Hyperhydration and Glycerol: Thermoregulatory Effects During Exercise in Hot Climates

2000 ◽  
Vol 25 (6) ◽  
pp. 536-545 ◽  
Author(s):  
William A. Latzka ◽  
Michael N. Sawka
Keyword(s):  
Heat Stress ◽  
Core Temperature ◽  
Body Water ◽  
Fluid Replacement ◽  
Whole Body ◽  
Threshold Temperature ◽  
Sweating Rate ◽  
Design Problems ◽  
Fluid Ingestion ◽  
Water Exercise

Hyperhydration or increasing body water content above normal (euhydration) level was thought to have some benefit during exercise heat-stress; however, attempts to overdrink have been minimized by a rapid diuretic response. The perception that hyperhydration might be beneficial for exercise performance and for thermoregulation arose from the adverse consequences of hypohydration. Many studies had examined the effects of hyperhydration on thermoregulation in the heat; however, most of them suffer from design problems that confound their results. The design problems included control conditions not representing euhydration but hypohydration, control conditions not adequately described, cold fluid ingestion that reduced core temperature, and/or changing heat acclimation status. Several investigators reported lower core temperatures during exercise after hyperhydration, while other studies do not. Some investigators reported higher sweating rates with hyperhydration, while other studies do not. Recent research that controlled for these confounding variables reported that hyperhydration (water or glycerol) did not alter core temperature, skin temperature, whole body sweating rate, local sweating rate, sweating threshold temperature, sweating sensitivity, or heart rate responces compared to euhydration trail. If euhydration is maintained during exercise-heat stress then hyperhydration appears to have no meaningful advantage. Key words: Hydration, fluid replacement, exercise heat-stress, total body water exercise

Hyperhydration: thermoregulatory effects during compensable exercise-heat stress

1997 ◽  
Vol 83 (3) ◽  
pp. 860-866 ◽  
Author(s):  
William A. Latzka ◽  
Michael N. Sawka ◽  
Scott J. Montain ◽  
Gary S. Skrinar ◽  
Roger A. Fielding ◽  
...  
Keyword(s):  
Heat Stress ◽  
Heat Loss ◽  
Lean Body Mass ◽  
Body Mass ◽  
Core Temperature ◽  
Whole Body ◽  
Threshold Temperature ◽  
Evaporative Heat Loss ◽  
Sweating Rate ◽  
Total Body

Latzka, William A., Michael N. Sawka, Scott J. Montain, Gary S. Skrinar, Roger A. Fielding, Ralph P. Matott, and Kent B. Pandolf.Hyperhydration: thermoregulatory effects during compensable exercise-heat stress. J. Appl. Physiol. 83(3): 860–866, 1997.—This study examined the effects of hyperhydration on thermoregulatory responses during compensable exercise-heat stress. The general approach was to determine whether 1-h preexercise hyperhydration [29.1 ml/kg lean body mass; with or without glycerol (1.2 g/kg lean body mass)] would improve sweating responses and reduce core temperature during exercise. During these experiments, the evaporative heat loss required (Ereq = 293 W/m2) to maintain steady-state core temperature was less than the maximal capacity (Emax = 462 W/m2) of the climate for evaporative heat loss (Ereq/Emax= 63%). Eight heat-acclimated men completed five trials: euhydration, glycerol hyperhydration, and water hyperhydration both with and without rehydration (replace sweat loss during exercise). During exercise in the heat (35°C, 45% relative humidity), there was no difference between hyperhydration methods for increasing total body water (∼1.5 liters). Compared with euhydration, hyperhydration did not alter core temperature, skin temperature, whole body sweating rate, local sweating rate, sweating threshold temperature, sweating sensitivity, or heart rate responses. Similarly, no difference was found between water and glycerol hyperhydration for these physiological responses. These data demonstrate that hyperhydration provides no thermoregulatory advantage over the maintenance of euhydration during compensable exercise-heat stress.

