses: 1) renal and segmental artery BV measured over the current standard of three cardiac cycles have good agreement with measurements over nine cardiac cycles ( study 1); and 2) renal and segmental artery BV measurements have relatively poor day-to-day reliability ( study 2). In study 1, there was excellent agreement between measurements over three and nine cardiac cycles for BV in both the renal and segmental arteries, as evidenced by BV measurements that were not statistically different ( P ≥ 0.68), were highly consistent ( r ≥ 0.99, P < 0.01), had a coefficient of variation ≤2.5 ± 1.8%, and 97% (renal artery) and 92% (segmental artery) of the individual differences fell within the 95% limits of agreement. In study 2, there was relatively good day-to-day reliability in renal artery BV as evidenced by no differences between three separate days ( P ≥ 0.30), an intraclass correlation coefficient (ICC) of 0.92 (0.78, 0.98), and 7.4 ± 5.5% coefficient of variation. The day-to-day reliability was relatively poor in the segmental artery with an ICC of 0.77 (0.41, 0.93) and 9.0 ± 5.6% coefficient of variation. These findings support measuring renal and segmental artery hemodynamics over three cardiac cycles and the utility in reporting renal BV across days. However, because of the variation across days, hemodynamic responses in the segmental arteries should be reported as changes from baseline when making comparisons across multiple days. NEW & NOTEWORTHY The present study indicates that Doppler ultrasound-derived measures of renal and segmental artery hemodynamics over three cardiac cycles have excellent agreement with those over nine cardiac cycles. These findings support the current practice of measuring renal and segmental artery blood velocity over three cardiac cycles. This study also demonstrates that there is excellent day-to-day reliability for measures of renal artery blood velocity, which supports reporting absolute values of renal artery blood velocity across days. However, it was also found that the day-to-day reliability of segmental artery measurements is relatively poor. Thus, to account for this variability, we suggest that segmental artery hemodynamics be compared as relative changes from baseline across separate days.

The present study examined the factor structure of the Personality Assessment Inventory Antisocial Features scale (PAI-ANT) in a non-forensic sample of 1257 undergraduate students. One to four-factor models were tested using exploratory factor analysis (EFA), with a four-factor solution exhibiting the best fitting model (Bentler 1995). Next examined was the convergent and discriminant validity of the PAI-ANT. Results indicated that the PAI-ANT four-factor model was significantly related to measures of general personality, pride, impulsivity, and attachment. Comparisons between the original three-factor model (as proposed by Morey 2007) and our derived four-factor model showed that both models generally had the expected pattern of relations for their respective factors although mixed findings were found for the sensation seeking and risk-taking scales. Findings for these scales indicated that individuals could crave excitement and also have some positive characteristics. The current findings suggest that the four-factor model of the PAI is the best way to interpret the PAI psychopathy scale, but that some caution is needed in interpreting the sensation seeking and risk-taking scales.

This study tested the hypotheses that compared to drinking water, consumption of a caffeinated soft drink sweetened with high‐fructose corn syrup (HFCS) attenuates the cutaneous vasodilatory response to local skin heating without (Protocol 1) and following ischemia‐reperfusion injury (Protocol 2). In a randomized, counterbalanced crossover design, 14 healthy adults (25 ± 3 year, 6 women) consumed 500 ml of water (water) or a caffeinated soft drink sweetened with HFCS (Mtn. Dew, DEW). Thirty minutes following beverage consumption local skin heating commenced on the right forearm (Protocol 1), while on the left forearm ischemia‐reperfusion commenced with 20 min of ischemia followed by 20 min of reperfusion and then local skin heating (Protocol 2). Local skin heating involved 40 min of heating to 39℃ followed by 20 min of heating to 44℃. Skin blood flow (SkBf, laser Doppler) data were normalized to mean arterial pressure and are presented as a cutaneous vascular conductance (CVC) and as percentage of the CVC response during heating to 44℃ (%CVCmax). Protocol 1: During local heating at 39℃, no differences were observed in CVC (water: 2.0 ± 0.6 PU/mmHg; DEW: 2.0 ± 0.8 PU/mmHg, p = 0.83) or %CVCmax (water: 59 ± 14%; DEW 60 ± 15%, p = 0.84) between trials. Protocol 2: During local skin heating at 39℃, no differences were observed in CVC (water: 1.7 ± 0.5 PU/mmHg; DEW: 1.5 ± 0.5 PU/mmHg, p = 0.33) or %CVCmax (water: 64 ± 15%; DEW 61 ± 15% p = 0.62) between trials. The cutaneous microvascular vasodilator response to local heating with or without prior ischemia‐reperfusion injury is not affected by acute consumption of a caffeinated soft drink sweetened with HFCS., We examined the effect of consumption of a caffeinated soft drink sweetened with high‐fructose corn syrup on the cutaneous vasodilatory response to local skin heating without and following ischemia‐reperfusion injury. We identified that the cutaneous microvascular vasodilator response to local heating with or without prior ischemia‐reperfusion injury is not affected by acute consumption of a caffeinated soft drink sweetened with high‐fructose corn syrup.

