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New Findings: What is the central question of this study? In male lowlanders, does hypoxia modulate thermoregulatory effector responses during repeated whole-body cold stress encountered in a single day? What is the main finding and its importance? A ∼10 h sustained exposure to hypoxia appears to mediate a gradual upregulation of endogenous heat production, preventing the progressive hypothermic response prompted by serial cold stimuli. Also, hypoxia progressively degrades mood, and compounds the perceived thermal discomfort, and sensations of fatigue and coldness., Abstract: We examined whether hypoxia would modulate thermoeffector responses during repeated cold stress encountered in a single day. Eleven men completed two ∼10 h sessions, while breathing, in normobaria, either normoxia or hypoxia ( P O 2 : 12 kPa). During each session, subjects underwent sequentially three 120 min immersions to the chest in 20°C water (CWI), interspersed by 120 min rewarming. In normoxia, the final drop in rectal temperature (T rec ) was greater in the third (∼1.2°C) than in the first and second (∼0.9°C) CWIs (P < 0.05). The first hypoxic CWI augmented the T rec fall (∼1.2°C; P = 0.002), but the drop in T rec did not vary between the three hypoxic CWIs (P = 0.99). In normoxia, the metabolic heat production ( M ̇ ) was greater during the first half of the third CWI than during the corresponding part of the first CWI (P = 0.02); yet the difference was blunted during the second half of the CWIs (P = 0.89). In hypoxia, by contrast, the increase in M ̇ was augmented by ∼25% throughout the third CWI (P < 0.01). Regardless of the breathing condition, the cold-induced elevation in mean arterial pressure was blunted in the second and third CWI (P < 0.05). Hypoxia aggravated the sensation of coldness (P = 0.05) and thermal discomfort (P = 0.04) during the second half of the third CWI. The present findings therefore demonstrate that prolonged hypoxia mediates, in a gradual manner, metabolic and thermoperceptual sensitization to repeated cold stress., (© 2020 The Authors. Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)

Purpose: The purpose was to examine whether associations exist between temperature responses in the fingers vs. toes and hand vs. foot during local cold-water immersion and rewarming phases., Methods: Seventy healthy subjects (58 males, 12 females) immersed their right hand or right foot, respectively, in 8 °C water for 30 min (CWI phase), followed by a 15-min spontaneous rewarming (RW) in 25 °C air temperature., Results: Temperature was lower in the toes than the fingers during the baseline phase (27.8 ± 3.0 vs. 33.9 ± 2.5 °C, p < 0.001), parts of the CWI phase (min 20-30: 8.8 ± 0.7 vs. 9.7 ± 1.4 °C, p < 0.001), and during the RW phase (peak temperature: 22.5 ± 5.1 vs. 32.7 ± 3.6 °C, p < 0.001). Cold-induced vasodilatation (CIVD) was more common in the fingers than in the toes (p < 0.001). Within the first 10 min of CWI, 61% of the subjects exhibited a CIVD response in the fingers, while only 6% of the subjects had a CIVD response in the toes. There was a large variability of temperature responses both within and between extremities, and there was a weak correlation between finger- and toe temperature both during the CWI (r = 0.21, p = 0.08) and the RW phases (r = 0.26, p = 0.03)., Conclusions: Results suggest that there is generally a lower temperature in the toes than the fingers after a short time of local cold exposure and that the thermal responses of the fingers/hands are not readily transferable to the toes/foot.

