Heat tolerance and the validity of occupational heat exposure limits in women during moderate-intensity work.

To mitigate excessive rises in core temperature (>1 °C) in non-heat acclimatized workers, the American Conference of Governmental Industrial Hygienists (ACGIH) provides heat stress limits (Action Limit Values; ALV), defined by the wet-bulb globe temperature (WBGT) and a worker's metabolic rate. However, since these limits are based on data from men, their suitability for women remains unclear. We therefore assessed core temperature and heart rate in men (n = 19; body surface area-to-mass ratio: 250 (SD 17) cm2/kg) and women (n = 15; body surface area-to-mass ratio: 268 (SD 24) cm2/kg) aged 18-45 years during 180 min of walking at a moderate metabolic rate (200 W/m2) in WBGTs below (16 and 24 °C) and above (28 and 32 °C) ACGIH ALV. Sex did not significantly influence (i) rises in core temperature, irrespective of WBGT, (ii) the proportion of participants with rises in core temperature >1 °C in environments below ACGIH limits, and (iii) work duration before rises in core temperature exceeded 1 °C or volitional termination in environments above ACGIH limits. Although further studies are needed, these findings indicate that for the purpose of mitigating rises in core temperature exceeding recommended limits (>1 °C), ACGIH guidelines have comparable effectiveness in non-heat acclimatized men and women during moderate-intensity work. Novelty: Sex did not appreciably influence thermal strain nor the proportion of participants with core temperatures exceeding recommended limits. Sex did not significantly influence tolerance to uncompensable heat stress. Despite originating from data obtained in only men, current occupational heat stress guidance offered comparable effectiveness in men and women.

Heat Tolerance and Occupational Heat Exposure Limits in Older Men with and without Type 2 Diabetes or Hypertension.

PURPOSE: To mitigate rises in core temperature >1°C, the American Conference of Governmental Industrial Hygienists (ACGIH) recommends upper limits for heat stress (action limit values [ALV]), defined by wet-bulb globe temperature (WBGT) and a worker's metabolic rate. However, these limits are based on data from young men and are assumed to be suitable for all workers, irrespective of age or health status. We therefore explored the effect of aging, type 2 diabetes (T2D), and hypertension (HTN) on tolerance to prolonged, moderate-intensity work above and below these limits. METHODS: Core temperature and heart rate were assessed in healthy, heat unacclimatized young (18-30 yr, n = 13) and older (50-70 yr) men (n = 14) and heat unacclimatized older men with T2D (n = 10) or HTN (n = 13) during moderate-intensity (metabolic rate: 200 W·m-2) walking for 180 min (or until termination) in environments above (28°C and 32°C WBGT) and below (16°C and 24°C WBGT) the ALV for continuous work at this intensity (25°C WBGT). RESULTS: Work tolerance in the 32°C WBGT was shorter in men with T2D (median [IQR]; 109 [91-173] min; P = 0.041) and HTN (120 [65-170] min; P = 0.010) compared with healthy older men (180 [133-180] min). However, aging, T2D, and HTN did not significantly influence (i) core temperature or heart rate reserve, irrespective of WBGT; (ii) the probability that core temperature exceeded recommended limits (>1°C) under the ALV; and (iii) work duration before core temperature exceeded recommended limits (>1°C) above the ALV. CONCLUSION: These findings demonstrate that T2D and HTN attenuate tolerance to uncompensable heat stress (32°C WBGT); however, these chronic diseases do not significantly impact thermal and cardiovascular strain, or the validity of ACIGH recommendations during moderate-intensity work.

Impact of uncomplicated controlled hypertension on thermoregulation during exercise-heat stress.

Exercise is promoted for management of hypertension and as a general healthy behavior, but environmental conditions are seldom considered in these recommendations. Hypertension may affect skin blood flow and sweating, two of the primary mechanisms which prevent continued elevations in core temperature by facilitating whole-body heat loss during exercise-heat stress. We show that during incremental exercise-heat stress (in hot-dry conditions), controlled and uncomplicated hypertension is unlikely to exert a meaningful effect on whole-body heat loss in individuals who are already physically active.

