Local Sweat Research Articles

INHIBITING PSEUDOMONAS AERUGINOSA GROWTH ASSOCIATED WITH PROSTHETIC LINERS

INTRODUCTION
 The conventional use of a prosthetic device by amputees involves contact of the residual limb tissue with the prosthetic socket using an intermediate elastomer liner. Roll-on gel liners are applied directly to the limb, and slide into the rigid hard socket; the gels are generally silicone or plastic. Regardless of the material, or the liner system used on a residual limb, problems occur because of direct skin and socket or liner contact.1 The skin tissue of the residual limb is subject to compressive, shear, and tensile forces through weight bearing against the interface wall. In addition the skin is subject to heat/sweat issues that may be seasonal and related to the insulation properties of the interface material. A common problem encountered by the prosthetic user is socket odor, or odor emanating from socket liners.2 Proper hygiene does not guarantee the reduction of strong socket or liner odor over time. In addition, skin problems among amputees include rashes, blistering, mold/fungal infections and other skin irritations. The socket/wall interface (regardless of material composition) is subject to local skin sloughing, sweat, and skin oils in a warm/moist dark environment over hours of use providing an ideal environment for fungal and bacterial growth.3 To address this problem, our team evaluated a titanium and silicone hybrid cleaning and coating technology containing a silver fatty acid complex against the odor producing, Gram-negative, facultative anaerobe, Pseudomonas aeruginosa.4
 Abstract PDF Link: https://jps.library.utoronto.ca/index.php/cpoj/article/view/32016/24435
 How to cite: Jarrell J.D, Garcia D.R, Born C.T. INHIBITING PSEUDOMONAS AERUGINOSA GROWTH ASSOCIATED WITH PROSTHETIC LINERS. CANADIAN PROSTHETICS & ORTHOTICS JOURNAL, VOLUME 1, ISSUE 2, 2018; ABSTRACT, POSTER PRESENTATION AT THE AOPA’S 101ST NATIONAL ASSEMBLY, SEPT. 26-29, VANCOUVER, CANADA, 2018. DOI: https://doi.org/10.33137/cpoj.v1i2.32016 
 Abstracts were Peer-reviewed by the American Orthotic Prosthetic Association (AOPA) 101st National Assembly Scientific Committee. 
 http://www.aopanet.org/

On exercise thermoregulation in females: interaction of endogenous and exogenous ovarian hormones.

One in two female athletes chronically take a combined, monophasic oral contraceptive pill (OCP). Previous thermoregulatory investigations proposed that an endogenous rhythm of the menstrual cycle still occurs with OCP usage. Forthcoming large international sporting events will expose female athletes to hot environments differing in their thermal profile, yet few data exist on how trained women will respond from both a thermoregulatory and performance stand-point. In the present study, we have demonstrated that a small endogenous rhythm of the menstrual cycle still affects Tcore and also that chronic OCP use attenuates the sweating response, whereas behavioural thermoregulation is maintained. Furthermore, humid heat affects both performance and thermoregulatory responses to a greater extent than OCP usage and the menstrual cycle does. We studied thermoregulatory responses of ten well-trained ( , 57± 7mLmin-1 kg-1 ) women taking a combined, monophasic oral contraceptive pill (OCP) (≥12months) during exercise in dry and humid heat, across their active OCP cycle. They completed four trials, each of resting and cycling at fixed intensities (125 and 150W), aiming to assess autonomic regulation, and then a self-paced intensity (30-min work trial) to assess behavioural regulation. Trials were conducted in quasi-follicular (qF) and quasi-luteal (qL) phases in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT) (27°C). During rest and exercise at 125W, rectal temperature was 0.15°C higher in qL than qF (P= 0.05) independent of environment (P= 0.17). The onset threshold and thermosensitivity of local sweat rate and forearm blood flow relative to mean body temperature was unaffected by the OCP cycle (both P> 0.30). Exercise performance did not differ between quasi-phases (qF: 268± 31kJ, qL: 263± 26kJ, P= 0.31) but was 5± 7% higher during DRY than during HUM (273± 29kJ, 258± 28kJ; P= 0.03). Compared to matched eumenorrhoeic athletes, chronic OCP use impaired the sweating onset threshold and thermosensitivity (both P< 0.01). In well-trained, OCP-using women exercising in the heat: (i) a performance-thermoregulatory trade-off occurred that required behavioural adjustment; (ii) humidity impaired performance as a result of reduced evaporative power despite matched WBGT; and (iii) the sudomotor but not behavioural thermoregulatory responses were impaired compared to matched eumenorrhoeic athletes.

Temperature of water ingested before exercise alters the onset of physiological heat loss responses.

