Interactive effects of exercise intensity and recovery posture on post-exercise hypotension.

Post-exercise reduction in blood pressure, termed post-exercise hypotension (PEH), is relevant for both acute and chronic health reasons and potentially for peripheral cardiovascular adaptations. We investigated the interactive effects of exercise intensity and recovery postures (seated, supine, and standing) on PEH. Thirteen normotensive men underwent a VO2max test on a cycle ergometer and 5 exhaustive constant load trials to determine critical power (CP) and the gas exchange threshold (GET). Subsequently, work-matched exercise trials were performed at two discrete exercise intensities (10% > CP and 10% < GET), with one hour of recovery in each of three postures. For both exercise intensities, standing posture resulted in a more substantial PEH (all P < 0.01). For both standing and seated recovery postures, the higher exercise intensity led to larger reductions in systolic, diastolic and mean arterial pressures (all P < 0.01), whereas in the supine recovery posture, the reduction in diastolic and mean arterial pressures was unaffected by prior exercise intensity (both P > 0.05). PEH is more pronounced during recovery from exercise performed above critical power versus below GET. However, the effect of exercise intensity on PEH is largely abolished when recovery is performed in the supine posture.

Acute moderate normobaric hypoxia does not modify circulating thyroid hormone concentrations induced by one hour of head out cold-water immersion.

This study tested the hypothesis that acute moderate normobaric hypoxia augments circulating thyroid hormone concentrations during and following one hour of cold head out water immersion (HOWI), compared to when cold HOWI is completed during normobaric normoxia. In a randomized crossover single blind design, 12 healthy adults (27 ± 2 y, 2 women) completed one hour of cold (22.0±0.1°C) HOWI breathing either normobaric normoxia (FiO2 = 0.21) or normobaric hypoxia (FiO2 = 0.14). Free and total thyroxine (T3) and triiodothyronine (T4), and thyroid stimulating hormone (TSH) concentrations were measured in venous blood samples obtained before (baseline), during (15-, 30-, and 60-min), and 15 min following HOWI (post-), and were corrected for changes in plasma volume. Arterial oxyhemoglobin saturation and core (rectal) temperature were measured continuously. Arterial oxyhemoglobin saturation was lower during hypoxia (90 ± 3%) compared to normoxia (98 ± 1%, p<0.001). Core temperature fell from baseline (normoxia: 37.2 ± 0.4°C, hypoxia: 37.2 ± 0.4°C) to post- cold HOWI (normoxia: 36.4 ± 0.5°C, hypoxia: 36.3 ± 0.5°C, p<0.001) in both conditions but did not change differently between conditions (condition x time: p=0.552). Circulating TSH, Total T3, Free T4, Total T3, and Free T4 concentrations demonstrated significant main effects of time (all p≤0.024), but these changes did not differ between normoxic and hypoxic conditions (condition x time: all p³0.163). These data indicate that acute moderate normobaric hypoxia does not modify the circulating thyroid hormone response during one hour of cold HOWI.

Relation between resting spleen volume and apnea-induced increases in hemoglobin mass.

