FRIESEN, BRIAN J.; CARTER, MIKE R.; POIRIER, MARTIN P.; KENNY, GLEN P.
Exertional heat stroke (EHS) is a medical condition that occurs when core temperature exceeds 40.0°C (3,8,32) and can lead to circulatory failure, multiorgan dysfunction, and most commonly central nervous system dysfunction (10). The early recognition of EHS and the rapid on-site cooling of the individual with EHS to a near normal resting core temperature is paramount to their survival and to minimize heat-related injury (3,6,8). Effective cooling modalities in the treatment of EHS must achieve a rectal temperature cooling rate exceeding 0.1°C·min−1–0.2°C·min−1 when cooling begins immediately and should be no less than 0.15°C·min−1 if cooling is delayed (8).
Cold water immersion (CWI) <10°C is considered the gold standard treatment for EHS patients (8), and circulated ice-water immersion (2°C) has been shown to provide some of the highest rectal temperature cooling rates (0.35°C·min−1), especially for the second-degree drop (note: the first and the second-degree cooling rate simply reflect the change in core temperature measured for the first- and the second-degree Celsius drop in core temperature after the start of immersion) in core temperature (0.50°C·min−1) (24). Despite the proven clinical benefits of CWI, Taylor et al. (28) recently showed that temperate water immersion (TWI) at 26°C provided near similar overall core cooling rates to that measured in much cooler water temperature conditions (24), and they concluded on this basis that TWI should be used to reduce the undesirable effects of CWI (i.e., cold shock response and elevated shivering response) while maintaining patient comfort. Although they showed that TWI resulted in esophageal cooling to 37.5°C in less than 3 min, they failed to consider the fact that a significant residual body heat load remained in the visceral organs as evidenced by a correspondingly elevated rectal temperature of approximately 39°C–39.5°C.
It is well established that physical characteristics such as adiposity, lean body mass, body surface area, and body surface area-to-mass ratio (AD/M) influence core cooling responses in previously resting normothermic individuals during CWI (1,2,4,15,16,20,23,29,31). However, it is unclear whether the pattern of response is similar when CWI is used in the treatment of individuals rendered hyperthermic by prolonged exercise in the heat. Some insight may be gleaned by recent reports showing that lean body mass, and not body adiposity, is an important factor affecting cooling rates during CWI (21,22). However, the one study (22) showing that differences in LBM was an important factor in determining core cooling rates in hyperthermic individuals during CWI was based on a comparison between males and females, whereby females demonstrated an approximately 1.7-fold greater rectal cooling rate during CWI relative to their male counterparts despite being matched for AD/M and having a greater body adiposity. In a secondary analysis, a significant correlation (r = 0.70, P = 0.001) was observed between rectal cooling rates and body surface area-to-lean body mass ratio (AD/LBM) when pooled data from male and females were examined. The authors surmised that AD/LBM may be a key factor affecting whole-body cooling rate during the treatment of hyperthermic individuals using water immersion (22).
Therefore, the purpose of this study was to evaluate the effect of differences in AD/LBM on core temperature cooling rates during CWI (2°C) and TWI (26°C) after exercise-induced hyperthermia (end-exercise rectal temperature of 40°C). We evaluated the hypothesis that individuals with a high (315.6 cm2·kg−1) AD/LBM would have greater core cooling rates compared with individuals with a low (275.6 cm2·kg−1) AD/LBM. Furthermore, we examined the hypothesis that core cooling rates during TWI would be lower in comparison with CWI and that CWI would minimize variations in core cooling rates and immersion times attributed to differences in AD/LBM.
The current experimental protocol was approved by the University of Ottawa Health Sciences and Science Research Ethics Board, in accordance with the Declaration of Helsinki. Written informed consent was obtained from all volunteers before their participation in the study.
Twenty adult males (18–35 yr) volunteered for one preliminary and two experimental sessions. Participants were healthy, physically active (exercised for a minimum of 30 min, three times per week at a moderate intensity), nonsmoking, and free of any known cardiovascular, metabolic, and respiratory diseases. During the preliminary session, training history, body height, mass, and density as well as maximum oxygen uptake were determined. Training history was assessed by having the participants quantify their physical activity levels using the quantitative (3 months) and 7-d physical activity recall questionnaires proposed by Kohl et al. (19). Maximum oxygen uptake (V˙O2max) was determined by indirect calorimetry (MOXUS system; Applied Electrochemistry, Pittsburgh, PA) during a progressive incremental treadmill exercise protocol in thermoneutral (22°C, 30% relative humidity) conditions (5). Body height was determined using a stadiometer (model 2391; Detecto, Webb City, MO), whereas body mass was measured using a digital high-performance weighing terminal (IND560; Mettler Toledo Inc., Mississauga, ON, Canada). Body surface area was subsequently calculated from the measurements of body height and mass (9). Body density was measured using the hydrostatic weighing technique and used to calculate body fat percentage (27). Lean body mass was calculated from the difference between body mass and absolute fat mass. Participants were then divided into high (315.6 ± 7.9 cm2·kg−1, n = 10) or low (275.6 ± 8.6 cm2·kg−1, n = 10) body surface area-to-lean body mass ratio (AD/LBM) groups. Participant’s physical characteristics are presented in Table 1.