This study sought to determine whether the temperature of water ingested before exercise alters the onset threshold and subsequent thermosensitivity of local vasomotor and sudomotor responses after exercise begins. Twenty men [24 (SD 4) yr of age, 75.8 (SD 8.1) kg body mass, 52.3 (SD 7.7) ml·min-1·kg-1 peak O2 consumption (V̇o2peak)] ingested 1.5°C, 37°C, or 50°C water (3.2 ml/kg), rested for 5 min, and then cycled at 50% V̇o2peak for 15 min at 23.0 (SD 0.9) °C and 32 (SD 10) % relative humidity. Mean body temperature (Tb), local sweat rate (LSR), and skin blood flow (SBF) were measured. In a subset of eight men [25 (SD 5) yr of age, 78.6 (SD 8.3) kg body mass, 48.9 (SD 11.1) ml·min-1·kg-1 V̇o2peak], blood pressure was measured and cutaneous vascular conductance (CVC) was determined. The change in Tb was greater at the onset of LSR measurement with ingestion of 1.5°C than 50°C water [ΔTb = 0.19 (SD 0.15) vs. 0.11 (SD 0.12) °C, P = 0.04], but not 37°C water [ΔTb = 0.14 (SD 0.14) °C, P = 0.23], but did not differ between trials for SBF measurement [ΔTb = 0.18 (SD 0.15) °C, 0.11 (SD 0.13) °C, and 0.09 (SD 0.09) °C with 1.5°C, 37°C, and 50°C water, respectively, P = 0.07]. Conversely, the thermosensitivity of LSR and SBF was not different [LSR = 1.11 (SD 0.75), 1.11 (SD 0.75), and 1.34 (SD 1.11) mg·min-1·cm-2·°C-1 with 1.5°C, 37°C, and 50°C ingested water, respectively ( P = 0.46); SBF = 717 (SD 882), 517 (SD 606), and 857 (SD 904) %baseline arbitrary units (AU)/°C with 1.5°C, 37°C, and 50°C ingested water, respectively ( P = 0.95)]. After 15 min of exercise, LSR and SBF were greater with ingestion of 50°C than 1.5°C water [LSR = 0.40 (SD 0.17) vs. 0.31 (SD 0.19) mg·min-1·cm-2 ( P = 0.02); SBF = 407 (SD 149) vs. 279 (SD 117) %baseline AU ( P < 0.001)], but not 37°C water [LSR = 0.50 (SD 0.22) mg·min-1·cm-2; SBF = 324 (SD 169) %baseline AU]. CVC was statistically unaffected [275 (SD 81), 340 (SD 114), and 384 (SD 160) %baseline CVC with 1.5°C, 37°C, and 50°C ingested water, respectively, P = 0.30]. Collectively, these results support the concept that visceral thermoreceptors modify the central drive for thermoeffector responses.

Sweating distribution and active sweat glands on the scalp of young males in hot-dry and hot-humid environments

We investigated the effects of humidity on regional sweating secretion and active sweat gland density on the scalp during passive heating in hot environments. Eight male subjects shaved their heads prior to expose to dry (30%RH; H30%) and humid (85%RH; H85%) conditions at an air temperature of 32°C. Total sweat rate, local sweat rates (frontal, vertex, temporal, and occipital regions), active sweat glands on the scalp (2 frontal, 2 parietal, 2 temporal, 1 occipital, and 1 vertex), and rectal and skin temperatures were measured during leg immersion in 42°C water for 60min. (1) Total sweat rates were greater for H30% (179.4 ± 35.6gh-1) than for H85% (148.1 ± 27.2gh-1) (P < 0.05). (2) Scalp sweat secretion tended to be greater in the H85% than the H30%. (3) Head sweat rates were greater on the frontal than on the vertex for both humidity conditions (P < 0.05). (4) Active sweat gland density on the scalp was greater for H85% (82 ± 13glandscm-2) than for H30% (62 ± 17glandscm-2) (P < 0.05). (5) No significant difference was found in rectal temperature between H30% and H85%, whereas mean skin temperature was significantly lower for H30% (34.8 ± 0.7°C) than for the H85% condition (36.0 ± 0.3°C) (P < 0.05). These results indicate that the thermoregulatory sweating responses for the scalp region were significantly increased in the hot-humid condition compared to the hot-dry condition. Among the regions on the scalp surface, the vertex was the least sensitive to the change in humidity.

Spatial and temporal migration of sweat: from skin to clothing

PurposeMoisture accumulation in clothing affects human performance and productivity through its impact on thermal balance and various aspects of discomfort. Building on our laboratory’s work on mapping sweat production across the body, this study aimed to obtain detailed spatial and temporal maps showing how this sweat migrates into a single clothing layer (T-shirt) during physical exercise.MethodEight male participants performed running exercise in a warm environment. Garment sweat absorption was mapped over a total running time of 50 min, in 10 separated running trials of different durations (5 min increments). After running, the garment was dissected into 22 different parts and local sweat absorption (ABSlocal) was quantified by weighing each garment part before and after drying. From ABSlocal, garment total sweat absorption (ABStotal) was estimated.ResultsAfter 50 min, Tcore rose from 37 ± 0.2 to 38.6 ± 0.3 °C, HR increased from 69 ± 15 to 163 ± 12 bpm (p < 0.001), GSL was 586 ± 86 g m−2. Clear patterns of sweat absorption reduction from superior-to-inferior and from medial-to-lateral T-shirt zones were observed, with the mid back medial and the low front hem showing the highest, respectively.ConclusionsQuantitative data on garment total and regional sweat absorption were obtained and considerable variation between different garment zones was identified. These data can support the development of sport and personal protective clothing with the end goal to prevent workers’ heat-related injuries as well as maximise human performance and productivity.