Introduction: Indigenous populations renowned for apneic diving have comparatively large spleen volumes. It has been proposed that a larger spleen translates to heightened apnea-induced splenic contraction and elevations in circulating hemoglobin mass (Hbmass), which, in theory, improves O2 carrying and/or CO2/pH buffering capacities. However, the relation between resting spleen volume and apnea- induced increases in Hbmass is unknown. Therefore, we tested the hypothesis that resting spleen volume is positively related to apnea-induced increases in total Hbmass. Methods: Fourteen healthy adults (six women; 29 ± 5 years) completed a two-minute carbon monoxide rebreathe procedure to measure pre-apneas Hbmass and blood volume. Spleen length, width, and thickness were measured pre-and post-five maximal apneas via ultrasound. Spleen volume was calculated via the Pilström equation (test-retest CV:2 ± 2%). Hemoglobin concentration ([Hb]; g/dl) and hematocrit (%) were measured pre- and post-apneas via capillary blood samples. Post-apneas Hbmass was estimated as post-apnea [Hb] x pre-apnea blood volume. Data are presented as mean ± SD. Results: Spleen volume decreased from pre- (247 ± 95 mL) to post- (200 ± 82 mL, p<0.01) apneas. [Hb] (14.6 ± 1.2 vs. 14.9 ± 1.2 g/dL, p<0.01), hematocrit (44 ± 3 vs. 45 ± 3%, p=0.04), and Hbmass (1025 ± 322 vs. 1046 ± 339 g, p=0.03) increased from pre- to post-apneas. Pre-apneas spleen volume was unrelated to post-apneas increases in Hbmass (r=-0.02, p=0.47). O2 (+28 ± 31 mL, p<0.01) and CO2 (+31 ± 35 mL, p<0.01) carrying capacities increased post-apneas. Conclusion: Larger spleen volume is not associated with a greater rise in apneas-induced increases in Hbmass in non-apnea-trained healthy adults.

Cool head-out water immersion does not alter cerebrovascular reactivity to hypercapnia despite elevated middle cerebral artery blood velocity: A pilot study.

Episodic increases in cerebral blood flow (CBF) are thought to contribute to improved cerebrovascular function and health. Head-out water immersion (HOWI) may be a useful modality to increase CBF secondary to the hydrostatic pressure placed on the body. However, it is unclear whether water temperatures common to the general public elicit similar cerebrovascular responses. We tested the hypothesis that mean middle cerebral artery blood velocity (MCAvmean) and cerebrovascular reactivity to CO2 (CVRCO2) would be higher during an acute bout of thermoneutral (TN; 35°C) vs. cool (COOL; 25°C) HOWI. Ten healthy participants (age: 23±3 y; 4 women) completed two randomized HOWI visits. Right MCAvmean, end-tidal CO2 (PETCO2) mean arterial pressure (MAP), and MCA conductance (MCAvmean/MAP) were continuously recorded. CVRCO2 was assessed using a stepped hypercapnia protocol before (PRE), at 30 minutes of HOWI (HOWI), immediately after HOWI (POST-1), and 45 minutes after HOWI (POST-2). Absolute values are reported as mean ± SD. MCAvmean, PETCO2, MAP, and CVRCO2 were not different between conditions at any timepoint (all P≥0.17). In COOL, MCAvmean increased from PRE (61±9 cm/s) during HOWI (68±11 cm/s), at POST-1 (69±11 cm/s), and POST-2 (72±8 cm/s) (all P<0.01), and in TN from PRE to POST-1 (66±13 vs. 71±14 cm/s; P = 0.05). PETCO2 did not change over time in either condition. In COOL, MAP increased from PRE (85±5 mmHg) during HOWI (101±4 mmHg), at POST-1 (97±7 mmHg), and POST-2 (96±9 mmHg), and in TN from PRE (88±5 mmHg) at HOWI (98±7 mmHg) and POST-1 (99±8 mmHg) (all P<0.01). In COOL, CVRCO2 increased from PRE to HOWI (1.66±0.55 vs. 1.92±0.52 cm/s/mmHg; P = 0.04). MCA conductance was not different between or within conditions. These data indicate that 30 minutes of cool HOWI augments MCAvmean and that the increase in MCAvmean persists beyond cool HOWI. However, cool HOWI does not alter CVRCO2 in healthy young adults.

Activation of cardiac parasympathetic and sympathetic activity occurs at different skin temperatures during face cooling.

