Heat Loss Responses Research Articles

Effect of Human Skin Grafts on Whole-Body Heat Loss During Heat Stress: A Case Study

Studies suggest that the local heat loss responses of sweating and skin blood flow are impaired in burn survivors with skin grafts. However, it is unknown how skin grafts alter whole-body heat exchange during exercise in the heat, particularly when the skin grafts cover a significant fraction of body surface area. PURPOSE: To compare differences in whole-body heat exchange between a burn survivor in which skin grafts represent 75% of body surface area, relative to the average response of 2 control participants matched for age, body composition and fitness. METHODS: One burn survivor, 17 years post injury, and 2 control participants performed 60 min of cycling exercise at a fixed metabolic heat production rate of 400 W in a calorimeter at 35°C, ∼20% relative humidity. Whole-body heat exchange (dry and evaporative) was measured by direct calorimetry, while concurrent indirect calorimetry was used to measure metabolic rate. Core (intestinal pill) and mean skin (non-grafted of controls; grafted of burn survivor) temperatures were measured throughout. RESULTS: Rate of metabolic heat production was similar between controls and burn survivor (394 ± 3 and 419 ± 3 W respectively). However, the maximum rate of total heat loss attained by the burn survivor only represented 67% of the average value attained by controls (253 vs. 379 ± 43 W). A dry heat gain (27 ± 10 W) was observed in the control participants. In contrast, a dry heat loss to the environment was observed in the burn survivor (17 W). Nonetheless, differences in total heat loss were primarily due to a lower evaporative heat loss for the burn survivor, which only represented 53% of the average peak value attained by controls (236 vs. 406 ± 53 W). Consequently, the increase in body heat content during exercise was greater in the burn survivor (663 κJ) compared to controls (224 ± 58 κJ). This was reflected by greater increases in core (1.22°C vs. 0.61 ± 0.19°C) and mean skin (2.05°C vs. 0.48 ± 0.21°C) temperatures for the burn survivor compared to controls. CONCLUSIONS: These data suggest that burn survivors in which skin grafts represent a significant fraction of body surface area are at a greater risk of heat stress during exercise in the heat, particularly due to reduced evaporative heat loss. Supported by NIH GM068865.

The independent effect of sex on whole‐body heat loss during exercise in the heat

Many studies have examined sex-related differences in thermoregulatory responses during exercise. However, no study has clearly established if such differences are due to either physical (body size and composition) or physiological (onset and sensitivity) factors. Therefore, we examined sex-related differences in whole-body heat loss after eliminating confounding differences in physical characteristics. Seven males (M) and 7 females (F, follicular phase), matched for body mass (M: 66.5±5.3, F: 66.1±7.0 kg) and surface area (M: 1.79±0.10, F: 1.76±0.10 m2), performed 90-min of cycling at a metabolic heat production of 500 W (35°C, 20% RH). Whole-body dry and evaporative heat exchange were measured by direct calorimetry. Mean body temperature (Tb) was calculated using the measurements of esophageal and mean skin temperatures. Despite similar rates of metabolic heat production between sexes during exercise (p=0.660), the peak rate of total heat loss attained was significantly lower in females (p≤0.05). These differences were entirely due to a lower evaporative heat loss in females (427±24 vs. 460±35 W, p=0.081), as there were no significant differences in dry heat exchange (−24±18 vs. −32±17 W, p=0.362). There were no significant differences between sexes in the mean Tb onset threshold for evaporative heat loss (p=0.159). However, there was a trend for a greater sensitivity of the evaporative heat loss response in males (642±121 vs. 516±124 W·°C−1, p=0.078). Sex independently modulates the physiological control of whole-body heat loss during exercise in the heat. Support: Natural Sciences and Engineering Research Council (Dr. G.P. Kenny)

Baroreceptors and thermal state modulate metaboreceptor reductions in local heat loss responses