Type 2 diabetes does not exacerbate body heat storage in older adults during brief, extreme passive heat exposure.

Aging exacerbates hyperthermia and cardiovascular strain during passive heat exposure, but it remains unclear whether those effects worsen in older adults with type 2 diabetes (T2D). We examined these responses in unacclimatized, physically active, older individuals with (n = 13, mean ± SD age: 60 ± 8 years, HbA1c: 7.0 ± 1.0%) and without (Control, n = 30, 62 ± 6 years) well-controlled T2D during a brief, 3-h passive exposure to extreme heat (44°C, 30% relative humidity). Metabolic heat production, dry heat gain, total heat gain (metabolic heat production + dry heat gain), evaporative heat loss, body heat storage (summation of heat gain/loss), rectal and mean skin temperatures as well as heart rate were measured continuously. No between-group differences were observed for metabolic heat production (T2D vs. Control; 53 ± 5 vs. 55 ± 7 W/m2), dry heat gain (48 ± 9 vs. 47 ± 11 W/m2), total heat gain (101 ± 10 vs. 102 ± 14 W/m2) and evaporative heat loss (83 ± 10 vs. 85 ± 12 W/m2) over the 3 h (all P > 0.05). Consequently, the changes in body heat storage (380 ± 93 vs. 358 ± 172 kJ, P = 0.67) were similar between groups. Moreover, no between-group differences in rectal and mean skin temperatures or heart rate were measured. We conclude that unacclimatized, physically active, older adults with well-controlled T2D do not experience greater hyperthermia and cardiovascular strain compared to their healthy counterparts while resting in extreme heat for a brief, 3-h period.

Heart rate variability dynamics during treatment for exertional heat strain when immediate response is not possible.

NEW FINDINGS: What is the central question of this study? Does a delay in cold water immersion treatment affect the cardiac autonomic control of exertionally heat-strained individuals? What is the main finding and its importance? Cold water immersion is effective for treating exertionally heat-strained individuals even when treatment is commenced with a significant delay. However, that treatment delay leads to only partial/transient restoration of cardiac autonomic control. Therefore, we recommend that exertional heatstroke patients are continuously monitored for several hours even after core temperature has returned to normal values. ABSTRACT: Immediate cold water immersion (CWI) is the gold-standard treatment for exertional heatstroke. In the field, however, treatment is often delayed, primarily owing to a delayed paramedic response and/or inaccurate diagnosis. We examined the effect of treatment (reduction of rectal temperature to 37.5°C) delays of 5 (short), 20 (moderate) and 40 (prolonged) min on cardiac autonomic control [as assessed via heart rate variability (HRV)] in eight exertionally heat-strained (40.0°C rectal temperature) individuals. Eleven HRV indices were computed that have been described commonly in the literature and characterize almost all known domains of the variability and complexity of the cardiopulmonary system. We found that the cardiac autonomic control (as assessed via HRV) of exertionally heat-strained individuals was significantly affected by the amount of time it took for the CWI treatment to be applied. Six out of 11 HRV indices studied, from all variability domains, displayed strong (P ≤ 0.005) time × delay interaction effects. Moreover, the number of significantly (P ≤ 0.005) abnormal (i.e. different from the short delay) HRV indices more than doubled (seven versus 15) from the moderate delay to the prolonged delay. Finally, our results demonstrated that a CWI treatment applied with delays of 20 and, primarily, 40 min did not lead to a full restoration of cardiac autonomic control of exertionally heat-strained individuals. In conclusion, this study supports CWI for treating exertionally heat-strained individuals even when applied with prolonged delay, but it highlights the importance of continued cardiac monitoring of patients who have suffered exertional heatstroke for several hours after restoration of core temperature to normal.