Introduction: Tonic carotid body (CB) activity is reduced during exposure to cold and hyperoxia. We tested the hypotheses that cold water diving lowers CB chemosensitivity and augments CO2 retention more than thermoneutral diving. Methods: Thirteen subjects (age: 26±4 y; BMI: 26±2 kg/m2) completed two, four-hour head out water immersion protocols in a hyperbaric chamber (1.6 ATA) in cold (15°C) and thermoneutral (25°C) water. CB chemosensitivity was assessed using brief hypercapnic ventilatory response (CBCO2) and hypoxic ventilatory response (CBO2) tests pre-dive, 80 and 160 min into the dives (D80 and D160, respectively), immediately following and 60 min post-dive. Data are reported as an absolute mean (SD) change from pre-dive. Results: End-tidal CO2 pressure increased during both the thermoneutral water dive (D160: +2(3) mmHg; p=0.02) and cold water dive (D160: +1(2) mmHg; p=0.03). Ventilationincreased during the cold water dive (D80: 4.13(4.38) and D160: 7.75(5.23) L·min-1; both pCO2 was unchanged during the dive (p=0.24) and was not different between conditions (p=0.23). CBO2 decreased during the thermonutral water dive (D80: -3.45(3.61) and D160: -2.76(4.04) L·min·mmHg-1; pO2 was not different between conditions (p=0.17). Conclusion: CB chemosensitivity was not attenuated during the cold stress diving condition and does not appear to contribute to changes in ventilation or CO2 retention.

Arterial hypercapnia reduces renal perfusion. Beetroot juice (BRJ) increases nitric oxide bioavailability and may improve renal blood flow. We tested the hypothesis that acute consumption of BRJ attenuates both decreases in blood velocity and increases in vascular resistance in the renal and segmental arteries during acute hypercapnia. In fourteen healthy young adults, blood velocity and vascular resistance were measured with Doppler ultrasound in the renal and segmental arteries during five minutes of breathing a carbon dioxide gas mixture (CO2) before and three hours after consuming 500 mL of BRJ. There was no difference between pre- and post-BRJ consumption in the increase in the partial pressure of end-tidal CO2 during CO2 breathing (pre: +4 ± 1 mmHg, post: +4 ± 2 mmHg, p = 0.4281). Segmental artery blood velocity decreased during CO2 breathing in both pre- (by −1.8 ± 1.9 cm/s, p = 0.0193) and post-BRJ (by −2.1 ± 1.9 cm/s, p = 0.0079), but there were no differences between pre- and post-consumption (p = 0.7633). Segmental artery vascular resistance increased from room air baseline during CO2 at pre-BRJ consumption (by 0.4 ± 0.4 mmHg/cm/s, p = 0.0153) but not post-BRJ (p = 0.1336), with no differences between pre- and post-consumption (p = 0.7407). These findings indicate that BRJ consumption does not attenuate reductions in renal perfusion during acute mild hypercapnia in healthy young adults.

