Sensitivity and specificity of using exercise heart rate in a thermoneutral environment to predict heat tolerance status.

OBJECTIVES: Following heat illness, a return to activity may require passing a heat tolerance test (HTT). However, there are several logistical limitations to the widespread use of the HTT. Thus, it would be advantageous to develop a test that could be conducted in a thermoneutral (~22°C) environment to predict heat tolerance status. The purpose of the current study was to determine the sensitivity and specificity of using the criteria of a heart rate (HR) ≥130 bpm following 30 min of thermoneutral exercise in detecting heat-intolerant and heat-tolerant individuals. MATERIAL AND METHODS: Sixty-five subjects visited the lab on 3 separate days. The first visit consisted of completing a maximal oxygen uptake (VO2 max) test to assess cardiovascular fitness. For lab visits 2 and 3, subjects randomly completed a 2-hour walking treadmill test in either a hot (40°C, 40% relative humidity [RH]) or thermoneutral (22°C, 40% RH) environment. RESULTS: Forty-eight subjects were classified as heat-intolerant and 17 subjects as heat-tolerant. Using the criterion of a HR ≥130 bpm at 30 min of exercise in the thermoneutral environment, specificity (54%) and sensitivity (100%) of passing the HTT was calculated. Secondary analysis using multiple regression revealed 3 significant variables for predicting ending HR during the HTT. They were: 1) absolute VO2 max (l/min), 2) age, and 3) HR at 30 min of exercise during thermoneutral exercise. CONCLUSIONS: Exercise in a thermoneutral environment had a positive predictive value of 100%, thus, if a subject has a HR ≥130 bpm at 30 min of exercise in a thermoneutral environment, they are very likely to fail a subsequent 2-hour HTT in the heat and be classified as heat-intolerant. Therefore, prior screening has the potential to save time and money, along with providing safety to a heat-intolerant subject. Int J Occup Med Environ Health. 2023;36(2):192-200.

The effect of heat acclimation on the sweat lactate concentration vs. sweat rate relationship.

It is well known that there is a high concentration of lactate in sweat. Interest in measuring sweat lactate has arisen from its potential role in several clinical and sport performance applications. However, the effect of heat acclimation on sweat lactate concentration is still under debate. This is partly because sweat lactate concentration is greatly affected by sweat rate, which is known to increase during heat acclimation. Thus, to better understand this issue it is necessary to account for sweat rate - which has not been done previously in the literature. Therefore, the purpose of the current study was to determine the effect of heat acclimation on the relationship between sweat rate vs. sweat lactate concentration. Six subjects completed a 7-day heat acclimation protocol. The daily 2-h exercise bout was split into three 40-min intervals with exercise intensity increasing with each successive interval. This was done to induce three different sweat rates to determine the sweat rate vs. sweat lactate concentration relationship before and after heat acclimation for each participant. A 2 (heat acclimation) x 3 (sweat rate) repeated measures ANOVA was conducted to determine statistical significance. There was a significant (p < 0.05) decrease in the grand mean sweat lactate concentration over the course of seven days of heat acclimation from 17.0 ± 5.0 to 11.3 ± 1.1 mmol/L (p < 0.05). A significant (p < 0.05) heat acclimation x sweat rate ordinal interaction was also found. The results of the current study show that heat acclimation significantly decreases the sweat lactate concentration. In addition, there was a significant ordinal interaction which suggests that the impact of sweat rate on sweat lactate concentration is decreased following heat acclimation.

Type 1 diabetes mellitus diagnosis in young adult preceded by years of elevated postprandial and fasting glucose but normal HbA1c: A clinical example of discordance.

Herein, a case study of an individual with fasting blood glucose (FBG), glycosylated hemoglobin (HbA1c), and postprandial blood glucose (PBG) measures from the 3 years preceding their type 1 diabetes mellitus diagnosis is used to highlight discordance among these common diagnostic tests. Data from the patient's own records, participation in clinical research, and healthcare provider were collated. Measures of FBG (90-160 mg/dL) and PBG (195-247 mg/dL) were elevated for 3 years with a normal HbA1c (5.0-5.4%) and without any symptoms. Overt symptoms, including polyuria, polydipsia, and unexplained weight loss, manifested 3 years later prompting the patient to contact their physician. Testing revealed an elevated HbA1c (9.8%) and presence of glutamic acid decarboxylase autoantibodies (GAD) (9 IU/mL). Daily body composition measures and weighed food logs from the 3 months preceding and 4 months after diagnosis illustrate the effects of glucose spilling and inadequate insulin levels. Both FBG and PBG indicated diabetes 3 years prior to HbA1c. While FBG, PBG, and HbA1c are considered equally appropriate for screening and diagnosing diabetes, this case study highlights the need to revisit important distinctions between these tests that explain their frequent discordance.