Studies show that activation of muscle metaboreceptors following isometric hand grip exercise (IHG) attenuates local sweating (LSR) and cutaneous vascular conductance (CVC). It is unclear however if: 1) concomitant changes in baroreceptor loading status and/or, 2) the level of thermal stress modulates this response. Twelve males performed 1-min of IHG at 60% of maximal voluntary contraction followed by 2-min of ischemia under simultaneous application of either lower body positive (LBPP, +40 mmHg), negative (LBNP, −20 mmHg) or no pressure (CON). On separate days, trials were repeated under no heat stress (NHS) and heat stress conditions of 0.6°C (MHS) and 1.2°C (HHS) increase in esophageal temperature (Tes). For all heat stress conditions, mean arterial pressure (MAP) remained greater during LBPP (p<0.001), and lower during LBNP (p<0.001) relative to CON during ischemia. Despite differences in baroreceptor loading status, no difference in LSR or CVC were observed under NS and MHS. However, during HHS, LBNP significantly reduced CVC by 16% (p=0.028) and LSR by 7% (p=0.036) relative to CON. In contrast, LBPP significantly elevated CVC by 23% relative to CON (p=0.013), albeit no differences in LSR were observed (p=0.909). These data suggest that baroreceptor loading status can modulate metaboreceptor-mediated changes in local heat loss responses but only under elevated levels of thermal stress (Tes ≥ 1.2°C). Support: Natural Sciences and Engineering Research Council (Dr. G. Kenny)

Hypoxia-induced hypothermia mediated by noradrenaline and nitric oxide in the rostromedial preoptic area

Central nitric oxide (NO) has an important role in hypothermia induced by hypoxia as well as in that elicited by noradrenaline (NA) microinjected into the rostromedial preoptic area (POA) of the hypothalamus. Here, I tested the hypothesis that activation of adrenoceptors and NO in the rostromedial POA is involved in hypoxia-induced hypothermia in urethane–chloralose-anesthetized, neuromuscularly blocked, artificially ventilated rats. Hypoxic ventilation (10% O 2–90% N 2, 5 min) evoked an increase in the tail skin temperature and a decrease in the colonic temperature, though these changes occurred at 30 s to 7 min after returning the rats to ventilation with room air. These responses were eliminated by prior bilateral transection of the carotid sinus nerves, but not by bilateral cervical vagotomy, suggesting the involvement of activated carotid chemoreceptors in the hypoxic ventilation-induced hypothermia. Such responses were also greatly attenuated by the microinjection of an NO synthase (NOS) inhibitor, N G -monomethyl- l -arginine ( l -NMMA, 25 nmol), but not by that of its inactive enantiomer, N G -monomethyl- d -arginine ( d -NMMA, 25 nmol), into the NA-sensitive, hypothermia-inducing site in the rostromedial POA. Pretreatment with the α 1 -adrenoceptor blocker prazosin (50 pmol), but not vehicle saline, also greatly attenuated the hypoxic ventilation-induced heat loss responses. These results suggest that this hypoxia-induced hypothermia was mediated, at least in part, by activation of α 1 -adrenoceptors and NOS in the rostromedial POA.

Exercise-rest cycles do not alter local and whole body heat loss responses

Previous studies have suggested that greater core temperatures during intermittent exercise (Ex) are due to attenuated sweating [upper back sweat rate (SR)] and skin blood flow (SkBF) responses. We evaluated the hypothesis that heat loss is not altered during exercise-rest cycles (ER). Ten male participants randomly performed four 120-min trials: 1) 60-min Ex and 60-min recovery (60ER); 2) 3 × 20-min Ex separated by 20-min recoveries (20ER); 3) 6 × 10-min Ex separated by 10-min recoveries (10ER), or 4) 12 × 5-min Ex separated by 5-min recoveries (5ER). Exercise was performed at a workload of 130 W at 35°C. Whole body heat exchange was determined by direct calorimetry. Core temperature, SR (by ventilated capsule), and SkBF (by laser-doppler) were measured continuously. Evaporative heat loss (EHL) progressively increased with each ER, such that it was significantly greater (P ≤ 0.05) at the end of the last compared with the first Ex for 5ER (299 ± 39 vs. 440 ± 41 W), 10ER (425 ± 51 vs. 519 ± 45 W), and 20ER (515 ± 63 vs. 575 ± 74 W). The slope of the EHL response against esophageal temperature significantly increased from the first to the last Ex within the 10ER (376 ± 56 vs. 445 ± 89 W/°C, P ≤ 0.05) and 20ER (535 ± 85 vs. 588 ± 28 W/°C, P ≤ 0.05) conditions, but not during 5ER (296 ± 96 W/°C vs. 278 ± 95 W/°C, P = 0.237). In contrast, the slope of the SkBF response against esophageal temperature did not significantly change from the first to the last Ex (5ER: 51 ± 23 vs. 54 ± 19%/°C, P = 0.848; 10ER: 53 ± 8 vs. 56 ± 21%/°C, P = 0.786; 20ER: 44 ± 20 vs. 50 ± 27%/°C, P = 0.432). Overall, no differences in body heat content and core temperature were observed. These results suggest that altered local and whole body heat loss responses do not explain the previously observed greater core temperatures during intermittent exercise.