We tested the hypothesis that thermal behavior resulting in reductions in mean skin temperature alleviates thermal discomfort and mitigates the rise in core temperature during light-intensity exercise. In a 27 ± 0°C, 48 ± 6% relative humidity environment, 12 healthy subjects (6 men, 6 women) completed 60 min of recumbent cycling. In both trials, subjects wore a water-perfused suit top continually perfusing 34 ± 0°C water. In the behavior trial, subjects maintained their upper body thermally comfortable by pressing a button to perfuse cool water (2.2 ± 0.5°C) through the top for 2 min per button press. Metabolic heat production (control: 404 ± 52 W, behavior: 397 ± 65 W; P = 0.44) was similar between trials. Mean skin temperature was reduced in the behavior trial (by −2.1 ± 1.8°C, P < 0.01) because of voluntary reductions in water-perfused top temperature ( P < 0.01). Whole body ( P = 0.02) and local sweat rates were lower in the behavior trial ( P ≤ 0.05). Absolute core temperature was similar ( P ≥ 0.30); however, the change in core temperature was greater in the behavior trial after 40 min of exercise ( P ≤ 0.03). Partitional calorimetry did not reveal any differences in cumulative heat storage (control: 554 ± 229, behavior: 544 ± 283 kJ; P = 0.90). Thermal behavior alleviated whole body thermal discomfort during exercise (by −1.17 ± 0.40 arbitrary units, P < 0.01). Despite lower evaporative cooling in the behavior trial, similar heat loss was achieved by voluntarily employing convective cooling. Therefore, thermal behavior resulting in large reductions in skin temperature is effective at alleviating thermal discomfort during exercise without affecting whole body heat loss. NEW & NOTEWORTHY This study aimed to determine the effectiveness of thermal behavior in maintaining thermal comfort during exercise by allowing subjects to voluntarily cool their torso and upper limbs with 2°C water throughout a light-intensity exercise protocol. We show that voluntary cooling of the upper body alleviates thermal discomfort while maintaining heat balance through convective rather than evaporative means of heat loss.

High environmental temperatures are associated with increased risk of acute kidney injury, which may be related to reductions in renal blood flow. The susceptibility of the kidneys may be increased because of heat stress-induced changes in renal vascular resistance (RVR) to sympathetic activation. We tested the hypotheses that, compared with normothermia, increases in RVR during the cold pressor test (CPT, a sympathoexcitatory maneuver) are attenuated during passive heating and exacerbated after cooling recovery. Twenty-four healthy adults (22 ± 2 yr; 12 women, 12 men) completed CPTs at normothermic baseline, after passive heating to a rise in core temperature of ~1.2°C, and after cooling recovery when core temperature returned to ~0.2°C above normothermic baseline. Blood velocity was measured by Doppler ultrasound in the distal segment of the right renal artery (Renal, n = 24 during thermal stress, n = 12 during CPTs) or the middle portion of a segmental artery (Segmental, n = 12). RVR was calculated as mean arterial pressure divided by renal or segmental blood velocity. RVR increased at the end of CPT during normothermic baseline in both arteries (Renal: by 1.0 ± 1.0 mmHg·cm−1·s, Segmental: by 2.2 ± 1.2 mmHg·cm−1·s, P ≤ 0.03), and these increases were abolished with passive heating ( P ≥ 0.76). At the end of cooling recovery, RVR in both arteries to the CPT was restored to that of normothermic baseline ( P ≤ 0.17). These data show that increases in RVR to sympathetic activation during passive heating are attenuated and return to that of normothermic baseline after cooling recovery. NEW & NOTEWORTHY Our data indicate that increases in renal vascular resistance to the cold pressor test (i.e., sympathetic activation) are attenuated during passive heating, but at the end of cooling recovery this response returns to that of normothermic baseline. Importantly, hemodynamic responses were assessed in arteries going to (renal artery) and within (segmental artery) the kidney, which has not been previously examined in the same study during thermal and/or sympathetic stressors.