Urine color expressed in CIE L*a*b* colorspace during rapid changes in hydration status.

Background: To investigate how rapid changes in hydration affect urine color expressed in CIE L*a*b* colorspace. Methods: This study was a two-day crossover design where subjects (N = 30) came in one visit dehydrated, after a 15 h overnight fluid deprivation, and rapidly rehydrated by drinking at least 1000 mL of water in 2 h. On the other visit subjects reported euhydrated and then rapidly dehydrated 2% by walking (3 mph) in a heat chamber (100°F, 50% humidity) for 2 h. Urine samples on both days were collected pre- and post-dehydration/rehydration. Urine osmolality, urine specific gravity, subjective urine color and objective urine color expressed in CIE L*a*b* colorspace were measured. Results: In the dehydration trial participants experienced a significant weight loss of approximately 2% of their starting, euhydrated body weight. The CIE urine color L*-value significantly decreased (-2.3 units) while the b*-value significantly increased (16 units). Subjective urine color significantly increased (1 unit). Urine osmolality increased (25 mmol/kg) and urine specific gravity increased (0.002 g/mL) between the pre- and post-dehydration conditions, however, neither of these changes were statistically significant. In the rehydration trial participants had a significant 1.5% increase in body weight after the ingestion of water. Significant increases were observed in the CIE urine color L*-value (7 units) and a*-value (1.1 units), while the b*-value significantly decreased (-24 units). Subjective urine color significantly decreased (-3 units). Urine osmolality (-600 mmol/kg) and urine specific gravity (-0.018 g/mL) significantly decreased between the pre- and post-rehydration conditions. Conclusions: Traditional markers of hydration, including urine osmolality and urine specific gravity, did not significantly change in the acute dehydration trial, suggesting that these values may not be responsive to rapid changes in hydration status. However, the CIE L*- and b*-values of urine color significantly decreased in the rapid dehydration trial and significantly increased in the rapid rehydration trial. Thus, the results of the current study suggest that urine color L*- and b*-values expressed in the CIE L*a*b* colorspace were more responsive to changes in hydration status during rapid dehydration than traditional indices of urine concentration and thus may be better markers under such conditions.

Exercise intensity influences plasma and sweat amino acid concentrations: a crossover trial.

BACKGROUND: The purpose of this study was to explore the relationship between concentrations of amino acid (AA) and related metabolites in plasma and sweat obtained before and after exercise performed at different intensities and therefore different rates of sweat loss. METHODS: Ten subjects completed a maximally ramped exercise test and three 30-min submaximal (45/60/75% VO2max) exercise bouts. Blood samples were collected before/after the exercise bouts and sweat was collected from the forearm throughout. Samples were analyzed for concentrations of AA and related molecules. RESULTS: Sweat AA excretion rate was higher during the 60% bout compared to the 45% bout but was similar in comparison to the 75% indicating a plateau in rates of sweat AA losses as sweat rate increased. Plasma concentrations of AAs, urea, ammonia, and other non-proteinogenic AAs were not significantly different between exercise bouts performed at 45% and 60%. Exercise at 75% tended to reduce concentrations of sweat amino acids with significantly depressed concentrations of glycine, lysine, serine, threonine, histidine, arginine, tryptophan, aspartate and ornithine. CONCLUSIONS: Overall, this research suggests that increasing exercise intensity increases AA metabolism as demonstrated by reduced plasma AA concentrations and increased excretion through sweat glands, which is mediated by a mechanism yet to be identified.

Acute normobaric hypoxia does not increase blood or plasma viscosity.