Sufficiently cold-water temperatures (<7°C) are needed to elicit the sympathetic response to the cold pressor test using the hand. However, it is not known if stimulating the trigeminal nerve via face cooling, which increases both sympathetic and cardiac parasympathetic activity, also has a threshold temperature. We tested the hypothesis that peak autonomic activation during a progressive face cooling challenge would be achieved when the stimulus temperature is ≤7°C. Twelve healthy participants (age: 25 ± 3 yr, four women) completed our study. Six pliable bags, each containing water or an ice slurry (34°C, 28°C, 21°C, 14°C, 7°C, and 0°C) were applied sequentially to participants' forehead, eyes, and cheeks for 5 min each. Mean arterial pressure (photoplethysmography; index of sympathetic activity) and heart rhythm (3-lead ECG) were averaged in 1-min increments at the end of baseline and throughout each temperature condition. Heart rate variability in the time [(root mean square of successive differences (RMSSD)] and frequency [high-frequency (HF) power] domains was used to estimate cardiac parasympathetic activity. Data are presented as the increase from baseline ± SD. Mean arterial pressure only increased from baseline in the 7°C (13.1 ± 10.3 mmHg; P = 0.018) and 0°C (25.2 ± 7.8 mmHg; P < 0.001) conditions. Only the 0°C condition increased RMSSD (160.6 ± 208.9 ms; P = 0.009) and HF power (11,450 ± 14,555 ms2; P = 0.014) from baseline. Our data indicate that peak increases in sympathetic activity during face cooling are initiated at a higher forehead skin temperature than peak increases in cardiac parasympathetic activity.

Diagnostic accuracy of thermal, hydration, and heart rate assessments in discriminating positive acute kidney injury risk following physical work in the heat.

Occupational heat stress increases the risk of acute kidney injury (AKI). This study presents a secondary analysis to generate novel hypotheses for future studies by investigating the diagnostic accuracy of thermal, hydration, and heart rate assessments in discriminating positive AKI risk following physical work in the heat in unacclimatized individuals. Unacclimatized participants (n = 13, 3 women, age: ∼23 years) completed four trials involving 2 h of exercise in a 39.7 ± 0.6 °C, 32 ± 3% relative humidity environment that differed by experimental manipulation of hyperthermia (i.e., cooling intervention) and dehydration (i.e., water drinking). Diagnostic accuracy was assessed via receiver operating characteristic curve analysis. Positive AKI risk was identified when the product of concentrations insulin-like growth factor binding protein 7 and tissue inhibitor of metalloproteinase-2 [IGFBP7∙TIMP-2] exceeded 0.3 (ng∙mL-1)2∙1000-1. Peak absolute core temperature had the acceptable discriminatory ability (AUC = 0.71, p = 0.009), but a relatively large variance (AUC 95% CI: 0.57-0.86). Mean body temperature, urine specific gravity, urine osmolality, peak heart rate, and the peak percent of both maximum heart rate and heart rate reserve had poor discrimination (AUC = 0.66-0.69, p ≤ 0.051). Mean skin temperature, percent change in body mass and plasma volume, and serum sodium and osmolality had no discrimination (p ≥ 0.072). A peak increase in mean skin temperature of >4.7 °C had a positive likelihood ratio of 11.0 which suggests clinical significance. These data suggest that the absolute value of peak core temperature and the increase in mean skin temperature may be valuable to pursue in future studies as a biomarker for AKI risk in unacclimatized workers.

Renal vascular control during normothermia and passive heat stress does not differ between healthy younger men and women.