Background: The Buffalo Concussion Treadmill Test (BCTT) is a graded exertion test for assessing exercise tolerance after concussion, but its utility is limited for certain populations. Hypothesis: We developed the Buffalo Concussion Bike Test (BCBT) and tested its comparability with the BCTT. We hypothesize that heart rate (HR) at symptom exacerbation on the BCBT will be equivalent to the BCTT. Study Design: Case-control study. Level of Evidence: Level 3. Methods: Adolescents with acute concussion (AC) (n = 20; mean age, 15.9 ± 1.1 years; 60% male) presenting to a concussion clinic within 10 days of injury and age- and sex-matched healthy controls (n = 20; mean age, 15.9 ± 1.1 years; 60% male) performed the BCTT at first visit and returned within 3 days to perform the BCBT. Test duration, HR, symptom severity (measured using a visual analog scale), and exertion (measured using the Borg Rating of Perceived Exertion) were collected during each test. Results: Adolescents with AC who were exercise intolerant on the BCTT were also intolerant on the BCBT, with symptom exacerbation occurring at a mean 8.1 ± 2.8 minutes on the BCTT versus 14.6 ± 6.0 minutes on the BCBT ( P < 0.01). Two 1-sided t tests showed that the HR at symptom exacerbation in AC patients (137 ± 28 bpm on BCTT vs 135 ± 25 bpm on BCBT; 95% CI, Conclusion: The HR at symptom exacerbation on BCBT is equivalent to the BCTT for the assessment of exercise tolerance after concussion in adolescents. Clinical Relevance: The BCBT can be used in patients with limited mobility or for research interventions that require limited participant motion.

Studies related to psychopathy and EEG have increased over the past decade making it a good time to examine where the field is on this topic as well as to determine future directions. The current study reviewed 68 research reports that focused on psychopathy and various components of EEG. We examined early, mid, and late level ERP processing as well as spectra analyses. The results indicate that psychopathic individuals exhibit generally unencumbered performance categorizing cognitive stimuli and demonstrate the typical facilitation of physical responses commensurate with an intact orienting response. Moreover, the results suggest that individuals with elevated psychopathic traits are especially adept at screening out distracting threat-related and other irrelevant information allowing them to allocate attention to stimuli that are goal-relevant. Those with elevated psychopathic traits also do not appear to have significant impairments in associative learning or error processing. Where psychopathic individuals diverge most from those with low levels of these traits is in relation to processing affect-laden content. In some contexts, psychopathic individuals appear to quickly terminate the processing of emotional information and in other contexts (e.g., seeing others in pain) they elaborately process emotional information both of which may help explain their prototypical lack of conscience. Much of the aberrant functioning of those with elevated psychopathic traits depends on the psychopathy factor being examined with F1 traits showing less cognitive impairment than F2 traits. Recommendations for future research are provided.

We tested the hypothesis that thermal behavior is greater during and after high- compared with moderate-intensity exercise. In a 27°C, 20% relative humidity environment, 20 participants (10 women, 10 men) cycled for 30 min at moderate [53% (SD 6) peak oxygen uptake (V̇o2peak) or high [78% (SD 6) V̇o2peak] intensity, followed by 120 min of recovery. Mean skin and core temperatures and mean skin wettedness were recorded continuously. Participants maintained thermally comfortable neck temperatures with a custom-made neck device. Neck device temperature provided an index of thermal behavior. The weighted average of mean skin and core temperatures and mean skin wettedness provided an indication of the afferent stimulus to thermally behave. Mean skin and core temperatures were greater at end-exercise in high intensity ( P < 0.01). Core temperature remained elevated in high intensity until 70 min of recovery ( P = 0.03). Mean skin wettedness and the afferent stimulus were greater at 10–20 min of exercise in high intensity ( P ≤ 0.03) and remained elevated until 60 min of recovery ( P < 0.01). Neck device temperature was lower during exercise in high versus moderate intensity ( P ≤ 0.02). There was a strong relation between the afferent stimulus and neck device temperature during exercise (high: R2 = 0.82, P < 0.01; moderate: R2 = 0.95, P < 0.01) and recovery (high: R2 = 0.97, P < 0.01; moderate: R2 = 0.93, P < 0.01). During exercise, slope ( P = 0.49) and y-intercept ( P = 0.91) did not differ between intensities. In contrast, slope was steeper ( P < 0.01) and y-intercept was higher ( P < 0.01) during recovery from high-intensity exercise. Thermal behavior is greater during high-intensity exercise because of the greater stimulus to behave. The withdrawal of thermal behavior is augmented after high-intensity exercise. NEW & NOTEWORTHY This is the first study to determine the effects of exercise intensity on thermal behavior. We show that exercise intensity does not independently modulate thermal behavior during exercise but is dependent on the magnitude of afferent stimuli. In contrast, the withdrawal of thermal behavior after high-intensity exercise is augmented. This may be a consequence of an attenuated perceptual response to afferent stimuli, which may be due to processes underlying postexercise hypoalgesia.