Sensory nerves and nitric oxide contribute to reflex cutaneous vasodilation in humans

2013 ◽  
Vol 304 (8) ◽  
pp. R651-R656 ◽  
Author(s):  
Brett J. Wong
Keyword(s):  
Nitric Oxide ◽  
Heat Stress ◽  
Core Temperature ◽  
Sensory Nerve ◽  
Sensory Nerves ◽  
Whole Body ◽  
Oral Temperature ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Reflex Cutaneous Vasodilation

We tested the hypothesis that inhibition of cutaneous sensory nerves would attenuate reflex cutaneous vasodilation in response to an increase in core temperature. Nine subjects were equipped with four microdialysis fibers on the forearm. Two sites were treated with topical anesthetic EMLA cream for 120 min. Sensory nerve inhibition was verified by lack of sensation to a pinprick. Microdialysis fibers were randomly assigned as 1) lactated Ringer (control); 2) 10 mM nitro-l-arginine methyl ester (l-NAME) to inhibit nitric oxide synthase; 3) EMLA + lactated Ringer; and 4) EMLA + l-NAME. Laser-Doppler flowmetry was used as an index of skin blood flow, and blood pressure was measured via brachial auscultation. Subjects wore a water-perfused suit, and oral temperature was monitored as an index of core temperature. The suit was perfused with 50°C water to initiate whole body heat stress to raise oral temperature 0.8°C above baseline. Cutaneous vascular conductance (CVC) was calculated and normalized to maximal vasodilation (%CVCmax). There was no difference in CVC between control and EMLA sites (67 ± 5 vs. 69 ± 6% CVCmax), but the onset of vasodilation was delayed at EMLA compared with control sites. The l-NAME site was significantly attenuated compared with control and EMLA sites (45 ± 5% CVCmax; P < 0.01). Combined EMLA + l-NAME site (25 ± 6% CVCmax) was attenuated compared with control and EMLA ( P < 0.001) and l-NAME only ( P < 0.01). These data suggest cutaneous sensory nerves contribute to reflex cutaneous vasodilation during the early, but not latter, stages of heat stress, and full expression of reflex cutaneous vasodilation requires functional sensory nerves and NOS.

scholarly journals Impaired sweating responses to a passive whole body heat stress in individuals with multiple sclerosis

2017 ◽  
Vol 118 (1) ◽  
pp. 7-14 ◽  
Author(s):  
Dustin R. Allen ◽  
Mu Huang ◽  
Iqra M. Parupia ◽  
Ariana R. Dubelko ◽  
Elliot M. Frohman ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Heat Stress ◽  
Core Temperature ◽  
Sweat Rate ◽  
Whole Body ◽  
Healthy Controls ◽  
Cutaneous Vasodilation ◽  
Whole Body Heat Stress ◽  
Reflex Control ◽  
Body Heat

Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system (CNS), disrupting autonomic function. The aim of this study was to test the hypothesis that individuals with MS have blunted control of thermoregulatory reflex increases in sweat rate (SR) and cutaneous vasodilation compared with controls during a passive whole body heat stress (WBH). Eighteen individuals with relapsing-remitting MS and 18 healthy controls (Con) participated in the study. Core temperature (Tcore), skin temperature, heart rate, arterial blood pressure (10-min intervals), skin blood flow (laser-Doppler flux, LDF), and SR were continuously measured during normothermic baseline (34°C water perfusing a tube-lined suit) and WBH (increased Tcore 0.8°C via 48°C water perfusing the suit). Following WBH, local heaters were warmed to 42°C, inducing peak cutaneous vasodilation at the site of LDF collection. Cutaneous vascular conductance (CVC) was calculated as the ratio of LDF to mean arterial pressure and expressed as a percentage of peak achieved during local heating. Individuals with MS had attenuated SR responses to WBH (ΔSR from baseline: Con, 0.65 ± 0.27; MS, 0.42 ± 0.17 mg·cm−2·min−1, P = 0.003), whereas Δ%CVC42C from baseline was similar between groups (Con, 42 ± 16%; MS, 38 ± 12%, P = 0.39). SR responses were blunted as a function of Tcore in MS (interaction: group × Tcore, P = 0.03), of which differences were evident at ΔTcore 0.7°C and 0.8°C ( P < 0.05). No interaction was observed in Δ%CVC42C. Taken together, the findings show MS blunts sweating responses, whereas control of the cutaneous vasculature is preserved, in response to WBH. NEW & NOTEWORTHY This study is the first to assess the reflex control of the thermoregulatory system in individuals living with multiple sclerosis (MS). The novel findings are twofold. First, attenuated increases in sweat rate in subjects with MS compared with healthy controls were observed in response to a moderate increase (0.8°C) in core temperature via passive whole body heat stress. Second, it appears the reflex control of the cutaneous vasculature is preserved in MS.

