Brachial and carotid hemodynamic response to hot water immersion in men and women.

This study sought to compare the brachial and carotid hemodynamic response to hot water immersion (HWI) between healthy young men and women. Ten women (W) and 11 men (M) (24 ± 4 yr) completed a 60-min HWI session immersed to the level of the sternum in 40°C water. Brachial and carotid artery hemodynamics (Doppler ultrasound) were measured at baseline (seated rest) and every 15 min throughout HWI. Within the brachial artery, total shear rate was elevated to a greater extent in women [+479 (+364, +594) s-1] than in men [+292 (+222, +361) s-1] during HWI (P = 0.005). As shear rate is inversely proportional to blood vessel diameter and directly proportional to blood flow velocity, the sex difference in brachial shear response to HWI was the result of a smaller brachial diameter among women at baseline (P < 0.0001) and throughout HWI (main effect of sex, P < 0.0001) and a greater increase in brachial velocity seen in women [+48 (+36, +61) cm/s] compared with men [+35 (+27, +43) cm/s] with HWI (P = 0.047) which allowed for a similar increase in brachial blood flow between sexes [M: +369 (+287, +451) mL/min, W: +364 (+243, +486) mL/min, P = 0.943]. In contrast, no differences were seen between sexes in carotid total shear rate, flow, velocity, or diameter at baseline or throughout HWI. These data indicate the presence of an artery-specific sex difference in the hemodynamic response to a single bout of HWI.

The effect of body surface area exposure to menthol on temperature regulation and perception in men.

INTRODUCTION: In warm conditions topical application of menthol increases cool sensations and influences deep body temperature. The purpose of this experiment was to explore whether different body surface areas (BSA) exposed to menthol influence these responses. It was hypothesized that the forcing function exerted by menthol will be proportionally related to BSA. METHOD: Using a within-participant design, 13 participants underwent three BSA exposures (Small [S; finger]; Medium [M; arm]; Large [L; upper/lower body]) to 4.13% menthol, and one Placebo exposure. During each exposure participants rested supine in a tent (30 °C, 50%rh) for 30-min before their intervention and 30-min thereafter. Measures included thermal sensation, thermal comfort, irritation, skin blood flow (finger SkBF; laser Doppler flowmetry), rectal temperature (Tre), and skin temperature (chest, forearm, thigh, calf). The Area Under the Curve from minute 30 to 60 was calculated and analyzed using a one-way ANOVA or Friedman's test with post-hoc testing (0.05 alpha level). RESULTS: There was no significant difference in any measure of thermometry (p > 0.05), while SKBF was significantly lowered in L, M, and S vs. P respectively (p < 0.05). Participants in L felt cooler vs. P and S (p < 0.05). Losses in thermal comfort were noted in L and M vs. P and S (p < 0.05), along with increased irritation in L vs. S (p < 0.05). CONCLUSIONS: Despite similar skin temperatures, larger BSA's exposed to menthol caused cooler sensations, likely due to the activation of a larger pool of menthol-sensitive neurons. This occurred in the absence of thermal discomfort and without perceptions of irritation exceeding 'weak'. Larger BSA's also exhibited greater alterations in Tre, likely driven by a reduction in SkBF, but despite this mean body temperature was regulated suggesting the thermoregulatory system can cope with the range of BSA exposures studied herein.