The purpose of this study was to test the hypothesis that consuming a soft drink (i.e., a high-fructose, caffeinated beverage) during and following exercise in the heat elevates biomarkers of acute kidney injury (AKI) in humans. Twelve healthy adults drank 2 liters of an assigned beverage during 4 h of exercise in the heat [35.1 (0.1)°C, 61 (5)% relative humidity] in counterbalanced soft drink and water trials, and ≥1 liter of the same beverage after leaving the laboratory. Stage 1 AKI (i.e., increased serum creatinine ≥0.30 mg/dl) was detected at postexercise in 75% of participants in the Soft Drink trial compared with 8% in Water trial ( P = 0.02). Furthermore, urinary neutrophil gelatinase-associated lipocalin (NGAL), a biomarker of AKI, was higher during an overnight collection period after the Soft Drink trial compared with Water in both absolute concentration [6 (4) ng/dl vs. 5 (4) ng/dl, P < 0.04] and after correcting for urine flow rate [6 (7) (ng/dl)/(ml/min) vs. 4 (4) (ng/dl)/(ml/min), P = 0.03]. Changes in serum uric acid from preexercise were greater in the Soft Drink trial than the Water trial at postexercise ( P < 0.01) and 24 h ( P = 0.05). There were greater increases from preexercise in serum copeptin, a stable marker of vasopressin, at postexercise in the Soft Drink trial ( P < 0.02) than the Water trial. These findings indicate that consuming a soft drink during and following exercise in the heat induces AKI, likely via vasopressin-mediated mechanisms.

This study tested the hypothesis that females rely on thermal behavior to a greater extent during and after exercise, relative to males.In a 24°C ± 1°C; (45% ± 10% RH) environment, 10 males (M) and 10 females (F) (22 ± 2 yr) cycled for 60 min (metabolic heat production: M, 117 ± 18 W·m; F, 129 ± 21 W·m), followed by 60-min recovery. Mean skin and core temperatures, skin blood flow and local sweat rates were measured continually. Subjects controlled the temperature of their dorsal neck to perceived thermal comfort using a custom-made device. Neck device temperature provided an index of thermal behavior and mean body temperature provided an index of the stimulus for thermal behavior. Data were analyzed for total area under the curve for exercise and recovery time points. To further isolate the effect of exercise on thermal behavior during recovery, data were also analyzed the minute mean body temperature returned to preexercise levels within a subject.There were no sex differences in metabolic heat production (P = 0.71) or body temperatures (P ≥ 0.10) during exercise. Area under the curve for neck device temperature during exercise was greater for F (-98.4°C·min ± 33.6°C·min vs -64.5°C·min ± 47.8°C·min, P = 0.04), but did not differ during recovery (F, 86.8°C·min ± 37.8°C·min; M, 65.6°C·min ± 35.9°C·min; P = 0.11). In M, mean skin (P = 0.90), core (P = 0.70) and neck device (P = 0.99) temperatures had recovered by the time that mean body temperature had returned to preexercise levels. However, in F, neck device temperature (P = 0.04) was reduced while core temperature remained elevated (P0.01).Females use thermal behavior during exercise to a greater extent than M. During recovery, thermal behavior may compensate for elevated core temperatures in F despite mean body temperatures returning to preexercise levels.