Divergent roles of plasma osmolality and the baroreflex on sweating and skin blood flow

2012 ◽  
Vol 302 (5) ◽  
pp. R634-R642 ◽  
Author(s):  
Aaron G. Lynn ◽  
Daniel Gagnon ◽  
Konrad Binder ◽  
Robert C. Boushel ◽  
Glen P. Kenny
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Core Temperature ◽  
Skin Blood Flow ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Plasma Osmolality ◽  
Whole Body ◽  
Lower Body ◽  
Change In Mean

Plasma hyperosmolality and baroreceptor unloading have been shown to independently influence the heat loss responses of sweating and cutaneous vasodilation. However, their combined effects remain unresolved. On four separate occasions, eight males were passively heated with a liquid-conditioned suit to 1.0°C above baseline core temperature during a resting isosmotic state (infusion of 0.9% NaCl saline) with (LBNP) and without (CON) application of lower-body negative pressure (−40 cmH2O) and during a hyperosmotic state (infusion of 3.0% NaCl saline) with (LBNP + HYP) and without (HYP) application of lower-body negative pressure. Forearm sweat rate (ventilated capsule) and skin blood flow (laser-Doppler), as well as core (esophageal) and mean skin temperatures, were measured continuously. Plasma osmolality increased by ∼10 mosmol/kgH2O during HYP and HYP + LBNP conditions, whereas it remained unchanged during CON and LBNP ( P ≤ 0.05). The change in mean body temperature (0.8 × core temperature + 0.2 × mean skin temperature) at the onset threshold for increases in cutaneous vascular conductance (CVC) was significantly greater during LBNP (0.56 ± 0.24°C) and HYP (0.69 ± 0.36°C) conditions compared with CON (0.28 ± 0.23°C, P ≤ 0.05). Additionally, the onset threshold for CVC during LBNP + HYP (0.88 ± 0.33°C) was significantly greater than CON and LBNP conditions ( P ≤ 0.05). In contrast, onset thresholds for sweating were not different during LBNP (0.50 ± 0.18°C) compared with CON (0.46 ± 0.26°C, P = 0.950) but were elevated ( P ≤ 0.05) similarly during HYP (0.91 ± 0.37°C) and LBNP + HYP (0.94 ± 0.40°C). Our findings show an additive effect of hyperosmolality and baroreceptor unloading on the onset threshold for increases in CVC during whole body heat stress. In contrast, the onset threshold for sweating during heat stress was only elevated by hyperosmolality with no effect of the baroreflex.

Control of thermoregulatory sweating during exercise in the heat

1989 ◽  
Vol 257 (2) ◽  
pp. R311-R316 ◽  
Author(s):  
M. N. Sawka ◽  
R. R. Gonzalez ◽  
A. J. Young ◽  
R. C. Dennis ◽  
C. R. Valeri ◽  
...  
Keyword(s):  
Heat Stress ◽  
Relative Humidity ◽  
Blood Volume ◽  
Treadmill Exercise ◽  
Threshold Temperature ◽  
Control Parameters ◽  
Esophageal Temperature ◽  
Stress Tests ◽  
Sweating Rate ◽  
Humidity Environment

The purposes of this study were the following: 1) to determine whether erythrocyte infusion alters the control of thermoregulatory sweating and 2) to demonstrate how increases and decreases of both plasma tonicity and blood volume influence the thermoregulatory control parameters of threshold temperature and sweating sensitivity. Six non-heat-acclimated and five heat-acclimated males attempted heat stress tests (HSTs) both before and shortly after (48-96 h) autologous erythrocyte infusion. The non-heat-acclimated subjects were euhydrated for both HSTs, whereas the heat-acclimated subjects were studied in a euhydrated and a hypohydrated (-5% body wt) condition both pre- and postinfusion (500 ml of solution containing approximately 60% hematocrit of autologous erythrocytes). The HSTs consisted of treadmill exercise (335 W.m-2) in a hot (35 degrees C, 45% relative humidity) environment, and esophageal temperature and local sweating rate were continuously measured during 25 min of exercise. These experiments resulted in a matrix of conditions where both plasma tonicity and blood volume were increased or decreased relative to control conditions (euhydration, preinfusion). The findings concerning thermoregulatory sweating during exercise in the heat were summarized as follows: 1) acute polycythemia decreases the threshold temperature and increases the sweating sensitivity, 2) both threshold temperature and sweating sensitivity are increased or decreased from control levels dependent on the combined influence of plasma tonicity and blood volume, and 3) equations are presented that describe how plasma tonicity and blood volume alter threshold temperature and sweating sensitivity values.