All experimental sessions were at the same time of day for a given participant and were separated by a minimum of 48 h. The participants were asked to drink 500 mL of water the night before as well as the morning of each experimental session and to limit food consumption 2 h before each experimental session. Participants were asked to refrain from ingesting alcohol, caffeine, and nonsteroidal anti-inflammatory drugs as well as exercising 24 h before experimentation. Upon arrival at the laboratory, participants inserted a temperature probe in their rectum, voided their bladder, and weighed themselves nude. Participants then changed into standardized athletic clothing (shorts and running shoes) and subsequently sat quietly for a 20 min instrumentation period at an ambient room temperature of 23°C. After instrumentation, the participant entered a thermal chamber (Can-Trol Environmental Systems Ltd., Markham, ON, Canada) regulated at 40.0°C, 20% relative humidity where they remained seated, resting for an additional 20 min. Thereafter, participants donned a nylon rain poncho covering the entire upper body and head to minimize evaporative heat loss and accelerate the heating process. Participants were then required to run on a treadmill (Desmo HP, Woodway, Waukesha, WI) at approximately 65% of their predetermined V˙O2max until rectal temperature (Tre) reached 40.0°C or until volitional fatigue.
After the cessation of exercise, participants donned neoprene boots (DuPont, Wilmington, DE) and, after 5 min, were transferred and immersed in an upright seated position with their legs extended to the nipples (arms and hands out of the water for safety reasons) in a circulated water bath (S-110-SL; Whitehall Manufacturing, City of Industry, CA) maintained at either 2°C (CWI) or 26°C (TWI). Participants remained in the water bath until Tre decreased to 37.5°C. Participants were then removed from the water bath and remained in an upright seated posture while they were towel dried. To ensure the safety of each participant, Tre was monitored for 30 min or until Tre returned within 0.5°C of baseline resting values. After the completion of the trial, a nude body weight measurement was completed to assess fluid loss.
Esophageal temperature (Tes) and Tre were measured using general purpose thermocouple temperature probes (Mon-a-therm General Purpose Temperature Probe; Mallinckrodt Medical Inc., St. Louis, MO). The rectal temperature probe was inserted approximately 15 cm past the anal sphincter. The esophageal temperature probe was inserted 40 cm past the entrance of the nostril while the participants sipped water (100–300 mL) through a straw. Skin temperature and dry heat exchange were measured at nine sites using T-type (copper/constantan) thermocouples integrated into heat flow sensors (Concept Engineering, Old Saybrook, CT) attached to the skin with surgical tape (3M™; Transpore™, St. Paul, MN). Mean skin temperature (MTsk) and mean dry heat loss (HD) were subsequently calculated using a nine-point weighting of the regional proportions determined by Hardy and Dubois (13). These were as follows: forehead, 9.39%; upper arm, 9.39%; upper back, 11.75%; chest, 11.75%; lower back, 11.75%; abdomen, 11.75%; quadriceps, 12.75%; hamstring, 12.75%; and front calf, 8.72%. Because the head, chest, upper back, upper arm, and forearm were not entirely immersed during water immersion, they were not used to calculate MTsk and HD (24). As such, the following weightings were used to calculate mean skin temperature (MTsk-im) and dry heat loss (HD-im) during water immersion: lower back, 20.35%; abdomen, 20.35%; quadriceps, 22.09%; hamstring, 22.09%; and front calf, 15.12%. Temperature data were collected using an HP Agilent data acquisition module (model 3497A) at a rate of one sample every 15 s and simultaneously displayed and recorded in spreadsheet format on a personal computer with a LabVIEW software (version 7.0; National Instruments, Austin, TX). Heart rate (HR) was measured continuously using a HR monitor (Model FS1; Polar Electro Oy, Kempele, Finland) in combination with a coded transmitter. HR was recorded every 5 min during the experimental trials. Measurements of nude body weight were obtained before and after each experimental trial using a digital high-performance weighing terminal (IND560; Mettler Toledo Inc.). Results were recorded to the nearest 0.01 kg.