The study examined the effects of a 10-day normobaric hypoxic confinement on the finger and toe temperature responses to local cooling. Eight male lowlanders underwent a normoxic (NC) and, in a separate occasion, a normobaric hypoxic confinement (HC; FO 2 : 0.154; simulated altitude ~3400m). Before and after each confinement, subjects immersed for 30min their right hand and, in a different session, their right foot in 8°C water, while breathing either room air (AIR) or a hypoxic gas mixture (HYPO). Throughout the cold-water immersion tests, thermal responses were monitored with thermocouples on fingers and toes. Neither confinement influenced thermal responses in the fingers during the AIR or HYPO test. In the foot, by contrast, HC, but not NC, reduced the average toe temperature by ~1.5°C (p=0.03), both during the AIR and HYPO test. We therefore conclude that a 10-day confinement to normobaric hypoxia per se augments cold-induced vasoconstriction in the toes, but not in the fingers. The mechanism underlying this dissimilarity remains to be established., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Purpose: Acute hypoxia alters the threshold for sensation of cutaneous thermal stimuli. We hypothesised that hypoxia-induced alterations in cutaneous temperature sensation may lead to modulation of the perception of temperature, ultimately influencing behavioural thermoregulation and that the magnitude of this effect could be influenced by daily physical training., Methods: Fourteen men were confined 10 days to a normobaric hypoxic environment (P I O 2  = 88.2 ± 0.6 mmHg, corresponding to 4175 m elevation). Subjects were randomly assigned to a non-exercising (Live-high, LH, N = 6), or exercising group (Live-high Train-high, LH-TH, N = 8) comprised of 1-h bouts of cycle ergometry, twice daily, at a work-rate equivalent to 50% hypoxic peak power output. A subset of subjects (N = 5) also completed a control trial under normoxic conditions. The thermal comfort zone (TCZ) was determined in normoxia, and during hypoxic confinement days 2 (HC2) and 10 (HC10) in both groups using a water-perfused suit in which water temperature was regulated by the subjects within a range, they deemed thermally comfortable. Mean skin temperature and proximal-distal temperature gradients (two sites: forearm-fingertip, calf-toe) were recorded each minute throughout the 60-min protocol., Results: The average width of the TCZ did not differ between the control group (9.0 ± 6.9 °C), and the LH and LH-TH groups on days HC2 (7.2 ± 4.2 °C) and HC10 (10.2 ± 7.5 °C) of the hypoxic exposure (p = 0.256). [Formula: see text] was marginally higher on HC2 (35.9 ± 1.0 °C) compared to control (34.9 ± 0.8 °C, p = 0.040), but not on HC10 (35.6 ± 1.0 °C), reflecting the responses of hand perfusion., Conclusion: There was a little systematic effect of hypoxia or exercise training on TCZ magnitude or boundary temperatures.

Future Lunar and Mars habitats will maintain a hypobaric hypoxic environment to minimise the risk of decompression sickness during the preparation for extra-vehicular activity. This study was part of a larger study investigating the separate and combined effects of inactivity associated with reduced gravity and hypoxia, on the cardiovascular, musculoskeletal, neurohumoural, and thermoregulatory systems. Eleven healthy normothermic young male subjects participated in three trials conducted on separate occasions: (1) Normobaric hypoxic ambulatory confinement, (2) Normobaric hypoxic bedrest and (3) Normobaric normoxic bedrest. Normobaric hypoxia was achieved by reduction of the oxygen fraction in the air (FiO2 = 0.141 ± 0.004) within the facility, while the effects of reduced gravity were simulated by confining the subjects to a horizontal position in bed, with all daily routines performed in this position for 21 days. The present study investigated the effect of the interventions on behavioural temperature regulation. The characteristics of the thermal comfort zone (TCZ) were assessed by a water-perfused suit, with the subjects instructed to regulate the sinusoidally varying temperature of the suit within a range considered as thermally comfortable. Measurements were performed 5 days prior to the intervention (D-5), and on days 10 (D10) and 20 (D20) of the intervention. no statistically significant differences were found in any of the characteristics of the TCZ between the interventions (HAMB, HBR and NBR), or between different measurement days (D-5, D10, D20) within each intervention. rectal temperature remained stable, whereas skin temperature (Tsk) increased during all interventions throughout the one hour trial. no difference in Tsk between D-5, D10 and D20, and between HAMB, HBR and NBR were revealed. subjects perceived the regulated temperature as thermally comfortable, and neutral or warm. we conclude that regulation of thermal comfort is not compromised by hypoxic inactivity., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

