Heat Loss Responses Research Articles

Ingesting carbonated water post-exercise in the heat transiently ameliorates hypotension and enhances mood state.

The objective was to assess if post-exercise ingestion of carbonated water in a hot environment ameliorates hypotension, enhances cerebral blood flow and heat loss responses, and positively modulates perceptions and mood states. Twelve healthy, habitually active young adults (five women) performed 60min of cycling at 45% peak oxygen uptake in a hot climate (35°C). Subsequently, participants consumed 4°C carbonated or non-carbonated (control) water (150 and 100mL for males and females regardless of drink type) at 20 and 40min into post-exercise periods. Mean arterial pressure decreased post-exercise at 20min only (P=0.032) compared to the pre-exercise baseline. Both beverages transiently (∼1min) increased mean arterial pressure and middle cerebral artery mean blood velocity (cerebral blood flow index) regardless of post-exercise periods (all P ≤ 0.015). Notably, carbonated water ingestion led to greater increases in mean arterial pressure (2.3±2.8mmHg vs. 6.6±4.4mmHg, P<0.001) and middle cerebral artery mean blood velocity (1.6±2.5cm/s vs. 3.8±4.1cm/s, P=0.046) at 20min post-exercise period compared to non-carbonated water ingestion. Both beverages increased mouth exhilaration and reduced sleepiness regardless of post-exercise periods, but these responses were more pronounced with carbonated water ingestion at 40min post-exercise (mouth exhilaration: 3.1±1.4vs. 4.7±1.7, P=0.001; sleepiness: -0.7±0.91vs. -1.9±1.6, P=0.014). Heat loss responses and other perceptions were similar between the two conditions throughout (all P ≥ 0.054). We show that carbonated water ingestion temporarily ameliorates hypotension and increases the cerebral blood flow index during the early post-exercise phase in a hot environment, whereas it enhances mouth exhilaration and reduces sleepiness during the late post-exercise phase.

GH and IGF-1 in skin interstitial fluid and blood are associated with heat loss responses in exercising young adults.

Sweat glands and cutaneous vessels possess growth hormone (GH) and insulin-like growth factor 1 (IGF-1) receptors. Here, we assessed if exercise increases GH and IGF-1 in skin interstitial fluid, and whether baseline and exercise-induced increases in GH and IGF-1 concentrations in skin interstitial fluid/blood are associated with heat loss responses of sweating and cutaneous vasodilation. Sixteen young adults (7 women) performed a 50-min moderate-intensity exercise bout (50% VO2peak) during which skin dialysate and blood samples were collected. In a sub-study (n = 7, 4 women), we administered varying concentrations of GH (0.025-4000ng/mL) and IGF-1 (0.000256-100µg/mL) into skin interstitial fluid via intradermal microdialysis. Sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC) were measured continuously for both studies. Exercise increased sweating and CVC (both P < 0.001), paralleled by increases of serum GH and skin dialysate GH and IGF-1 (all P ≤ 0.041) without changes in serum IGF-1. Sweating was positively correlated with baseline dialysate and serum GH levels, as well as exercise-induced increases in serum GH and IGF-1 (all P ≤ 0.044). Increases in CVC were not correlated with any GH and IGF-1 variables. Exogenous administration of GH and IGF-1 did not modulate resting sweat rate and CVC. (1) Exercise increases GH and IGF-1 levels in the skin interstitial fluid, (2) exercise-induced sweating is associated with baseline GH in skin interstitial fluid and blood, as well as exercise-induced increases in blood GH and IGF-1, and (3) cutaneous vasodilation during exercise is not associated with GH and IGF-1 in skin interstitial fluid and blood.

Serum, interstitialand sweat ATP in humans exposed to heat stress: Insights into roles of ATP in the heat loss responses.

Hyperthermia increases intravascular adenosine triphosphate (ATP) and is associated with greater hyperthermia-induced cutaneous vasodilation. Hyperthermia may also increase skin interstitial fluid ATP thereby activating cutaneous vascular smooth muscle cells and sweat glands. We evaluated the hypothesis that whole-body heating would increase skin interstitial fluid ATP, and this response would be associated with an increase in cutaneous vasodilation and sweating. Nineteen (8 females) young adults underwent whole-body heating using a water-perfusion suit to increase core temperature by ~1°C during which time cutaneous vascular conductance (CVC, ratio of laser-Doppler blood flow to mean arterial pressure) and sweat rate (ventilated capsule technique) were measured at four forearm skin sites to minimize between-site variations. Dialysate from the skin sites were collected via intradermal microdialysis. Heating increased serum ATP, CVC, and sweat rate (all p ≤ 0.031). However, heating did not modulate dialysate ATP (median, baseline vs. end-heating: 2.38 vs. 2.70 nmol/ml) (p = 0.068), though the effect size was moderate (Cohen's d = 0.566). While the heating-induced increase in CVC was not correlated with changes in serum ATP (r = 0.439, p = 0.060), we observed a negative correlation (rs = -0.555, p = 0.017) between dialysate ATP and CVC. We did not observe a significant correlation between the heating-induced sweating and serum, dialysate, or sweat ATP (rs = 0.091 to -0.322, all p ≥ 0.222). Altogether, we showed that passive heating increases ATP in blood and possibly skin interstitial fluid, with the latter potentially blunting cutaneous vasodilation. However, ATP does not appear to modulate sweating.

