Electric fan use during heat waves: Turn off for the elderly?

Comment on: Ravanelli NM, Jay O. Electric fan use in heat waves: Turn on or turn off? Temperature. 2016;3:358–360. doi:10.1080/23328940.2016.1211073

Hyperthermia Does Not Alter Baroreflex Control Of Heart Rate During Central Hypovolemia Associated With Simulated Hemorrhage. .

Baroreceptors modulate arterial blood pressure through neural control of cardiac output and peripheral vascular resistance. Hyperthermia reduces tolerance to central hypovolemia, however hyperthermia itself does not alter baroreflex control of heart rate or muscle sympathetic nerve activity. The combined influence of hyperthermia and profound central hypovolemia on baroreflex function remains unknown. This study tested the hypothesis that baroreflex sensitivity (as indexed from ∆ heart rate /∆ blood pressure) would be reduced in hyperthermia compared to normothermia during central hypovolemia. Twelve healthy males (32 ± 5 y) underwent central hypovolemia to pre-syncope, which was induced via progressive lower body negative pressure (LBNP), during normothermia and, on a separate day (randomized, counter balanced) during hyperthermia (+1.2 ± 0.1°C increase in internal temperature). Baroreflex sensitivity was assessed during the final full stage of LBNP completed, and during a 30 second period immediately preceding any bradycardia prior to pre-syncope. LBNP during hyperthermia reduced tolerance by ~58% relative to LBNP during normothermia (normothermia: 72mmHg ±20 vs hyperthermia: 42mmHg± 13; P\u3c0.001). During the final full LBNP stage, baroreflex sensitivity was not different between thermal conditions (hyperthermia: 1.9 ± 1.6 bpm/mmHg, normothermia: 2.4 ± 1.5 bpm/mmHg, p=0.46). Likewise, just prior to pre-syncope baroreflex sensitivity between thermal conditions was not different (hyperthermia: 1.0±1.3 bpm/mmHg, normothermia: 1.5±1.1 bpm/mmHg; p=0.10). These data indicate that during profound central hypovolemia baroreflex control of heart rate is unaffected by hyperthermia. Thus, reductions in the capacity to tolerate central hypovolemia while hyperthermic is not related to altered baroreflex control of heart rate

Alterations in Human Baroreceptor Reflex Regulation of Blood Pressure Following 15 Days of Simulated Microgravity Exposure

Prolonged exposure to microgravity is known to invoke physiological changes which predispose individuals to orthostatic intolerance upon readaptation to the earth's gravitational field. Attenuated baroreflex responsiveness has been implicated in contributing to this inability to withstand orthostatic stress. To test this hypothesis, eight individuals were exposed to 15 days of simulated microgravity exposure using the 6° head-down bed rest model. Prior to, and after the simulated microgravity exposure, the following were assessed: a) aortic baroreflex function; b) carotid baroreflex function; c) cardiopulmonary baroreflex function; and d) the degree of interaction between the cardiopulmonary and carotid baroreflexes

Inhibition of Nitric Oxide Inhibition of Nitric Oxide Synthase Does Not Alter Dynamic Cerebral Autoregulation in Humans

The aim of this study was to determine whether inhibition of nitric oxide synthase (NOS) alters dynamic cerebral autoregulation in humans. Beat-to-beat blood pressure (BP) and cerebral blood flow (CBF) velocity (transcranial Doppler) were measured in eight healthy subjects in the supine position and during 60° head-up tilt (HUT). NOS was inhibited by intravenous N G-monomethyl-L-arginine (L-NMMA) infusion. Dynamic cerebral autoregulation was quantified by transfer function analysis of beat-to-beat changes in BP and CBF velocity. Pressor effects of L-NMMA on cerebral hemodynamics were compared with those of phenylephrine infusion. In the supine position, L-NMMA increased mean BP from 83 ± 3 to 94 ± 3 mmHg (P \u3c 0.01). However, CBF velocity remained unchanged. Consequently, cerebrovascular resistance index (CVRI) increased by 15% (P \u3c 0.05). BP and CBF velocity variability and transfer function gain at the low frequencies of 0.07-0.20 Hz did not change with L-NMMA infusion. Similar changes in mean BP, CBF velocity, and CVRI were observed after phenylephrine infusion, suggesting that increase in CVRI after L-NMMA was mediated myogenically by increase in arterial pressure rather than a direct effect of cerebrovascular NOS inhibition. During baseline tilt without L-NMMA, steady-state BP increased and CBF velocity decreased. BP and CBF velocity variability at low frequencies increased in parallel by 277% and 217%, respectively (P \u3c 0.05). However, transfer function gain remained unchanged. During tilt with L-NMMA, changes in steady-state hemodynamics and BP and CBF velocity variability as well as transfer gain and phase were similar to those without L-NMMA. These data suggest that inhibition of tonic production of NO does not appear to alter dynamic cerebral autoregulation in humans

