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.

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.

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 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.

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.

Meta-inflammation and cardiometabolic disease in obesity: Can heat therapy help?

Obesity and associated metabolic dysfunction have reached epidemic proportions worldwide. The current theory linking metabolic disease and obesity involves ischemic adipose tissue initiating an inflammatory cascade that results in systemic insulin resistance and may eventually lead to type II diabetes mellitus. Diabetes and associated metabolic dysfunction increase the risk of developing cardiovascular disease and fatal cardiovascular events. By targeting key steps in this process, ischemia and inflammation, this cascade may be prevented or reversed and thus metabolic and cardiovascular health may be preserved in obesity. Regular heat exposure (termed 'heat therapy') offers potential to improve cardiometabolic health in obese individuals through a variety of mechanisms that include but are not limited to heat shock proteins, hypoxia-inducible factor 1α, and hemodynamic effects. The purpose of this review is to highlight the cardiometabolic decline in obese individuals stemming from adipose tissue dysfunction, and examine the ways in which heat therapy and associated cellular and systemic adaptations can intersect with this decline in function to improve or restore cardiovascular and metabolic health.

Physiological Responses to Overdressing and Exercise-Heat Stress in Trained Runners.

Heat acclimation is the best strategy to improve performance in a hot environment. Many athletes seeking the benefits of heat acclimation lack access to a hot environment for exercise and, thus, rely on overdressing to simulate environmental heat stress. It is currently unknown whether this approach produces the requisite thermoregulatory strain necessary for heat acclimation in trained men and women. PURPOSE: To compare physiological and cellular responses to exercise in a hot environment (HOT; 40°C, 30% RH) with minimal clothing (clo = 0.87) and in a temperate environment (CLO; 15°C, 50% RH) with overdressing (clo = 1.89) in both men and women. METHODS: HR, rectal temperature (Tre), mean skin temperature (Tsk), sweating rate (SR), and extracellular heat shock protein (eHSP)72 were measured in 13 (7 males, 6 females) well-trained runners (V˙O2max: 58.7 ± 10.7 mL·kg·min) in response to ~60 min of treadmill running at 50%-60% V˙O2max in HOT and CLO. RESULTS: Tre increased in both conditions, but the increase was greater in HOT (ΔTre HOT: 2.6°C ± 0.1°C; CLO 2.0°C ± 0.1°C; P = 0.0003). SR was also higher in HOT (1.41 ± 0.1 L h; CLO: 1.16 ± 0.1 L·h; P = 0.0001). eHSP72 increased in HOT (% change: 59% ± 11%; P = 0.03) but not in CLO (6% ± 2%; P = 0.31). Mean Tsk and HR were not different between HOT and CLO in men but were higher in HOT for women. CONCLUSION: These data support the idea that overdressing during exercise in a temperate environment may produce the high Tre, Tsk, HR, and SR necessary for adaptation, but these responses do not match those in hot, dry environments. It is possible that greater exercise stimulus, warmer environment, or more clothing may be required to allow for a similar level of acclimation.

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.

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.

Effect of Hypohydration on Muscle Endurance, Strength, Anaerobic Power and Capacity and Vertical Jumping Ability: A Meta-Analysis.

BACKGROUND: How hypohydration impacts non-bodyweight (BW)-dependent muscle performance and vertical jumping ability remains to be determined using meta-analytic procedures. OBJECTIVES: Our objective was to determine the impact of hypohydration on muscle endurance, strength, anaerobic power and capacity and vertical jumping ability using a meta-analytic approach. DATA SOURCES: Studies were located using database searches and cross-referencing. SYNTHESIS METHODS: Effect summaries were obtained using random-effects models; method of moments mixed-effects analysis-of-variance-like procedures were used to determine differences between groups; and restricted maximum likelihood random-effects meta-regressions were performed to determine relationships between variables, impact of confounders, and interaction effects. RESULTS: A total of 28 manuscripts met the inclusion criteria, producing six (upper body muscle endurance), ten (lower body muscle endurance), 14 (upper body muscle strength), 25 (lower body muscle strength), nine (muscle anaerobic power), nine (muscle anaerobic capacity), and 12 (vertical jumping ability) effect estimates. Hypohydration impaired overall muscle endurance by 8.3 ± 2.3% (P < 0.05), with no significant difference between upper body (-8.4 ± 3.3%) and lower body (-8.2 ± 3.2%). As a whole, muscle strength fell by 5.5 ± 1.0% (P < 0.05) with hypohydration; the difference between lower (-3.7 ± 1.8%) and upper (-6.2 ± 1.1%) body was non-significant. Anaerobic power (-5.8 ± 2.3%) was significantly altered with hypohydration, but anaerobic capacity (-3.5 ± 2.3%) and vertical jumping ability (0.9 ± 0.7%) were not. No significant correlations were observed between the changes in any of the muscle performance variables or vertical jumping ability and the changes in hypohydration level. Using an active procedure to dehydrate participants decreased muscle performance by an additional 5.4 ± 1.9% (2.76-fold) (P = 0.02) compared with using a passive dehydration procedure. Trained individuals demonstrated a 3.3 ± 1.7% (1.76-fold) (P = 0.06) lesser decrease in muscle performance with hypohydration than did untrained individuals. CONCLUSION: Hypohydration, or factors associated with dehydration, are likely to be associated with practically important decrements in muscle endurance, strength, and anaerobic power and capacity. However, their impact on non-BW-dependent muscle performance is substantially mitigated in trained individuals or when hypohydration is induced passively. Conversely, it is possible that body water loss (~3% BW) may improve performance in BW-dependent tasks such as vertical jumping ability.