Induction and decay of seasonal acclimatization on whole body heat loss responses during exercise in a hot humid environment with different air velocities.

Whether whole body heat loss and thermoregulatory function (local sweat rate and skin blood flow) are different between summer and autumn and between autumn and winter seasons during exercise with different air flow in humid heat remain unknown. We therefore tested the hypotheses that whole body sweat rate (WBSR), evaporated sweat rate, and thermoregulatory function during cycling exercise in autumn would be higher than in winter but would be lower than in summer under hot-humid environment (32 C, 75% RH). We also tested the hypothesis that the increase of air velocity would enhance evaporated sweat rate and sweating efficiency across winter, summer, and autumn seasons. Eight males cycled for 1 h at 40% V̇o2max in winter, summer, and autumn seasons. Using an electric fan, air velocity increased from 0.2 m/s to 1.1 m/s during the final 20 min of cycling. The autumn season resulted in a lower WBSR, unevaporated sweat rate, and a higher sweating efficiency compared with summer (all P ≤ 0.05) but WBSR and unevaporated sweat rate in autumn were higher than in winter and thus sweating efficiency was lower when compared with winter only at the air velocity of 0.2 m/s (All P ≤ 0.05). Furthermore, evaporated sweat rate and core temperature (Tcore) were not different among winter, summer, and autumn seasons (All P > 0.19). In conclusion, changes in WBSR across different seasons do not alter Tcore during exercise in a hot humid environment. Furthermore, increasing air velocity enhances evaporated sweat rate and sweating efficiency across all seasons.

Ingestion of carbonated water increases middle cerebral artery blood velocity and improves mood states in resting humans exposed to ambient heat stress

Sugar-free carbonated water is consumed worldwide. The consumption of carbonated water is high in summer, when the heat loss responses of sweating and skin vasodilation are activated, and thermal perceptions (thermal sensation and comfort) and mood states are negatively modulated. However, whether ingesting carbonated water under ambient heat exposure modulates cerebral blood flow index, heat loss responses, thermal perceptions, and mood states remains to be determined. In this study, 17 healthy, habitually active, young adults (eight women) ingested 4 °C noncarbonated or carbonated water under 37 °C ambient heat-stressed resting conditions. Both drinks increased the middle cerebral artery mean blood velocity, an index of cerebral blood flow, and mean arterial pressure, with carbonated water exhibiting higher elevations than noncarbonated water (P < 0.05). However, the heart rate, sweat rate, and skin blood flow during and after drinking remained unchanged between the two conditions (P > 0.05). The thermal sensation and comfort after drinking remained unchanged between the two conditions (P > 0.05); but, a drink-induced reduction in sleepiness was higher, and drink-induced elevations in motivation and exhilaration were higher after ingesting carbonated water than those after ingesting noncarbonated water (P < 0.05). The analyses suggest that in humans under ambient heat-stressed resting conditions, ingestion of cold carbonated water increases the cerebral blood flow index, blood pressure, motivation, and exhilaration, whereas it decreases sleepiness relative to ingestion of noncarbonated cold water. However, ingestion of cold carbonated water fails to modulate thermoregulatory responses and thermal perception as opposed to noncarbonated cold water.

Cutaneous TRPV4 Channels Activate Warmth-Defense Responses in Young and Adult Birds.

Transient receptor potential vanilloid 4 (TRPV4) channels are sensitive to warm ambient temperatures (Tas), triggering heat loss responses in adult rats in a Tas range of ∼26–30°C. In birds, however, the thermoregulatory role of TRPV4 has never been shown. Here, we hypothesized that stimulation of TRPV4 induces thermolytic responses for body temperature (Tb) maintenance in birds, and that this function is already present in early life, when the Ta range for TRPV4 activation does not represent a warm condition for these animals. We first demonstrated the presence of TRPV4 in the dorsal and ventral skin of chickens (Gallus gallus domesticus) by immunohistochemistry. Then, we evaluated the effects of the TRPV4 agonist, RN1747, and the TRPV4 antagonists, HC067047 and GSK2193874, on Tb and thermoeffectors at different Tas in 5-day-old chicks and 60-day-old adult chickens. For the chicks, RN1747 transiently reduced Tb both in thermoneutrality (31°C) and in a cold Ta for this phase (26°C), which relied on huddling behavior inhibition. The TRPV4 antagonists alone did not affect Tb or thermoeffectors but blocked the Tb decrease and huddling inhibition promoted by RN1747. For the adults, TRPV4 antagonism increased Tb when animals were exposed to 28°C (suprathermoneutral condition for adults), but not to 19°C. In contrast, RN1747 decreased Tb by reducing metabolic rate and activating thermal tachypnea at 19°C, a Ta below the activation range of TRPV4. Our results indicate that peripheral TRPV4 receptors are functional in early life, but may be inhibited at that time when the range of activation (∼26–30°C) represents cold Ta for chicks, and become physiologically relevant for Tb maintenance when the activation Ta range for TRPV4 becomes suprathermoneutral for adult chickens.

TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation in humans in vivo.

What is the central question of this study? Do transmembrane member 16A (TMEM16A) blockers modulate the activation of heat loss responses of sweating and cutaneous vasodilatation? What are the main finding and its importance? Relative to the vehicle control site, TMEM16A blockers T16Ainh-A01 and benzbromarone had no effect on sweat rate or cutaneous vascular conductance during whole-body heating inducing a 1.1±0.1°C increase in core temperature above baseline resting levels. These results suggest that TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation during whole-body heat stress. Animal and in vitro studies suggest that transmembrane member 16A (TMEM16A), a Ca2+ -activated Cl- channel, contributes to regulating eccrine sweating. However, direct evidence supporting this possibility in humans is lacking. We assessed the hypothesis that TMEM16A blockers attenuate sweating during whole-body heating in humans. Additionally, we assessed the associated changes in the heat loss response of cutaneous vasodilatation to determine if a functional role of TMEM16A may exist. Twelve young (24±2years) adults (six females) underwent whole-body heating using a water-perfused suit to raise core temperature 1.1±0.1°C above baseline. Sweat rate and cutaneous vascular conductance (normalized to maximal conductance via administration of sodium nitroprusside) were evaluated continuously at four forearm skin sites treated continuously by intradermal microdialysis with (1) lactated Ringer's solution (control), (2) 5% dimethyl sulfoxide (DMSO) serving as a vehicle control, or (3) TMEM16A blockers 1mM T16Ainh-A01 or 2mM benzbromarone dissolved in 5% DMSO solution. All drugs were administered continuously via intradermal microdialysis. Whole-body heating increased core temperature progressively and this was paralleled by an increase in sweat rate and cutaneous vascular conductance at all skin sites. However, sweat rate (all P>0.318) and cutaneous vascular conductance (all P≥0.073) did not differ between the vehicle control site relative to the TMEM16A blocker-treated sites. Collectively, our findings indicate that TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation during whole-body heating in young adults in vivo.

The effect of acute intradermal administration of ascorbate on heat loss responses in older adults with uncomplicated controlled hypertension.

What is the central question of this study? Does acute intradermal administration of the antioxidant ascorbate augment local forearm cutaneous vasodilatation and sweating via nitric oxide synthase (NOS)-dependent mechanisms during exercise-heat stress in older adults with uncomplicated controlled hypertension? What is the main finding and its importance? Relative to the control site, ascorbate had no effect on forearm cutaneous vascular conductance (CVC) and sweat rate, although CVC was reduced with NOS inhibition in older adults with hypertension. Acute local administration of ascorbate to forearm skin does not modulate heat loss responses during exercise-heat stress in older adults with hypertension. Nitric oxide synthase (NOS) contributes to the heat loss responses of cutaneous vasodilatation and sweating during exercise. However, the contribution of NOS may be attenuated in individuals with uncomplicated, controlled hypertension due to elevated oxidative stress, which can reduce NO bioavailability. We evaluated the hypothesis that the acute local intradermal administration of the antioxidant ascorbate would enhance cutaneous vasodilatation and sweating via NOS-dependent mechanisms during an exercise-heat stress in adults with hypertension. Habitually active adults who were normotensive (n=14, 7 females, 62±4years) or had uncomplicated, controlled hypertension (n=13, 6 females, 62±5years) performed 30min of moderate-intensity (50% of their pre-determined peak oxygen uptake) semi-recumbent cycling in the heat (35°C, 20% relative humidity). Cutaneous vascular conductance (CVC) and sweat rate were assessed at four forearm skin sites continuously perfused with (1) lactated Ringer solution (Control), (2) 10mM antioxidant ascorbate, (3) 10mMNG -nitro-l-arginine methyl ester (l-NAME), a non-selective NOS inhibitor, or (4) a combination of ascorbate and l-NAME. Relative to Control, no effect of ascorbate was observed on CVC or sweating in either group (P=0.619). However, l-NAME reduced CVC relative to Control in both groups (P≤0.038). No effect of any treatment on sweating was observed (P≥0.306). Thus, acute local administration of ascorbate to forearm skin does not enhance the activation of heat loss responses of cutaneous vasodilatation and sweating in older adults, and those with hypertension during an exercise-heat stress.