Contact skin temperature measurements and associated effects of obstructing local sweat evaporation during mild exercise-induced heat stress

Objective: Locally increasing evaporative resistance is one mechanism by which contact skin temperature (Tsk) sensors and their attachments may disturb the temperature of the skin site being measured. We aimed to determine the extent to which an obstruction of evaporation affects local Tsk during exercise-induced sweating and how this compares to the Tsk measured using a conventional contact Tsk sensor. Approach: Twelve adult males each completed one experimental session (~24 °C, ~46% relative humidity) involving seated rest and exercise (cycle ergometer). Air velocity was ~0.5 m · s−1 during rest and ~1 m · s−1 during exercise. Tsk of the right posterolateral forearm was measured using fine-wire thermocouples (0.125 mm diameter; chosen for minimal sensor-related disturbance) under two concurrent experimental conditions: uncovered or directly covered by a moisture-impermeable matte-black aluminium foil (thickness 0.08 mm, area 15 mm × 22 mm). The adjacent Tsk was also measured using an iButton attached with a nonwoven medical tape. Changes in next-to-skin absolute vapour pressure were used to estimate the onset of sweating. Main results: During exercise, covered thermocouple temperatures were consistently warmer than those uncovered. These differences were small before the onset of sweating (0.1 °C, p = 0.16), but increased thereafter (0.6 and 1.0 °C by minutes 15 and 30 of exercise, respectively; p ⩽ 0.03). For change scores from baseline rest, the iButton-measured Tsk was as much as 0.7 °C warmer than uncovered and −0.4 °C cooler than covered thermocouples during sweating, but differences were not statistically supported and with wide 95% limits of agreement (up to ±3.1 °C). Significance: When delineated, a small obstruction of evaporation itself caused an overestimation of Tsk during exercise although, while demonstrable, these effects were less clear in the context of using a conventional contact Tsk sensor and attachment.

Postsynaptic cutaneous vasodilation and sweating: influence of adiposity and hydration status.

Obesity and hypohydration independently affect postsynaptic endothelial function, but it is unknown if hypohydration affects lean and obese individuals differently. To examine the effect of hypohydration on postsynaptic cutaneous vasodilation and sweating in men with high and low adiposity (HI- and LO-BF, respectively). Ten males with LO-BF and ten with HI-BF were instrumented for forearm microdialysis when euhydrated and hypohydrated. Changes in cutaneous vascular conductance (CVC) with intradermal infusion of sodium nitroprusside (SNP) and methacholine chloride (MCh) were assessed. Local sweat rate (LSR) was simultaneously assessed at the MCh site. At the end of the last dose, maximal CVC was elicited by delivering a maximal dose of SNP for 30min to both sites with simultaneous local heating at the SNP site. The concentration of drug needed to elicit 50% of the maximal response (EC50) was compared between groups and hydration conditions. When euhydrated, EC50 of MCh-induced CVC was not different between LO- vs. HI-BF [- 3.04 ± 0.12 vs. - 2.98 ± 0.19 log (MCh) M, P = 0.841]. EC50 of SNP-induced CVC was higher in euhydrated HI- vs. LO-BF (- 1.74 ± 0.17 vs. - 2.13 ± 0.06 log (SNP) M, P = 0.034). Within each group, hydration status did not change MCh- or SNP-induced CVC (P > 0.05). LSR was not different between groups or hydration condition (P > 0.05). These data suggest reduced sensitivity of endothelium-independent vasodilation in individuals with high adiposity when euhydrated. However, hypohydration does not affect cutaneous vasodilation or local sweat rate differently between individuals with low or high adiposity.

Heart Failure Modulates Thermoregulatory Control Independently Of Differences In Physical Characteristics And Metabolic Heat Production

PURPOSE: Heart failure (HF) patients appear to exhibit altered thermoregulatory responses during exercise in the heat. However, the extent to which these responses are altered due to physiological impairments independently of biophysical factors associated with differences in metabolic heat production (Hprod), evaporative heat balance requirements (Ereq) and/or body size, is presently unclear. Therefore, we examined thermoregulatory responses in 10 HF and 10 age-matched controls (CON) similar in body size during exercise at a fixed rate of Hprod, and thus Ereq, in a 30°C environment. METHODS: Rectal temperature (Trec), local sweat rate (LSR), and cutaneous vascular conductance (CVC) were measured during 60-min of cycle ergometry. Whole-body sweat rate (WBSR) was estimated from pre-post nude body weight corrected for fluid intake. Hprod and Ereq, as well as dry heat loss (Hdry) and evaporative heat loss from the skin (Esk) ─ assuming all secreted sweat evaporated, were calculated using partitional calorimetry. RESULTS: Despite exercising at the same rate of Hprod (HF: 338±43; CON: 323±31W, p=0.25), Trec was greater (p<0.01) in HF (0.81±0.16°C) than CON (0.49±0.27°C). In keeping with a similar Ereq (HF: 285±40; CON: 274±28W, p=0.35), no differences in WBSR (HF: 0.45±0.11; CON: 0.41±0.07L/h, p=0.38) or LSR (HF: 0.96±0.17; CON: 0.79±0.15mg/cm2/min, p=0.50) were observed between groups. Similarly, Hdry was comparable between groups (HF: 22.9±3.2; CON: 20.4±5.0W, p=0.14). Consequently, the cumulative body heat storage was similar between groups (HF: 154±106; CON: 196±174kJ, p=0.44). Furthermore, CVC was lower in HF than CON (HF: 0.83±0.42; CON: 2.10±0.79au/mmHg, p<0.01). CONCLUSIONS: Collectively, these findings demonstrate that HF patients exhibit an impaired skin blood flow response, but no differences in sweating. Given that HF had similar body heat storage to CON at the same Hprod, their greater rise in core temperature can be attributed to a less uniform internal distribution of heat between the body core and periphery.