The potentiated exercise-sweating rate observed during acute hypoxia is diminished after a sleep-high train-low (SH-TL) regimen. We tested the hypothesis that this attenuation of the sweating response after SH-TL is compensated for by an increase in heat loss via vasodilatation. Nine male subjects participated in a 28-day SH-TL regimen. Before (pre-), and after (post-) the SH-TL protocol, they performed an VO2peak test under normoxia and hypoxia. Additionally, pre- and post-SH-TL they completed three 30-min constant-work rate trials on a cycle ergometer. In one trial, the subjects inspired room air while exercising at 50% of normoxic VO2peak (CT). In the remaining trials, subjects exercised in hypoxia (F(I)O2 12.5%), either at the same absolute (HAT) or relative (50% of hypoxic VO2peak work rate (HRT) as in CT. Despite similar exercise core temperature responses between pre- and post-SH-TL trials, sweating rate was potentiated in HAT pre-SH-TL [CT: 1.97 (0.42); HRT: 1.86 (0.31); HAT: 2.55 (0.53) mg cm(-2) min(-1); p < 0.05]. Post-SH-TL exercise sweating rate was increased for CT, and remained unchanged in HRT and HAT [CT: 2.42 (0.76); HRT: 2.01 (0.33); HAT: 2.59 (0.30) mg cm(-2) min(-1)]. Pre-SH-TL, the forearm-fingertip skin temperature difference (Tsk(f-f)) was higher in HAT than in CT and HRT by ~3.5 °C (p < 0.05). The inter-condition differences in Tsk(f-f) were diminished post-SH-TL. In conclusion, the decrease in sweating rate during hypoxic exercise, following a SH-TL regimen, was countered by an increase in vasodilatation (reduced Tsk(f-f)), whereas SH-TL enhanced the sweating response during normoxic exercise. The mechanisms underlying these SH-TL-induced alterations in thermoregulatory responses remain to be settled.

Introduction: Bed rest is a terrestrial experimental analogue of unloading experienced during exposure to microgravity. Such unloading causes atrophy predominantly of the postural muscles, especially those of the lower limbs., Methods: We tested the hypothesis that 35 d horizontal bed rest alters thermoregulatory responses of subjects (N = 10) immersed in 15 degrees C water, particularly the heat produced by the shivering tremor of the skeletal muscles. Before and after bed rest we measured the thickness of the gastrocnemius medialis (GM), vastus lateralis (VL), tibialis anterior (TA), and biceps brachii (BB) muscles by ultrasonography. During the immersions, we monitored rectal and skin temperatures, heat flux, heart rate, and oxygen uptake., Results: After bed rest, muscle thickness decreased significantly by 12.2 +/- 8.8% and 8.0 +/- 9.1% in the GM and VL, respectively. No changes were observed in the TA and BB muscles. The 35-d bed rest caused a significant reduction in aerobic power, as reflected in maximal oxygen uptake. There were no significant differences in any of the observed thermoregulatory responses between the pre- and post-bed rest immersions., Conclusions: Cardiovascular and muscular deconditioning had no effect on the heat production and heat loss responses. Due to the significant reduction in the mass of the muscles in the lower limbs, concomitant with no change in heat production, we conclude that leg muscles do not play a significant role in shivering thermogenesis.