Heat therapy improves glucose tolerance and adipose tissue insulin signaling in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is associated with high rates of obesity and metabolic dysfunction. Repeated passive heat exposure (termed heat therapy) is a novel lifestyle intervention for improving health in obese women with PCOS. The purpose of this study was to examine changes in metabolic function in obese women with PCOS following heat therapy. Eighteen age- and BMI-matched obese women with PCOS (age: 27 ± 1 yr, BMI: 41.3 ± 1.1 kg/m-2) were assigned to heat therapy (HT) or time control (CON). HT participants underwent 30 one-hour hot tub sessions over 8-10 wk, while CON participants completed all testing but did not undergo heat therapy. Before (Pre), at the mid-point (Mid), and following (Post) 8-10 wk of heat therapy, metabolic health was assessed using a 2-h oral glucose tolerance test, a subcutaneous abdominal fat biopsy (Pre-Post only), and other blood markers relating to metabolic function. HT participants exhibited improved fasting glucose (Pre: 105 ± 3, Post: 89 ± 5mg/dl; P = 0.001), glucose area under the curve (AUC) (Pre: 18,698 ± 1,045, Post: 16,987 ± 1,017 mg·dl-1·min-1; P = 0.028) and insulin AUC (Pre: 126,924 ± 11,730, Post: 91,233 ± 14,429 IU l-1·min-1; P = 0.012). Adipocyte insulin signaling (p-AKT at Ser-473 with 1.2 nM insulin) increased in HT (Pre: 0.29 ± 0.14, Post: 0.93 ± 0.29 AU; P = 0.021). Additionally, serum testosterone declined in HT participants (Pre: 51 ± 7, Post: 34 ± 4 ng/dl; P = 0.033). No parameters changed over time in CON, and no change in BMI was observed in either group. HT substantially improved metabolic risk profile in obese women with PCOS. HT also reduced androgen excess and may improve PCOS symptomology.

Heat therapy reduces sympathetic activity and improves cardiovascular risk profile in women who are obese with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) affects up to 15% of women and is associated with increased risk of obesity and cardiovascular disease. Repeated passive heat exposure [termed "heat therapy" (HT)] is a lifestyle intervention with the potential to reduce cardiovascular risk in obesity and PCOS. Women with obesity (n = 18) with PCOS [age 27 ± 4 yr, body mass index (BMI) 41.3 ± 4.7 kg/m2] were matched for age and BMI, then assigned to HT (n = 9) or time control (CON; n = 9). HT subjects underwent 30 one-hour hot tub sessions over 8-10 wk, whereas CON subjects did not undergo HT. Muscle sympathetic nerve activity (MSNA), blood pressure, cholesterol, C-reactive protein, and markers of vascular function were assessed at the start (Pre) and end (Post) of 8-10 wk. These measures included carotid and femoral artery wall thickness and flow-mediated dilation (FMD), measured both before and after 20 min of ischemia-20 min of reperfusion (I/R) stress. HT subjects exhibited reduced MSNA burst frequency (Pre: 20 ± 8 bursts/min, Post: 13 ± 5 bursts/min, P = 0.012), systolic (Pre: 124 ± 5 mmHg, Post: 114 ± 6 mmHg; P < 0.001) and diastolic blood pressure (Pre: 77 ± 6 mmHg, Post: 68 ± 3 mmHg; P < 0.001), C-reactive protein (Pre: 19.4 ± 13.7 nmol/L, Post: 15.2 ± 12.3 nmol/L; P = 0.018), total cholesterol (Pre: 5.4 ± 1.1 mmol/L, Post: 5.0 ± 0.8 mmol/L; P = 0.028), carotid wall thickness (Pre: 0.054 ± 0.005 cm, Post: 0.044 ± 0.005 cm; P = 0.010), and femoral wall thickness (Pre: 0.056 ± 0.009 cm, Post: 0.042 ± 0.005 cm; P = 0.003). FMD significantly improved in HT subjects over time following I/R (Pre: 5.6 ± 2.5%, Post: 9.5 ± 1.7%; P < 0.001). No parameters changed over time in CON, and BMI did not change in either group. These findings indicate that HT reduces sympathetic nerve activity, provides protection from I/R stress, and substantially improves cardiovascular risk profiles in women who are obese with PCOS.

Passive heat therapy improves endothelial function, arterial stiffness and blood pressure in sedentary humans.