Seven days of cold acclimation substantially reduces shivering intensity and increases nonshivering thermogenesis in adult humans.

Daily compensable cold exposure in humans reduces shivering by ~20% without changing total heat production, partly by increasing brown adipose tissue thermogenic capacity and activity. Although acclimation and acclimatization studies have long suggested that daily reductions in core temperature are essential to elicit significant metabolic changes in response to repeated cold exposure, this has never directly been demonstrated. The aim of the present study is to determine whether daily cold-water immersion, resulting in a significant fall in core temperature, can further reduce shivering intensity during mild acute cold exposure. Seven men underwent 1 h of daily cold-water immersion (14°C) for seven consecutive days. Immediately before and following the acclimation protocol, participants underwent a mild cold exposure using a novel skin temperature clamping cold exposure protocol to elicit the same thermogenic rate between trials. Metabolic heat production, shivering intensity, muscle recruitment pattern, and thermal sensation were measured throughout these experimental sessions. Uncompensable cold acclimation reduced total shivering intensity by 36% (P = 0.003), without affecting whole body heat production, double what was previously shown from a 4-wk mild acclimation. This implies that nonshivering thermogenesis increased to supplement the reduction in the thermogenic contribution of shivering. As fuel selection did not change following the 7-day cold acclimation, we suggest that the nonshivering mechanism recruited must rely on a similar fuel mixture to produce this heat. The more significant reductions in shivering intensity compared with a longer mild cold acclimation suggest important differential metabolic responses, resulting from an uncompensable compared with compensable cold acclimation. NEW & NOTEWORTHY Several decades of research have been dedicated to reducing the presence of shivering during cold exposure. The present study aims to determine whether as little as seven consecutive days of cold-water immersion is sufficient to reduce shivering and increase nonshivering thermogenesis. We provide evidence that whole body nonshivering thermogenesis can be increased to offset a reduction in shivering activity to maintain endogenous heat production. This demonstrates that short, but intense cold stimulation can elicit rapid metabolic changes in humans, thereby improving our comfort and ability to perform various motor tasks in the cold. Further research is required to determine the nonshivering processes that are upregulated within this short time period.

Heat Loss Is Impaired in Older Men on the Day after Prolonged Work in the Heat.

PURPOSE: Prolonged work in the heat may exacerbate the rise in core temperature on the next work day, especially in older workers who display impairments in whole-body heat loss that increase body heat storage and core temperature relative to young adults during heat stress. We therefore evaluated whether whole-body heat loss in older adults was impaired on the day after prolonged work in the heat. METHODS: Whole-body heat exchange and heat storage were assessed in nine older (53-64 yr) men during three 30-min bouts of semirecumbent cycling at fixed rates of metabolic heat production (150 [Ex1], 200 [Ex2], 250 W·m [Ex3]), each separated by 15-min recovery, in hot-dry conditions (40°C, 20% relative humidity), immediately before (day 1), and on the day after (day 2) a prolonged, work simulation (~7.5 h) involving moderate-intensity intermittent exercise in hot-dry conditions (38°C, 34% relative humidity). Total heat loss (evaporative ± dry heat exchange) and metabolic heat production were measured using direct and indirect calorimetry, respectively. Body heat storage was quantified as the temporal summation of heat production and loss. RESULTS: Total heat loss (mean ± SD) during Ex1 did not differ between days 1 and 2 (151 ± 15 and 147 ± 14 W·m, respectively; P = 0.27), but was attenuated on day 2 during Ex2 (181 ± 15 W·m) and Ex3 (218 ± 16 W·m) relative to day 1 (192 ± 14 and 230 ± 19 W·m, respectively; both P < 0.01). Consequently, body heat storage throughout the protocol on day 2 (276 ± 114 kJ) was 31% greater than on day 1 (191 ± 87 kJ; P < 0.01). CONCLUSIONS: Prolonged work in the heat causes next-day impairments in whole-body heat loss, which exacerbate heat storage and may elevate the risk of heat injury on the following day in older workers.