For each trial, Tre, Tes, and MTsk values during the rest period were averaged for the last 5 min. The rates for whole-body heating during exercise [change in (Δ) temperature / exercise time] and core cooling during water immersion (Δ temperature / immersion time) were calculated for both Tre and Tes. The core cooling rates were calculated from start-immersion temperature to end-immersion temperature for both Tre and Tes. In addition, the core cooling rates for the first (start immersion temperature − 1°C) and the second degree Celsius [(start immersion temperature − 1°C) − 1°C] reductions in temperature were also calculated for Tre and Tes. The time to reach a temperature of 39.5°C, 39.0°C, 38.5°C, 38.0°C, and 37.5°C during immersion and the time to reach the nadir after immersion were calculated for Tre and Tes. During the immersion period, MTsk-im and HD-im were calculated in minute averages. Segmental linear regression analysis was conducted to analyze the break point (lag) period (min) at which core temperature (Tre and Tes) decreased after the start of immersion. The two slope method was used using Graph Pad Prism software version 5.0 (GraphPad Software Inc., La Jolla, CA).
All analyses were performed using the Statistical Package for the Social Sciences for Windows (version 20.0; SPSS Inc., Chicago, IL). The physical characteristics of the two experimental groups (high and low AD/LBM) were analyzed using independent-sample t-tests. A 2 × 2 mixed model ANOVA was used to analyze the data between groups (levels: high and low AD/LBM) and between conditions (levels: 2°C and 26°C) for the following dependent variables: core temperatures (Tre and Tes), MTsk, and HR (time points: rest, start exercise, end exercise, start immersion, end immersion, and nadir). Further, exercise and immersion times, weight loss, heating rates (Tre and Tes), cooling rates (overall, the first- and the second-degree decrease in Tre and Tes), segmental regression at the start of immersion, and time to reach Tre and Tes nadir during recovery after immersion were also analyzed using this method. A three-way mixed-model ANOVA was used to analyze MTsk-im and HD-im during the immersion period. The analysis was conducted using the repeated factors of time (i.e., levels: 0, 1, 2, 3, 4, 5, 6 min to last common point at end immersion) and water temperature (levels: 2°C and 26°C) and the nonrepeated factor of AD/LBM (levels: high and low AD/LBM). Similar analysis was conducted with the time to reach a core temperature of 39.5°C, 39.0°C, 38.5°C, 38.0°C, and 37.5°C during immersion for both Tre and Tes. The level of statistical significance was set at 0.05, and an alpha level was adjusted during multiple comparisons to maintain the rate of type I error at 5% during the Holm–Bonferroni post hoc analysis.
By design, there were significant differences between groups for AD/LBM (P < 0.001). There were also significant differences in lean body mass (P = 0.001) and % body fat (P = 0.039) between groups. No differences were found in terms of body mass (P = 0.256), absolute fat mass (P = 0.217), body surface area (P = 0.302), body surface area-to-mass ratio (P = 0.174), or relative maximum oxygen consumption (P = 0.920) between groups (Table 1).
There were no differences between groups or conditions in resting Tre, Tes, MTsk, and HR before the start of exercise (all P > 0.05; Table 2). No differences were observed in the exercise time taken to reach the end-exercise Tre of 40.0°C between groups (P = 0.836) and between conditions (P = 0.638). Exercise times were similar between groups for both the CWI (high AD/LBM: 41.4 ± 10.0 min vs low AD/LBM: 41.9 ± 10.0 min) and the TWI (high AD/LBM: 43.6 ± 6.3 vs low AD/LBM: 41.7 ± 8.5 min) conditions. As such, the rate of Tre increase (heating rate) was similar between groups (P = 0.661) and between conditions (P = 0.432). Similarly, no differences in the rate of Tes was measured between groups (P = 0.933) and between conditions (P = 0.543) (Table 3). Exercise also resulted in similar Tre increases from rest for both groups (P = 0.795) and conditions (P = 0.573). Increases in Tre during the CWI trial were 2.96°C ± 0.34°C versus 3.02°C ± 0.16°C, and increases during the TWI trial were 3.03°C ± 0.38°C versus 3.03°C ± 0.17°C for the high and low AD/LBM groups, respectively. Similarly for Tes, increases in temperature during exercise were similar for both groups (P = 0.595) and conditions (P = 0.678). Increases in Tes during the CWI trial were 3.43°C ± 0.56°C versus 3.12°C ± 0.64°C, and increases during the TWI trial were 3.17°C ± 0.58°C versus 3.24°C ± 0.63°C for the high and low AD/LBM groups, respectively. End-exercise MTsk was similar between groups (P = 0.161) and between conditions (P = 0.700) (Table 2). End-exercise HR was elevated above resting values to a similar magnitude for both groups (P = 0.874) and treatment conditions (P = 0.057) (Table 2).