Serotonin release in the preoptic area and anterior hypothalamus is not involved in thermoregulation during low-intensity exercise in a warm environment

The aim of the present study was to assess the response of serotonin (5-hydroxytryptamine; 5-HT) in the preoptic area and anterior hypothalamus (PO/AH) to thermoregulation during exercise in a warm environment. In addition, it was investigated whether a rapid increase in extracellular 5-HT levels in the PO/AH modifies the thermoregulatory response under the same exercise conditions. Rats were made to run for 120 min at 10 m min −1 on a treadmill at the ambient temperature of 30 °C. Body core temperature ( T core) was monitored using a biotelemetry system, and tail skin temperature ( T tail) was simultaneously measured as an index of heat loss response. Microdialysis in combination with HPLC was used to measure concentrations of monoamines in the PO/AH. Both T core and T tail increased during the first 20 min of exercise and remained stable until the end of the exercise period. Low-intensity exercise did not induce any changes in 5-HT release in the PO/AH, although the levels of norepinephrine and dopamine were increased. Moreover, increased extracellular 5-HT by local perfusion of 1 μM citalopram (selective 5-HT reuptake inhibitor; SSRI) in the PO/AH had no effect on the thermoregulatory response during acute low-intensity exercise in a warm environment. These results suggest that enhanced release of only 5-HT in the PO/AH may not intervene thermoregulation during exercise in a warm environment.

Non-thermal modification of heat-loss responses during exercise in humans

This review focuses on the characteristics of heat-loss responses during exercise with respect to non-thermal factors. In addition, the effects of physical training on non-thermal heat-loss responses are discussed. When a subject is already sweating the sweating rate increases at the onset of dynamic exercise without changes in core temperature, while cutaneous vascular conductance (skin blood flow) is temporarily decreased. Although exercise per se does not affect the threshold for the onset of sweating, it is possible that an increase in exercise intensity induces a higher sensitivity of the sweating response. Exercise increases the threshold for cutaneous vasodilation, and at higher exercise intensities, the sensitivity of the skin-blood-flow response decreases. Facilitation of the sweating response with increased exercise intensity may be due to central command, peripheral reflexes in the exercising muscle, and mental stimuli, whereas the attenuation of skin-blood-flow responses with decreased cutaneous vasodilation is related to many non-thermal factors. Most non-thermal factors have negative effects on magnitude of cutaneous vasodilation; however, several of these factors have positive effects on the sweating response. Moreover, thermal and non-thermal factors interact in controlling heat-loss responses, with non-thermal factors having a greater impact until core temperature elevations become significant, after which core temperature primarily would control heat loss. Finally, as with thermally induced sweating responses, physical training seems to also affect sweating responses governed by non-thermal factors.

Is there evidence for nonthermal modulation of whole body heat loss during intermittent exercise?

This study compared the effect of active, passive, and inactive recoveries on whole body evaporative and dry heat loss responses during intermittent exercise at an air temperature of 30 degrees C and a relative humidity of 20%. Nine males performed three 15-min bouts of upright seated cycling at a fixed external workload of 150 W. The exercise bouts were separated by three 15-min recoveries during which participants 1) performed loadless pedaling (active recovery), 2) had their lower limbs passively compressed with inflatable sleeves (passive recovery), or 3) remained upright seated on the cycle ergometer (inactive recovery). Combined direct and indirect calorimetry was employed to measure rates of whole body evaporative heat loss (EHL) and metabolic heat production (M-W). Mean body temperature (T(b)) was calculated from esophageal and mean skin temperatures, and mean arterial pressure (MAP) was measured continuously. Active and passive recoveries both reversed the reduction in MAP associated with inactive recovery (P <or= 0.05). This response was paralleled by greater levels of EHL during active (207 +/- 53 W) and passive recoveries (203 +/- 55 W) compared with the inactive condition (168 +/- 53 W, P <or= 0.05). However, the greater rate of EHL during active recovery was paralleled by a greater M-W (194 +/- 16 W) compared with inactive recovery (149 +/- 27 W, P <or= 0.001). In contrast, M-W during passive recovery (139 +/- 20 W) was not significantly different from the inactive condition (P = 0.468). Furthermore, there were no differences in T(b) between inactive and passive conditions during the recovery periods (P = 0.820). As such, passive recovery resulted in greater levels of EHL for a given change in T(b) compared with inactive recovery (P <or= 0.05). These results strongly suggest that the progressive increase in core temperature during successive exercise/rest cycles is primarily the result of a baroreflex-mediated attenuation of postexercise whole body evaporative heat loss.