KEY POINTS: A recent 30 year prospective study showed that lifelong sauna use reduces cardiovascular-related and all-cause mortality; however, the specific cardiovascular adaptations that cause this chronic protection are currently unknown. We investigated the effects of 8 weeks of repeated hot water immersion ('heat therapy') on various biomarkers of cardiovascular health in young, sedentary humans. We showed that, relative to a sham group which participated in thermoneutral water immersion, heat therapy increased flow-mediated dilatation, reduced arterial stiffness, reduced mean arterial and diastolic blood pressure, and reduced carotid intima media thickness, with changes all on par or greater than what is typically observed in sedentary subjects with exercise training. Our results show for the first time that heat therapy has widespread and robust effects on vascular function, and as such, could be a viable treatment option for improving cardiovascular health in a variety of patient populations, particularly those with limited exercise tolerance and/or capabilities. ABSTRACT: The majority of cardiovascular diseases are characterized by disorders of the arteries, predominantly caused by endothelial dysfunction and arterial stiffening. Intermittent hot water immersion ('heat therapy') results in elevations in core temperature and changes in cardiovascular haemodynamics, such as cardiac output and vascular shear stress, that are similar to exercise, and thus may provide an alternative means of improving health which could be utilized by patients with low exercise tolerance and/or capabilities. We sought to comprehensively assess the effects of 8 weeks of heat therapy on biomarkers of vascular function in young, sedentary subjects. Twenty young, sedentary subjects were assigned to participate in 8 weeks (4-5 times per week) of heat therapy (n = 10; immersion in a 40.5°C bath sufficient to maintain rectal temperature ≥ 38.5°C for 60 min per session) or thermoneutral water immersion (n = 10; sham). Eight weeks of heat therapy increased flow-mediated dilatation from 5.6 ± 0.3 to 10.9 ± 1.0% (P < 0.01) and superficial femoral dynamic arterial compliance from 0.06 ± 0.01 to 0.09 ±0.01 mm(2)  mmHg(-1) (P = 0.03), and reduced (i.e. improved) aortic pulse wave velocity from 7.1 ± 0.3 to 6.1 ± 0.3 m s(-1) (P = 0.03), carotid intima media thickness from 0.43 ± 0.01 to 0.37 ± 0.01 mm (P < 0.001), and mean arterial blood pressure from 83 ± 1 to 78 ± 2 mmHg (P = 0.02). No changes were observed in the sham group or for carotid arterial compliance, superficial femoral intima media thickness or endothelium-independent dilatation. Heat therapy improved endothelium-dependent dilatation, arterial stiffness, intima media thickness and blood pressure, indicating improved cardiovascular health. These data suggest heat therapy may provide a simple and effective tool for improving cardiovascular health in various populations.

Acute hot water immersion is protective against impaired vascular function following forearm ischemia-reperfusion in young healthy humans.

Ischemia-reperfusion (I/R) injury is a primary cause of poor outcomes following ischemic cardiovascular events. We tested whether acute hot water immersion protects against forearm vascular I/R. Ten (5 male, 5 female) young (23 ± 2 yr), healthy subjects participated in two trials in random order 7-21 days apart, involving: 1) 60 min of seated rest (control), or 2) 60 min of immersion in 40.5°C water (peak rectal temperature: 38.9 ± 0.2°C). I/R was achieved 70 min following each intervention by inflating an upper arm cuff to 250 mmHg for 20 min followed by 20 min of reperfusion. Brachial artery flow-mediated dilation (FMD) and forearm postocclusive reactive hyperemia (RH) were measured as markers of macrovascular and microvascular function at three time points: 1) preintervention, 2) 60 min postintervention, and 3) post-I/R. Neither time control nor hot water immersion alone affected FMD (both, P > 0.99). I/R reduced FMD from 7.4 ± 0.7 to 5.4 ± 0.6% (P = 0.03), and this reduction was prevented following hot water immersion (7.0 ± 0.7 to 7.7 ± 1.0%; P > 0.99). I/R also impaired RH (peak vascular conductance: 2.6 ± 0.5 to 2.0 ± 0.4 ml·min-1·mmHg-1, P = 0.003), resulting in a reduced shear stimulus (SRAUC·10-3: 22.5 ± 2.4 to 16.9 ± 2.4, P = 0.04). The post-I/R reduction in peak RH was prevented by hot water immersion (2.5 ± 0.4 to 2.3 ± 0.4 ml·min-1·mmHg-1; P = 0.33). We observed a decline in brachial artery dilator function post-I/R, which may be (partly) related to damage incurred downstream in the microvasculature, as indicated by impaired RH and shear stimulus. Hot water immersion was protective against reductions in FMD and RH post-I/R, suggesting heat stress induces vascular changes consistent with reducing I/R injury following ischemic events.

Assessment of extracellular dehydration using saliva osmolality.