Core temperature (Tre and Tes) remained significantly elevated above baseline resting levels before the start of immersion. There were no differences in the core temperature response between groups (Tre, P = 0.248; Tes, P = 0.384) and conditions (Tre, P = 0.712; Tes, P = 0.481) at the start of immersion (Table 2). No differences in preimmersion HR were observed between groups (P = 0.742) or treatment conditions (P = 0.209) (Table 2). Water immersion resulted in similar decreases in Tre for both groups (P = 0.243) and conditions (P = 0.845). Decreases in Tre during CWI were 2.50°C ± 0.23°C versus 2.58°C ± 0.19°C, and decreases during TWI were 2.51°C ± 0.34°C versus 2.60°C ± 0.05°C for the high and low AD/LBM groups, respectively. This was expected given that exit temperature was defined as Tre = 37.5°C. However, differences in the decrease in Tes were observed between conditions (P < 0.001) but not between groups (P = 0.627), with a greater Tes decrease observed during CWI. Decreases in Tes during CWI were 4.02°C ± 1.19°C versus 4.12°C ± 0.89°C, whereas decreases during TWI were 2.60°C ± 0.41°C versus 2.76°C ± 0.55°C for the high and low AD/LBM groups, respectively. Immersion times were significantly different between groups (P = 0.001) and treatment conditions (P < 0.001). Immersion times during the 2°C trial were 11.1 ± 5.4 min versus 19.7 ± 7.7 min for the high and low AD/LBM groups, respectively. Further, immersion times during the 26°C trial were 29.3 ± 14.5 min versus 52.1 ± 20.7 min for the high and low AD/LBM groups, respectively. The time (min) taken to cool to a Tre of 39.5°C, 39.0°C, 38.5°C, 38.0°C, and 37.5°C is presented in Figure 1. Responses were significantly different between groups (all P < 0.05) as well as conditions (all P < 0.05), where the time taken to reach the aforementioned temperature points was less during CWI compared with TWI, and individuals with a low AD/LBM took longer to reach all temperature points relative to those with a high AD/LBM.
Overall Tre cooling rates were significantly different between groups (P = 0.005) as well as conditions (P < 0.001). Greater Tre cooling rates were observed during CWI relative to TWI, and individuals with a low AD/LBM had slower overall Tre cooling rates compared with those with a high AD/LBM. Similar differences were observed during the first-degree Tre cooling rates between groups (P = 0.006) as well as conditions (P = 0.001). In contrast, no differences in the second-degree Tre cooling rates were measured between groups (P = 0.136). However, the second-degree Tre cooling rates were different between conditions (P < 0.001), with faster second-degree Tre cooling rates observed during CWI (Table 3).
Overall Tes cooling rates were significantly different between groups (P = 0.002) and conditions (P < 0.001), with faster Tes cooling rates observed during CWI relative to TWI, and individuals with a low AD/LBM had slower overall Tes cooling rates compared with those with a high AD/LBM (Table 3). Further, differences in the first-degree Tes cooling rates were observed between conditions (P < 0.001). Although a difference between groups (P = 0.001) was measured for the CWI condition (P < 0.001), there were no differences between groups for the TWI condition (P = 0.786). Significant differences in the second-degree Tes cooling rates were measured between conditions (P < 0.001), but responses did not differ between groups (P = 0.067).
The break point (lag) period (min) at which Tre started to decrease after the start of immersion was significantly different between groups (P = 0.002), with a greater lag time observed in the low AD/LBM group. However, no differences were found in the lag time at the start of immersion between conditions (P = 0.855). The Tre lag period during CWI was 2.34 ± 2.43 versus 5.85 ± 2.80 min for the high and low AD/LBM groups, respectively. The lag period during TWI was comparable with CWI (3.16 ± 1.55 vs 4.74 ± 2.64 min for high and low AD/LBM groups, respectively). In contrast, no differences in Tes break point were measured between groups (P = 0.163) or conditions (P = 0.935). The Tes lag period during CWI was 0.96 ± 1.48 versus 1.48 ± 0.38 min for the high and low AD/LBM groups, respectively, with similar responses measured in the TWI condition (1.02 ± 0.70 vs 1.48 ± 1.33 min for high and low AD/LBM groups, respectively).