Calcium‐activated Chloride Channel TMEM16A/ANO1 Does Not Mediate the Regulation of Sweating and Cutaneous Vasodilation in Humans In Vivo

The regulation of human body temperature during a heat stress is dependent on the activation of the heat loss responses of cutaneous vasodilation and eccrine sweating. While significant advancements have been made in our understanding of the mechanisms governing their regulation, new potential modifiers such as transmembrane member 16A (TMEM16A), a Ca2+‐activated Cl‐ channel also known as anoctamin 1 (ANO1), continue to be identified. In vitro and animal studies suggest a role for TMEM16A in the regulation of sweat secretion and vascular tone. For example, Ca2+ induced Cl‐current was abolished in TMEM16A deficit, but not BEST2 deficit, NCL‐SG3 human eccrine sweat gland cell lines. Further, animal models showed the activation of TMEM16A on vascular smooth muscle cells blunts vasodilation. However, direct evidence supporting a role of TMEM16 in mediating cutaneous vasodilation as well as eccrine sweating in humans in vivo remains to be established. Therefore, we evaluated the hypothesis that TMEM16A mediates the regulation of sweating and cutaneous vasodilation during a whole‐body heat stress in young adults.Twelve young (24 ± 2 years) adults (6 females) underwent a whole‐body heat stress induced by a water‐perfused suit to raise core temperature 1.1±0.1ºC above baseline resting levels. Sweat rate (ventilated capsule) and cutaneous vascular conductance (assessed as skin blood flow/mean arterial pressure and normalised to maximal conductance achieved via simultaneous local skin heating to 44°C and administration of sodium nitroprusside) were assessed at four skin sites on the forearm treated with 1) lactated Ringers (control), 2) 5 % dimethyl sulfoxide serving as a vehicle control, 3) 1 mM T16Ainh‐A01 (a TMEM16A blocker) or 4) 2 mM benzbromarone (another TMEM16A blocker). All drugs were administered continuously via intradermal microdialysis.Sweat rate increased as heating continued at all skin sites (P &lt; 0.001 for a main effect of heating stage). Neither the main effect of treatment site nor the interaction between treatment site and heating stage was significant (both P ≥ 0.318). Cutaneous vascular conductance increased in parallel to elevations in core temperature (P &lt; 0.001 for a main effect of heating stage). Although no main effect of treatment site was observed (P = 0.109), a significant interaction between heating stage and treatment site was measured (P &lt; 0.001). Post‐hoc analysis revealed that cutaneous vascular conductance at the DMSO‐treated site was higher than the control site at baseline (P = 0.047). By contrast, cutaneous vascular conductance at moderate elevations in core temperature (i.e., ≥0.4‐0.8 °C) was greater at the control site relative to the DMSO‐treated site (all P ≤ 0.013). Importantly, no differences were measured in cutaneous vascular conductance between the DMSO‐treated site and TMEM16A blocker‐treated sites (all P ≥ 0.073).Taken together, our findings demonstrate for the first time that TMEM16A does not contribute to the regulation of sweating and cutaneous vasodilation during whole‐body heating in young adults in vivo.

Heat loss responses at rest and during exercise in pregnancy: A scoping review.

The teratogenic risk associated with maternal hyperthermia (i.e., core temperature ≥39.0°C) has been a crucial motive in understanding thermoregulatory responses in pregnancy. To date, a substantial number of studies have focused on core temperature responses in a wide range of exercise intensities, duration, and ambient temperatures. Fortunately, none have reported core temperatures exceeding 39.0°C. Nonetheless, there are limited studies that have provided substantial insight into both dry and evaporative heat loss mechanisms involved in facilitating the maintenance of core temperature (≥39.0°C) during heat stress in pregnant women. The purpose of this scoping review was to summarize the available literature that has assessed heat loss responses in studies of human pregnancy. A search strategy was developed combining the terms pregnancy, thermoregulation, and adaptation. A systematic search was performed in the following databases: PubMed, Embase, Scopus, and ProQuest. Studies eligible for inclusion included pregnant women between the ages of 18-40 years old, and at least one measurement of the following: sweating, blood flow, skin temperature, and behavioural responses. Retrieved data were categorized as evaporative (sweating), dry or behavioural heat loss responses and summarized narratively. Thirty-three studies were included in this review (twenty-nine measured physiological responses and four measured behavioural responses). Studies suggest that during exercise, evaporative (sweating) and dry (skin blood flow and temperature) heat loss responses increase from early to late pregnancy in addition to greater cardiac output, blood volume and reduced vascular resistance. Behavioural practices related to heat loss responses are also influenced by cultural/religious expectations, personal preferences and sociodemographics. The findings from this review suggest that pregnancy modifies evaporative (sweating), dry and behavioural heat loss. However, future studies have an opportunity to compare heat loss measurements accounting for gestational weight gain and thermal sensation/comfort scale to associate physiological responses with perceptual responses across pregnancy.