A Preliminary Investigation Into The Effect Of Nauseogenic Vection And Whole‐Body Heating On Motion Sickness Severity: A Combined And Individual Stressors Approach

INTRODUCTIONThe use of virtual reality for training, medical and recreational applications is limited by the side effects of prolonged exposure to vection. Secondary factors such as environmental temperature may be crucial in modulating the onset and severity of these side effects. To understand the role of environmental temperature in modulating nausea in virtual reality, this preliminary investigation explored the differential impacts of ambient temperature and vection on motion sickness severity using an individual and combined stressors approach.METHODSThirteen healthy individuals (eight female, five male, 24.8 ± 3.1 yrs) watched a 22 min pre‐recorded driving simulator video in four different conditions, which included: 1) Computer screen in a neutral temperature of 22°C, 50% rH; 2) Virtual reality in a neutral temperature of 22°C, 50% rH; 3) Computer screen in a hot temperature of 35°C, 50% rH; 4) Virtual reality in a hot temperature of 35°C, 50% rH. Subjective measures for visually induced motion sickness were explored using the fast motion sickness scale (FMS; 0–20 visual analogue scale) and the simulator sickness questionnaire (SSQ) both during and following exposure to each condition. To explore the effect of vection and whole‐body heating on physiological indices of motion sickness, local sweat rate (via ventilated sweat capsules), rectal temperature, skin blood flow (via laser Doppler flowmetry), skin temperature, blood pressure and heart rate were examined.RESULTSThe results from FMS ratings indicate that, when taken independently, vection significantly increased sickness severity (computer screen, 0.6 ± 0.8 vs. virtual reality, 4.3 ± 3.1; p&lt;0.001), with an onset time of ~3.5 mins across VR trials. A significant independent influence of ambient temperature was also observed on FMS ratings (neutral conditions, 2.1 ± 2.3 vs. hot conditions, 2.8 ± 3.4; p=0.04). However, no interaction between vection and ambient temperature was observed (p=0.2), indicating an additive response between factors. The SSQ ratings immediately following each trial paralleled FMS observations, demonstrating significant independent main effects for vection (p&lt;0.001) and ambient temperature (p=0.009) on reported motion sickness severity, yet without interaction (p=0.07). No main effects were seen in SSQ rating 2 hrs post trials. Local sweat rate, skin temperature, and heart rate each increased (p&lt;0.03) with whole‐body heating (17.4 ± 10.5 ml.m−2.hr−1; 2.7 ± 6.5 °C; 4.1 ± 9.0 bpm), but were not affected by vection (p&gt;0.6); furthermore, with no interactions observed (p&gt;0.4). No main effects were observed for blood flow, mean arterial pressure or rectal temperature (p&gt;0.1).CONCLUSIONThis preliminary study shows no interaction between ambient temperature and a mild‐moderate vection stimulus on motion sickness severity. Investigations into true motion, responders and non‐responders, as well as stimulus strength, may better highlight any interactions that may exist in this area.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Circadian Rhythm Does Not Alter the Sweating Response to Exercise in Thermoneutral and Warm Ambient Temperatures