Can targeting glutamate receptors with long-term heat acclimation improve outcomes following hypoxic injury?

Long-term heat acclimation appears to improve tolerance to hypoxic insults in various tissues, including brain, providing a promising avenue to improve functional outcomes following cerebrovascular events. Glutamate discharge is implicated in dysfunction following hypoxic stress and thus, targeting glutamate receptors with heat acclimation could improve cognitive outcomes following hypoxic injury.

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.

Heat acclimation and cross tolerance to hypoxia: Bridging the gap between cellular and systemic responses.

Recent research has suggested a potential for some of the physiological and cellular responses to heat acclimation to carry over to improved tolerance of the novel stresses of another environment. This cross-tolerance is evident in heat-acclimated animals that exhibit enhanced tolerance to either hypoxic or ischemic stress, and is primarily attributed to shared cellular stress response pathways. These pathways include Hypoxia-Inducible Factor-1 (HIF-1) and Heat Shock Proteins (HSP). Whether these shared cellular stress response pathways translate to systemic cross-tolerance (improved exercise tolerance, reduced risk of environment-associated illness) has not been clearly shown, particularly in humans. This review highlights the HIF-1 and HSP pathways and their relationship with systemic acclimation responses, and further examines the potential cellular and systemic adaptations that may result in cross-tolerance between hot and hypoxic environments.

Water-deficit equation: systematic analysis and improvement.

BACKGROUND: The water-deficit equation {WD(1) = 0.6 × B(m) × [1 - (140 ÷ Na(+))]; B(m) denotes body mass} is used in medicine and nutrition to estimate the volume (L) of water required to correct dehydration during the initial stages of fluid-replacement therapy. Several equation assumptions may limit its accuracy, but none have been systematically tested. OBJECTIVES: We quantified the potential error in WD(1) for the estimation of free water (FW) and total body water (TBW) losses and systematically evaluated its assumptions. DESIGN: Thirty-six euhydrated volunteers were dehydrated (2.2-5.8% B(m)) via thermoregulatory sweating. Assumptions within WD(1) were tested by substituting measured euhydrated values for assumed or unknown values. These included the known (premorbid) B(m) (WD(2)), a proposed correction for unknown B(m) (WD(3)), the TBW estimated from body composition (WD(4)), the actual plasma sodium (WD(5)), the substitution of plasma osmolality (Posm) for sodium (WD(6)), and actual Posm (WD(7)). RESULTS: Dehydration reduced TBW by 3.49 ± 0.91 L, 57% of which (2.02 ± 0.96 L) was FW loss, and increased plasma sodium from 139 (range: 135-143 mmol/L) to 143 (range: 141-148 mmol/L) mmol/L. Calculations for WD(1) through WD(7) all underestimated TBW loss by 1.5-2.5 L (P < 0.05). WD(1) through WD(5) underestimated FW by 0.5 L to 1.0 L (P < 0.05), but WD(6) and WD(7) estimated FW loss to within 0.06-0.16 L (P > 0.05). CONCLUSIONS: WD(1) grossly underestimates TBW and FW losses. Corrections for unknowns and assumptions (WD(2) through WD(5)) improved estimates little. The use of WD(6) = 0.6 × B(m) × [1 - (290 ÷ Posm)] accurately estimates FW but still underestimates TBW losses by >40%.

Hypohydration does not alter standing balance.

We examined the effect of body water deficits on standing balance and sought to determine if plasma hyperosmolality (P(osm)) and/or volume reduction (%ΔV(plasma)) exerted independent effects. Nine healthy volunteers completed three experimental trials which consisted of a euhydration (EUH) balance test, a water deficit session and a hypohydration (HYP) balance test. Hypohydration was achieved both by exercise-heat stress to 3% and 5% body mass loss (BML), and by a diuretic to 3% BML. Standing balance was assessed during quiet standing on a force platform with eyes open and closed. With eyes closed, hypohydration significantly decreased medial-lateral sway path and velocity by 13% (both p < .040). However, 95% confidence intervals for the mean difference between EUH and HYP were all within the coefficient of variation of EUH measures, indicating limited practical importance. Neither V(plasma) loss nor P(osm) increases were associated with changes in balance. We concluded that standing balance was not altered by hypohydration.