Nitric Oxide Synthase Inhibition Does Not Affect Regulation of Muscle Sympathetic Nerve Activity During Head-Up Tilt

To test the hypothesis that systemic inhibition of nitric oxide (NO) synthase does not alter the regulation of sympathetic outflow during head-up tilt in humans, in eight healthy subjects NO synthase was blocked by intravenous infusion of NG-monomethyl-L-arginine (L-NMMA). Blood pressure, heart rate, cardiac output, total peripheral resistance (TPR), and muscle sympathetic nerve activity (MSNA) were recorded in the supine position and during 60° head-up tilt. In the supine position, infusion of L-NMMA increased blood pressure, via increased TPR, and inhibited MSNA. However, the increase in MSNA evoked by head-up tilt during L-NMMA infusion (change in burst rate: 24 ± 4 bursts/min; change in total activity: 209 ± 36 U/min) was similar to that during head-up tilt without L-NMMA (change in burst rate: 23 ± 4 bursts/min; change in total activity: 251 ± 52 U/min, n = 6, all P \u3e 0.05). Moreover, changes in TPR and heart rate during head-up tilt were virtually identical between the two conditions. These results suggest that systemic inhibition of NO synthase with L-NMMA does not affect the regulation of sympathetic outflow and vascular resistance during head-up tilt in humans

1972 Ruby Yearbook

A digitized copy of the 1972 Ruby, the Ursinus College yearbook.https://digitalcommons.ursinus.edu/ruby/1075/thumbnail.jp

Sex, But Not Spontaneous Cardiovagal Baroreflex Sensitivity, Predicts Tolerance To Simulated Hemorrhage

Some, but not all studies, suggest that spontaneous cardiovagal baroreflex sensitivity (cBRS; i.e., autonomic control of heart rate) is lower in females. However, it is unknown whether cBRS values are associated with hemorrhagic tolerance, which has repeatedly been demonstrated to be lower in females. PURPOSE: Therefore, the purpose of this study was to test the hypothesis that resting spontaneous cBRS is lower in females and that cBRS is associated with differences in hemorrhagic tolerance between the sexes. METHODS: 25 females (age: 26 ± 6 years) and 27 males (age: 30 ± 5 years) completed a progressive lower-body negative pressure (LBNP – a simulation of hemorrhage) protocol starting at -40 mmHg, which was reduced by 10 mmHg every 3 minutes until presyncope. Presyncope was defined by the subject feeling faint and/or nauseous; a rapid decline in blood pressure (BP) \u3c systolic BP of 80 mmHg; and/or a relative bradycardia accompanied by narrowing of pulse pressure. LBNP tolerance was quantified as cumulative stress index (CSI; mmHg*min). Heart rate (HR) and beat-to-beat BP (finometer) were measured continuously. Spontaneous cBRS was analyzed using the sequence method (i.e., ≥ 3 consecutive cardiac cycles of concordant changes in R-R interval and systolic BP, r2 ≥ 0.8 for such sequences). Data were compared between sexes using a Mann-Whitney U test. A least squares multiple linear regression was used to compare the effect of sex and cBRS on CSI. Data are presented as median ± IQR. RESULTS: Resting BP and HR were not different between the sexes (p \u3e 0.36 for both). Resting cBRS was not different between females and males (21 ± 16 vs. 22 ± 11 ms/mmHg, respectively, p = 0.73). As expected, females had a lower tolerance to LBNP (Females: 385 ± 322, Males: 918 ± 418 mmHg*min, p \u3c 0.0001). Multiple linear regression analysis revealed a significant effect of sex (β = 408, p= 0.04), but not resting cBRS (β = 2.4, p = 0.69) or sex*cBRS (i.e., interaction; β = 1.32, p = 0.87), on CSI. When data from both sexes were combined, there was no correlation between resting cBRS and CSI (r = 0.05, p = 0.71). CONCLUSION: Our cohort did not exhibit sex-related differences in resting cBRS. As expected, females had a lower tolerance to simulated hemorrhage. Importantly, we demonstrated that resting cBRS does not explain the observed sex differences in hemorrhagic tolerance