The Influence of Baroreceptor Loading Status on Muscle Metaboreceptor Modulation of Heat Loss Responses

Muscle metaboreceptors have been shown to have a profound effect on the control of the local heat loss responses of sweating (LSR) and skin blood flow (SkBF). Under experimental conditions which employ the ischemic isometric hand-grip exercise (IHG) model, muscle metaboreceptors tend to reduce active vasodilation and attenuate sweating. However, it remains unclear if non-pharmacologically-induced changes in baroreceptor status may mitigate this response. PURPOSE: To evaluate the influence of baroreceptor loading status on LSR and SkBF during postexercise ischemia. METHODS: Seven physically active males (19-24 years) completed two experimental trials under a normothermic (NS) and hyperthermic (whole-body warming, HS) state. Subjects performed 1-min of IHG exercise at 60% of their maximal voluntary contraction followed by 2-min of ischemia under simultaneous lower body positive pressure (LBPP, +40 mm Hg), negative pressure (LBNP, -20 mm Hg) and no pressure (CON). The sequence of these conditions was performed in random order with a 20-min recovery period between conditions to minimize muscular fatigue. RESULTS: No significant differences were observed during baseline rest or at the end of the IHG exercise. Under both NS and HS, mean arterial pressure (MAP) was increased above baseline resting during ischemia. However, the magnitude of increase in MAP was greater during LBPP for both NS (p<0.001) and HS (p<0.002), but lower during LBNP (p<0.028) under HS relative to CON. Despite differences in baroreceptor loading status under NS, no significant difference in LSR or SkBF were observed. In HS, no differences in SkBF were measured between CON and LBPP. However, SkBF response during ischemia was significantly reduced during LBNP as compared to CON (p=0.015) and LBPP (p=0.023). No differences in LSR were observed between CON and LBNP during ischemia. However, a marked reduction in LSR was measured in LBPP relative to CON (p=0.024) but not LBNP (p=0.092). CONCLUSIONS: These results suggest that baroreceptor loading status can mitigate muscle metaboreceptor-induced changes in local heat loss responses. However, this only appears to occur in a hyperthermic state. Funding support from the Natural Sciences and Engineering Research Council of Canada (held by Dr. G. Kenny).

Effects of Type 2 Diabetes on Body Heat Storage During Exercise in the Heat

Type 2 diabetes (T2DM) is associated with metabolic, cardiovascular, and neurological dysfunctions which may impair thermoregulatory mechanisms during heat exposure escalating the risk of heat-related illnesses and injuries. The risks may be greater where these individuals perform exercise in hot environments, as the ability to maintain core temperature during heat stress becomes compromised. PURPOSE: To examine the effects of diabetes-related decreases in local heat loss responses of skin blood flow (SkBF) and sweating (LSR) on the rates of whole-body evaporative and dry heat loss and change in body heat content (DHb) during and following exercise performed under heat stress. METHODS: Fourteen adults age 45 to 65 years with (n=7) and without (n=7, CON) T2DM (>5 years duration) were matched for age, fitness, body fat, and body surface area/mass ratio. Participants cycled for 60-min at a constant rate of heat production of ∼325 W (∼56% VO2peak) followed by 60-min of recovery in a whole-body direct calorimeter at 24°C (temperate) and 30°C (hot) ambient conditions. Rectal temperature (Tre), LSR and SkBF were measured continuously. RESULTS: After 60-min exercise, average DHb was similar between groups at 24°C (+266±72 kJ and +247±44 kJ for CON and T2DM) and 30°C (+260±72 kJ and +248±30 kJ for CON and T2DM). Similar increases in whole-body heat loss, Tre, LSR and SkBF were also found. No differences in the DHb was measured between groups during the 60-min recovery (24°C: -129±66 kJ and -156±41 kJ; 30°C: -111±48 kJ and -123±38 kJ for CON and T2DM). A net positive DHb remained at end of recovery for both groups under both ambient conditions (p<0.05). This was paralleled by a sustained elevation in Tre in both groups at the 30°C ambient condition only (0.18±0.18°C and 0.21±0.08°C for CON and T2DM; p<0.05). No group differences in whole-body or local (LSR and SkBF) responses were observed. CONCLUSION: Despite previous suggestions of an impaired thermoregulatory response during heat exposure in T2DM, no differences were observed in whole-body heat loss and DHb during exercise performed in temperate or hot ambient conditions relative to matched-controls. Further studies are required to examine these responses under greater levels of thermal stress. Funding support: Natural Sciences and Engineering Research Council of Canada.