The present study sought to determine whether the diurnal fluctuation in core temperature alters the sweating response to exercise in thermoneutral (23°C) and warm (33°C) environments. Six healthy males exercised on a semi‐recumbent ergometer at a fixed evaporative requirement for heat balance (200W/m2) for 60 min at two different times of day and two ambient temperatures matched for absolute humidity (1.3 kPa); i) 0800h/23°C, ii) 0800h/33°C, iii) 1600h/23°C, and iv) 1600h/33°C. Esophageal temperature (Tes), mean body temperature (Tb), local sweat rate (LSR) measured at the arm and upper back, and whole body sweat loss (WBSL) were measured. Resting absolute Tes was higher at 1600h compared to 0800h at 23°C (0800h: 36.7±0.2°C, 1600h: 36.9±0.2°C; P=0.04) and 33°C (0800h: 36.6±0.2°C, 1600h 36.9±0.2°C; P=0.005). Similarly, end‐exercise (steady‐state) absolute Tes was higher at 1600h relative to 0800h at 23°C (0800h: 37.4±0.2°C, 1600h: 37.6±0.2°C; P=0.04) and 33°C (0800h: 37.0±0.2°C, 1600h 37.2±0.2°C; P=0.01). However the change in Tes was similar irrespective of the time of day at both 23°C (0800h: 0.7±0.1°C, 1600h: 0.7±0.2°C; P=0.37) and 33°C (0800h: 0.4±0.1°C, 1600h: 0.3±0.1°C; P=0.35). Further, mean steady‐state LSR of arm and back after 60 min of exercise was similar irrespective of time at both 23°C (0800h: 0.66±0.06 mg/cm2/min, 1600h: 0.65±0.13 mg/cm2/min; P=0.74) and 33°C (0800h: 0.62±0.11 mg/cm2/min, 1600 h: 0.58±0.11 mg/cm2/min, P=0.50). Likewise, WBSL at steady‐state (46 to 60 min) was similar between morning and afternoon trials at 23°C (0800h: 156±28 g, 1600h: 162±36 g; P=0.38) and 33°C (0800h: 147±29 g, 1600h: 158±34 g, P=0.55). While sweating commenced prior to exercise in 33°C, the onset threshold for sweating occurred at a higher Tb at 1600h compared to 800h at 23°C (0800h: 35.6±0.1°C, 1600h 35.9±0.2°C; P=0.03), however the change in Tb was similar at 23°C regardless of time of day (0800h: 0.14±0.07°C, 1600h 0.17±0.12°C; P=0.47). Lastly, sudomotor thermosensitivity (LSR‐Tb) was similar at both 23°C (0800h: 0.80±0.26 mg/cm2/min/°C, 1600h: 0.82±0.30 mg/cm2/min/°C; P=0.80) and 33°C (0800h: 0.81±0.18 mg/cm2/min, 1600h: 0.90±0.40 mg/cm2/min, P=0.87). Taken together, preliminary data suggests the difference in absolute core temperature (~0.3°C) associated with diurnal fluctuation does not alter the sweating response at a fixed evaporative requirement for heat balance in both thermoneutral and warm conditions.Support or Funding InformationN.R. was supported by an NSERC Postgraduate Scholarship‐Doctoral and a University of Ottawa Excellence Scholarship.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The Sweating and Core Temperature Response to Compensable and Uncompensable Heat Stress Following Heat Acclimation

While a greater maximal sweat rate following heat acclimation has been suggested to mitigate the rise in core temperature during uncompensable heat stress, it remains unclear whether heat acclimation will alter the core temperature response to compensable heat stress wherein heat balance is attainable. Thus, the primary aim of the present study was to evaluate the influence of complete heat acclimation on sweating and core temperature response to exercise in a compensable and uncompensable environment. A total of 8 (6 males, 2 females) unacclimated individuals were recruited. On separate days, participants exercised at a fixed rate of heat production (450 W) for 45‐mins of compensable heat stress (CHS; 37°C, 30% RH) and 60‐min of uncompressible heat stress (UCHS; 37°C, 60% RH) before and after heat acclimation. Core temperature [esophageal (Tes) and rectal (Tre)], local sweat rate of the arm (LSRarm) and back (LSRback), and whole body sweat loss (WBSL) were measured during experimental trials. Heat acclimation included an 8‐wk aerobic training intervention followed by 10 consecutive days of up to 90 minutes of treadmill walking in hot and humid conditions (38°C, 65% RH). Prior to CHS or UCHS, resting absolute Tes and Tre were lower following heat acclimation (Tes: 36.6±0.2°C; Tre: 36.8±0.1°C) relative to unacclimated (Tes: 36.9±0.2°C, P=0.002; Tre: 37.1±0.2°C, P=0.003). During CHS, the change in Tes and Tre were similar following heat acclimation (ΔTes: 0.4±0.1°C; ΔTre: 0.7±0.1°C) compared to unacclimated (ΔTes: 0.4±0.2°C, P=0.72; ΔTre: 0.7±0.1°C, P=0.61). Cumulative WBSL during CHS was marginally greater with acclimation (557±40 g) relative to unacclimated (494±59 g, P=0.01). Despite no difference in LSRback following 45‐min of CHS with or without heat acclimation (P=0.94), stead‐state LSRarm was slightly higher with acclimation (0.75±0.16 mg/cm2/min) compared to unacclimated (0.61±0.15 mg/cm2/min, P&lt;0.001). In contrast, the change in Tes and Tre during UCHS was significantly smaller following heat acclimation (ΔTes: 0.7±0.2°C; ΔTre: 0.9±0.2°C) relative to an unacclimated state (ΔTes: 1.1±0.3°C, P=0.04; ΔTre: 1.1±0.2°C, P&lt;0.001). WBSL was far greater during UCHS post‐heat acclimation (913±126 g) in comparison to prior to acclimation (671±83 g, P&lt;0.001). Further, end‐exercise LSRback and LSRarm were higher post‐heat acclimation (LSRback: 1.48±0.28 mg/cm2/min; LSRarm: 1.20±0.33 mg/cm2/min) relative to pre‐acclimation (LSRback: 1.21±0.26, P&lt;0.001; LSRarm: 0.91±0.26 mg/cm2/min, P&lt;0.001) during UCHS. Taken together, the core temperature response to compensable heat stress is similar irrespective of acclimation status, despite marginal greater whole‐body sweat rates. However, the large increases local and whole body sweat rate following heat acclimation clearly mitigated the rise in core temperature during uncompensable heat stress.Support or Funding InformationThis research was supported by a Discovery Grant from the Natural Sciences and Engineering Research Council (NSERC) of Canada (#386143‐2010, held by O.J.). N.R. was supported by an NSERC Postgraduate Scholarship‐Doctoral and a University of Ottawa Excellence Scholarship.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Thermoeffector Responses at a Fixed Rate of Heat Production in Heart Failure Patients.