BACKGROUND: It has previously been reported that chronic hypoxia increases blood viscosity. The increase is usually attributed to polycythemia-induced increases in hematocrit. However, the effect of acute hypoxia in humans on blood viscosity is unknown. OBJECTIVE: Therefore, the purpose of this study was to determine the effect of acute hypoxia, independent of changes in hematocrit, on blood and plasma viscosity. METHODS: Nine healthy volunteers breathed room air for 30 min, followed by 30 min of breathing 15% oxygen. Blood samples were collected at the end of both the normoxic and hypoxic conditions. Blood viscosity, plasma viscosity, and hematocrit were measured in each sample. RESULTS: The mean±SD hemoglobin oxygen saturation significantly (P < 0.05) decreased from 98±1% during normoxia to 87±2% during hypoxia. Hematocrit was essentially identical for the two conditions (42.1% vs. 42.0%). Blood viscosity was not significantly different for the two conditions with a mean of 2.89±0.17 cP during normoxia and 2.83±0.19 cP during hypoxia. Likewise, plasma viscosity was not significantly different for the two conditions with a mean of 1.19±0.04 cP during normoxia and 1.19±0.05 cP during hypoxia. CONCLUSION: Such results suggest that acute normobaric hypoxia, independent of changes in hematocrit, does not increase blood or plasma viscosity.

The Effect of Hydration on Urine Color Objectively Evaluated in CIE L*a*b* Color Space.

Urine color has been shown to be a viable marker of hydration status in healthy adults. Traditionally, urine color has been measured using a subjective color scale. In recent years, tristimulus colorimetry developed by the International Commission on Illumination (CIE L*a*b*) has been widely adopted as the reference method for color analysis. In the L*a*b* color space, L* indicates lightness ranging from 100 (white) to 0 (black), while a* and b* indicate chromaticity. a* and b* are color directions: -a* is the green axis, +a* is the red axis, -b* is the blue axis, and +b* is the yellow axis. The L*a*b* color space model is only accurately represented in three-dimensional space. Considering the above, the purpose of the current study was to evaluate urine color during different hydration states, with the results expressed in CIE L*a*b* color space. The study included 28 healthy participants (22 males and 6 females) ranging between the age of 20 and 67 years (28.6 ± 11.3 years). One hundred and fifty-one urine samples were collected from the subjects in various stages of hydration, including morning samples after 7-15 h of water deprivation. Osmolality and CIE L*a*b* parameters were measured in each sample. As the urine osmolality increased, a significant linear increase in b* values was observed as the samples became more pronouncedly yellow (τb = 0.708). An increase in dehydration resulted in darker and significantly more yellow urine, as L* values decreased in lightness and b* values increased along the blue-yellow axis. However, as dehydration increased, a notable polynomial trend in color along the green-red axis was observed as a* values initially decreased, indicating a green hue in slightly dehydrated urine, and then increased as urine became more concentrated and thus more dehydrated. It was determined that 74% of the variance seen in urine osmolality was due to CIE L*a*b* variables. This newfound knowledge about urine color change along with the presented regression model for predicting urine osmolality provides a more detailed and objective perspective on the effect of hydration on urine color, which to our knowledge has not been previously researched.

Haemoconcentration, not decreased blood temperature, increases blood viscosity during cold water immersion.

INTRODUCTION: Prolonged cold-water immersion (CWI) has the potential to cause significant hypothermia and haemoconcentration; both of which have previously been shown to independently increase blood viscosity in vitro. The purpose of this study was to determine the effect of CWI on blood viscosity and examine the relative contribution of decreased blood temperature and haemoconcentration. METHODS: Ten healthy volunteers were immersed to mid-sternum in 10°C water for 90 minutes. Gastrointestinal (GI) temperature, haematocrit (Hct), and blood viscosity were measured pre- and post-CWI. RESULTS: CWI caused mean (SD) GI temperature to decrease from 37.5 (0.3)°C to 36.2 (0.7)°C (P < 0.05). CWI also caused mean Hct to increase from 40.0 (3.5)% to 45.0 (2.9)% (P < 0.05). As a result of the haemoconcentration and decreased GI temperature during CWI the mean blood viscosity increased by 19% from 2.80 (0.28) mPa·s⁻¹ to 3.33 (0.42) mPa·s⁻¹ (P < 0.05). However, when the pre-CWI blood sample was measured at the post-CWI GI temperature (36.2°C) there was no significant difference in the blood viscosity when compared to the pre-CWI (37.5°C) blood sample (2.82 (0.20) mPa·s-1 and 2.80 (0.28) mPa·s-1 respectively). Furthermore, the changes in Hct and blood viscosity during CWI were significantly correlated with an r = 0.84. CONCLUSION: The results of the current study show that prolonged, severe CWI causes a significant 19% increase in blood viscosity. In addition, the results strongly suggest that almost all of the increased blood viscosity seen following CWI is the result of haemoconcentration, not decreased blood temperature.