Postexercise whole-body sweating increases during muscle metaboreceptor activation in young men.

We assessed the effect of metaboreceptor activation on whole-body evaporative heat loss (WB-EHL) in 12 men (aged 24 ± 4 years) in the early-to-late stages of a 60-min exercise recovery in the heat. Metaboreceptor activation induced by 1-min isometric-handgrip (IHG) exercise followed by 5-min forearm ischemia to trap metabolites increased WB-EHL by 25%-31% and 26%-34% during the ischemic period relative to IHG-only and control (natural recovery only), respectively, throughout recovery. We show that metaboreceptor activation enhances WB-EHL in recovery.

Work Rate during Self-paced Exercise is not Mediated by the Rate of Heat Storage.

PURPOSE: To date, there have been mixed findings on whether greater anticipatory reductions in self-paced exercise intensity in the heat are mediated by early differences in rate of body heat storage. The disparity may be due to an inability to accurately measure minute-to-minute changes in whole-body heat loss. Thus, we evaluated whether early differences in rate of heat storage can mediate exercise intensity during self-paced cycling at a fixed rate of perceived exertion (RPE of 16; hard-to-very-hard work effort) in COOL (15°C), NORMAL (25°C), and HOT (35°C) ambient conditions. METHODS: On separate days, nine endurance-trained cyclists exercised in COOL, NORMAL, and HOT conditions at a fixed RPE until work rate (measured after first 5 min of exercise) decreased to 70% of starting values. Whole-body heat loss and metabolic heat production were measured by direct and indirect calorimetry, respectively. RESULTS: Total exercise time was shorter in HOT (57 ± 20 min) relative to both NORMAL (72 ± 23 min, P = 0.004) and COOL (70 ± 26 min, P = 0.045). Starting work rate was lower in HOT (153 ± 31 W) compared with NORMAL (166 ± 27 W, P = 0.024) and COOL (170 ± 33 W, P = 0.037). Rate of heat storage was similar between conditions during the first 4 min of exercise (all P > 0.05). Thereafter, rate of heat storage was lower in HOT relative to NORMAL and COOL until 30 min of exercise (last common time-point between conditions; all P < 0.05). Further, rate of heat storage was significantly higher in COOL compared with NORMAL at 15 min (P = 0.026) and 20 min (P = 0.020) of exercise. No differences were measured at end exercise. CONCLUSIONS: We show that rate of heat storage does not mediate exercise intensity during self-paced exercise at a fixed RPE in cool to hot ambient conditions.

Does a Prolonged Work Day in the Heat Impair Heat Loss on the Next Day in Young Men?

PURPOSE: Heat strain is known to be exacerbated on the second of consecutive work days. We therefore evaluated whether prolonged work in the heat would impair whole-body heat loss capacity on the next day. METHODS: To evaluate this possibility, we assessed changes in whole-body heat exchange and heat storage in eight young (26 ± 4 yr) men during heat stress tests performed on the same day before (day 1) and on the day after (day 2) a prolonged work simulation. Each heat stress test involved three, 30-min bouts of semirecumbent cycling at fixed rates of metabolic heat production (200 W·m (Ex1), 250 W·m (Ex2), and 300 W·m (Ex3)), each separated by 15-min recovery, under hot, dry conditions (40°C, 20% relative humidity). The work simulation (7.5 h) involved three moderate-intensity intermittent work bouts (2 h), each separated by 30-min rest breaks, under similarly hot, dry conditions (38°C, 34% relative humidity). Total heat loss (evaporative ± dry heat exchange) and metabolic heat production were measured using direct and indirect calorimetry, respectively. Body heat storage was quantified as the temporal summation of heat production and loss. RESULTS: Total heat loss did not differ between days 1 and 2 (P = 0.66) and averaged (mean ± 95% confidence interval) 185 ± 7 W (Ex1), 233 ± 7 W (Ex2), and 261 ± 5 W (Ex3) across test days. Consequently, the change in body heat storage was also similar between days 1 and 2 (P = 0.32), averaging 133 ± 15 kJ (Ex1), 99 ± 16 kJ (Ex2), and 184 ± 15 kJ (Ex3) across test days. CONCLUSIONS: When assessed under controlled laboratory conditions in young men, prolonged work in the heat does not seem to impair whole-body heat loss or exacerbate heat storage on the following day.