Men are likely at greater risk for heat-induced acute kidney injury compared with women, possibly due to differences in vascular control. We tested the hypothesis that the renal vasoconstrictor and vasodilator responses will be greater in younger women compared with men during passive heat stress. Twenty-five healthy adults [12 women (early follicular phase) and 13 men] completed two experimental visits, heat stress or normothermic time-control, assigned in a block-randomized crossover design. During heat stress, participants wore a water-perfused suit perfused with 50°C water. Core temperature was increased by ∼0.8°C in the first hour before commencing a 2-min cold pressor test (CPT). Core temperature remained clamped and at 1-h post-CPT, subjects ingested a whey protein shake (1.2 g of protein/kg body wt), and measurements were taken pre-, 75 min, and 150 min post-protein. Beat-to-beat blood pressure (Penaz method) was measured and segmental artery vascular resistance (VR, Doppler ultrasound) was calculated as segmental artery blood velocity ÷ mean arterial pressure. CPT-induced increases in segmental artery VR did not differ between trials (trial effect: P = 0.142) nor between men (heat stress: 1.5 ± 1.0 mmHg/cm/s, normothermia: 1.4 ± 1.0 mmHg/cm/s) and women (heat stress: 1.4 ± 1.2 mmHg/cm/s, normothermia: 2.1 ± 1.1 mmHg/cm/s) (group effect: P = 0.429). Reductions in segmental artery VR following oral protein loading did not differ between trials (trial effect: P = 0.080) nor between men (heat stress: -0.6 ± 0.8 mmHg/cm/s, normothermia: -0.6 ± 0.6 mmHg/cm/s) and women (heat stress: -0.5 ± 0.5 mmHg/cm/s, normothermia: -1.1 ± 0.6 mmHg/cm/s) (group effect: P = 0.204). Renal vasoconstrictor responses to the cold pressor test and vasodilator responses following an oral protein load during heat stress or normothermia do not differ between younger men and younger women in the early follicular phase of the menstrual cycle.NEW & NOTEWORTHY The mechanisms underlying greater heat-induced acute kidney injury risk in men versus women remain unknown. This study examined renal vascular control, including both vasodilatory (oral protein load) and vasoconstrictor (cold presser test) responses, during normothermia and heat stress and compared these responses between men and women. The results indicated that in both conditions neither renal vasodilatory nor vasoconstrictor responses differ between younger men and younger women.

Arterial oxygen desaturation during moderate hypoxia hinders sensorimotor performance.

INTRODUCTION: Moderate hypoxia may impact cognitive and sensorimotor performance prior to self-recognized impairments. Therefore, rapid and objective assessment tools to identify people at risk of impaired function during moderate hypoxia is needed. PURPOSE: Test the hypothesis that reductions in arterial oxygen saturation during moderate normobaric hypoxia (FiO2 = 14%) decreases gamified sensorimotor performance as measured by alterations of motor acuity. METHODS: Following three consecutive days of practice, thirty healthy adults (25 ± 5 y, 10 females) completed three bouts of the tablet-based gamified assessment (Statespace Labs, Inc.) of motor acuity at Baseline and 60 and 90 min after exposure to 13.8 ± 0.2% (hypoxia) and 20.1 ± 0.4% (normoxia) oxygen. The gamified assessment involved moving the tablet to aim and shoot at targets. Both conditions were completed on the same day and were administered in a single-blind, block randomized manner. Performance metrics included shot time and shot variability. Arterial oxyhemoglobin saturation estimated via forehead pulse oximetry (SpO2). Data were analyzed using linear mixed effects models. RESULTS: Compared to normoxia (99±1%), SpO2 was lower (p<0.001) at 60 (89±3%) and 90 (90±2%) min of hypoxia. Shot time was unaffected by decreases in SpO2 (0.012, p = 0.19). Nor was shot time affected by the interaction between SpO2 decrease and baseline performance (0.006, p = 0.46). Shot variability was greater (i.e., less precision, worse performance) with decreases in SpO2 (0.023, p = 0.02) and depended on the interaction between SpO2 decrease and baseline performance (0.029, p< 0.01). CONCLUSION: Decreases in SpO2 during moderate hypoxic exposure hinders sensorimotor performance via decreased motor acuity, i.e., greater variability (less precision) with no change in speed with differing decreases in SpO2. Thus, personnel who are exposed to moderate hypoxia and have greater decreases in SpO2 exhibit lower motor acuity, i.e., less precise movements even though decision time and movement speed are unaffected.

Strategies to mitigate acute kidney injury risk during physical work in hot environments.