Hyperhydration: tolerance and cardiovascular effects during uncompensable exercise-heat stress

1998 ◽  
Vol 84 (6) ◽  
pp. 1858-1864 ◽  
Author(s):  
William A. Latzka ◽  
Michael N. Sawka ◽  
Scott J. Montain ◽  
Gary S. Skrinar ◽  
Roger A. Fielding ◽  
...  
Keyword(s):  
Heat Stress ◽  
Lean Body Mass ◽  
Body Mass ◽  
Core Temperature ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Temperature Tolerance ◽  
Whole Body ◽  
Evaporative Heat Loss ◽  
Water Glycerol

This study examined the efficacy of glycerol and water hyperhydration (1 h before exercise) on tolerance and cardiovascular strain during uncompensable exercise-heat stress. The approach was to determine whether 1-h preexercise hyperhydration (29.1 ml H2O/kg lean body mass with or without 1.2 g/kg lean body mass of glycerol) provided a physiological advantage over euhydration. Eight heat-acclimated men completed three trials (control euhydration before exercise, and glycerol and water hyperhydrations) consisting of treadmill exercise-heat stress (ratio of evaporative heat loss required to maximal capacity of climate = 416). During exercise (∼55% maximal O2 uptake), there was no difference between glycerol and water hyperhydration methods for increasing ( P < 0.05) total body water. Glycerol hyperhydration endurance time (33.8 ± 3.0 min) was longer ( P < 0.05) than for control (29.5 ± 3.5 min), but was not different ( P > 0.05) from that of water hyperhydration (31.3 ± 3.1 min). Hyperhydration did not alter ( P > 0.05) core temperature, whole body sweating rate, cardiac output, blood pressure, total peripheral resistance, or core temperature tolerance. Exhaustion from heat strain occurred at similar core and skin temperatures and heart rates in each trial. Symptoms at exhaustion included syncope and ataxia, fatigue, dyspnea, and muscle cramps ( n = 11, 10, 2, and 1 cases, respectively). We conclude that 1-h preexercise glycerol hyperhydration provides no meaningful physiological advantage over water hyperhydration and that hyperhydration per se only provides the advantage (over euhydration) of delaying hypohydration during uncompensble exercise-heat stress.

scholarly journals Thermoregulatory adaptations with progressive heat acclimation are predominantly evident in uncompensable, but not compensable, conditions

2019 ◽  
Vol 127 (4) ◽  
pp. 1095-1106 ◽  
Author(s):  
Nicholas Ravanelli ◽  
Geoff Coombs ◽  
Pascal Imbeault ◽  
Ollie Jay
Keyword(s):  
Heat Stress ◽  
Core Temperature ◽  
Heat Dissipation ◽  
Sweat Rate ◽  
Heat Acclimation ◽  
Whole Body ◽  
Evaporative Heat Loss ◽  
Physiological Limits ◽  
Physiological Capacity ◽  
Uncompensable Heat Stress