Hyperthermia and cardiovascular strain during an extreme heat exposure in young versus older adults.

We examined whether older individuals experience greater levels of hyperthermia and cardiovascular strain during an extreme heat exposure compared to young adults. During a 3-hour extreme heat exposure (44°C, 30% relative humidity), we compared body heat storage, core temperature (rectal, visceral) and cardiovascular (heart rate, cardiac output, mean arterial pressure, limb blood flow) responses of young adults (n = 30, 19-28 years) against those of older adults (n = 30, 55-73 years). Direct calorimetry measured whole-body evaporative and dry heat exchange. Body heat storage was calculated as the temporal summation of heat production (indirect calorimetry) and whole-body heat loss (direct calorimetry) over the exposure period. While both groups gained a similar amount of heat in the first hour, the older adults showed an attenuated increase in evaporative heat loss (p < 0.033) in the first 30-min. Thereafter, the older adults were unable to compensate for a greater rate of heat gain (11 ± 1 ; p < 0.05) with a corresponding increase in evaporative heat loss. Older adults stored more heat (358 ± 173 kJ) relative to their younger (202 ± 92 kJ; p < 0.001) counterparts at the end of the exposure leading to greater elevations in rectal (p = 0.043) and visceral (p = 0.05) temperatures, albeit not clinically significant (rise < 0.5°C). Older adults experienced a reduction in calf blood flow (p < 0.01) with heat stress, yet no differences in cardiac output, blood pressure or heart rate. We conclude, in healthy habitually active individuals, despite no clinically observable cardiovascular or temperature changes, older adults experience greater heat gain and decreased limb perfusion in response to 3-hour heat exposure.

Heart rate variability during high heat stress: a comparison between young and older adults with and without Type 2 diabetes.

We examined whether older individuals with and without Type 2 diabetes (T2D) experience differences in heart rate variability (HRV) during a 3-h exposure to high heat stress compared with young adults. Young (Young; n = 22; 23 ± 3 yr) and older individuals with (T2D; n = 11; 59 ± 9 yr) and without (Older; n = 25; 63 ± 5 yr) T2D were exposed to heat stress (44°C, 30% relative humidity) for 3 h. Fifty-five HRV measures were assessed for 15 min at baseline and at minutes 82.5-97.5 (Mid) and minutes 165-180 (End) during heat stress. When compared with Young, a similar number of HRV indices were significantly different (P < 0.05) in Older (Baseline: 35; Mid: 29; End: 32) and T2D (Baseline: 31; Mid: 30; End: 27). In contrast, the number of HRV indices significantly different (P < 0.05) between Older and T2D were far fewer (Baseline: 13, Mid: 1, End: 3). Within-group analyses demonstrated a greater change in the Young group's HRV during heat stress compared with Older and T2D; the number of significantly different (P < 0.05) HRV indices between baseline and End were 42, 29, and 20, for Young, Older, and T2D, respectively. Analysis of specific HRV domains suggest that the Young group experienced greater sympathetic activity during heat stress compared with Older and T2D. In conclusion, when compared with young, older individuals with and without T2D demonstrate low HRV at baseline and less change in HRV (including an attenuated sympathetic response) during 3 h high heat stress, potentially contributing to impaired thermoregulatory function.

The Influence of Arc-Flash and Fire-Resistant Clothing on Thermoregulation during Exercise in the Heat.