Effects of Isomaltulose Ingestion on Thermoregulatory Responses during Exercise in a Hot Environment.

Isomaltulose is a low glycemic and insulinemic carbohydrate available as a constituent of sports drinks. However, it remains unclear whether thermoregulatory responses (sweating and cutaneous vasodilation) after isomaltulose drink ingestion differ from those of sucrose and water during exercise in a hot environment. Ten young healthy males consumed 10% sucrose, 10% isomaltulose, or water drinks. Thirty-five minutes after ingestion, they cycled for fifteen minutes at 75% peak oxygen uptake in a hot environment (30 °C, 40% relative humidity). Sucrose ingestion induced greater blood glucose concentration and insulin secretion at the pre-exercise state, compared with isomaltulose and/or water trials, with no differences during exercise in blood glucose. Change in plasma volume did not differ between the three trials throughout the experiment, but both sucrose and isomaltulose ingestions similarly increased plasma osmolality, as compared with water (main beverage effect, p = 0.040)—a key response that potentially delays the onset of heat loss responses. However, core temperature thresholds and slopes for heat loss responses were not different between the trials during exercise. These results suggest that ingestion of isomaltulose beverages induces low glycemic and insulinemic states before exercise but does not alter thermoregulatory responses during exercise in a hot environment, compared with sucrose or water.

The effect of seasonal acclimatization on whole body heat loss response during exercise in a hot humid environment with different air velocity.

Seasonal acclimatization from winter to summer is known to enhance thermoeffector responses in hot-dry environments during exercise whereas its impact on sweat evaporation and core temperature (Tcore) responses in hot-humid environments remains unknown. We, therefore, sought to determine whether seasonal acclimatization is able to modulate whole body sweat rate (WBSR), evaporated sweat rate, sweating efficiency, and thermoregulatory function during cycling exercise in a hot-humid environment (32°C, 75% RH). We also determined whether the increase in air velocity could enhance evaporated sweat rate and sweating efficiency before and after seasonal acclimatization. Twelve males cycled for 1 h at 40% V̇o2max in winter (preacclimatization) and repeated the trial again in summer (after acclimatization). For the last 20 min of cycling at a steady-state of Tcore, air velocity increased from 0.2 (0.04) m/s to 1.1 (0.02) m/s by using an electric fan located in front of the participant. Seasonal acclimatization enhanced WBSR, unevaporated sweat rate, local sweat rate and mean skin temperature compared with preacclimatization state (all P < 0.05) whereas sweating efficiency was lower (P < 0.01) until 55 min of exercise. Tcore and evaporated sweat rate were unaltered by acclimatization status (all P > 0.70). In conclusion, seasonal acclimatization enhances thermoeffector responses but does not attenuate Tcore during exercise in a hot-humid environment. Furthermore, increasing air velocity enhances evaporated sweat rate and sweating efficiency irrespective of acclimated state. NEW & NOTEWORTHY Seasonal acclimatization to humid heat enhances eccrine sweat gland function and thus results in a higher local and whole body sweat rate but does not attenuate Tcore during exercise in a hot-humid environment. Sweating efficiency is lower after seasonal acclimatization to humid heat compared with preacclimatization with and without the increase of air velocity. However, having a lower sweating efficiency does not mitigate the Tcore response during exercise in a hot-humid environment.

Effects of short-term heat acclimation on whole-body heat exchange and local nitric oxide synthase- and cyclooxygenase-dependent heat loss responses in exercising older men.