The kidneys' integrative responses to heat stress aid thermoregulation, cardiovascular control, and water and electrolyte regulation. Recent evidence suggests the kidneys are at increased risk of pathological events during heat stress, namely acute kidney injury (AKI), and that this risk is compounded by dehydration and exercise. This heat stress related AKI is believed to contribute to the epidemic of chronic kidney disease (CKD) occurring in occupational settings. It is estimated that AKI and CKD affect upwards of 45 million individuals in the global workforce. Water and electrolyte disturbances and AKI, both of which are representative of kidney-related pathology, are the two leading causes of hospitalizations during heat waves in older adults. Structural and physiological alterations in aging kidneys likely contribute to this increased risk. With this background, this comprehensive narrative review will provide the first aggregation of research into the integrative physiological response of the kidneys to heat stress. While the focus of this review is on the human kidneys, we will utilize both human and animal data to describe these responses to passive and exercise heat stress, and how they are altered with heat acclimation. Additionally, we will discuss recent studies that indicate an increased risk of AKI due to exercise in the heat. Lastly, we will introduce the emerging public health crisis of older adults during extreme heat events and how the aging kidneys may be more susceptible to injury during heat stress.

We tested the hypothesis that ingestion of a caffeinated soft drink sweetened with high‐fructose corn syrup acutely increases arterial stiffness. In a randomized counterbalanced, crossover design, fourteen healthy adults (25 ± 3 years, 6 women) reported to the laboratory for two experimental visits where 500 ml of tap water (H2O) or 500 ml of Mountain Dew® (a caffeinated soft drink sweetened with high‐fructose corn syrup (HFCS)) were consumed. Arterial stiffness (carotid‐to‐femoral pulse wave velocity (cfPWV)), peripheral and central blood pressures were measured pre‐consumption, 30 min post‐consumption, and 120 min post‐consumption. Prior to each measurement period, beat‐to‐beat hemodynamic measures were collected. Changes in heart rate, blood pressure, and cardiac output from pre‐consumption did not differ between trials at any timepoint (p ≥ 0.06). Moreover, changes in peripheral or central blood pressures from pre‐consumption did not differ between trials (p ≥ 0.84). Likewise, changes in cfPWV from pre‐consumption to 30 min post‐consumption (HFCS: 0.2 ± 0.3 m/s, H2O: 0.0 ± 0.3 m/s, p = 0.34) and 120 min post‐consumption (HFCS: 0.3 ± 0.4 m/s, H2O: 0.2 ± 0.3 m/s, p = 0.77) did not differ. Changes in aortic augmentation pressure, augmentation index, augmentation index corrected to a heart rate of 75 bpm, and reflection magnitude did not differ between conditions at 30 min post‐ (p ≥ 0.55) or 120 min post‐ (p ≥ 0.18) consumption. In healthy young adults, ingesting 500 ml of a commercially available caffeinated soft drink sweetened with high‐fructose corn syrup does not acutely change indices of arterial stiffness and wave reflection., This study investigated whether the ingestion of a caffeinated soft drink sweetened with high‐fructose corn syrup acutely modified arterial stiffness. In a randomized counterbalanced, crossover design, fourteen young healthy adults consumed 500 ml of tap water or a caffeinated soft drink sweetened with high‐fructose corn syrup, after which carotid‐to‐femoral pulse wave velocity was measured. This study found that ingesting 500 ml of a commercially available caffeinated soft drink sweetened with high‐fructose corn syrup does not acutely change indices of arterial stiffness.

Concussions have been shown to result in autonomic dysfunction and altered cerebral vascular function. We tested the hypothesis that concussed athletes (CA) would have altered cerebral vascular function during acute decreases and increases in blood pressure compared to healthy controls (HC). Ten CA (age: 20 ± 2 y, 7 females) and 10 HC (age: 21 ± 2 y, 6 females) completed 5 min of lower body negative pressure (LBNP; −40 mmHg) and 5 min of lower body positive pressure (LBPP; 20 mmHg). Protocols were randomized and separated by 10 min. Mean arterial pressure (MAP) and middle cerebral artery blood velocity (MCAv) were continuously recorded. Cerebral vascular resistance (CVR) was calculated as MAP/MCAv. Values are reported as change from baseline to the last minute achieved (LBNP) or 5 min (LBPP). There were no differences in baseline values between groups. During LBNP, there were no differences in the change for MAP (CA: −23 ± 18 vs. HC: −21 ± 17 cm/s; P = 0.80) or MCAv (CA: −13 ± 8 vs. HC: −18 ± 9 cm/s; P = 0.19). The change in CVR was different between groups (CA: −0.08 ± 0.26 vs. HC: 0.18 ± 0.24 mmHg/cm/s; P = 0.04). Total LBNP time was lower for CA (204 ± 92 s) vs. HC (297 ± 64 s; P = 0.04). During LBPP, the change in MAP was not different between groups (CA: 13 ± 6 vs. HC: 10 ± 7 mmHg; P = 0.32). The change in MCAv (CA: 7 ± 6 vs. HC: −4 ± 13 cm/s; P = 0.04) and CVR (CA: −0.06 ± 0.27 vs. HC: 0.38 ± 0.41 mmHg/cm/s; P = 0.03) were different between groups. CA exhibited impaired tolerance to LBNP and had a different cerebral vascular response to LBPP compared to HC.