Heart failure (HF) patients seem to exhibit altered thermoregulatory responses during exercise in the heat. However, the extent to which these responses are altered due to physiological impairments independently of biophysical factors associated with differences in metabolic heat production (Hprod), evaporative heat balance requirements (Ereq), and/or body size is presently unclear. Therefore, we examined thermoregulatory responses in 10 HF patients and 10 age-matched controls (CON) similar in body size during exercise at a fixed rate of Hprod and therefore Ereq in a 30°C environment. Rectal temperature, local sweat rate, and cutaneous vascular conductance were measured throughout 60 min of cycle ergometry. Whole-body sweat rate was estimated from pre-post nude body weight corrected for fluid intake. Despite exercising at the same rate of Hprod (HF, 338 ± 43 W; CON, 323 ± 31 W; P = 0.25), the rise in rectal temperature was greater (P < 0.01) in HF (0.81°C ± 0.16°C) than in CON (0.49°C ± 0.27°C). In keeping with a similar Ereq (HF, 285 ± 40 W; CON, 274 ± 28 W; P = 0.35), no differences in whole-body sweat rate (HF, 0.45 ± 0.11 L·h; CON, 0.41 ± 0.07 L·h; P = 0.38) or local sweat rate (HF, 0.96 ± 0.17 mg·cm·min; CON, 0.79 ± 0.15 mg·cm·min; P = 0.50) were observed between groups. However, the rise in cutaneous vascular conductance was lower in HF than in CON (HF, 0.83 ± 0.42 au·mm Hg; CON, 2.10 ± 0.79 au·mm Hg; P < 0.01). In addition, the cumulative body heat storage estimated from partitional calorimetry was similar between groups (HF, 154 ± 106 kJ; CON, 196 ± 174 kJ; P = 0.44). Collectively, these findings demonstrate that HF patients exhibit a blunted skin blood flow response, but no differences in sweating. Given that HF patients had similar body heat storage to that of CON at the same Hprod, their greater rise in core temperature can be attributed to a less uniform internal distribution of heat between the body core and periphery.

Skin-interfaced systems for sweat collection and analytics.

Recent interdisciplinary advances in materials, mechanics, and microsystem designs for biocompatible electronics, soft microfluidics, and electrochemical biosensors establish the foundations for emerging classes of thin, skin-interfaced platforms capable of capturing, storing, and performing quantitative, spatiotemporal measurements of sweat chemistry, instantaneous local sweat rate, and total sweat loss. This review summarizes scientific and technical progress in this area and highlights the implications in real time and ambulatory modes of deployment during physical activities across a broad range of contexts in clinical health, physiology research, fitness/wellness, and athletic performance.

Thermal behavior remains engaged following exercise despite autonomic thermoeffector withdrawal

We tested the hypothesis that thermal behavior during the exercise recovery compensates for elevated core temperatures despite autonomic thermoeffector withdrawal. In a thermoneutral environment, 6 females and 6 males (22 ± 1 y) cycled for 60 min (225 ± 46 W metabolic heat production), followed by 60 min passive recovery. Mean skin and core temperatures, skin blood flow, and local sweat rate were measured continually. Subjects controlled the temperature of their dorsal neck to perceived thermal comfort using a custom-made neck device. Neck device temperature provided an index of thermal behavior. Mean body temperature, calculated as the average of mean skin and core temperatures, provided an index of the stimulus for thermal behavior. To isolate the independent effect of exercise on thermal behavior during recovery, data were analyzed post-exercise the exact minute mean body temperature recovered to pre-exercise levels within a subject. Mean body temperature returned to pre-exercise levels 28 ± 20 min into recovery (Pre: 33.5 ± 0.2, Post: 33.5 ± 0.2 °C, P = 0.20), at which point, mean skin temperature had recovered (Pre: 29.6 ± 0.4, Post: 29.5 ± 0.5 °C, P = 0.20) and core temperature (Pre: 37.3 ± 0.2, Post: 37.5 ± 0.3 °C, P = 0.01) remained elevated. Post-exercise, skin blood flow (Pre: 59 ± 78, Post: 26 ± 25 PU, P = 0.10) and local sweat rate (Pre: 0.05 ± 0.25, Post: 0.13 ± 0.14 mg/cm2 min−1, P = 0.09) returned to pre-exercise levels, while neck device temperature was depressed (Pre: 27.4 ± 1.1, Post: 21.6 ± 7.4 °C, P = 0.03). These findings suggest that thermal behavior compensates for autonomic thermoeffector withdrawal in the presence of elevated core temperatures post-exercise.