What is the central question of this study? Does short-term heat acclimation enhance whole-body evaporative heat loss and augment nitric oxide synthase (NOS)-dependent cutaneous vasodilatation and NOS- and cyclooxygenase (COX)-dependent sweating, in exercising older men? What is the main finding and its importance? Our preliminary data (n=8) demonstrated that short-term heat acclimation improved whole-body evaporative heat loss, but it did not influence the effects of NOS and/or COX inhibition on cutaneous vasodilatation or sweating in older men during an exercise-heat stress. These outcomes might imply that although short-term heat acclimation enhances heat dissipation in older men, it does not modulate NOS- and COX-dependent control of cutaneous vasodilatation or sweating on the forearm. Ageing is associated with decrements in whole-body heat loss (evaporative+dry heat exchange), which might stem from alterations in nitric oxide synthase (NOS)- and cyclooxygenase (COX)-dependent cutaneous vasodilatation and sweating. We evaluated whether short-term heat acclimation would (i) enhance whole-body heat loss primarily by increasing evaporative heat loss, and (ii) augment NOS-dependent cutaneous vasodilatation and NOS- and COX-dependent sweating, in exercising older men. Eight older men [mean (SD) age, 59(8)years] completed a calorimetry and microdialysis trial before and after 7days of exercise-heat acclimation. For the calorimetry trials, whole-body evaporative and dry heat exchange were assessed using direct calorimetry during 30min bouts of cycling at light, moderate and vigorous metabolic heat productions (150, 200 and 250W/m2 , respectively) in dry heat (40°C, 20% relative humidity). For the microdialysis trials, local cutaneous vascular conductance and sweat rate were assessed during 60min exercise in the heat (35°C, 20% relative humidity) at four dorsal forearm skin sites treated with lactated Ringer solution (control), NOS inhibitor, COX inhibitor or combined NOS and COX inhibitors, via microdialysis. Evaporative heat loss during moderate (P=0.036) and vigorous (P=0.021) exercise increased after acclimation. Inhibition of NOS alone reduced cutaneous vascular conductance to a similar extent before and after acclimation (P<0.040), whereas separate and combined NOS and COX inhibition had no significant effects on sweating relative to the control site (P=0.745). Our preliminary results might suggest that short-term heat acclimation improves evaporative heat loss, but does not significantly modulate the contributions of NOS or COX to cutaneous vasodilatation or sweating on the forearm in older men during an exercise-heat stress.

Phenotypic flexibility in heat production and heat loss in response to thermal and hydric acclimation in the zebra finch, a small arid-zone passerine

To maintain constant body temperature (Tb) over a wide range of ambient temperatures (Ta) endothermic animals require large amounts of energy and water. In hot environments, the main threat to endothermic homeotherms is insufficient water to supply that necessary for thermoregulation. We investigated flexible adjustment of traits related to thermoregulation and water conservation during acclimation to hot conditions or restricted water availability, or both, in the zebra finch, Taeniopygia guttata a small arid-zone passerine. Using indirect calorimetry, we measured changes in whole animal metabolic rate (MR), evaporative heat loss (EHL) and Tb before and after acclimation to 23 or 40 °C, with different availability of water. Additionally, we quantified changes in partitioning of EHL into respiratory and cutaneous avenues in birds exposed to 25 and 40 °C. In response to heat and water restriction zebra finches decreased MR, which together with unchanged EHL resulted in increased efficiency of evaporative heat loss. This facilitated more precise Tb regulation in heat-acclimated birds. Acclimation temperature and water availability had no effect on the partitioning of EHL into cutaneous or respiratory avenues. At 25 °C, cutaneous EHL accounted for ~ 60% of total EHL, while at 40 °C, its contribution decreased to ~ 20%. Consistent among-individual differences in MR and EHL suggest that these traits, provided that they are heritable, may be a subject to natural selection. We conclude that phenotypic flexibility in metabolic heat production associated with acclimation to hot, water-scarce conditions is crucial in response to changing environmental conditions, especially in the face of current and predicted climate change.

Heat shock protein 90 modulates cutaneous vasodilation during an exercise-heat stress, but not during passive whole-body heating in young women.

Heat shock protein 90 (HSP90) modulates exercise‐induced cutaneous vasodilation in young men via nitric oxide synthase (NOS), but only when core temperature is elevated ~1.0°C. While less is known about modulation of this heat loss response in women during exercise, sex differences may exist. Further, the mechanisms regulating cutaneous vasodilation can differ between exercise‐ and passive‐heat stress. Therefore, in 11 young women (23 ± 3 years), we evaluated whether HSP90 contributes to NOS‐dependent cutaneous vasodilation during exercise (Protocol 1) and passive heating (Protocol 2) and directly compared responses between end‐exercise and a matched core temperature elevation during passive heating. Cutaneous vascular conductance (CVC%max) was measured at four forearm skin sites continuously treated with (a) lactated Ringers solution (control), (b) 178 μM Geldanamycin (HSP90 inhibitor), (c) 10 mM L‐NAME (NOS inhibitor), or (d) combined 178 μM Geldanamycin and 10 mM L‐NAME. Participants completed both protocols during the early follicular (low hormone) phase of the menstrual cycle (0–7 days). Protocol 1: participants rested in the heat (35°C) for 70 min and then performed 50 min of moderate‐intensity cycling (~55% VO2peak) followed by 30 min of recovery. Protocol 2: participants were passively heated to increase rectal temperature by 1.0°C, comparable to end‐exercise. HSP90 inhibition attenuated CVC%max relative to control at end‐exercise (p < .05), but not during passive heating. While NOS inhibition and combined HSP90 + NOS inhibition attenuated CVC%max relative to control for both protocols (all p < .05), they did not differ from each other. We show that HSP90 modulates cutaneous vasodilation NOS‐dependently during exercise in young women, with no effect during passive heating, despite a similar NOS contribution.