Short-term exercise training does not improve whole-body heat loss when rate of metabolic heat production is considered

We evaluated the effects of an 8-week exercise training program in previously sedentary individuals on whole-body heat balance during exercise at a constant rate of metabolic heat production. Prior to and after 8 weeks of training, ten participants performed 60-min of cycling exercise at a constant rate of heat production (approximately 450 W) followed by 60-min of recovery, at 30 degrees C and 15% relative humidity. Rate of total heat loss was measured directly by whole-body calorimetry, while rate of metabolic heat production was measured simultaneously by indirect calorimetry. Esophageal (T(es)), skin blood flow (SkBF) and local sweat rate (LSR) were also measured continuously. The 8-week exercise training program elicited a 10% increase in maximal aerobic capacity (P < 0.001). Furthermore, exercise training reduced (P <or= 0.05) baseline (37.10 +/- 0.28 vs. 36.95 +/- 0.24 degrees C) and end-exercise (37.85 +/- 0.30 vs. 37.55 +/- 0.20 degrees C) values for T (es) as well as onset thresholds for LSR (37.23 +/- 0.26 vs. 36.96 +/- 0.22 degrees C, P < 0.001) and SkBF (37.16 +/- 0.38 vs. 36.83 +/- 0.26 degrees C, P < 0.001). However, these improvements in thermoregulatory function did not translate into a greater rate of total heat loss between the pre- and post-training exercise trials (P = 0.762). Furthermore, there were no differences in SkBF (P = 0.546) and LSR (P = 0.475) from pre- to post-training. Although physical training resulted in significant improvements of cardiorespiratory and thermoregulatory functions, these adaptations did not improve whole-body and local heat loss responses during exercise performed at a given rate of metabolic heat production.

Human thermoregulation: separating thermal and nonthermal effects on heat loss

Human thermoregulatory control during heat stress has been studied at rest, during exercise and more recently during exercise recovery. Heat balance in the body is maintained by changes in the rate of heat loss via adjustments in skin blood flow and sweating. Independent of thermal control, the actions of nonthermal factors have important consequences in the control of heat loss responses during and following exercise. While the effect of these nonthermal factors is largely considered to be an inhibitory or excitatory stimulus which displaces the set-point about which temperature is regulated, their effects on human thermoregulatory control are far reaching. Many factors can affect the relative contribution of thermal and nonthermal influences to heat balance including exercise intensity, hemodynamic status, and the level of hyperthermia imposed. This review will characterize the physiological responses associated with heat stress and discuss the thermal and nonthermal influences on sweating and skin blood flow in humans. Further, recent calorimetric evidence for the understanding of thermal and nonthermal contributions to human heat balance will also be discussed.

Nitric oxide mediates noradrenaline-induced hypothermic responses and opposes prostaglandin E 2-induced fever in the rostromedial preoptic area

Noradrenaline (NA) microinjected into the rostromedial preoptic area (POA) elicits heat loss responses and opposes prostaglandin E 2-induced fever. Here, I tested the hypothesis that local synthesis and release of nitric oxide (NO) mediates the NA-induced effects. The unilateral microinjection of the NO donor sodium nitroprusside (SNP, 8.4 nmol), but not that of saline solution, into the NA-sensitive site elicited an increase in tail skin temperature and decreases in the whole-body O 2 consumption rate, heart rate, and colonic temperature simultaneously in urethane–chloralose-anesthetized rats. Pretreatment with SNP greatly attenuated the thermogenic, tachycardic, and hyperthermic effects of prostaglandin E 2 (140 fmol) microinjected into the same site. Furthermore, the NA-induced hypothermic responses were largely blocked by a prior microinjection of an NO synthase inhibitor N G-monomethyl- l-arginine ( l-NMMA, 5 nmol), but not by that of its inactive enantiomer, N G-monomethyl- d-arginine ( d-NMMA, 5 nmol), at the same site. These results suggest that the hypothermic and antipyretic effects of NA are mediated by NO in the rostromedial POA.