We evaluated the effect of arc-flash and fire-resistant (AFR) clothing ensembles (CE) on whole-body heat dissipation during work in the heat. On 10 occasions, 7 males performed four 15-min cycling bouts at a fixed rate of metabolic heat production (400 W) in the heat (35°C), each separated by 15-min of recovery. Whole-body heat loss and metabolic heat production were measured by direct and indirect calorimetry, respectively. Body heat storage was calculated as the temporal summation of heat production and heat loss. Responses were compared in a semi-nude state and while wearing two CE styles: (1) single-piece (coveralls) and (2) two-piece (workpant + long-sleeve shirt). For group 1, there was one non-AFR single-piece CE (CE1STD) and three single-piece CE with AFR properties (CE2AFR, CE3AFR, CE4AFR). For group 2, there was one non-AFR two-piece CE (CE5STD) and four two-piece CE with AFR properties (CE6AFR, CE7AFR, CE8AFR, CE9AFR). The workpants for CE6AFR were not AFR-rated, while a cotton undershirt was also worn for conditions CE8AFR and CE9AFR and for all single-piece CE. Heat storage for all conditions (CE1STD: 328 ± 55, CE2AFR: 335 ± 87, CE3AFR: 309 ± 95, CE4AFR: 403 ± 104, CE5STD: 253 ± 78, CE6AFR: 268 ± 89, CE7AFR: 302 ± 70, CE8AFR: 360 ± 36, CE9AFR: 381 ± 99 kJ) was greater than the semi-nude state (160 ± 124 kJ) (all p ≤ 0.05). No differences were measured between single-piece uniforms (p = 0.273). Among the two-piece uniforms, heat storage was greater for CE8AFR and CE9AFR relative to CE5STD and CE6AFR (all p ≤ 0.05), but not CE7AFR (both p > 0.05). Differences between clothing styles were measured such that greater heat storage was observed in both CE1STD and CE2-4AFR relative to CE5STD. Further, heat storage was greater in CE2AFR and CE4AFR relative to CE6AFR, while it was greater in CE4AFR compared to CE7AFR. Body heat storage during work in the heat was not influenced by the use of AFR fabrics in the single- or two-piece uniforms albeit less heat was stored in the two-piece uniforms when no undershirt was worn. However, heat storage was comparable between clothing styles when an undershirt was worn with the two-piece uniform.

Temperature of Ingested Water during Exercise Does Not Affect Body Heat Storage.

PURPOSE: The objective of this study was to examine the effect of ingested water temperature on heat balance during exercise as assessed by direct calorimetry. METHODS: Ten healthy males (25 ± 4 yr) cycled at 50% V˙O2peak (equivalent rate of metabolic heat production (M-W) of 523 ± 84 W) for 75 min under thermocomfortable conditions (25°C, 25% relative humidity) while consuming either hot (50°C) or cold (1.5°C) water. Four 3.2 mL·kg⁻¹ boluses of hot or cold water were consumed 5 min before and at 15, 30, and 45 min after the onset of exercise. Total heat loss (HL = evaporative heat loss (HE) ± dry heat exchange (HD)) and M-W were measured by direct and indirect calorimetry, respectively. Change in body heat content (ΔHb) was calculated as the temporal summation of M-W and HL and adjusted for changes in heat transfer from the ingested fluid (Hfluid). RESULTS: The absolute difference for HL (209 ± 81 kJ) was similar to the absolute difference of Hfluid (204 ± 36 kJ) between conditions (P = 0.785). Furthermore, the difference in HL was primarily explained by the corresponding changes in HE (hot: 1538 ± 393 kJ; cold: 1358 ± 330 kJ) because HD was found to be similar between conditions (P = 0.220). Consequently, no difference in ΔHb was observed between the hot (364 ± 152 kJ) and cold (363 ± 134 kJ) conditions (P = 0.971) during exercise. CONCLUSION: We show that ingestion of hot water elicits a greater HL relative to cold water ingestion during exercise. However, this response was only compensated for the heat of the ingested fluid as evidenced by similar ΔHb between conditions. Therefore, our findings indicate that relative to cold water ingestion, consuming hot water does not provide a thermoregulatory advantage. Both hot and cold water ingestion results in the same amount of heat stored during prolonged moderate-intensity exercise.