Prolonged physical work in the heat can reduce renal function and increase the risk of acute kidney injury (AKI). This is concerning given that the latest climate change projections forecast a rise in global temperature as well as the frequency, intensity, and duration of heatwaves. This means that outdoor and indoor workers in the agriculture or construction industries will be exposed to higher heat stress in the years ahead. Several studies indicate a higher incidence of chronic kidney disease from nontraditional origins (CKDnt) in individuals exposed to high temperatures, intense physical work, and/or recurrent dehydration. It has been proposed that prolonged physical work in the heat accompanied by dehydration results in recurrent episodes of AKI that ultimately lead to permanent kidney damage and the development of CKDnt. Thus, there is a need to identify and test strategies that can alleviate AKI risk during physical work in the heat. The purpose of this review is to present strategies that might prevent and mitigate the risk of AKI induced by physical work in the heat.

Grass-Fed and Non-Grass-Fed Whey Protein Consumption Do Not Attenuate Exercise-Induced Muscle Damage and Soreness in Resistance-Trained Individuals: A Randomized, Placebo-Controlled Trial.

Eccentric muscle contractions can cause structural damage to muscle cells resulting in temporarily decreased muscle force production and soreness. Prior work indicates pasture-raised dairy products from grass-fed cows have greater anti-inflammatory and antioxidant properties compared to grain-fed counterparts. However, limited research has evaluated the utility of whey protein from pasture-raised, grass-fed cows to enhance recovery compared to whey protein from non-grass-fed cows. Therefore, using a randomized, placebo-controlled design, we compared the effect of whey protein from pasture-raised, grass-fed cows (PRWP) to conventional whey protein (CWP) supplementation on indirect markers of muscle damage in response to eccentric exercise-induced muscle damage (EIMD) in resistance-trained individuals. Thirty-nine subjects (PRWP, n = 14; CWP, n = 12) completed an eccentric squat protocol to induce EIMD with measurements performed at 24, 48, and 72 h of recovery. Dependent variables included: delayed onset muscle soreness (DOMS), urinary titin, maximal isometric voluntary contraction (MIVC), potentiated quadriceps twitch force, countermovement jump (CMJ), and barbell back squat velocity (BBSV). Between-condition comparisons did not reveal any significant differences (p ≤ 0.05) in markers of EIMD via DOMS, urinary titin, MIVC, potentiated quadriceps twitch force, CMJ, or BBSV. In conclusion, neither PRWP nor CWP attenuate indirect markers of muscle damage and soreness following eccentric exercise in resistance-trained individuals.

Aerobic exercise performance is reduced following prolonged cold-water immersion.

Background: We tested the hypotheses that self-paced aerobic exercise performance is reduced following four hours of cold-water immersion when breathing air and further reduced when breathing 100% oxygen (O2). Nine healthy adults (four women; age 24 ± 3 years; body fat 17.9 ± 6.4%; VO2max 48±9 mL • kg • minute⁻¹) completed three visits: a no-immersion control trial and two experimental trials consisting of a four-hour cold-water immersion (20.1±0.3°C) either breathing air (FIO2 = 0.21) or O2 (FIO2 = 1.0). During the no-immersion control trial and following immersion in the experimental trials, subjects first completed a 60-minute ruck-march carrying 20% of body mass in a rucksack, immediately followed by an unweighted, self-paced 5-km time trial on a motorized treadmill. Core temperature, heart rate, and rating of perceived exertion were recorded every 1,000 meters during the 5-km time trial. Data are presented mean± SD. Time trial performance was reduced following immersion in both the 100% O2 trial (32±6 minutes; p=0.01) and air trial (32±5 minutes; p=0.01) compared to the control trial (28± 4 minutes). However, there was no difference between the 100% O2 and air trials (p=0.86). Heart rate, core temperature, and rating of perceived exertion increased during the time trial (time effect: p≺0.01), but were not different between trials (trial effect: p≥0.33). These findings suggest that prolonged cold-water immersion attenuates self-paced aerobic exercise performance, but does not appear to be further affected by breathing gas type.