Influence of nonthermal baroreceptor modulation of heat loss responses during uncompensable heat stress

We evaluated the hypothesis that with increasing levels of hyperthermia, thermal influences would predominate over nonthermal baroreceptor control of cutaneous vascular conductance (CVC) and local sweat rate (LSR). On separate days, eight male participants were positioned in either an upright seated posture (URS) or a 15 degrees head-down tilt (HDT) posture in a thermoneutral condition and during passive heating, until mean body temperature (T(body)) increased by 1.5 degrees C. Hemodynamic [heart rate (HR), cardiac output, mean arterial pressure (MAP)] and thermal responses [T(re), CVC, LSR] were measured continuously. MAP showed a gradual decrease in the early- to mid-stages of heating for both HDT and URS. At a T(body) > 0.6 degrees C, MAP achieved a stable, albeit reduced level from baseline resting for the duration of the heating, whereas MAP decreased significantly throughout the heating period in the URS position (p < 0.001). CVC increased rapidly in the early stages of heating and achieved a stable elevated level in both HDT and URS at the mid-stage of heating (T(body) increase <or= 0.45 degrees C) for the duration of the heating period (i.e., to a T(body) increase of 1.5 degrees C). A similar pattern of response was observed in LSR. A rapid increase in LSR was observed in the early- to mid-stages of heating (T(body) increase <or= 0.75 degrees C), followed by a slower increase until the end of heating. Responses were similar between conditions. We conclude that despite a significant nonthermal drive, as evidenced by a significant difference in MAP between conditions in the late stages of heating, the thermoeffector activity governing CVC and LSR responses are primarily modulated by thermal input.

Heat loss responses and blockade of prostaglandin E2-induced thermogenesis elicited by α1-adrenergic activation in the rostromedial preoptic area

The unilateral microinjection of noradrenaline (NA), but not vehicle solution, into the rostromedial preoptic area (POA) elicited simultaneous increases in cutaneous temperatures of the tail and sole of the foot and decreases in the whole-body O2 consumption rate, heart rate, and colonic temperature in urethane–chloralose-anesthetized rats, suggesting a coordinate increase in heat loss and decrease in heat production. The magnitude of these responses increased dose-dependently over the range of 1–100 pmol, except for the metabolic and bradycardic responses. Similar hypothermic responses were elicited by the microinjection of 40 pmol methoxamine (an α1-adrenergic agonist), but not by that of clonidine (an α2-agonist) or isoproterenol (a β-agonist). Sites at which microinjection of NA elicited hypothermic responses were in the vicinity of the organum vasculosum of the lamina terminalis including the median preoptic nucleus, whereas no thermal or metabolic response was elicited when NA was microinjected into the lateral POA or caudal part of the medial POA. The microinjection of 130 fmol prostaglandin (PG) E2 into the NA-sensitive site always elicited thermogenic, tachycardic, and hyperthermic responses. Furthermore, the PGE2-induced febrile responses were greatly attenuated by prior administration of NA at the same site. These results demonstrate that NA in the rostromedial POA exerts α1-adrenoceptor-mediated hypothermic effects and opposes PGE2-induced fever.

Cutaneous Vasodilation Response to a Linear Increase in Air Temperature from 28°C to 40°C in Prepubertal Boys and Young Men

The cutaneous vasodilation and sweating responses of prepubertal children to heat stress were examined. Seven prepubertal boys (9-11 years old) and 9 young men (20-24 years old) were seated wearing only swimming trunks while the air temperature (T(a)) was linearly increased from 28 degrees C to 40 degrees C over 50 min and then maintained at 40 degrees C for an additional 10 min. Skin temperature, cutaneous vascular conductance (CVC), and local sweating rate (m(sw)) were measured at multiple sites on the body. The boys had a significantly greater mean surface area-to-mass ratio compared with the young men. The rectal temperature did not change in either group with increasing T(a), although it was significantly higher in the boys. During the first half of the exposure period, when T(a) was less than the mean skin temperature (T(sk)), the boys had significantly higher CVC on the chest and significantly lower m(sw) on the chest and thigh as compared with the young men. During the latter half of the exposure, when heat stress was increased as T(a) exceeded mean T(sk), the boys had significantly higher mean T(sk), greater CVC on the chest and finger, greater rate of increase in the CVC on the forehead and finger, lower m(sw) on the chest and thigh, greater increase in heart rate, and higher thermal sensation. The mean body temperature at the onset of sweating was significantly greater in the boys than in the men. These results suggest that, compared with young men, prepubertal boys manifest greater physiological and perceptual strain under heat stress induced by T(a) exceeding mean T(sk), which is most probably attributable to a combination of lower evaporative heat loss, as evidenced by lower m(sw), and greater heat gain owing to a larger surface area-to-mass ratio. The maturation-related differences in heat loss responses vary according to body site.