Hand heating lowers postprandial blood glucose concentrations: A double-blind randomized controlled crossover trial.

OBJECTIVES: Examine effect of single hand heating with and without negative pressure on fasting blood glucose (FBG) and postprandial blood glucose (PBG). DESIGN: Double-blind randomized controlled trial with crossover design. SUBJECTS: FBG experiment: 17 healthy subjects (4 males). PBG experiment: 13 healthy subjects (1 males). INTERVENTIONS: Devices included one providing heat only, one heat and negative pressure, and one acting as a sham. For the FBG experiment the devices were used for 30 min. For the PBG experiment the devices were used for one hour during an oral glucose tolerance test (OGTT). OUTCOME MEASURES: Blood glucose measurements were used to determine change in FBG, peak PBG, area under the curve (AUC), and incremental AUC (iAUC). RESULTS: Temperature: Change in tympanic temperature was ≤ 0.15 °C for all trials. FBG: There was no effect on FBG. PBG: Compared to the sham device the heat plus vacuum and heat only device lowered peak blood glucose by 16(31)mg/dL, p = 0.092 and 18(28)mg/dL, p = 0.039, respectively. AUC and iAUC: Compared to the sham device, the heat plus vacuum device and heat only device lowered the AUC by 5.1(15.0)%, p = 0.234 and 7.9(11.1)%, p = 0.024 respectively and iAUC by 17.2(43.4)%, p = 0.178 and 20.5(34.5)%, p = 0.054, respectively. CONCLUSIONS: Heating a single hand lowers postprandial blood glucose in healthy subjects.

Rating of perceived exertion increases synergistically during prolonged exercise in a combined heat and hypoxic environment.

The purpose of this study was to determine the cardiovascular, thermoregulatory, and perceived exertion responses during 2 h of moderate intensity exercise in a combined high heat (38 °C, 40% relative humidity) and hypoxic (15% O2) environment. Ten healthy volunteers completed 2 h of treadmill walking at 40% of maximal oxygen uptake in four different conditions, each separated by approximately 1 week: (1) control, 23 °C/20.9% O2, (2) heat, 38 °C/20.9% O2, (3) hypoxia, 23 °C/15% O2, and (4) combined heat/hypoxia, 38 °C/15% O2. Compared to the responses seen in each condition alone, heart rate (HR) and core temperature (Tcore) showed an additive increase in the combined heat and hypoxic environment after 2 h of moderate intensity exercise. The most important new finding was that the mean rating of perceived exertion (RPE) increased synergistically 3.3 units when exercising in the combined high heat and hypoxic environment, compared to 1.9 units in the heat condition alone. The results suggest that RPE is a conscious perception of effort that plays a regulatory function to ensure that the work rate remains at an intensity that can be safely sustained, rather than simply a marker of exercise intensity. Such results also support previous anecdotal reports that exercise on hot days at altitude seem unusually difficult.

Evaluation of cognitive performance and neurophysiological function during repeated immersion in cold water.

Exposure to cold causes disturbances in cognitive performance that can have a profound impact on the safety, performance, and success of populations that frequent cold environments. It has recently been suggested that repeated cold stress, resulting in cold acclimation, may be a potential strategy to mitigate the cognitive impairments frequently seen upon exposure to cold temperatures. The purpose of this study, therefore, was to examine cognitive and neurophysiological function during repeated cold water immersion. Twelve healthy participants consisting of 8 males and 4 females (mean ±â€¯SD age: 26 ±â€¯5 years, height: 174.0 ±â€¯8.9 cm, weight: 75.6 ±â€¯13.1 kg) completed seven 90-minute immersions in 10 °C water, each separated by 24 h. During immersions 1, 4, and 7, a double-digit addition task and a computer-based psychomotor vigilance task (PVT) were administered to assess cognitive performance, while neurophysiological function was assessed using electroencephalography (EEG) measurements collected during the PVT. Findings suggest that participants experienced an insulative type of cold acclimation, evidenced by greater heat retention and less shivering, with possible improvements in cognitive performance. Participants had more correct responses on the double-digit addition task on Immersion 7 (39 ±â€¯5) compared with Immersion 1 (33 ±â€¯6); p < 0.001, yet no differences were observed for reaction time between Immersion 7 (286 ±â€¯31 ms) and Immersion 1 (281 ±â€¯19 ms); p = 0.59. Additionally, EEG analyses indicate no beneficial changes in neurophysiological function. Results demonstrate that individuals who are frequently exposed to cold water may be more suited to handle certain cognitive challenges after several exposures, although additional investigations are needed to provide neurophysiological support for this.