Whole-body heat exchange during heat acclimation and its decay.

PURPOSE: The purpose of this study was to quantify how much whole-body heat loss increases during heat acclimation and the decay in these improvements after heat acclimation. METHODS: Ten males underwent a 14-d heat acclimation protocol that consisted of 90 min of cycling in the heat (40°C, 20% relative humidity) at approximately 50% of maximum oxygen consumption. Before (day 0), during (day 7), and at the end (day 14) of the heat acclimation protocol as well as 7 and 14 d after heat acclimation (days 21 and 28), whole-body heat exchange (evaporative and dry) was measured using direct calorimetry during three bouts of 30-min exercise at 300 (Ex1), 350 (Ex2), and 400 W·m (Ex3), each separated by 10 and 20 min of recovery, respectively, at 35°C and 16% relative humidity. Concurrent measurements of metabolic heat production (indirect calorimetry) allowed for the direct calculation of change in body heat content (ΔHb). RESULTS: After accounting for an increase in net dry heat gain, increases in whole-body evaporative heat loss were evident for Ex2 and Ex3 on day 7 (Ex2, 4.9 ± 5.6%; Ex3, 9.0 ± 6.0%; both P ≤ 0.05) and all heat loads on day 14 (Ex1, 7.6 ± 8.3%; Ex2, 7.7 ± 5.5%; Ex3, 11.2 ± 4.6%; all P ≤ 0.05) relative to day 0 (Ex1, 494 ± 27 W; Ex2, 583 ± 21 W; Ex3, 622 ± 36 W). As a result, a lower cumulative ΔHb was measured on day 7 (-18 ± 8%, P ≤ 0.001) and day 14 (-26 ± 10%, P ≤ 0.001) compared with that measured on day 0 (1062 ± 123 kJ). Most of these improvements were retained after 2 wk of nonexposure to the heat. CONCLUSIONS: This is the first study to quantify how much 14 d of heat acclimation can increase whole-body evaporative heat loss, which can improve by as much as approximately 11%.

Treatment of exertional heat stress developed during low or moderate physical work.

PURPOSE: We examined whether treatment for exertional heat stress via ice water immersion (IWI) or natural recovery is affected by the intensity of physical work performed and, thus, the time taken to reach hyperthermia. METHODS: Nine adults (18-45 years; 17.9 ± 2.8 percent body fat; 57.0 ± 2.0 mL kg(-1) min(-1) peak oxygen uptake) completed four conditions incorporating either walking or jogging at 40 °C (20 % relative humidity) while wearing a non-permeable rain poncho. Upon reaching 39.5 °C rectal temperature (Tre), participants recovered either via IWI in 2 °C water or via natural recovery (seated in a ~29 °C environment) until T re returned to 38 °C. RESULTS: Cooling rates were greater in the IWI [Tre: 0.24 °C min(-1); esophageal temperature (Tes): 0.24 °C min(-1)] than the natural recovery (Tre and Tes: 0.03 °C min(-1)) conditions (p < 0.001) with no differences between the two moderate and the two low intensity conditions (p > 0.05). Cooling rates for T re and T es were greater in the 39.0-38.5 °C (Tre: 0.19 °C min(-1); Tes: 0.31 °C min(-1)) compared with the 39.5-39.0 °C (Tre: 0.11 °C min(-1); Tes: 0.13 °C min(-1)) period across conditions (p < 0.05). Similar reductions in heart rate and mean arterial pressure were observed during recovery across conditions (p > 0.05), albeit occurred faster during IWI. Percent change in plasma volume at the end of natural recovery and IWI was 5.96 and 9.58%, respectively (p < 0.001). CONCLUSION: The intensity of physical work performed and, thus, the time taken to reach hyperthermia does not affect the effectiveness of either IWI treatment or natural recovery. Therefore, while the path to hyperthermia may be different for each patient, the path to recovery must always be immediate IWI treatment.