INTRODUCTION: When substantial solute losses accompany body water an isotonic hypovolemia (extracellular dehydration) results. The potential for using blood or urine to assess extracellular dehydration is generally poor, but saliva is not a simple ultra-filtrate of plasma and the autonomic regulation of salivary gland function suggests the possibility that saliva osmolality (Sosm) may afford detection of extracellular dehydration via the influence of volume-mediated factors. PURPOSE: This study aimed to evaluate the assessment of extracellular dehydration using Sosm. In addition, two common saliva collection methods and their effects on Sosm were compared. METHODS: Blood, urine, and saliva samples were collected in 24 healthy volunteers during paired euhydration and dehydration trials. Furosemide administration and 12 h fluid restriction were used to produce extracellular dehydration. Expectoration and salivette collection methods were compared in a separate group of eight euhydrated volunteers. All comparisons were made using paired t-tests. The diagnostic potential of body fluids was additionally evaluated. RESULTS: Dehydration (3.1 ± 0.5% loss of body mass) decreased PV (-0.49 ± 0.12 L; -15.12 ± 3.94% change), but Sosm changes were marginal (<10 mmol/kg) and weakly correlated with changes in absolute or relative PV losses. Overall diagnostic accuracy was poor (AUC = 0.77-0.78) for all body fluids evaluated. Strong agreement was observed between Sosm methods (Expectoration: 61 ± 10 mmol/kg, Salivette: 61 ± 8 mmol/kg, p > 0.05). CONCLUSIONS: Extracelluar dehydration was not detectable using plasma, urine, or saliva measures. Salivette and expectoration sampling methods produced similar, consistent results for Sosm, suggesting no methodological influence on Sosm.

Modeling thermoregulatory responses during high-intensity exercise in warm environments.

The six cylinder thermoregulatory model (SCTM) has been validated thoroughly for resting humans. This type of modeling is helpful to predict and develop guidance for safe performance of work and recreational activities. In the context of a warming global climate, updating the accuracy of the model for intense exercise in warm environments will help a wide range of individuals in athletic, recreational, and military settings. Three sets of previously collected data were used to determine SCTM accuracy. Dataset 1: two groups [large (LG) 91.5 kg and small (SM) 67.7 kg] of individuals performed 60 min of semirecumbent cycling in temperate conditions (25.1°C) at metabolic rates of 570-700 W. Dataset 2: two LG (100 kg) and SM (65.8 kg) groups performed 60 min of semirecumbent cycling in warm/hot environmental conditions (36.2°C) at metabolic rates of 590-680 W. Dataset 3: seven volunteers completed 8-km track trials (∼30 min) in cool (17°C) and warm (30°C) environments. The volunteers' metabolic rates were estimated to be 1,268 W and 1,166 W, respectively. For all datasets, SCTM-predicted core temperatures were found to be similar to the observed core temperatures. The root mean square deviations (RMSDs) ranged from 0.06 to 0.46°C with an average of 0.2°C deviation, which is less than the acceptance threshold of 0.5°C. Thus, the present validation shows that SCTM predicts core temperatures with acceptable accuracy during intense exercise in warm environments and successfully captures core temperature differences between large and small individuals.NEW & NOTEWORTHY The SCTM has been validated thoroughly for resting humans in warm and cold environments and during water immersion. The present study further demonstrated that SCTM predicts core temperatures with acceptable accuracy during intense exercise up to 1,300 W in temperate and warm environments and captures core temperature differences between large and small individuals. SCTM is potentially useful to develop guidance for safe operation in athletic, military, and occupational settings during exposure to warm or hot environments.

Hypohydration and acute thermal stress affect mood state but not cognition or dynamic postural balance.

