Thermoregulatory, cardiovascular, and psychophysical response to alcohol in men in 40 degrees C water

1992 ◽  
Vol 72 (6) ◽  
pp. 2099-2107 ◽  
Author(s):  
T. G. Allison ◽  
W. E. Reger

The goals of the study were to test the hypotheses that ethyl alcohol (ETOH) in low-to-moderate doses would alter thermo-regulation and/or disrupt the normal relationship between physiological and psychophysical indexes of heat stress during 40 degrees C water immersion and to characterize the cardiovascular response to the combined stimuli of heat, water immersion, and ETOH. Six healthy men underwent three trials of 21 min of immersion in water at 40.0 +/- 0.1 degrees C after consuming 0, 0.27, or 0.54 g ETOH/kg. Esophageal temperature (Tes) rose by approximately 1.0 degrees C during immersion for each trial. Per unit of Tes rise, changes during immersion in skin temperature, sweat rate, heart rate, systolic and diastolic blood pressure, and psychophysical assessments of comfort and overheating did not differ significantly by trial. Across trials, there was an apparent threshold for activation of thermoregulatory responses at an approximately 0.5 degrees C increase in Tes occurring after approximately 9 min of immersion. This threshold was identified psychophysically by increased ratings of overheating and decreased comfort. Above the threshold, there was an attenuation of the rate of increase of Tes. Cardiovascular stress was mild (rate-pressure product approximately 12,000) and not significantly increased by ETOH. Hypotension and tachycardia when subjects stood to exit the tub were observed. The data suggest that ETOH at the doses administered does not affect thermoregulatory, cardiovascular, or psychophysical indexes of heat stress during 40 degrees C water immersion.

2017 ◽  
Vol 312 (5) ◽  
pp. R637-R642 ◽  
Author(s):  
Matthew A. Tucker ◽  
Ashley Six ◽  
Nicole E. Moyen ◽  
Alf Z. Satterfield ◽  
Matthew S. Ganio

Hypohydration decreases cutaneous vasodilation and sweating during heat stress, but it is unknown if these decrements are from postsynaptic (i.e., sweat gland/blood vessel) alterations. The purpose of this study was to determine if hypohydration affects postsynaptic cutaneous vasodilation and sweating responses. Twelve healthy men participated in euhydrated (EU) and hypohydrated (HY) trials, with hypohydration induced via fluid restriction and passive heat stress. Changes in cutaneous vascular conductance (CVC; %max) in response to incremental intradermal infusion of the endothelium-independent vasodilator sodium nitroprusside (SNP) and the endothelium-dependent vasodilator methacholine chloride (MCh) were assessed by laser Doppler flowmetry. Local sweat rate (LSR) was simultaneously assessed at the MCh site via ventilated capsule. At the end of the last dose, maximal CVC was elicited by delivering a maximal dose of SNP (5 × 10−2 M) for 30 min to both sites with simultaneous local heating (~44°C) at the SNP site. The concentration of drug needed to elicit 50% of the maximal response (log EC50) was compared between hydration conditions. The percent body mass loss was greater with HY vs. EU (−2.2 ± 0.7 vs. −0.1 ± 0.7%, P < 0.001). Log EC50 of endothelium-dependent CVC was lower with EU (−3.62 ± 0.22) vs. HY (−2.93 ± 0.08; P = 0.044). Hypohydration did not significantly alter endothelium-independent CVC or LSR (both P > 0.05). In conclusion, hypohydration attenuated endothelium-dependent CVC but did not affect endothelium-independent CVC or LSR responses. These data suggest that reductions in skin blood flow accompanying hypohydration can be partially attributed to altered postsynaptic function.


1992 ◽  
Vol 73 (4) ◽  
pp. 1340-1350 ◽  
Author(s):  
S. J. Montain ◽  
E. F. Coyle