There was no difference in MTsk before the start of immersion between groups (P = 0.760) and conditions (P = 0.177) (Table 2). Reductions in MTsk-im became gradually less as a function of time (P < 0.001), and no differences between groups were observed (P = 0.094). However, differences were found between conditions (P < 0.001) where MTsk-im was lower during CWI after the first minute of immersion.
At the start of immersion, there was a marked increase in HD-im followed by gradual reduction as a function of time throughout the immersion period (P < 0.001). No differences in HD-im were observed between groups (P = 0.826). Conversely, differences in HD-im were found between conditions (P < 0.001), where HD-im was higher during CWI relative to TWI (Fig. 2). When HD-im was averaged for the entire immersion period (minute averages), there were no differences between groups (P = 0.137). However, there were differences between conditions (P < 0.001), where the average HD-im was higher during CWI. The average HD-im for the 2°C trial was 1217.9 ± 406.1 versus 969.6 ± 238.9 W·m−2 for the high and low AD/LBM groups, respectively. Further, the average HD-im during the 26°C trial was 471.8 ± 213.6 versus 392.8 ± 180.5 W·m−2 for the high and low AD/LBM groups, respectively.
No differences in Tre were observed between groups (P = 0.839) and conditions (P = 0.202) at the end of immersion. This was expected given that exit temperature was defined as a Tre of 37.5°C. The corresponding changes in Tes were different between conditions such that Tes at end of immersion during CWI was significantly lower (P < 0.001). However, Tes was similar between groups (P = 0.244) at the end of immersion. HR at the end of immersion was similar between groups (P = 0.387) but was lower during TWI as compared with CWI (P = 0.010) but not different between groups (Table 2).
There were no differences in the Tre nadir after immersion between groups (P = 0.259). However, differences were found between conditions (P < 0.001), and the Tre nadir after CWI was lower (Table 2). Although the Tre nadir between groups was similar, the time (min) to reach the Tre nadir was significantly different between groups (P = 0.037) and conditions (P < 0.001). During both CWI and TWI, the time to reach Tre nadir was greater for the low relative to the high AD/LBM groups. However, the time to reach Tre nadir for both groups was reduced in the TWI condition (CWI: 20.1 ± 7.9 vs 13.9 ± 6.7 min and TWI: 8.3 ± 6.5 vs 4.9 ± 4.8 min). Similarly, Tes nadir was different between conditions (P < 0.001). However, no differences between groups (P = 0.727) were observed.
Changes in body mass as assessed pre- and post-trial were similar between groups (P = 0.346) and conditions (P = 0.284). The change in body mass during the 2°C trial was 1.38 ± 0.31 versus 1.59 ± 0.51 kg for the high and low AD/LBM groups, respectively. A similar magnitude of change was observed during the 26°C trial, where reductions in body mass were 1.53 ± 0.30 versus 1.61 ± 0.34 kg for the high versus low AD/LBM groups, respectively.
In accordance with our hypothesis, we show that AD/LBM influences core cooling rates during both CWI and TWI after exercise-induced hyperthermia (Tre of 40°C). Individuals with a high AD/LBM had an approximately 1.7-fold greater overall rectal cooling rate relative to those individuals with a low AD/LBM during both CWI and TWI. Further, overall rectal cooling rates during CWI were approximately 2.7-fold faster than during TWI for both the high and low AD/LBM groups. Further, the time to reach a rectal temperature of 39.5°C, 39.0°C, 38.5°C, 38.0°C, and 37.5°C was greater in the low versus high AD/LBM group, with CWI producing the fast cooling times for both groups relative to TWI.
Death related to EHS is preventable through early recognition and rapid on-site cooling with CWI (3,6,8). Growing evidence suggests that CWI (i.e., <10°C) is the most efficacious treatment modality for EHS patients (8) with 2°C ice-water immersion yielding some of the highest overall cooling rates, especially for the second-degree decrease in core temperature (24). This treatment modality has a proven clinical track record with 100% survivability if the cooling is initiated within 5 min (7). The effectiveness of CWI is mainly attributed to high levels of conductive and convective heat loss between the skin surface and water, where the colder the water, the greater the skin-water thermal gradient to facilitate heat transfer (24). Despite the proven clinical benefits of CWI, some experts continue to argue against the use of CWI in the treatment of EHS patients (28). The premise of their argument is that when peripheral circulation is viable (patient is not under circulatory collapse), a temperate water bath of approximately 26°C should be used (7,28) because it minimizes patient discomfort and the potential adverse effects (cold shock response, elevated shivering and marked vasoconstriction reducing core cooling rate, cold injury, etc.) associated with CWI while at the same time providing comparable core cooling rates with that of CWI (7,28). Their findings have led to the misguided conclusion that TWI should be used in the treatment of hyperthermic victims.