Precooling and Warm-Up Effects on Time Trial Cycling During Heat Stress

Heat stress limits endurance exercise performance. Combining precooling and warm-up prior to endurance exercise in the heat may exploit the benefits of both strategies while avoiding the potential negative consequences of each. This study tested the hypothesis that precooling combined with warm-up improves time trial cycling performance in the heat relative to either treatment alone. Nine healthy men completed three 16.1-km time trials in 33°C after: 1) precooling (ice slurry and ice vest) alone (PREC); 2) warm-up alone (WU); or 3) PREC plus WU (COMBO). Tre was lower after PREC compared to WU throughout exercise and lower than COMBO for the first 12 km; COMBO was lower than WU for the first 4 km. Tsk during PREC was lower than COMBO and WU for the first 8 km, and lower in COMBO than WU for the first 4 km. PREC lowered pre-exercise heart rate relative to COMBO and WU (68 ± 10, 106 ± 12, 101 ± 13 bpm, respectively), but it increased similarly during exercise. Local sweat rate (SR) was lower in PREC (0.1 ± 0.1 mg · cm-2 · min-1) than COMBO (0.5 ± 0.2 mg · cm-2 · min-1) and WU (0.6 ± 0.2 mg · cm-2 · min-1) for the first 4 km. Treatments did not differentially affect performance (PREC = 31.9 ± 1.9 min, COMBO = 32.6 ± 2.7 min, WU = 33.1 ± 2.9 min). We conclude precooling alone or with warm-up mitigated thermal strain during exercise, but did not significantly improve 16.1-km cycling time trial performance.Al-horani RA, Wingo JE, Ng J, Bishop P, Richardson M. Precooling and warm-up effects on time trial cycling during heat stress. Aerosp Med Hum Perform. 2018; 89(2):87-93.

Maximum Skin Wettedness after Aerobic Training with and without Heat Acclimation.

To quantify how maximum skin wettedness (ωmax); that is, the determinant of the boundary between compensable and uncompensable heat stress, is altered by aerobic training in previously unfit individuals and further augmented by heat acclimation. Eight untrained individuals completed an 8-wk aerobic training program immediately followed by 8 d of hot/humid (38°C, 65%RH) heat acclimation. Participants completed a humidity ramp protocol pretraining (PRE-TRN), posttraining (POST-TRN), and after heat acclimation (POST-HA), involving treadmill marching at a heat production of 450 W for 105 min in 37.5°C, 2.0 kPa (35%RH). After attaining a steady-state esophageal temperature (Tes), humidity increased 0.04 kPa·min. An upward inflection in Tes indicated the upper limit of physiological compensability (Pcrit), which was then used to quantify ωmax. Local sweat rate, activated sweat gland density, and sweat gland output on the back and arm were simultaneously measured throughout. Peak aerobic capacity increased POST-TRN by approximately 14% (PRE-TRN: 45.8 ± 11.8 mL·kg·min; POST-TRN: 52.0 ± 11.1 mL·kg·min, P < 0.001). ωmax values became progressively greater from PRE-TRN (0.72 ± 0.06) to POST-TRN (0.84 ± 0.08; P = 0.02), to POST-HA (0.95 ± 0.05; P = 0.03). These shifts in ωmax were facilitated by a progressively greater local sweat rate and activated sweat gland density from PRE-TRN (0.84 ± 0.21 mg·cm·min; 67 ± 20 glands per square centimeter) to POST-TRN (0.96 ± 0.21 mg·cm·min, P = 0.03; 86 ± 27 glands per square centimeter; P = 0.009), to POST-HA (1.15 ± 0.21 mg·cm·min; P < 0.001; 98 ± 35 glands per square centimeter; P < 0.001). No differences in sweat gland output were observed. A greater ωmax occurred after 8 wk of aerobic training, but ωmax was further augmented with heat acclimation, indicating only a partially increased heat loss capacity with training. These ωmax values may assist future predictions of heat stress risk in untrained/trained unacclimated individuals and trained heat-acclimated individuals.

Decreased thermal sweating of central sudomotor mechanism in African and Korean men.

Tropical natives sweat less and preserve more body fluid than temperate natives, tolerating heat stress. However, the mechanisms involved in such sweating reduction have not been fully elucidated. We examined the sudomotor responses of men of African (n = 36) and Korean (n = 41) ancestry during hot water (43 °C) leg immersion (central sudomotor response). Correlations between mean body temperature, basal metabolic rate (BMR), and sweat rate were also examined. All procedures were done in an automated climate chamber. Local skin temperatures and BMR were measured and mean body temperature was calculated. Sweating activities which include evaporative loss rate, sweat onset time, sweat rate, sweat volume, and whole-body sweat loss volume were examined. In the heat load test, Africans showed lower mean body and local skin temperatures than Koreans before and after heating. Before and after heating, BMR declined significantly in Africans, while that of Koreans declined less. Local sweat onset time increased more in Africans than in Koreans. Local evaporative loss rate, local sweat volume, local sweat rate, and whole body sweat loss volume were reduced in Africans compared with Koreans. There were positive associations of mean body temperature and resting BMR with mean sweat rate. In conclusion, we observed a larger reduction of sudomotor activity in tropical Africans than in temperate Koreans, which was associated with their lower mean body temperature and lower resting BMR.

Oxidative stress does not influence local sweat rate during high-intensity exercise.