This investigation determined the effect of different rates of dehydration, induced by ingesting different volumes of fluid during prolonged exercise, on hyperthermia, heart rate (HR), and stroke volume (SV). On four different occasions, eight endurance-trained cyclists [age 23 +/- 3 (SD) yr, body wt 71.9 +/- 11.6 kg, maximal O2 consumption 4.72 +/- 0.33 l/min] cycled at a power output equal to 62-67% maximal O2 consumption for 2 h in a warm environment (33 degrees C dry bulb, 50% relative humidity, wind speed 2.5 m/s). During exercise, they randomly received no fluid (NF) or ingested a small (SF), moderate (MF), or large (LF) volume of fluid that replaced 20 +/- 1, 48 +/- 1, and 81 +/- 2%, respectively, of the fluid lost in sweat during exercise. The protocol resulted in graded magnitudes of dehydration as body weight declined 4.2 +/- 0.1, 3.4 +/- 0.1, 2.3 +/- 0.1, and 1.1 +/- 0.1%, respectively, during NF, SF, MF, and LF. After 2 h of exercise, esophageal temperature (Tes), HR, and SV were significantly different among the four trials (P < 0.05), with the exception of NF and SF. The magnitude of dehydration accrued after 2 h of exercise in the four trials was linearly related with the increase in Tes (r = 0.98, P < 0.02), the increase in HR (r = 0.99, P < 0.01), and the decline in SV (r = 0.99, P < 0.01). LF attenuated hyperthermia, apparently because of higher skin blood flow, inasmuch as forearm blood flow was 20–22% higher than during SF and NF at 105 min (P < 0.05). There were no differences in sweat rate among the four trials. In each subject, the increase in Tes from 20 to 120 min of exercise was highly correlated to the increase in serum osmolality (r = 0.81-0.98, P < 0.02-0.19) and the increase in serum sodium concentration (r = 0.87-0.99, P < 0.01-0.13) from 5 to 120 min of exercise. In summary, the magnitude of increase in core temperature and HR and the decline in SV are graded in proportion to the amount of dehydration accrued during exercise.


1998 ◽  
Vol 84 (5) ◽  
pp. 1731-1739 ◽  
Author(s):  
Stephen S. Cheung ◽  
Tom M. McLellan

—The purpose of the present study was to determine the separate and combined effects of aerobic fitness, short-term heat acclimation, and hypohydration on tolerance during light exercise while wearing nuclear, biological, and chemical protective clothing in the heat (40°C, 30% relative humidity). Men who were moderately fit [(MF); <50 ml ⋅ kg−1 ⋅ min−1maximal O2 consumption; n = 7] and highly fit [(HF); >55 ml ⋅ kg−1 ⋅ min−1maximal O2 consumption; n = 8] were tested while they were euhydrated or hypohydrated by ∼2.5% of body mass through exercise and fluid restriction the day preceding the trials. Tests were conducted before and after 2 wk of daily heat acclimation (1-h treadmill exercise at 40°C, 30% relative humidity, while wearing the nuclear, biological, and chemical protective clothing). Heat acclimation increased sweat rate and decreased skin temperature and rectal temperature (Tre) in HF subjects but had no effect on tolerance time (TT). MF subjects increased sweat rate but did not alter heart rate, Tre, or TT. In both MF and HF groups, hypohydration significantly increased Tre and heart rate and decreased the respiratory exchange ratio and the TT regardless of acclimation state. Overall, the rate of rise of skin temperature was less, while ΔTre, the rate of rise of Tre, and the TT were greater in HF than in MF subjects. It was concluded that exercise-heat tolerance in this uncompensable heat-stress environment is not influenced by short-term heat acclimation but is significantly improved by long-term aerobic fitness.


2017 ◽  
Vol 23 (5) ◽  
pp. 380-384
Author(s):  
Márcio Rabelo Mota ◽  
Sandro Nobre Chaves ◽  
Maurílio Tiradentes Dutra ◽  
Ricardo Jacó de Oliveira ◽  
Renata Aparecida Elias Dantas ◽  
...  

ABSTRACT Introduction: Pre-prandial exercise promotes greater mobilization of fat metabolism due to the increased release of catecholamines, cortisol, and glucagon. However, this response affects how the cardiovascular system responds to exercise. Objective: To evaluate the response of systolic, diastolic, and mean blood pressure, heart rate (HR) and rate-pressure product (RPP) to pre- and postprandial exercise. Methods: Ten physically active male subjects (25.50 ± 2.22 years) underwent two treadmill protocols (pre- and postprandial) performed for 36 minutes at 65% of VO2max on different days. On both days, subjects attended the laboratory on a 10-hour fasting state. For the postprandial session, volunteers ingested a pre-exercise meal of 349.17 kcal containing 59.3 g of carbohydrates (76.73%), 9.97 g of protein (12.90%), and 8.01 g of lipids (10.37%). Blood pressure, HR and RPP were measured before and after exercise. The 2x2 factorial Anova with the multiple comparisons test of Bonferroni was applied to analyze cardiovascular variables in both moments (pre- vs. postprandial). The significance level was set at p<0.05. Results: Systolic (121.70 ± 7.80 vs. 139.78 ± 12.91 mmHg) and diastolic blood pressure (66.40 ± 9.81 vs. 80.22 ± 8.68 mmHg) increased significantly after exercise only in the postprandial session (p<0.05). HR increased significantly (p<0.05) after both protocols (64.20 ± 15.87 vs. 141.20 ± 10.33 bpm pre-prandial and 63.60 ± 8.82 vs. 139.20 ± 10.82 bpm postprandial). RPP had a similar result (8052.10 ± 1790.68 vs. 18382.60 ± 2341.66 mmHg.bpm in the pre-prandial session and 7772.60 ± 1413.76 vs. 19564.60 ± 3128.99 mmHg.bpm in the postprandial session). Conclusion: These data suggest that fasted exercise does not significantly alter the blood pressure. Furthermore, the meal provided before the postprandial exercise may promote a greater blood pressure responsiveness during exercise.