Gamified assessment of cognitive performance during moderate hypoxia.

INTRODUCTION: There is a need for rapid and objective assessment tools to identify people at risk of impaired cognitive function during hypoxia. PURPOSE: To test the hypotheses that performance on gamified cognitive tests examining the cognitive domains of executive function (Gridshot), working memory (Capacity) and spatial tracking (Multitracker) will be reduced during normobaric exposure to moderate normobaric hypoxia. METHODS: Following three consecutive days of practice, twenty-one healthy adults (27 ± 5 y, 9 females) completed five 1-min rounds of the tablet-based games Gridshot, Capacity, and Multitracker (Statespace Labs, Inc.) at Baseline and 60 and 90 min after exposure to 14.0 ± 0.2% (hypoxia) and 20.6 ± 0.3% (normoxia) oxygen. Both conditions were completed on the same day and were administered in a single-blind, block randomized manner. Arterial oxyhemoglobin saturation was estimated via forehead pulse oximetry (SpO2). Data were analyzed using ANCOVA with a covariate of Baseline. RESULTS: Compared to normoxia (98 ± 1%), SpO2 was lower (p < 0.001) at 60 (91 ± 3%) and 90 (91 ± 2%) min of hypoxia. No condition x time interaction effects were identified for any gamified cognitive tests (p ≥ 0.32). A main effect of condition was identified for Capacity (p = 0.05) and Multitracker (p = 0.04), but not Gridshot (p = 0.33). Post hoc analyses of the composite scores for both Capacity (p = 0.11) and Multitracker (p = 0.73) demonstrated no difference between conditions. CONCLUSION: Performance on gamified cognitive tests was not consistently affected by acute normobaric moderate hypoxic exposure.

Water consumption patterns impact hydration markers in males working in accordance with the National Institute for Occupational Safety and Health recommendations.

The impact of water consumption bolus volume and frequency on hydration biomarkers during work in the heat is unknown. In a randomized, crossover fashion, eight males consumed either 500 mL of water every 40 min or 237 mL of water every 20 min during 2 hr of continuous walking at 6.4 kph, 1.0% grade in a 34 °C/30% relative humidity environment, followed by 2 hr of rest. Hydration biomarkers and variables were assessed pre-work, post-work, and after the 2 hr recovery. There were no differences in body mass between trials at any time point (all p > 0.05). Percent change in plasma volume during work was not different when 237 mL of water was repeatedly consumed (-1.6 ± 8.2%) compared to 500 mL of water (-1.3 ± 3.0%, p = 0.92). Plasma osmolality was maintained over time (p = 0.55) with no difference between treatments (p = 0.21). When consuming 500 mL of water repeatedly, urine osmolality was lower at recovery (205 ± 108 mOsmo/L) compared to pre-work (589 ± 95 mOsmo/L, p < 0.01), different from repeatedly consuming 237 mL of water which maintained urine osmolality from pre-work (548 ± 144 mOsmo/L) through recovery (364 ± 261 mOsmo/L, p = 0.14). Free water clearance at recovery was greater with repeated consumption of 500 mL of water (1.2 ± 1.0 mL/min) compared to 237 mL of water (0.4 ± 0.8 mL/min, p = 0.02). Urine volume was not different between treatments post-work (p = 0.62), but greater after 2 hr of recovery when repeatedly consuming 500 mL of water compared to 237 mL (p = 0.01), leading to greater hydration efficiency upon recovery with repeated consumption of 237 mL of water (68 ± 12%) compared to 500 mL (63 ± 14%, p = 0.01). Thirst and total gastrointestinal symptom scores were not different between treatments at any time point (all p > 0.05). Body temperatures and heart rate were not different between treatments at any time point (all p > 0.05). Drinking larger, less frequent water boluses or drinking smaller, more frequent water boluses are both reasonable strategies to promote adequate hydration and limit changes in body mass in males completing heavy-intensity work in the heat.

Fluid balance during physical work in the heat is not modified by the menstrual cycle when fluids are freely available.