It is important to note that the evidence in support of the aforementioned argument is primarily based on a study by Taylor et al. (28), who showed that temperate water (26°C) provided similar esophageal cooling rates to that measured in 14°C cold water (0.71°C·min−1 and 0.88°C·min−1 for 26°C and 14°C water immersion, respectively) based on the time it took to reduce esophageal temperature to 37.5°C. However, the authors failed to consider that although esophageal temperature was reduced to 37.5°C in less than 3 min, a significant amount of residual heat remained in the deep visceral organs as evidenced by a corresponding rectal temperature of approximately 39°C–39.5°C at that time (7). From a clinical perspective, using TWI would have a detrimental effect on the survival of EHS patients as the length of time core temperature remains above critical values is the main criteria determining the survival of individuals with EHS (3,14). Our study clearly demonstrates that CWI provides rectal cooling rates that far exceed TWI by approximately 2.7-fold for individuals in both the high and the low AD/LBM groups. This is consistent with the findings of Proulx et al. (24), who reported that rectal cooling rates during 2°C CWI (0.35°C·min−1) were almost two times greater than during water temperatures of 8°C, 14°C, and 20°C (0.19°C·min−1, 0.15°C·min−1, and 0.19°C·min−1, respectively). Further, the overall esophageal cooling rates were significantly greater during CWI as compared with TWI for both the high and the low AD/LBM groups. Our results demonstrate that CWI cools both rectal and esophageal temperature more rapidly than during TWI. From a clinical perspective, a more rapid attenuation of both visceral (represented by rectal temperature) and central nervous system (represented by esophageal temperature) is critical to maximizing the chances of surviving exertional heatstroke (3,12,26,30).
Our results support the suggestion by Lemire et al. (22) that AD/LBM may be an important physical determinant of whole-body cooling rate during water immersion in hyperthermic individuals. This is evidenced by our observation that 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 and TWI. Moreover, we show that differences in AD/LBM are more pronounced with a warmer water immersion temperature because there was an 8.6-min immersion time difference between groups during CWI (11.1 ± 5.4 vs 19.7 ± 7.7 min for high and low AD/LBM, respectively) and a 22.8-min difference between groups during TWI (29.3 ± 14.5 vs 52.1 ± 20.7 min for high and low AD/LBM, respectively). These results provide strong support to the previous suggestions (7) that CWI can minimize variations in core cooling caused by large differences in physical characteristics.
The differences in core temperature cooling rates observed between the high and the low AD/LBM groups can be largely explained by differences in LBM as a significant (∼13 kg) difference in LBM between high (63.29 kg) and low (75.96 kg) groups was observed. It is important to note that there were no differences between groups in body surface area or AD/M. Although an approximately 7% (high: 20.24% ±7.64 % vs 13.26% ± 6.31%) difference in body adiposity was observed between high and low AD/LBM groups, previous studies show that moderate differences in adiposity do not affect core cooling rates in hyperthermic individuals (21,22). Regardless, we show that core cooling rates were greater in the high AD/LBM group despite a greater adiposity. In light of marked differences in LBM between groups, it is likely that differences in core cooling rate between groups are attributed to differences in the residual heat load in muscle. Previous studies show that a significant residual heat load remains in muscle tissue after dynamic exercise in the heat (17,18). For example, Kenny et al. (18) demonstrated that only 53% of the heat stored during 60 min of exercise was dissipated after 60 min of recovery, with most residual heat stored in muscle tissue. This is supported in part by our observation of a greater lag time in the decrease in rectal temperature at the start of immersion in individuals with a low AD/LBM relative to individuals with a high AD/LBM.