1984 ◽  
Vol 56 (5) ◽  
pp. 1283-1288 ◽  
Author(s):  
J. M. Johnson ◽  
D. S. O'Leary ◽  
W. F. Taylor ◽  
M. K. Park

To find whether sweat rate (SR) and forearm skin blood flow ( SkBF ) were reflexly affected by skin temperature (Tsk) we used water-perfused suits to rapidly elevate Tsk during exercise. With this elevation in Tsk, there was a period of little net change in esophageal temperature (Tes) but marked responses in SR and SkBF . During this period a rise in Tsk of 4.2 +/- 0.3 degrees C was associated with an increase in SR of 0.44 +/- 0.09 mg X cm-2 X min-1 and an increase in SkBF of 3.27 +/- 0.42 ml X 100 ml-1 X min-1. Multiple linear regression analysis as well as comparison with control studies in which Tsk was kept cool also reveal a consistent role for Tsk in the reflex regulation of SR and SkBF . Responses in SR and FBF were much more marked at levels of Tsk below 33 degrees C. Below a Tsk of 33 degrees C, SR rose 0.30 +/- 0.06 mg X cm-2 X min-1 per degrees C rise in Tsk, whereas above 33 degrees SR rose only 0.05 +/- 0.01 mg X cm2 X min per degrees C. FBF rose 2.81 +/- 0.60 and 0.77 +/- 0.18 ml X 100 ml-1 X min-1 per degrees C rise in Tsk at the lower and upper ranges of Tsk, respectively.


1988 ◽  
Vol 65 (6) ◽  
pp. 2709-2713 ◽  
Author(s):  
K. D. Mittleman ◽  
I. B. Mekjavic

Recent studies using inanimate and animal models suggest that the afterdrop observed upon rewarming from hypothermia is based entirely on physical laws of heat flow without involvement of the returning cooled blood from the limbs. During the investigation of thermoregulatory responses to cold water immersion (15 degrees C), blood flow to the limbs (minimized by the effects of hydrostatic pressure and vasoconstriction) was occluded in 17 male subjects (age, 29.0 +/- 3.3 yr). Comparisons of rectal (Tre) and esophageal temperature (Tes) responses were made during the 5 min before occlusion, during the 10-min occlusion period, and for 5 min immediately after the release of the cuffs (postocclusion). In the preocclusion phase, Tre and Tes showed similar cooling rates. The occlusion of blood flow to the extremities significantly arrested the cooling of Tes (P less than 0.05) with little effect on Tre. Upon release of the pressure cuffs, the returning extremity blood flow resulted in an increased rate of cooling, that was three times greater at the esophageal site (-0:149 +/- 0.052 vs. -0.050 +/- 0.026 degrees C.min-1). These results suggest that the cooled peripheral circulation, minimized during cold water immersion, may dramatically affect esophageal temperature and the complete neglect of the circulatory component to the afterdrop phenomenon is not warranted.


2015 ◽  
Vol 309 (1) ◽  
pp. R36-R42 ◽  
Author(s):  
Nicole E. Moyen ◽  
Hannah M. Anderson ◽  
Jenna M. Burchfield ◽  
Matthew A. Tucker ◽  
Melina A. Gonzalez ◽  
...  