Enhanced heat loss responses induced by short‐term endurance training in exercising women

We investigated the effects of short-term endurance training and detraining on sweating and cutaneous vasodilatation during exercise in young women, taking into account changes in maximal oxygen uptake (VO2max) and the phase of the menstrual cycle. Eleven untrained women participated in endurance training; cycle exercise at approximately 60% VO2max for 60 min day(-1), 4-5 days week(-1) (30 degrees C, 45% relative humidity) for three complete menstrual cycles. The standard exercise test consisted of exercise at 50% VO2max for 30 min (25 degrees C, 45% relative humidity), and was conducted before training (Pre), during training sessions (T1, T2 and T3) and after cessation of training (D1 and D2). Values of VO2max increased significantly from 32.7 +/- 1.2 to 37.8 +/- 1.2 ml min(-1) kg(-1) at the end of the training. Local sweat rate in the chest and thigh, but not in the back and forearm, were significantly greater during T1 and T2 only in women who started training from the midfollicular phase. Cutaneous blood flow did not change with training. The threshold oesophageal temperatures for heat loss responses were significantly decreased during T1 versus Pre (averaged values for each body site: sweating, 37.49 +/- 0.08 versus 37.22 +/- 0.12 degrees C; and cutaneous vasodilatation, 37.40 +/- 0.07 versus 37.17 +/- 0.10 degrees C) and maintained through T3; the sensitivities of heat loss responses were not altered. These changes returned to the Pre level by D1. Our data indicate that physical training improves heat loss responses by decreasing the threshold temperatures and that these effects occur within a month of training and disappear within a month after cessation of training. The degree of increase in sweating with training differs among body sites and might be affected by the phase of the menstrual cycle.

Calorimetric Measurement of Postexercise Net Heat Loss and Residual Body Heat Storage

Previous studies have shown a rapid reduction in postexercise local sweating and blood flow despite elevated core temperatures. However, local heat loss responses do not illustrate how much whole-body heat dissipation is reduced, and core temperature measurements do not accurately represent the magnitude of residual body heat storage. Whole-body evaporative (H(E)) and dry (H(D)) heat loss as well as changes in body heat content (DeltaH(b)) were measured using simultaneous direct whole-body and indirect calorimetry. Eight participants cycled for 60 min at an external work rate of 70 W followed by 60 min of recovery in a calorimeter at 30 degrees C and 30% relative humidity. Core temperature was measured in the esophagus (T(es)), rectum (T(re)), and aural canal (T(au)). Regional muscle temperature was measured in the vastus lateralis (T(vl)), triceps brachii (T(tb)), and upper trapezius (T(ut)). After 60 min of exercise, average DeltaH(b) was +273 +/- 57 kJ, paralleled by increases in T(es), T(re), and T(au) of 0.84 +/- 0.49, 0.67 +/- 0.36, and 0.83 +/- 0.53 degrees C, respectively, and increases in T(vl), T(tb), and T(ut) of 2.43 +/- 0.60, 2.20 +/- 0.64, and 0.80 +/- 0.20 degrees C, respectively. After a 10-min recovery, metabolic heat production returned to pre-exercise levels, and H(E) was only 22.9 +/- 6.9% of the end-exercise value despite elevations in all core temperatures. After a 60-min recovery, DeltaH(b) was +129 +/- 58 kJ paralleled by elevations of T(es) = 0.19 +/- 0.13 degrees C, T(re) = 0.20 +/- 0.03 degrees C, T(au) = 0.18 +/- 0.04 degrees C, Tvl = 1.00 +/- 0.43 degrees C, T(tb) = 0.92 +/- 0.46 degrees C, and T(ut) = 0.31 +/- 0.27 degrees C. Despite this, H(E) returned to preexercise levels. Only minimal changes in H(D) occurred throughout. We confirm a rapid reduction in postexercise whole-body heat dissipation by evaporation despite elevated core temperatures. Consequently, only 53% of the heat stored during 60 min of exercise was dissipated after 60 min of recovery, with the majority of residual heat stored in muscle tissue.