Water immersion in the treatment of exertional hyperthermia: physical determinants.

PURPOSE: We examined the effect of differences in body surface area-to-lean body mass ratio (AD/LBM) on core temperature cooling rates during cold water immersion (CWI, 2°C) and temperate water immersion (TWI, 26°C) after exercise-induced hyperthermia. METHODS: Twenty male participants were divided into two groups: high (315.6 ± 7.9 cm·kg, n = 10) and low (275.6 ± 8.6 cm·kg, n = 10) AD/LBM. On two separate occasions, participants ran on a treadmill in the heat (40.0°C, 20% relative humidity) wearing an impermeable rain suit until rectal temperature reached 40.0°C. After exercise, participants were immersed up to the nipples (arms remained out of the water) in either a CWI (2°C) or a TWI (26°C) circulated water bath until rectal temperature returned to 37.5°C. RESULTS: Overall rectal cooling rates were significantly different between experimental groups (high vs low AD/LBM, P = 0.005) and between immersion conditions (CWI vs TWI, P < 0.001). Individuals with a high AD/LBM had an approximately 1.7-fold greater overall rectal cooling rate relative to those with low AD/LBM during both CWI (high: 0.27°C·min ± 0.10°C·min vs low: 0.16°C·min ± 0.10°C·min) and TWI (high: 0.10°C·min ± 0.05°C·min vs low: 0.06°C·min ± 0.02°C·min). Further, the overall rectal cooling rates during CWI were approximately 2.7-fold greater than during TWI for both the high (CWI: 0.27°C·min ± 0.10°C·min vs TWI: 0.10°C·min ± 0.05°C·min) and the low (CWI: 0.16°C·min ± 0.10°C·min vs TWI: 0.06°C·min ± 0.02°C·min) AD/LBM groups. CONCLUSION: We show that individuals with a low AD/LBM have a reduced rectal cooling rate and take longer to cool than those with a high AD/LBM during both CWI and TWI. However, CWI provides the most effective cooling treatment irrespective of physical differences.

Influence of circulating cytokines on prolactin during slow vs. fast exertional heat stress followed by active or passive recovery.

Prolactin (PRL) has been suggested as an indicator of fatigue during exertional heat stress (EHS), given its strong relationship with body core temperature (T(c)); however, the strength of this relationship during different rates of T(c) increase and subsequent recovery is unknown. In addition, given the influence that systemic cytokines, such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α, have on the pituitary gland, it would be of interest to determine the relationship between PRL, IL-6, and TNF-α during EHS. The purpose was to examine the PRL, IL-6, and TNF-α heat stress responses during slow and fast heating and subsequent resting or cold water immersion recovery. On 4 days, nine individuals walked at ≈ 45% (slow heating) or ran at ≈ 65% (fast heating) maximal oxygen consumption on a treadmill in the heat (40°C, 30% relative humidity) until rectal temperature (T(re)) reached 39.5°C (esophageal temperature; fast = 39.41 ± 0.04°C, slow = 39.82 ± 0.09°C). Post-EHS, subjects were either immersed in 2°C water or rested seated until T(re) returned to 38.0°C. Venous blood, analyzed for PRL, IL-6, and TNF-α, was obtained at rest, during exercise (T(re) 38.0, 39.0, 39.5°C), the start of recovery (≈ 5 min after 39.5°C), and subsequent recovery (T(re) 39.0, 38.0°C). IL-6 exhibited myokine properties, given the greater increases with slow heating and lack of increase in TNF-α. A strong temperature-dependent PRL response during slow and fast heating provides additional support for the use of PRL as a peripheral marker of impending fatigue, which is independent of IL-6 and TNF-α cytokine responses.