The purpose of this study was to compare smokers and nonsmokers' sudomotor and cutaneous vascular responses to whole body passive heat stress. Nine regularly smoking (SMK: 29 ± 9 yr; 10 ± 6 cigarettes/day) and 13 nonsmoking (N-SMK: 27 ± 8 yr) males were passively heated until core temperature (TC) increased 1.5°C from baseline. Forearm local sweat rate (LSR) via ventilated capsule, sweat gland activation (SGA), sweat gland output (SGO), and cutaneous vasomotor activity via laser-Doppler flowmetry (CVC) were measured as mean body temperature increased (ΔTb) during passive heating using a water-perfused suit. Compared with N-SMK, SMK had a smaller ΔTb at the onset of sweating (0.52 ± 0.19 vs. 0.35 ± 0.14°C, respectively; P = 0.03) and cutaneous vasodilation (0.61 ± 0.21 vs. 0.31 ± 0.12°C, respectively; P < 0.01). Increases in LSR and CVC per °C ΔTb (i.e., sensitivity) were similar in N-SMK and SMK (LSR: 0.63 ± 0.21 vs. 0.60 ± 0.40 Δmg/cm2/min/°C ΔTb, respectively, P = 0.81; CVC: 82.5 ± 46.2 vs. 58.9 ± 23.3 Δ%max/°C ΔTb, respectively; P = 0.19). However, the plateau in LSR during whole body heating was higher in N-SMK vs. SMK (1.00 ± 0.13 vs. 0.79 ± 0.26 mg·cm−2·min−1; P = 0.03), which was likely a result of higher SGO (8.94 ± 3.99 vs. 5.94 ± 3.49 μg·gland−1·min−1, respectively; P = 0.08) and not number of SGA (104 ± 7 vs. 121 ± 9 glands/cm2, respectively; P = 0.58). During whole body passive heat stress, smokers had an earlier onset for forearm sweating and cutaneous vasodilation, but a lower local sweat rate that was likely due to lower sweat output per gland. These data provide insight into local (i.e., forearm) thermoregulatory responses of young smokers during uncompensatory whole body passive heat stress.


2005 ◽  
Vol 98 (3) ◽  
pp. 829-837 ◽  
Author(s):  
Yoshi-Ichiro Kamijo ◽  
Kichang Lee ◽  
Gary W. Mack

The role of skin temperature in reflex control of the active cutaneous vasodilator system was examined in six subjects during mild graded heat stress imposed by perfusing water at 34, 36, 38, and 40°C through a tube-lined garment. Skin sympathetic nerve activity (SSNA) was recorded from the peroneal nerve with microneurography. While monitoring esophageal, mean skin, and local skin temperatures, we recorded skin blood flow at bretylium-treated and untreated skin sites by using laser-Doppler velocimetry and local sweat rate by using capacitance hygrometry on the dorsal foot. Cutaneous vascular conductance (CVC) was calculated by dividing skin blood flow by mean arterial pressure. Mild heat stress increased mean skin temperature by 0.2 or 0.3°C every stage, but esophageal and local skin temperature did not change during the first three stages. CVC at the bretylium tosylate-treated site (CVCBT) and sweat expulsion number increased at 38 and 40°C compared with 34°C ( P < 0.05); however, CVC at the untreated site did not change. SSNA increased at 40°C ( P < 0.05, different from 34°C). However, SSNA burst amplitude increased ( P < 0.05), whereas SSNA burst duration decreased ( P < 0.05), at the same time as we observed the increase in CVCBT and sweat expulsion number. These data support the hypothesis that the active vasodilator system is activated by changes in mean skin temperature, even at normal core temperature, and illustrate the intricate competition between active vasodilator and the vasoconstrictor system for control of skin blood flow during mild heat stress.


1984 ◽  
Vol 246 (3) ◽  
pp. R321-R324 ◽  
Author(s):  
L. A. Stephenson ◽  
C. B. Wenger ◽  
B. H. O'Donovan ◽  
E. R. Nadel

To characterize the changes in the control of the heat loss responses associated with the circadian variation in body temperature, we studied five men during 20 min of exercise in 25 degrees C on 6 separate days. Experiments were conducted at six times, equally spaced over the 24-h day. Esophageal temperature (Tes) and chest sweat rate (msw) were measured continuously, and forearm blood flow (FBF) was measured one to two times per minute. The thresholds for sweating and forearm vasodilation were significantly higher at 1600 and 2000 than at 2400 and 0400, averaging 0.57 and 0.65 degrees C higher, respectively, at 1600 than at 0400. Resting Tes and the Tes thresholds for cutaneous vasodilation and sweating during exercise all showed a similar circadian rhythm. The level at which core temperature is regulated therefore varies over the 24-h day with the zenith occurring around 1600 and the nadir at 0400. However, whereas the slope of the msw-to-Tes relation did not change over the 24-h day, the slope of the FBF-to-Tes relation tended to increase between 0400 and 2400, implying that the circadian rhythm may be more complex than just a shift in the central reference temperature.


2014 ◽  
Vol 31 (2) ◽  
pp. 145-149 ◽  
Author(s):  
Wanda Pilch ◽  
Zbigniew Szyguła ◽  
Tomasz Palka ◽  
Paweł Pilch ◽  
Tomasz Cison ◽  
...  

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