Equivocal findings have been reported in the few studies that examined the impact of ambient temperature (T a) and hypohydration on cognition and dynamic balance. The purpose of this study was to determine the impact of acute exposure to a range of ambient temperatures (T(a) 10-40 °C) in euhydration (EUH) and hypohydration (HYP) states on cognition, mood and dynamic balance. Thirty-two men (age 22 ± 4 years, height 1.80 ± 0.05 m, body mass 85.4 ± 10.8 kg) were grouped into four matched cohorts (n = 8), and tested in one of the four T(a) (10, 20, 30, 40 °C) when EUH and HYP (-4 % body mass via exercise-heat exposure). Cognition was assessed using psychomotor vigilance, 4-choice reaction time, matching to sample, and grammatical reasoning. Mood was evaluated by profile of mood states and dynamic postural balance was tested using a Biodex Balance System. Thermal sensation (TS), core (T core) and skin temperature (T(sk)) were obtained throughout testing. Volunteers lost -4.1 ± 0.4 % body mass during HYP. T sk and TS increased with increasing T(a), with no effect of hydration. Cognitive performance was not altered by HYP or thermal stress. Total mood disturbance (TMD), fatigue, confusion, anger, and depression increased during HYP at all T(a). Dynamic balance was unaffected by HYP, but 10 °C exposure impaired balance compared to all other T(a). Despite an increase in TMD during HYP, cognitive function was maintained in all testing environments, demonstrating cognitive resiliency in response to body fluid deficits. Dynamic postural stability at 10 °C appeared to be hampered by low-grade shivering, but was otherwise maintained during HYP and thermal stress.

Individualized monitoring of heat illness risk: novel adaptive physiological strain index to assess exercise-heat strain from athletes to fully encapsulated workers.

Objective. Exercise-heat strain estimation approaches often involve combinations of body core temperature (Tcore), skin temperature (Tsk) and heart rate (HR). A successful existing measure is the 'Physiological Strain Index' (PSI), which combines HR and Tcore values to estimate strain. However, depending on variables such as aerobic fitness and clothing, the equation's 'maximal/critical' Tcore must be changed to accurately represent the strain, in part because high Tsk (small Tcore-Tsk) can increase cardiovascular strain and thereby negatively affect performance. Here, an 'adaptive PSI' (aPSI) is presented where the original PSI Tcorecriticalvalue is 'adapted' dynamically by the delta between Tcore and Tsk.Approach. PSI and aPSI were computed for athletes (ELITE,N= 11 male and 8 female, 8 km time-trial) and soldiers in fully encapsulating personal protective equipment (PPE,N= 8 male, 2 km approach-march). While these were dissimilar events, it was anticipated given that the clothing and work rates would elicit similar very-high exercise-heat strain values.Main results. Mean end HR values were similar (∼180 beats min-1) with higher Tcore = 40.1 ± 0.4 °C for ELITE versus PPE 38.4 ± 0.6 °C (P< 0.05). PSI end values were different between groups (P< 0.01) and appeared 'too-high' for ELITE (11.4 ± 0.8) and 'too-low' for PPE (7.6 ± 2.0). However, aPSI values were not different (9.9 ± 1.4 versus 9.0 ± 2.5 versus;p> 0.05) indicating a 'very high' level of exercise-heat strain for both conditions.Significance. A simple adaptation of the PSI equation, which accounts for differences in Tcore-to-Tsk gradients, provides a physiological approach to dynamically adapt PSI to provide a more accurate index of exercise-heat strain under very different working conditions.

Biological and analytical variation of the human sweating response: implications for study design and analysis.

Appropriate quantification of analytical and biological variation of thermoregulatory sweating has important practical utility for research design and statistical analysis. We sought to examine contributors to variability in local forearm sweating rate (SR) and sweating onset (SO) and to evaluate the potential for using bilateral measurements. Two women and eight men (26 ± 9 yr; 79 ± 12 kg) completed 5 days of heat acclimation and walked (1.8 l/min VO(2)) on three occasions for 30 min in 40°C, 20% RH, while local SR and SO were measured. Local SR measures among days were not different (2.14 ± 0.72 vs. 2.02 ± 0.79 vs. 2.31 ± 0.72 mg·cm(2)·min(-1), P = 0.19) nor was SO (10.47 ± 2.54 vs. 10.04 ± 2.97 vs. 9.87 ± 3.44 min P = 0.82). Bilateral SR (2.14 ± 0.72 vs. 2.16 ± 0.71 mg·cm(2)·min(-1), P = 0.56) and SO (10.47 ± 2.54 vs. 10.83 ± 2.48 min, P = 0.09) were similar and differences were ≤ 1 SD of day-to-day differences for a single forearm. Analytical imprecision (CV(a)), within (CV(i))-, and between (CV(g))-subjects' coefficient of variation for local SR were 2.4%, 22.3%, and 56.4%, respectively, and were 0%, 9.6%, and 41%, respectively, for SO. We conclude: 1) technologically, sweat capsules contribute negligibly to sweat measurement variation; 2) bilateral measures of SR and SO appear interchangeable; 3) when studying potential factors affecting sweating, changes in SO afford a more favorable signal-to-noise ratio vs. changes in SR. These findings provide a quantitative basis for study design and optimization of power/sample size analysis in the evaluation of thermoregulatory sweating.