Menstrual cycle and oral contraceptive use do not modify postexercise heat loss responses

It is unknown whether menstrual cycle or oral contraceptive (OC) use influences nonthermal control of postexercise heat loss responses. We evaluated the effect of menstrual cycle and OC use on the activation of heat loss responses during a passive heating protocol performed pre- and postexercise. Women without OC (n = 8) underwent pre- and postexercise passive heating during the early follicular phase (FP) and midluteal phase (LP). Women with OC (n = 8) underwent testing during the active pill consumption (high exogenous hormone phase, HH) and placebo (low exogenous hormone phase, LH) weeks. After a 60-min habituation at 26 degrees C, subjects donned a liquid conditioned suit. Mean skin temperature was clamped at approximately 32.5 degrees C for approximately 15 min and then gradually increased, and the absolute esophageal temperature at which the onset of forearm vasodilation (Th(vd)) and upper back sweating (Th(sw)) were noted. Subjects then cycled for 30 min at 75% Vo(2 peak) followed by a 15-min seated recovery. A second passive heating was then performed to establish postexercise values for Th(vd) and Th(sw). Between 2 and 15 min postexercise, mean arterial pressure (MAP) remained significantly below baseline (P < 0.05) by 10 +/- 1 and 11 +/- 1 mmHg for the FP/LH and LP/HH, respectively. MAP was not different between cycle phases. During LP/HH, Th(vd) was 0.16 +/- 0.24 degrees C greater than FP/LH preexercise (P = 0.020) and 0.15 +/- 0.23 degrees C greater than FP/LH postexercise (P = 0.017). During LP/HH, Th(sw) was 0.17 +/- 0.23 degrees C greater than FP/LH preexercise (P = 0.016) and 0.18 +/- 0.16 degrees C greater than FP/LH postexercise (P = 0.001). Postexercise thresholds were significantly greater (P < or = 0.001) than preexercise during both FP/LH (Th(vd), 0.22 +/- 0.03 degrees C; Th(sw), 0.13 +/- 0.03 degrees C) and LP/HH (Th(vd), 0.21 +/- 0.03 degrees C; Th(sw), 0.14 +/- 0.03 degrees C); however, the effect of exercise was similar between LP/HH and FP/LH. No effect of OC use was observed. We conclude that neither menstrual cycle nor OC use modifies the magnitude of the postexercise elevation in Th(vd) and Th(sw).

Can supine recovery mitigate the exercise intensity dependent attenuation of post-exercise heat loss responses?

Cutaneous vascular conductance (CVC) and sweat rate are subject to non-thermal baroreflex-mediated attenuation post-exercise. Various recovery modalities have been effective in attenuating these decreases in CVC and sweat rate post-exercise. However, the interaction of recovery posture and preceding exercise intensity on post-exercise thermoregulation remains unresolved. We evaluated the combined effect of supine recovery and exercise intensity on post-exercise cardiovascular and thermal responses relative to an upright seated posture. Seven females performed 15 min of cycling ergometry at low- (LIE, 55% maximal oxygen consumption) or high-(HIE, 85% maximal oxygen consumption) intensity followed by 60 min of recovery in either an upright seated or supine posture. Esophageal temperature, CVC, sweat rate, cardiac output, stroke volume, heart rate, total peripheral resistance, and mean arterial pressure (MAP) were measured at baseline, at end-exercise, and at 2, 5, 12, 20, and every 10 min thereafter until the end of recovery. MAP and stroke volume were maintained during supine recovery to a greater extent relative to an upright seated recovery following HIE (p <or= 0.05) and were paralleled by an elevated CVC and sweat rate response (p <or= 0.05). A significantly lower esophageal temperature was subsequently observed when supine throughout recovery (p <or= 0.05). Although we observed a reflex bradycardia and increased stoke volume with supine recovery following LIE, no differences were observed for MAP, CVC, sweat rate or esophageal temperature. Supine recovery attenuates the post-exercise reductions in MAP, CVC, and sweat rate in a manner dependent directly on exercise intensity. This effect is likely attributable to a non-thermal baroreceptor mechanism.