This study assessed whether, notwithstanding lower resting absolute core temperatures, alterations in time-dependent changes in thermoregulatory responses following partial and complete heat acclimation (HA) are only evident during uncompensable heat stress. Eight untrained individuals underwent 8 wk of aerobic training (i.e., partial HA) followed by 6 days of HA in 38°C/65% relative humidity (RH) (i.e., complete HA). On separate days, esophageal temperature (Tes), arm (LSRarm), and back (LSRback) sweat rate, and whole body sweat rate (WBSR) were measured during a 45-min compensable (37°C/30% RH) and 60-min uncompensable (37°C/60% RH) heat stress trial pre-training (PRE-TRN), post-training (POST-TRN), and post–heat acclimation (POST-HA). For compensable heat stress trials, resting Tes was lower POST-TRN (36.74 ± 0.27°C, P = 0.05) and POST-HA (36.60 ± 0.27°C, P = 0.001) compared with PRE-TRN (36.99 ± 0.19°C); however, ΔTes was similar in all trials (PRE-TRN:0.40 ± 0.23°C; POST-TRN:0.42 ± 0.20°C; POST-HA:0.43 ± 0.12°C, P = 0.97). While LSRback was unaltered by HA ( P = 0.94), end-exercise LSRarm was higher POST-TRN (0.70 ± 0.14 mg·cm−2·min−1, P < 0.001) and POST-HA (0.75 ± 0.16 mg·cm−2·min−1, P < 0.001) compared with PRE-TRN (0.61 ± 0.15 mg·cm−2·min−1). Despite matched evaporative heat balance requirements, steady-state WBSR (31st–45th min) was greater POST-TRN (12.7 ± 1.0 g/min, P = 0.02) and POST-HA (12.9 ± 0.8 g/min, P = 0.004), compared with PRE-TRN (11.7 ± 0.9 g/min). For uncompensable heat stress trials, resting Tes was lower POST-TRN (36.77 ± 0.22°C, P = 0.05) and POST-HA (36.62 ± 0.15°C, P = 0.03) compared with PRE-TRN (36.86 ± 0.24°C). But ΔTes was smaller POST-TRN (0.77 ± 0.19°C, P = 0.05) and POST-HA (0.75 ± 0.15°C, P = 0.04) compared with PRE-TRN (1.10 ± 0.32°C). LSRback and LSRarm increased with HA ( P < 0.007), supporting the greater WBSR with HA (POST-TRN:14.4 ± 2.4 g/min, P < 0.001; POST-HA:16.8 ± 2.8 g/min, P < 0.001) compared with PRE-TRN (12.7 ± 3.2 g/min). In conclusion, the thermal benefits of HA are primarily evident when conditions challenge the physiological capacity to dissipate heat. NEW & NOTEWORTHY We demonstrate that neither partial nor complete heat acclimation alters the change in core temperature during compensable heat stress compared with an unacclimated state, despite a marginally greater whole body sweat rate. However, the greater local and whole body sweat rate with partial and complete heat acclimation reduced the rise in core temperature during 60 min of uncompensable heat stress compared with an unacclimated state, suggesting the improvements in heat dissipation associated with heat acclimation are best observed when the upper physiological limits for evaporative heat loss are challenged.

scholarly journals Heat Stress and Cardiovascular, Hormonal, and Heat Shock Proteins in Humans

2012 ◽  
Vol 47 (2) ◽  
pp. 184-190 ◽  
Author(s):  
Masaki Iguchi ◽  
Andrew E. Littmann ◽  
Shuo-Hsiu Chang ◽  
Lydia A. Wester ◽  
Jane S. Knipper ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Heat Shock ◽  
Body Temperature ◽  
Controlled Trial ◽  
Whole Body ◽  
Cord Injury ◽  
Whole Body Heat Stress ◽  
Body Heat

Context: Conditions such as osteoarthritis, obesity, and spinal cord injury limit the ability of patients to exercise, preventing them from experiencing many well-documented physiologic stressors. Recent evidence indicates that some of these stressors might derive from exercise-induced body temperature increases. Objective: To determine whether whole-body heat stress without exercise triggers cardiovascular, hormonal, and extra-cellular protein responses of exercise. Design: Randomized controlled trial. Setting: University research laboratory. Patients or Other Participants: Twenty-five young, healthy adults (13 men, 12 women; age = 22.1 ± 2.4 years, height = 175.2 ± 11.6 cm, mass = 69.4 ± 14.8 kg, body mass index = 22.6 ± 4.0) volunteered. Intervention(s): Participants sat in a heat stress chamber with heat (73°C) and without heat (26°C) stress for 30 minutes on separate days. We obtained blood samples from a subset of 13 participants (7 men, 6 women) before and after exposure to heat stress. Main Outcome Measure(s): Extracellular heat shock protein (HSP72) and catecholamine plasma concentration, heart rate, blood pressure, and heat perception. Results: After 30 minutes of heat stress, body temperature measured via rectal sensor increased by 0.8°C. Heart rate increased linearly to 131.4 ± 22.4 beats per minute (F6,24 = 186, P &lt; .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F6,24 = 10.1, P &lt; .001) and 5 mm Hg (F6,24 = 5.4, P &lt; .001), respectively. Norepinephrine (F1,12 = 12.1, P = .004) and prolactin (F1,12 = 30.2, P &lt; .001) increased in the plasma (58% and 285%, respectively) (P &lt; .05). The HSP72 (F1,12 = 44.7, P &lt; .001) level increased with heat stress by 48.7% ± 53.9%. No cardiovascular or blood variables showed changes during the control trials (quiet sitting in the heat chamber with no heat stress), resulting in differences between heat and control trials. Conclusions: We found that whole-body heat stress triggers some of the physiologic responses observed with exercise. Future studies are necessary to investigate whether carefully prescribed heat stress constitutes a method to augment or supplement exercise.

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