Exercise and Heat Stress in Well-Healed Burn Survivors:Effects of Cooling Modalities on Thermal and Perceptual Responses

PURPOSE: Burn injuries that require grafting impair thermoregulation, which may dissuade individuals with such injuries from being physically active. We tested the hypothesis that cooling modalities attenuate core temperature elevations and perceptions of heat stress during physical activity in the heat among adults with well-healed burn injuries.METHODS: Adults with no burn injuries (non-burned), 20-40% body surface area burn injuries (moderate burn), and &gt; 40% body surface area burn injuries (large burn) performed 1 hour of moderate intensity exercise (2.5 ± 0.2 mph and 2% grade) on four different occasions in two environmental conditions (30 °C &amp; 39 °C, 40% relative humidity). Within each environmental condition, we applied one of the following cooling modalities, random assigned, for each visit: no cooling (control), fan at 4 m/s (fan), water spray every 5 min (water spray; scaled to burn area size), or a combination of water spray + fan.RESULTS: In 30 °C, perceptual strain index (PeSI) was reduced in the non-burned and moderate burn groups with water spray + fan, whereas PeSI was reduced with all cooling modalities in the large burn group. The cooling modalities did not affect core temperature responses. In the 39 °C environment, water spray and water spray + fan attenuated the elevation in core temperature (p ≤ 0.007) only in the large burn group. In the moderate burn group, PeSI was decreased with water spray + fan (p = 0.017). In the large burn group, both water spray alone and water spray + fan (p ≤ 0.041) lowered PeSI.CONCLUSIONS: For both environments across burn groups, the applied cooling modalities were generally more effective at reducing indices of perceptual strain relative to indices of thermal strain (e.g., core temperature).</p

Baroreflex sensitivity following acute upper-body exercise in the cold among stable coronary artery disease patients

Background: A cold environment and exercise separately affect the autonomic nervous system (ANS), baroreflex sensitivity (BRS), and blood pressure variability (BPV) but their combined effects on post-exercise recovery are not known. Our cross-over trial examined these responses following upper-body static and dynamic exercise performed in a cold and neutral environment in patients with coronary artery disease (CAD). Methods: 20 patients with stable coronary artery disease performed both graded static (10%–30% of maximal voluntary contraction) and dynamic (light, moderate and high perceived intensity) upper-body exercise at −15°C and +22°C for 30 min. Electrocardiogram and continuous blood pressure were measured to compute post-exercise (10 and 30 min after exercise) spectral powers of heart rate (HR), blood pressure variability and BRS at low (0.04–0.15 Hz) and high (0.15–0.4 Hz) frequencies. Results: Static upper-body exercise performed in a cold environment increased post-exercise high frequency (HF) spectral power of heart rate (HF RR) (p Conclusion: Static upper-body exercise in the cold increased post-exercise BRS and overall vagal activity but without reduced systolic blood pressure. Dynamic upper-body exercise in the cold reduced post-exercise vagal BRS but did not affect the other parameters. The influence of cold exposure on post-exercise autonomic and cardiovascular responses following static upper-body exercise require further studies. This information helps understanding why persons with cardiovascular diseases are vulnerable to low environmental temperature. ClinicalTrials.gov: NCT02855905 (04/08/2016)