Hydration assessment using the cardiovascular response to standing.

The cardiovascular response to standing (sit-to-stand change in heart rate; SSΔHR) is commonly employed as a screening tool to detect hypohydration (body water deficit). No study has systematically evaluated SSΔHR cut points using different magnitudes or different types of controlled hypohydration. The objective of this study was to determine the diagnostic accuracy of the often proposed 20 b/min SSΔHR cut point using both hypertonic and isotonic models of hypohydration. Thirteen healthy young adults (8M, 5F) underwent three bouts of controlled hypohydration. The first bout used sweating to elicit large losses of body water (mass) (>3 % sweat). The second two bouts were matched to elicit 3 % body mass losses (3 % diuretic; 3 % sweat). A euhydration control trial (EUH) was paired with each hypohydration trial for a total of six trials. Heart rate was assessed after 3-min sitting and after 1-min standing during all trials. SSΔHR was compared among trials, and receiver operator characteristic curve analysis was used to determine diagnostic accuracy of the 20 b/min SSΔHR cut point. Volunteers lost 4.5 ± 1.1, 3.0 ± 0.6, and 3.2 ± 0.6 % body mass during >3 % sweat, 3 % diuretic, and 3 % sweat trials, respectively. SSΔHR (b/min) was 9 ± 8 (EUH), 20 ± 12 (>3 % sweat; P < 0.05 vs. EUH), 17 ± 7 (3 % diuretic; P < 0.05 vs. EUH), and 13 ± 11 (3 % sweat). The 20 beats/min cut point had high specificity (90 %) but low sensitivity (44 %) and overall diagnostic accuracy of 67 %. SSΔHR increased significantly in response to severe hypertonic hypohydration and moderate isotonic hypohydration, but not moderate hypertonic hypohydration. However, the 20 beats/min cut point afforded only marginal diagnostic accuracy.

Reference change values for monitoring dehydration.

BACKGROUND: Dehydration is a common medical problem requiring heuristic evaluation. Our aim was to develop a quantitative and graphical tool based on serial changes in either plasma osmolality (P(osm)), urine specific gravity (U(sg)), or body mass (B(m)) to aid in determining the probability that a person has become dehydrated. A secondary purpose was to validate use of the tool by dehydrating a group of volunteers. METHODS: Basic data were obtained from a recent study of biological variation in common hydration status markers. Four reference change values (RCV) were calculated for each variable (P(osm), U(sg), B(m)) using four statistical probabilities (0.80, 0.90, 0.95, and 0.99). The probability derived from the Z-score for any given change can be calculated from: Z=change/[2(1/2)(CV(a)(2)+CV(i)(2))(1/2)]. This calculation was simplified to require one input (measured change) by plotting the RCV against probability to generate both an empirical equation and a dual quantitative-qualitative graphic. RESULTS: Eleven volunteers were dehydrated by moderate levels (-2.1% to -3.5% B(m)). Actual probabilities were obtained by substituting measured changes in P(osm), U(sg), and B(m) for X in the exponential equation, Y=1-e(-K·X), where each variable has a unique K constant. Median probabilities were 0.98 (P(osm)), 0.97 (U(sg)), and 0.97 (B(m)), which aligned with 'very likely' to 'virtually certain' qualitative probability categories for dehydration. CONCLUSIONS: This investigation provides a simple quantitative and graphical tool that can aid in determining the probability that a person has become dehydrated when serial measures of P(osm), U(sg), or B(m) are made.

DEET insect repellent: effects on thermoregulatory sweating and physiological strain.