Local inhibition of carbonic anhydrase does not decrease sweat rate.

BACKGROUND: The purpose of this study was to measure sweat rate during exercise in the heat after directly inhibiting carbonic anhydrase (CA) in eccrine sweat glands via transdermal iontophoresis of acetazolamide. It was hypothesized that if CA was important for sweat production, local administration of acetazolamide, without the confounding systemic effects of dehydration typically associated with past studies, would have a significant effect on sweat rate during exercise. METHODS: Ten healthy subjects volunteered to exercise in the heat following acetazolamide or distilled water iontophoresis on the forearm. RESULTS: The distilled water iontophoresis site had a mean sweat rate during exercise in the heat of 0.59±0.31 µL/cm2/min, while the acetazolamide iontophoresis site had a mean sweat rate of 0.63±0.36 µL/cm2/min (p>0.05). CONCLUSIONS: The most important finding of the current study was that iontophoresis of acetazolamide did not significantly decrease sweat rate during exercise in the heat. Such results suggest that in past studies it was systemic dehydration, and not CA inhibition at the level of the sweat gland, that caused the reported decreased sweat rate.

Impairment of exercise performance following cold water immersion is not attenuated after 7 days of cold acclimation.

PURPOSE: It is well-documented that severe cold stress impairs exercise performance. Repeated immersion in cold water induces an insulative type of cold acclimation, wherein enhanced vasoconstriction leads to greater body heat retention, which may attenuate cold-induced exercise impairments. The purpose of this study, therefore, was to investigate changes in exercise performance during a 7-day insulative type of cold acclimation. METHODS: Twelve healthy participants consisting of eight males and four females (mean ± SD age: 25.6 ± 5.2 years, height: 174.0 ± 8.9 cm, weight: 75.6 ± 13.1 kg) performed a 20 min self-paced cycling test in 23 °C, 40% humidity without prior cold exposure. Twenty-four hours later they began a 7-day cold acclimation protocol (daily 90 min immersion in 10 °C water). On days one, four, and seven of cold acclimation, participants completed the same cycling test. Measurements of work completed, core and skin temperatures, heart rate, skin blood flow, perceived exertion, and thermal sensation were measured during each cycling test. RESULTS: Successful insulative cold acclimation was observed. Work produced during the baseline cycling test (220 ± 70 kJ) was greater (p < 0.001) than all three tests that were performed following immersions (195 ± 58, 197 ± 60, and 194 ± 62 kJ) despite similar ratings of perceived exertion during each test, suggesting that cold exposure impaired cycling performance. This impairment, however, was not attenuated over the cold acclimation period. CONCLUSIONS: Results suggest that insulative cold acclimation does not attenuate impairments in exercise performance that were observed following acute cold water immersion.

Heat acclimation causes a linear decrease in sweat sodium ion concentration.

The purpose of this study was to determine the time course for the previously reported reduction in sweat sodium ion concentration during heat acclimation. Four healthy volunteers completed 7 consecutive days of heat acclimation which included 2h of treadmill walking in a 40°C and 40% relative humidity environment. A modified constant hyperthermia protocol was used as workloads were increased each day to maintain a constant core temperature over the 7 days of heat acclimation. Forearm sweat was collected 3 times during each 2h exercise bout on days 1, 3, 5, and 7 of heat acclimation. Forearm sweat rate and sweat sodium ion concentration were determined from each sample. The results showed that there was a significant (p < 0.05) downward shift in the mean sweat rate vs. sweat sodium ion concentration relationship on days 3, 5, and 7 of heat acclimation, as compared to the pre-heat acclimation (day 1) data. Thus, at any given sweat rate, heat acclimation resulted in a significantly lower sweat sodium ion concentration. The response was very rapid and occurred following only 2 consecutive days of heat exposure (i.e., day 3 vs. day 1 data). Furthermore, the calculated sweat sodium ion concentration, at a sweat rate of 1µl/cm2/min, decreased linearly (r = - 0.50, p < 0.05) during the 7 days of heat acclimation. Such results suggest that heat acclimation rapidly improves sodium ion reabsorption from the eccrine sweat gland duct as evidenced by significant reductions in the sweat sodium ion concentration.