The current guidelines of the treatment of EHS patients suggest that cooling modalities must achieve a rectal temperature cooling rate exceeding 0.1°C·min−1–0.2°C·min−1 when cooling begins immediately and should be no less than 0.15°C·min−1 if cooling is delayed (8). Our results suggest that CWI effectively surpasses this standard even in the presence of large physical differences, achieving overall rectal cooling rates of 0.27°C·min−1 and 0.16°C·min−1 for the high and low AD/LBM groups, respectively. On the other hand, rectal cooling rates during TWI were markedly lower at 0.10°C·min−1 and 0.06°C·min−1 for individuals with a high and low AD/LBM, respectively. It is noteworthy that individuals with a high AD/LBM just met the minimum cooling guidelines of 0.1°C·min−1, whereas individuals in the low AD/LBM group fell short of this lower limit. Taken together, our findings clearly demonstrate that TWI cannot provide sufficient cooling to meet the current cooling guidelines for individuals of all body morphologies, especially when treatment is delayed and cooling modalities with higher core cooling rates (0.15°C·min−1) are recommended.
An important consideration when using CWI is ensuring that rectal temperature is measured continuously during the immersion period to prevent excessive overcooling. Previous studies show that there is a marked afterdrop in core temperature after CWI when hyperthermic individuals are immersed in cold water to near resting temperatures (11,24,25). This core temperature afterdrop has been attributed primarily to the fact that the heat lost during immersion is greater than the heat gained during exercise (11,25). Further, there is a delayed response of conductive and convective heat transfer from the periphery to the core during CWI (11). To avoid excessive afterdrop after CWI, safe cooling limits have been proposed, whereby individuals should be removed from the water bath when Tre reaches 38.6°C to ensure the removal of 100% of the heat gained by exercise while reducing the risk of hypothermia (11,25). With respect to the latter, we observed a similar nadir (afterdrop Tre of 36.3°C and 36.0°C for individuals with a high and low AD/LBM, respectively) to that reported by Proulx et al. (24) after 2°C CWI (35.7°C). Thus, we confirm the previous recommendations (11,25) that a similar exit temperature be used irrespective of physical differences.
In summary, we show that individuals with a high AD/LBM had an approximately 1.7-fold greater overall rectal cooling rate compared with those with a low AD/LBM during both CWI and TWI after exercise-induced hyperthermia. Furthermore, overall rectal cooling rates were approximately 2.7-fold greater during CWI compared with TWI for both the high and the low AD/LBM groups. Taken together, 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 for all EHS patients irrespective of physical differences as it minimizes the time patients remain severely hyperthermic.
This research was supported by the Natural Sciences and Engineering Research Council (RGPIN-298159-2009, held by Dr. Glen P. Kenny) and the Leaders Opportunity Fund from the Canada Foundation for Innovation (22529, held by Dr. Glen P. Kenny). Dr. Glen P. Kenny was supported by a University of Ottawa Research Chair Award.
The provision of financial support does not in any way infer or imply endorsement of the research findings by either agency.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
The authors declare no conflict of interest.
The authors thank all of the participants who volunteered for this study as well as Mr. Mark Carlson, Dr. Daniel Gagnon, and Dr. Heather Wright for their technical assistance.
1. Anderson GS. Human morphology and temperature regulation. Int J Biometeorol
. 1999; 43 (3): 99–109.
2. Anderson GS, Ward R, Mekjavic IB. Gender differences in physiological reactions to thermal stress. Eur J Appl Physiol
. 1995; 71 (2–3): 95–101.
3. Armstrong LE, Casa DJ, Millard-Stafford M, Moran DS, Pyne SW, Roberts WO. American College of Sports Medicine Position Stand. Exertional heat illness during training and competition. Med Sci Sports Exerc
. 2007; 39 (3): 556–72.
4. Baker PT, Daniels F Jr. Relationship between skinfold thickness and body cooling for two hours at 15 degrees C. J Appl Physiol
. 1956; 8 (4): 409–16.
5. Canadian Society for Exercise Physiology. Chapter II: determination of aerobic power. In: Certified Fitness Appraiser Resource Manual
. Gloucester, Ontario; 1986, p. 1–32.
6. Casa DJ, Armstrong LE, Kenny GP, O’Connor FG, Huggins RA. Exertional heat stroke: new concepts regarding cause and care. Curr Sports Med Rep
. 2012; 11 (3): 115–23.
7. Casa DJ, Kenny GP, Taylor NA. Immersion treatment for exertional hyperthermia: cold or temperate water? Med Sci Sports Exerc
. 2010; 42 (7): 1246–52.
8. Casa DJ, McDermott BP, Lee EC, Yeargin SW, Armstrong LE, Maresh CM. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev
. 2007; 35 (3): 141–9.
9. Dubois D, Dubois E. Clinical calorimetry. A formula to estimate the approximate surface area if height and weight be known. Arch Int Med
. 1916; 17: 863–71.