Endurance Exercise Capacity &amp; Heat-loss Responses Are Greater In The Late Evening Than Morning

Endurance Exercise Capacity &amp; Heat-loss Responses Are Greater In The Late Evening Than Morning

Surface heat loss and chemical kinetic response in deflagration-to-detonation transition in microchannels

We examine how heat loss at walls affects the deflagration-to-detonation transition. We find that in the adiabatic case, autoignition near the wall produces fast flames in the boundary layer, while autoignition does not occur in the boundary layer for the case with heat loss at the walls.

Heat acclimation does not modify autonomic responses to core cooling and the skin thermal comfort zone.

Exercise heat acclimation (HA) is known to magnify the sweating response by virtue of a lower threshold as well as increased gain and maximal capacity of sweating. However, HA has been shown to potentiate the shivering response in a cold-air environment. We investigated whether HA would alter heat loss and heat production responses during water immersion. Twelve healthy male participants underwent a 10-day HA protocol comprising daily 90-min controlled-hyperthermia (target rectal temperature, Tre 38.5°C) exercise sessions. Preceding and following HA, the participants performed a maximal exercise test in thermoneutral conditions (ambient temperature 23°C, relative humidity 50%) and were, following exercise, immersed in 28°C water for 60min. Thermal comfort zone (TCZ) was also assessed with participants regulating the temperature of a water-perfused suit during heating and cooling. Baseline pre-immersion Tre was similar pre- and post-HA (pre: 38.33±0.33°C vs post: 38.12±0.36°C, p=0.092). The Tre cooling rate was identical pre-to post-HA (-0.03±0.01°C·min-1, p=0.31), as was the vasomotor response reflected in the forearm-fingertip temperature difference. Shivering thresholds (p=0.43) and gains (p=0.61) were not affected by HA. TCZ was established at similar temperatures, with the magnitude in regulated water temperature being 7.6 (16.3) °C pre-HA and 5.1 (24.7) °C post-HA (p=0.65). The present findings suggest that heat production and heat loss responses during whole body cooling as well as the skin thermal comfort zone remained unaltered by a controlled-hyperthermia HA protocol.

The Effects of Local NOS‐inhibition and Ascorbate Administration on Cutaneous Vasodilation and Sweating During Exercise‐heat Stress in Adults With and Without Hypertension

Aging is associated with oxidative stress in the skin resulting from an accumulation of radical oxygen species. Hypertension exacerbates oxidative stress, leading to a reduced contribution of nitric oxide (NO) to cutaneous vasodilation during whole‐body passive heat stress. We recently demonstrated that local administration of the non‐selective anti‐oxidant ascorbate did not modify NO‐dependent cutaneous vasodilation and sweating in older adults exercising in the heat (35°C). The effect of ascorbate on those responses in individuals with hypertension, however, remains uncertain. We therefore evaluated the hypothesis that local ascorbate administration improves NO‐dependent cutaneous vasodilation and sweating in adults with hypertension. Middle‐aged adults with (HYPE, mean [SD] age: 60 [5] years; n=7, 5 women) and without (CON, age: 63 [6] years; n=7, 2 women) hypertension performed two 30‐min bouts of cycling in the heat (35°C, 20% RH) at an external work rate eliciting ~50% peak aerobic power. The first (Ex1) and second (Ex2) bouts were separated by a 20‐min recovery. Four skin sites were perfused continuously via microdialysis with either 1) lactated Ringer’s (control site); 2) 10 mM ascorbate (anti‐oxidant treated); 3) 10 mM L‐NAME (NO‐inhibited); or 4) a combination of both agents. Cutaneous vascular conductance (CVC; presented as a % of maximum during sodium nitroprusside administration, CVCmax) and sweat rate were measured at each site. The effect of each treatment (i.e., change from the control site) was evaluated separately within each group. No differences in CVC at the control site were observed between HYPE (Ex1: 68 [20]%CVCmax; Ex2: 74 [25]%CVCmax) and CON (Ex1: 63 [16]%CVCmax; Ex2: 68 [20]%CVCmax; both p&gt;.74). In the HYPE, ascorbate augmented CVC during Ex1 (7 [4]%CVCmax, P=.003) and Ex2 (8 [6]%CVCmax, P=.014‐‐). By contrast, L‐NAME reduced CVC alone (Ex1: −26 [19]%CVCmax; Ex2: −29 [16]%CVCmax; both p&lt;.013) and when administered with ascorbate (Ex1: −19 [15]%CVCmax; Ex2: −19 [14]%CVCmax; both p&lt;.017). In CON, an effect of ascorbate was not observed (Ex1: −5 [20]%CVCmax; Ex2: −11 [21]%CVCmax; both p&gt;.18) and L‐NAME attenuated CVC with (Ex1: −22 [18]%CVCmax; Ex2: −23 [22]%CVCmax; both p&lt;.026) and without ascorbate (Ex1: −24 [14]%CVCmax; Ex2: −22 [23]%CVCmax; both p&lt;.031). Sweat rate was reduced in the HYPE compared to CON group during Ex1 (.39 [15] vs .78 [.31] mg·min−1 ·cm−2; p=.011) and Ex2 (.39 [15] vs .78 [.31] mg·min−1 ·cm−2; p=.011) at the control site. Sweating was not influenced by any treatment in HYPE (all p&gt;.07). In CON, ascorbate augmented sweating during Ex 1 (.14 [.16] mg·min−1 ·cm−2; p=.038) but not Ex2 (.09 [.23] mg·min−1 ·cm−2; p=.31). No effect on sweating was seen at either NO‐inhibited site in CON (all p&gt;.13). Therefore, in individuals with hypertension exercising in the heat, local administration of ascorbate augments NO‐dependent cutaneous vasodilation but not sweating, while in individuals without hypertension, ascorbate did not affect either heat loss response.Support or Funding InformationNatural Sciences and Engineering Research Council of Canada.