Cold acclimation and cognitive performance: A review.

Athletes, occupational workers, and military personnel experience cold temperatures through cold air exposure or cold water immersion, both of which impair cognitive performance. Prior work has shown that neurophysiological pathways may be sensitive to the effects of temperature acclimation and, therefore, cold acclimation may be a potential strategy to attenuate cold-induced cognitive impairments for populations that are frequently exposed to cold environments. This review provides an overview of studies that examine repeated cold stress, cold acclimation, and measurements of cognitive performance to determine whether or not cold acclimation provides beneficial protection against cold-induced cognitive performance decrements. Studies included in this review assessed cognitive measures of reaction time, attention, logical reasoning, information processing, and memory. Repeated cold stress, with or without evidence of cold acclimation, appears to offer no added benefit of improving cognitive performance. However, research in this area is greatly lacking and, therefore, it is difficult to draw any definitive conclusions regarding the use of cold acclimation to improve cognitive performance during subsequent cold exposures. Given the current state of minimal knowledge on this topic, athletes, occupational workers, and military commands looking to specifically enhance cognitive performance in cold environments would likely not be advised to spend the time and effort required to become acclimated to cold. However, as more knowledge becomes available in this area, recommendations may change.

Cold Acclimation Does Not Alter Physiological or Perceptual Responses During Subsequent Exercise in the Heat.

INTRODUCTION: Warfighters often train and conduct operations in cold environments. Specifically, military trainees and divers that are repeatedly exposed to cold water may experience inadvertent cold acclimatization, which results in body heat retention. These same warfighters can quickly switch between environments (cold to hot or hot to cold) given the nature of their work. This may present a risk of early onset of hyperthermia when cold-acclimatized warfighters are subsequently exposed to physiological insults that increase body temperature, such as exercise and heat stress. However, there is currently no evidence that suggests this is the case. The purpose of this work, therefore, is to determine what impact, if any, repeated immersion in cold water has on subsequent exercise in the heat. MATERIALS AND METHODS: Twelve healthy subjects (values in mean ± SD: age, 25.6 ± 5.2 years; height, 174.0 ± 8.9 cm; weight, 75.6 ± 13.1 kg) voluntarily provided written informed consent in accordance with the San Diego State University Institutional Review Board. They first completed 120 minutes of moderate treadmill walking in 40°C and 40% relative humidity. During this trial, subjects' physiological and perceptual responses were recorded. Twenty-four hours later, subjects began a cold acclimation protocol, which consisted of seven, 90-minute immersions in cold water (10°C, water level to chest). Each immersion was also separated by 24 hours. Subjects then repeated a subsequent trial of exercise in the heat 24 hours after the final immersion of the cold acclimation protocol. RESULTS: Results from cold acclimation revealed no change in core temperature, a decrease in skin temperature, and attenuated shivering and lactate responses, which supports a successful insulative-hypothermic cold acclimation response. This type of cold acclimation response primarily results in heat retention with associated energy conservation. Findings for heat trials (pre-cold acclimation and post-cold acclimation) revealed no differences between trials for all measurements, suggesting that cold acclimation did not influence physiological or perceptual responses during exercise in the heat. CONCLUSION: Our findings indicate that military divers or trainees that are frequently exposed to cold water, and hence have the ability to experience cold acclimatization, will likely not be at greater risk of increased thermal strain when subsequently exposed to physical activity in hot environments. In this study, no physiological or perceptual differences were observed between trials before and after cold acclimation, suggesting that cold acclimation does not present a greater hyperthermia risk during subsequent exercise in the heat.

Transition duration of ingested deuterium oxide to eccrine sweat during exercise in the heat.

The time necessary for the initial appearance of ingested water as sweat during exercise in the heat remains unknown. Based on the current literature, we estimated fluid transition through the body, from ingestion to appearance as sweat, to have a minimum time duration of approximately three minutes. The purpose of this study was to test this prediction and identify the time necessary for the initial enrichment of deuterium oxide (D2O) in sweat following ingestion during exercise in the heat. Eight participants performed moderate intensity (40% of maximal oxygen uptake) treadmill exercise in an environmental chamber (40°C, 40% rH) to induce active sweating. After fifteen minutes, while continuing to walk, participants consumed D2O (0.15mlkg-1) in a final volume of 50ml water. Scapular sweat samples were collected one minute prior to and ten minutes post-ingestion. Samples were analyzed for sweat D2O concentration using isotope ratio mass spectrometry and compared to baseline. Mean±SD ∆ sweat D2O concentration at minutes one and two post-ingestion were not significantly higher than baseline (0min). Minutes three (9±3ppm) through ten (23±11ppm) post-ingestion had ∆ sweat D2O concentrations significantly (P<0.05) higher than baseline. Such results suggest that ingested water rapidly transports across the mucosal membrane of the alimentary canal into the vasculature space, enters the extravascular fluid, and is actively secreted by the eccrine sweat glands onto the surface of the skin for potential evaporation in as little as three minutes during exercise in the heat.