Insect repellents (e.g. N,N-diethyl-m-toluamide or DEET) applied to the skin can potentially interfere with sweat production and evaporation, thus increasing physiological strain during exercise-heat stress. The purpose was to determine the impact of 33% DEET lotion on sweating responses, whole body thermoregulation and thermal sensation during walking exercise in the heat. Nine volunteers (2 females, 7 males; 22.1 ± 4.9 years; 176.4 ± 10.0 cm; 79.9 ± 12.9 kg) completed 5 days of heat acclimation (45°C, 20% rh; 545 watts; 100 min/day) and performed three trials: control (CON); DEET applied to forearm (DEET(LOC), 12 cm(2)); and DEET applied to ~13% body surface area (DEET(WB),). Trials consisted of 30 min walking (645 watts) in 40°C, 20% rh environment. Local sweat rate (SR), onset and skin wettedness were measured in DEET(LOC), and heart rate (HR), rectal temperature (T (re)), skin temperature (T (sk)), RPE, and thermal sensations (TS) were measured during DEET(WB). No differences (p > 0.05) were observed between DEET(LOC) versus CON, respectively, for steady state SR (1.89 ± 0.44 vs. 2.09 ± 0.84 mg/cm(2)/min), SR area under the curve (46.9 ± 11.7 vs. 55.0 ± 20.8 mg/cm(2)), sweating onset, or skin wettedness. There were no differences (p > 0.05) in HR, T (re), T (sk), Physiological Strain Index, RPE or TS between DEET(WB) versus CON. DEET did not impact measures of local forearm sweating and when applied according to military doctrine, did not adversely impact physiological responses during exercise-heat stress. DEET can be safely worn during military, occupational and recreational activities in hot, insect infested environments.

Hypohydration reduces vertical ground reaction impulse but not jump height.

This study examined vertical jump performance using a force platform and weighted vest to determine why hypohydration (approximately 4% body mass) does not improve jump height. Measures of functional performance from a force platform were determined for 15 healthy and active males when euhydrated (EUH), hypohydrated (HYP) and hypohydrated while wearing a weighted vest (HYP(v)) adjusted to precisely match water mass losses. HYP produced a significant loss of body mass [-3.2 +/- 0.5 kg (-3.8 +/- 0.6%); P < 0.05], but body mass in HYP(v) was not different from EUH. There were no differences in absolute or relative peak force or power among trials. Jump height was not different between EUH (0.380 +/- 0.048 m) and HYP (0.384 +/- 0.050 m), but was 4% lower (P < 0.05) in HYP(v) (0.365 +/- 0.52 m) than EUH due to a lower jump velocity between HYP(v) and EUH only (P < 0.05). However, vertical ground reaction impulse (VGRI) was reduced in both HYP and HYP(v) (2-3%) compared with EUH (P < 0.05). In conclusion, this study demonstrates the failure to improve jump height when HYP can be explained by offsetting reductions in both VGRI and body mass.

A simple and valid method to determine thermoregulatory sweating threshold and sensitivity.

Sweating threshold temperature and sweating sensitivity responses are measured to evaluate thermoregulatory control. However, analytic approaches vary, and no standardized methodology has been validated. This study validated a simple and standardized method, segmented linear regression (SReg), for determination of sweating threshold temperature and sensitivity. Archived data were extracted for analysis from studies in which local arm sweat rate (m(sw); ventilated dew-point temperature sensor) and esophageal temperature (T(es)) were measured under a variety of conditions. The relationship m(sw)/T(es) from 16 experiments was analyzed by seven experienced raters (Rater), using a variety of empirical methods, and compared against SReg for the determination of sweating threshold temperature and sweating sensitivity values. Individual interrater differences (n = 324 comparisons) and differences between Rater and SReg (n = 110 comparisons) were evaluated within the context of biologically important limits of magnitude (LOM) via a modified Bland-Altman approach. The average Rater and SReg outputs for threshold temperature and sensitivity were compared (n = 16) using inferential statistics. Rater employed a very diverse set of criteria to determine the sweating threshold temperature and sweating sensitivity for the 16 data sets, but interrater differences were within the LOM for 95% (threshold) and 73% (sensitivity) of observations, respectively. Differences between mean Rater and SReg were within the LOM 90% (threshold) and 83% (sensitivity) of the time, respectively. Rater and SReg were not different by conventional t-test (P > 0.05). SReg provides a simple, valid, and standardized way to determine sweating threshold temperature and sweating sensitivity values for thermoregulatory studies.