10. Epstein Y, Roberts WO. The pathophysiology of heat stroke: an integrative view of the final common pathway. Scan J Med Sci Sports
. 2011; 21 (6): 742–8.
11. Gagnon D, Lemire BB, Casa DJ, Kenny GP. Cold-water immersion and the treatment of hyperthermia: using 38.6 degrees C as a safe rectal temperature cooling limit. J Athl Train
. 2010; 45 (5): 439–44.
12. Gagnon D, Lemire BB, Jay O, Kenny GP. Aural canal, esophageal, and rectal temperatures during exertional heat stress and the subsequent recovery period. J Athl Train
. 2010; 45 (2): 157–63.
13. Hardy JD, Dubois EF. The technique of measuring radiation and convection. J Nutr
. 1938; 15: 461–75.
14. Hubbard RW, Bowers WD, Matthew WT, et al. Rat model of acute heatstroke mortality. J Appl Physiol
. 1977; 42 (6): 809–16.
15. Keatinge WR. The effects of subcutaneous fat and of previous exposure to cold on the body temperature, peripheral blood flow and metabolic rate of men in cold water. J Physiol
. 1960; 153: 166–78.
16. Keatinge WR, Sloan RE. Effect of swimming in cold water on body temperatures of children. J Physiol
. 1972; 226 (2): 55P–6P.
17. Kenny GP, Jay O. Sex differences in postexercise esophageal and muscle tissue temperature response. Am J Physiol
. 2007; 292 (4): R1632–40.
18. Kenny GP, Webb P, Ducharme MB, Reardon FD, Jay O. Calorimetric measurement of postexercise net heat loss and residual body heat storage. Med Sci Sports Exerc
. 2008; 40 (9): 1629–36.
19. Kohl HW, Blair SN, Paffenbarger RS, Macera CA, Kronenfeld JJ. A mail survey of physical activity habits as related to measured physical fitness. Am J Epidemiol
. 1988; 127 (6): 1228–39.
20. Kollias J, Bartlett L, Bergsteinova V, Skinner JS, Buskirk ER, Nicholas WC. Metabolic and thermal responses of women during cooling in water. J Appl Physiol
. 1974; 36: 577–80.
21. Lemire BB, Gagnon D, Jay O, Dorman L, DuCharme MB, Kenny GP. Influence of adiposity on cooling efficiency in hyperthermic individuals. Eur J Appl Physiol
. 2008; 104 (1): 67–74.
22. Lemire BB, Gagnon D, Jay O, Kenny GP. Differences between sexes in rectal cooling rates after exercise-induced hyperthermia. Med Sci Sports Exerc
. 2009; 41 (8): 1633–9.
23. McArdle WD, Magel JR, Gergley TJ, Spina RJ, Toner MM. Thermal adjustment to cold-water exposure in resting men and women. J Appl Physiol
. 1984; 56 (6): 1565–71.
24. Proulx CI, Ducharme MB, Kenny GP. Effect of water temperature on cooling efficiency during hyperthermia in humans. J Appl Physiol
. 2003; 94 (4): 1317–23.
25. Proulx CI, Ducharme MB, Kenny GP. Safe cooling limits from exercise-induced hyperthermia. Eur J Appl Physiol
. 2006; 96 (4): 434–45.
26. Shiraki K, Konda N, Sagawa S. Esophageal and tympanic temperature responses to core blood temperature-changes during hyperthermia. J Appl Physiol
. 1986; 61 (1): 98–102.
27. Siri WE. The gross composition of the body. Adv Biol Med Phys
. 1956; 4: 239–80.
28. Taylor NA, Caldwell JN, Van den Heuvel AM, Patterson MJ. To cool, but not too cool: that is the question—immersion cooling for hyperthermia. Med Sci Sports Exerc
. 2008; 40 (11): 1962–9.
29. Veicsteinas A, Ferretti G, Rennie DW. Superficial shell insulation in resting and exercising men in cold water. J Appl Physiol
. 1982; 52 (6): 1557–64.
30. Whitby JD, Dunkin LJ. Cerebral, oesophageal and nasopharyngeal temperatures. Br J Anaesth
. 1971; 43 (7): 673–6.
31. White MD, Ross WD, Mekjavic IB. Relationship between physique and rectal temperature cooling rate. Undersea Biomed Res
. 1992; 19 (2): 121–30.
32. Yaqub B, Al Deeb S. Heat strokes: aetiopathogenesis, neurological characteristics, treatment and outcome. J Neurol Sci
. 1998; 156 (2): 144–51.