Background Ultrasound inferior vena cava (IVC) diameter has been shown to decrease in response to hemorrhage. IVC diameter cut points to identify moderate and severe blood loss have not been established. Objectives This study sought to find ultrasound IVC diameter cut points to identify moderate and severe hemorrhage and assess the performance of these cut points vs. vital sign abnormalities. Methods This is a secondary analysis of data from a study that described changes in vital signs and sonographic measurements of the IVC during a lower body negative pressure model of hemorrhage. Using receiver operator curve analyses, optimal cut points for identifying moderate and severe hemorrhage were identified. The ability of these cut points to identify hemorrhage in patients with no vital sign abnormalities was then assessed. Results In both long- and short-axis views, maximum and minimum IVC diameters (IVCmax and IVCmin) were significantly lower than baseline in severe blood loss. The optimal cut point for IVCmax in both axes was found to be ≤ 0.8 cm. This cut point is able to distinguish between no blood loss vs. moderate blood loss, and no blood loss vs. severe blood loss. The optimal cut point for IVCmin was variable between axes and blood loss severity. IVC diameter cut points obtained were able to identify hemorrhage in patients with no vital sign abnormalities. Conclusion An ultrasound IVCmax of ≤ 0.8 cm may be useful in identifying moderate and severe hemorrhage before vital sign abnormalities are evident.

Background On March 17, 2020 an expert ASRM task force recommended the temporary suspension of new, non-urgent fertility treatments during an ongoing world-wide pandemic of Covid-19. We surveyed at the time of resumption of fertility care the psychological experience and coping strategies of patients pausing their care due to Covid-19 and examined which factors were associated and predictive of resilience, anxiety, stress and hopefulness. Methods Cross sectional cohort patient survey using an anonymous, self-reported, single time, web-based, HIPPA compliant platform (REDCap). Survey sampled two Northeast academic fertility practices (Yale Medicine Fertility Center in CT and Montefiore’s Institute for Reproductive Medicine and Health in NY). Data from multiple choice and open response questions collected demographic, reproductive history, experience and attitudes about Covid-19, prior infertility treatment, sense of hopefulness and stress, coping strategies for mitigating stress and two validated psychological surveys to assess anxiety (six-item short-form State Trait Anxiety Inventory (STAl-6)) and resilience (10-item Connor-Davidson Resilience Scale, (CD-RISC-10). Results Seven hundred thirty-four patients were sent invitations to participate. Two hundred fourteen of 734 (29.2%) completed the survey. Patients reported their fertility journey had been delayed a mean of 10 weeks while 60% had been actively trying to conceive > 1.5 years. The top 5 ranked coping skills from a choice of 19 were establishing a daily routine, going outside regularly, exercising, maintaining social connection via phone, social media or Zoom and continuing to work. Having a history of anxiety (p p p p p p = 0.035) to be predictive of more resilience while variables predictive of less resilience were being a full-time homemaker (p = 0.03), having received oral medication as prior infertility treatment (p = 0.003) and having higher scores on the STAI-6 ( Conclusions Prior to and in anticipation of further pauses in treatment the clinical staff should consider pretreatment screening for psychological distress and provide referral sources. In addition, utilization of a patient centered approach to care should be employed.