We tested the hypothesis that women may be more at risk of becoming dehydrated during physical work in the heat in the early follicular phase (EF), compared with the late follicular (LF) and mid-luteal (ML) phases of the menstrual cycle when allowed free access to drink. Twelve healthy, eumenorrheic, unacclimated women (26 ± 5 yr) completed three trials (EF, LF, and ML phases) involving 4 h of exposure to 33.8 ± 0.8 °C, 54 ± 1% relative humidity. Each hour, participants walked on a treadmill for 30 min at a rate of metabolic heat production of 338 ± 9 W. Participants drank a cool, flavor-preferred non-caloric sport drink ad libitum. Nude body weight was measured pre- and post-exposure, and percent changes in body weight loss were interpreted as an index of changes in total body water. Total fluid intake and urine output were measured and sweat rate was estimated from changes in body mass corrected for fluid intake and urine output. Fluid intake was not different between phases (EF: 1,609 ± 919 mL; LF: 1,902 ± 799 mL; ML: 1,913 ± 671; P = 0.202). Total urine output (P = 0.543) nor sweat rate (P = 0.907) differed between phases. Percent changes in body mass were not different between phases (EF: -0.5 ± 0.9%; LF: -0.3 ± 0.9%; ML: -0.3 ± 0.7%; P = 0.417). This study demonstrates that the normal hormonal fluctuations that occur throughout the menstrual cycle do not alter fluid balance during physical work in the heat.NEW & NOTEWORTHY The effect of the menstrual cycle on fluid balance during physical work in the heat when fluids are freely available is unknown. This study demonstrates that fluid balance is not modified in women across three distinct phases of the menstrual cycle during physical work in the heat These results indicate that when women have free access to cool fluid during physical work in the heat, they respond similarly across all three phases to maintain fluid homeostasis across the menstrual cycle.

Elevations in sweat sodium concentration following ischemia-reperfusion injury during passive heat stress.

Renal ischemia-reperfusion (I/R) injury results in damage to the renal tubules and causes impairments in sodium [Na+] reabsorption. Given the inability to conduct mechanistic renal I/R injury studies in vivo in humans, eccrine sweat glands have been proposed as a surrogate model given the anatomical and physiological similarities. We tested the hypothesis that sweat Na+ concentration is elevated following I/R injury during passive heat stress. We also tested the hypothesis that I/R injury during heat stress will impair cutaneous microvascular function. Fifteen young healthy adults completed ∼160 min of passive heat stress using a water-perfused suit (50°C). At 60 min of whole body heating, one upper arm was occluded for 20 min followed by a 20-min reperfusion. Sweat was collected from each forearm via an absorbent patch pre- and post-I/R. Following the 20-min reperfusion, cutaneous microvascular function was measured via local heating protocol. Cutaneous vascular conductance (CVC) was calculated as red blood cell flux/mean arterial pressure and normalized to CVC during local heating to 44°C. Na+ concentration was log-transformed and data were reported as a mean change from pre-I/R (95% confidence interval). Changes in sweat sodium concentration from pre-I/R differed between arms post-I/R (experimental arm: +0.97 [+0.67 - 1.27] [LOG] Na+; control arm: +0.68 [+0.38 - 0.99] [LOG] Na+; P < 0.01). However, CVC during the local heating was not different between the experimental (80 ± 10%max) and control arms (78 ± 10%max; P = 0.59). In support of our hypothesis, Na+ concentration was elevated following I/R injury, but likely not accompanied by alterations in cutaneous microvascular function.NEW & NOTEWORTHY In the present study, we have demonstrated that sweat sodium concentration is elevated following ischemia-reperfusion injury during passive heat stress. This does not appear to be mediated by reductions in cutaneous microvascular function or active sweat glands, but may be related to alterations in local sweating responses during heat stress. This study demonstrates a potential use of eccrine sweat glands to understand sodium handling following ischemia-reperfusion injury, particularly given the challenges of in vivo studies of renal ischemia-reperfusion injury in humans.