What is the central question of this study? We evaluated whether oxidative stress attenuates the contribution of nitric oxide to sweating during high-intensity exercise. What is the main finding and its importance? In contrast to our previous report of an oxidative stress-mediated reduction in nitric oxide-dependent cutaneous vasodilatation in this cohort during intense exercise, we demonstrated no influence of local ascorbate administration on the sweating response during moderate- (∼51% peak oxygen uptake) or high-intensity exercise (∼72% peak oxygen uptake). These new findings provide important mechanistic insight into how exercise-induced oxidative stress impacts sudomotor activity. Nitric oxide (NO)-dependent sweating is diminished during high- but not moderate-intensity exercise. We evaluated whether this impairment stems from increased oxidative stress during high-intensity exercise. On two separate days, 11 young (24±4years) men cycled in the heat (35°C) at a moderate [500W; 52±6% peak oxygen uptake (V̇O2 peak )] or high (700W; 71±5% V̇O2 peak ) rate of metabolic heat production. Each session included two 30min exercise bouts separated by a 20min recovery period. Local sweat rate was monitored at four forearm skin sites continuously perfused via intradermal microdialysis with the following: (i) lactated Ringer solution (Control); (ii) 10mm ascorbate (Ascorbate; non-selective antioxidant); (iii) 10mm NG -nitro-l-arginine methyl ester (l-NAME; NO synthase inhibitor); or (iv) 10mm ascorbate plus 10mm l-NAME (Ascorbate + l-NAME). During moderate exercise, sweat rate was attenuated at the l-NAME and Ascorbate + l-NAME sites (both ∼1.0mgmin-1 cm-2 ; all P<0.05) but not at the Ascorbate site (∼1.1mgmin-1 cm-2 ; both P≥0.28) in comparison to the Control site (∼1.1mgmin-1 cm-2 ). However, no differences were observed between treatment sites (∼1.4mgmin-1 cm-2 ; P=0.75) during high-intensity exercise. We conclude that diminished NO-dependent sweating during intense exercise occurs independent of oxidative stress.

Age Modulates Physiological Responses during Fan Use under Extreme Heat and Humidity.

We examined the effect of electric fan use on cardiovascular and thermoregulatory responses of nine young (26 ± 3 yr) and nine aged (68 ± 4 yr) adults exposed to extreme heat and humidity. While resting at a temperature of 42°C, relative humidity increased from 30% to 70% in 2% increments every 5 min. On randomized days, the protocol was repeated without or with fan use. HR, core (Tcore) and mean skin (Tsk) temperatures were measured continuously. Whole-body sweat loss was measured from changes in nude body weight. Other measures of cardiovascular (cardiac output), thermoregulatory (local cutaneous and forearm vascular conductance, local sweat rate), and perceptual (thermal and thirst sensations) responses were also examined. When averaged over the entire protocol, fan use resulted in a small reduction of HR (-2 bpm, 95% confidence interval [CI], -8 to 3), and slightly greater Tcore (+0.05°C; 95% CI, -0.13 to 0.23) and Tsk (+0.03°C; 95% CI, -0.36 to 0.42) in young adults. In contrast, fan use resulted in greater HR (+5 bpm; 95% CI, 0-10), Tcore (+0.20°C; 95% CI, 0.00-0.41), and Tsk (+0.47°C; 95% CI, 0.18-0.76) in aged adults. A greater whole-body sweat loss during fan use was observed in young (+0.2 kg; 95% CI, -0.2 to 0.6) but not aged (0.0 kg; 95% CI, -0.2 to 0.2) adults. Greater local sweat rate and cutaneous vascular conductance were observed with fan use in aged adults. Other measures of cardiovascular, thermoregulatory, and perceptual responses were unaffected by fan use in both groups. During extreme heat and humidity, fan use elevates physiological strain in aged, but not young, adults.

Fluid replacement modulates oxidative stress- but not nitric oxide-mediated cutaneous vasodilation and sweating during prolonged exercise in the heat.

The roles of nitric oxide synthase (NOS), reactive oxygen species (ROS), and angiotensin II type 1 receptor (AT1R) activation in regulating cutaneous vasodilation and sweating during prolonged (≥60 min) exercise are currently unclear. Moreover, it remains to be determined whether fluid replacement (FR) modulates the above thermoeffector responses. To investigate, 11 young men completed 90 min of continuous moderate intensity (46% V̇o2peak) cycling performed at a fixed rate of metabolic heat production of 600 W (No FR condition). On a separate day, participants completed a second session of the same protocol while receiving FR to offset sweat losses (FR condition). Cutaneous vascular conductance (CVC) and local sweat rate (LSR) were measured at four intradermal microdialysis forearm sites perfused with: 1) lactated Ringer (Control); 2) 10 mM NG-nitro-l-arginine methyl ester (l-NAME, NOS inhibition); 3) 10 mM ascorbate (nonselective antioxidant); or 4) 4.34 nM losartan (AT1R inhibition). Relative to Control (71% CVCmax at both time points), CVC with ascorbate (80% and 83% CVCmax) was elevated at 60 and 90 min of exercise during FR (both P < 0.02) but not at any time during No FR (all P > 0.31). In both conditions, CVC was reduced at end exercise with l-NAME (60% CVCmax; both P < 0.02) but was not different relative to Control at the losartan site (76% CVCmax; both P > 0.19). LSR did not differ between sites in either condition (all P > 0.10). We conclude that NOS regulates cutaneous vasodilation, but not sweating, irrespective of FR, and that ROS influence cutaneous vasodilation during prolonged exercise with FR.