Blunted Effects of Elevated Serum Osmolality on Whole‐body Heat Loss and Rectal Temperature in Middle‐aged‐to‐older Men Exercising in Dry Heat

We recently demonstrated that sweating‐induced hypohydration attenuated whole‐body heat loss (via reduced sweat evaporation) in young but not middle‐aged men during exercise‐heat stress. In that work, we reasoned that this divergent response may stem from an attenuated influence of intravascular osmolality (elevated during hypohydration) on heat dissipation in the middle‐aged. This hypothesis is supported by previous studies showing i) increased osmolality attenuates sweating in young adults and ii) fluid‐regulatory responses to osmotic stimuli are blunted with aging. However, the independent effect of intravascular osmolality on whole‐body heat loss and thermal strain in middle‐aged men during exercise has not been directly evaluated. On two separate occasions, six young (25 years [SD 4]) and eight middle‐aged‐to‐older (61 years) men underwent a 90‐min intravenous infusion of either 0.9% saline (200 [5] μmL·min−1·kg−1; ISO) or 3.0% saline (125 μmL·min−1·kg−1; HYP). Participants then performed 60 min of cycling at a fixed metabolic heat production of 250 W·m−2 in dry heat (40ºC, ~15% relative humidity). Serum osmolality and plasma volume responses were determined from venous blood samples procured at baseline (prior to infusion) and end‐exercise (60‐min). Heat production and whole‐body heat loss (evaporative + dry heat loss) were measured via indirect and direct calorimetry, respectively. Rectal temperature was monitored continuously. End‐exercise serum osmolality was elevated in HYP compared to ISO in the young (309 [4] vs 299 [3] mOsm·kg−1; p&lt;.001) and middle‐aged‐to‐older (312 [2] vs 300 [4] mOsm·kg−1; p&lt;.001) men and was similar between age‐groups (both p≥.07). In the young, the reduction in plasma volume from baseline at end‐exercise was greater in ISO relative to HYP (−8 [3] vs −4 [3]%; p=.014). By contrast, no differences in the plasma volume response were detected between ISO and HYP in the older group (−9 [4] vs −4 [6]%; p=.14). Changes in plasma volume were similar between age‐groups in each condition (both p≥.75). Whole‐body heat loss was attenuated in HYP compared to ISO in the young (233 [13] vs 251 [15] W·m−2; p=.012), whereas no effect of osmolality was observed in the middle‐aged‐to‐older men (225 [14] vs 227 [16] W·m−2; p=.74). Further, heat loss was attenuated in the middle‐aged‐to‐older vs young in ISO (p=.017) but was comparable between groups in HYP (p=.26). Similarly, a greater end‐exercise rectal temperature was noted in HYP vs ISO in the young (38.2 [0.3]°C vs 37.9 [0.3] °C; p=.037) but not the middle‐aged‐to‐older men (38.3 [0.3]°C vs 38.3 [0.3]°C; p=.88). The rectal temperature response was greater in the middle‐aged‐to‐older during ISO (p=.013) whereas no difference between age‐groups was observed in HYP (p=.59). Our findings indicate that whole‐body heat loss and rectal temperature responses to exercise in dry‐heat are not appreciably modified by increased serum osmolality in middle‐aged‐to‐older men. An age‐related reduction in osmotic sensitivity may therefore explain the blunted effect of hypohydration on heat loss previously observed in this population.Support or Funding InformationNatural Sciences and Engineering Research Council of Canada.