Acute beetroot juice consumption does not alter cerebral autoregulation or cardiovagal baroreflex sensitivity during lower-body negative pressure in healthy adults.

Introduction: Beetroot juice (BRJ) improves peripheral endothelial function and vascular compliance, likely due to increased nitric oxide bioavailability. It is unknown if BRJ alters cerebrovascular function and cardiovagal baroreflex control in healthy individuals. Purpose: We tested the hypotheses that BRJ consumption improves cerebral autoregulation (CA) and cardiovagal baroreflex sensitivity (cBRS) during lower-body negative pressure (LBNP). Methods: Thirteen healthy adults (age: 26 ± 4 years; 5 women) performed oscillatory (O-LBNP) and static LBNP (S-LBNP) before (PRE) and 3 h after consuming 500 mL of BRJ (POST). Participants inhaled 3% CO2 (21% O2, 76% N2) during a 5 min baseline and throughout LBNP to attenuate reductions in end-tidal CO2 tension (PETCO2). O-LBNP was conducted at ∼0.02 Hz for six cycles (-70 mmHg), followed by a 3-min recovery before S-LBNP (-40 mmHg) for 7 min. Beat-to-beat middle cerebral artery blood velocity (MCAv) (transcranial Doppler) and blood pressure were continuously recorded. CA was assessed using transfer function analysis to calculate coherence, gain, and phase in the very-low-frequency (VLF; 0.020-0.070 Hz) and low-frequency bands (LF; 0.07-0.20 Hz). cBRS was calculated using the sequence method. Comparisons between POST vs. PRE are reported as mean ± SD. Results: During O-LBNP, coherence VLF was greater at POST (0.55 ± 0.06 vs. 0.46 ± 0.08; P < 0.01), but phase VLF (P = 0.17) and gain VLF (P = 0.69) were not different. Coherence LF and phase LF were not different, but gain LF was lower at POST (1.03 ± 0.20 vs. 1.12 ± 0.30 cm/s/mmHg; P = 0.05). During S-LBNP, CA was not different in the VLF or LF bands (all P > 0.10). Up-cBRS and Down-cBRS were not different during both LBNP protocols. Conclusion: These preliminary data indicate that CA and cBRS during LBNP in healthy, young adults is largely unaffected by an acute bolus of BRJ.

Physical symptoms provoked by normobaric hot and humid disabled pressurized rescue module scenarios.

We tested the hypothesis that thermal discomfort will be greater, mood will be worse, and physical symptoms of heat illness will be exacerbated with elevations in dry bulb temperature during exposure to >95% relative humidity disabled pressurized rescue module simulation. On three occasions, 15 healthy males (23 ± 3 years) 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 eight hours. Thermal discomfort (visual analog scale), mood (profile of mood states), and physical symptoms of heat illness, ear-nose-throat, and muscle discomfort (environmental symptoms questionnaire) were assessed before and following each hour of exposure. Thermal discomfort was greater throughout the exposure in 35°C versus both 32°C and 33°C (p ≥ 0.03) and did not differ between the latter conditions (p ≥ 0.07). Mood worsened over time in all trials (p ≺ 0.01) and was worse in 35°C compared to 32°C and 33°C after five hours of exposure (p ≤ 0.05). Heat illness symptoms increased over time in all trials and was greater in 35°C versus 32°C and 33°C throughout the exposure (p ≤ 0.04). Ear-nose-throat and muscle discomfort symptoms increased over time in all trials (p < 0.01) and were higher in 35°C versus 32°C and 33°C after the sixth hour of exposure (p ≤ 0.02). In support of our hypothesis, mood was worse, physical symptoms of heat illness, and ear-nose-throat and muscle discomfort symptoms were exacerbated, and thermal discomfort was greater with elevations in dry bulb temperature during an eight-hour exposure to a >95% relative humidity disabled PRM simulation.