Leaching from the stratum corneum does not explain the previously reported elevated potassium ion concentration in sweat.

BACKGROUND: The purpose of this study was to determine if K+ is leached from the stratum corneum when sweat is present on the skin's surface. The results will help address whether sweat [K+] previously reported in the literature are artifactually elevated as a result of K+ leaching. METHODS: Twelve (six female, six male) healthy volunteers participated in this study. After thorough skin cleansing and preparation with isopropyl alcohol and high-performance liquid chromatography-grade distilled water, three sites were chosen and a 50 µL drop of artificial sweat was pipetted directly onto the skin. The artificial sweat had a [K+] of 4 mEq·L-1, an osmolality of 120 mosm·L-1, and a pH of 6.0. Immediately following, a clear plastic cover slip (~6 cm2) with a shallow 0.8 cm2 convex impression in the center was applied over each drop, preventing evaporation. Each sample was allowed to sit on the forearm, under the plastic cover slip, for 10 min. RESULTS: The mean (±SD) [K+] in 'artificial' sweat not exposed to the skin was measured to be 4.2±0.4 mEq·L-1. After 10 min of exposure to the stratum corneum of the forearm, the artificial sweat had a mean (±SD) [K+] of 3.9±0.3 mEq·L-1. There was no significant difference (p>0.05) in the [K+] between the control artificial sweat and the samples collected after 10 min of exposure to forearm skin. CONCLUSIONS: These results do not support the hypothesis that significant K+ leaching from the stratum corneum into standing sweat is the cause for the previously reported elevated sweat [K+].

Increases in core temperature counterbalance effects of haemoconcentration on blood viscosity during prolonged exercise in the heat.

NEW FINDINGS: What is the central question of this study? The purpose of the present study was to determine the effects of exercise-induced haemoconcentration and hyperthermia on blood viscosity. What is the main finding and its importance? Exercise-induced haemoconcentration, increased plasma viscosity and increased blood aggregation, all of which increased blood viscosity, were counterbalanced by increased red blood cell (RBC) deformability (e.g. RBC membrane shear elastic modulus and elongation index) caused by the hyperthermia. Thus, blood viscosity remained unchanged following prolonged moderate-intensity exercise in the heat. Previous studies have reported that blood viscosity is significantly increased following exercise. However, these studies measured both pre- and postexercise blood viscosity at 37 °C even though core and blood temperatures would be expected to have increased during the exercise. Consequently, the effect of exercise-induced hyperthermia on mitigating change in blood viscosity may have been missed. The purpose of this study was to isolate the effects of exercise-induced haemoconcentration and hyperthermia and to determine their combined effects on blood viscosity. Nine subjects performed 2 h of moderate-intensity exercise in the heat (37 °C, 40% relative humidity), which resulted in significant increases from pre-exercise values for rectal temperature (from 37.11 ± 0.35 to 38.76 ± 0.13 °C), haemoconcentration (haematocrit increased from 43.6 ± 3.6 to 45.6 ± 3.5%) and dehydration (change in body weight = -3.6 ± 0.7%). Exercise-induced haemoconcentration significantly (P < 0.05) increased blood viscosity by 9% (from 3.97 to 4.33 cP at 300 s(-1)), whereas exercise-induced hyperthermia significantly decreased blood viscosity by 7% (from 3.97 to 3.69 cP at 300 s(-1)). When both factors were considered together, there was no overall change in blood viscosity (from 3.97 to 4.03 cP at 300 s(-1)). The effects of exercise-induced haemoconcentration, increased plasma viscosity and increased red blood cell aggregation, all of which increased blood viscosity, were counterbalanced by increased red blood cell deformability (e.g. red blood cell membrane shear elastic modulus and elongation index) caused by the hyperthermia. Thus, blood viscosity remained unchanged following prolonged moderate-intensity exercise in the heat.