Motion sickness (MS) has been identified as a non-thermal factor that can moderate autonomic thermoregulatory responses. It has been shown that MS exaggerates core cooling during immersion in cold (15 °C) and luke-warm (28 °C) water by attenuating cold-induced vasoconstriction. The aim of the present study was to investigate whether MS affects thermal balance in a thermoneutral air environment. Eleven subjects were exposed to rotation in two conditions, control (CN) and MS. In the CN condition subjects refrained from head movements, whereas in the MS condition they performed a sequence of maximal head movements (left, right, up, down) at 15-s intervals until they were very nauseous. Sweating rate, rectal temperature (T(re)), the difference in temperature between the right forearm and tip of the second finger (T(ff)) as an index of cutaneous vasomotor tone, perceived MS, thermal comfort and temperature perception were recorded before and during rotation, and during 90-min post-rotation. During the post-rotation period, T(re) dropped and sweating rate increased in the MS but not in the CN condition. The T(ff) response suggests that MS-induced peripheral vasodilatation which, together with the sweating resulted in increased heat loss. During rotation, subjects perceived temperature to be uncomfortably high, suggesting that MS may also affect thermoregulatory behaviour. It thus appears that also in a thermoneutral air environment MS may substantially affect thermal balance.

Motion sickness (MS) exaggerates body cooling during cold-water immersion. The aim of the present study was to investigate whether such MS-induced predisposition to hypothermia is influenced by two anti-MS drugs: the histamine-receptor blocker dimenhydrinate (DMH) and the muscarine-receptor blocker scopolamine (Scop). Nine healthy male subjects were immersed in 15 degrees C water for a maximum of 90min in five conditions: (1) control (CN): no medication, no MS provocation; (2) MS-control (MS-CN): no medication, MS provocation; (3) MS-placebo (MS-P): placebo DMH and placebo Scop, MS provocation; (4) MS-DMH: DMH and placebo Scop, MS provocation; (5) MS-Scop: Scop and placebo DMH, MS provocation. MS was induced by use of a rotating chair. Throughout the experiments rectal temperature (T(re)), the difference in temperature between the non-immersed right forearm and third finger (T(ff)) as an index of peripheral vasoconstriction, and oxygen uptake (VO(2)) as a measure of shivering thermogenesis, were recorded. DMH and Scop were similarly efficacious in ameliorating nausea. The fall in T(re) was greater in the MS-CN and MS-P conditions than in the CN condition. DMH, but not Scop, prevented the MS-induced increase in body-core cooling. MS attenuated the cold-induced vasoconstriction, an effect which was fully prevented by DMH but only partially by Scop. MS provocation did not affect VO(2) in any condition. The results suggest that the MS-induced predisposition to hypothermia is predominantly mediated by histaminergic mechanisms and that DMH might be useful in conjunction with maritime accidents or other scenarios where exposure to cold and MS are imminent features., (Copyright (c) 2010 Elsevier Inc. All rights reserved.)

The present study investigated the effect of 21 days of horizontal bed rest on cutaneous cold and warm sensitivity, and on behavioural temperature regulation. Healthy male subjects (N = 10) were accommodated in a hospital ward for the duration of the study and were under 24-h medical care. All activities (eating, drinking, hygiene, etc.) were conducted in the horizontal position. On the 1st and 22nd day of bed rest, cutaneous temperature sensitivity was tested by applying cold and warm stimuli of different magnitudes to the volar region of the forearm via a Peltier element thermode. Behavioural thermoregulation was assessed by having the subjects regulate the temperature of the water within a water-perfused suit (T (wps)) they were wearing. A control unit established a sinusoidal change in T (wps), such that it varied from 27 to 42 degrees C. The subjects could alter the direction of the change of T (wps), when they perceived it as thermally uncomfortable. The magnitude of the oscillations towards the end of the trial was assumed to represent the upper and lower boundaries of the thermal comfort zone. The cutaneous threshold for detecting cold stimulus decreased (P < 0.05) from 1.6 (1.0) degrees C on day 1 to 1.0 (0.3) degrees C on day 22. No effect was observed on the ability to detect warm stimuli or on the regulated T (wps). We conclude that although cold sensitivity increased after bed rest, it was not of sufficient magnitude to cause any alteration in behavioural thermoregulatory responses.

Heat-loss responses during steady-load exercise are affected by an increase in relative work rate induced by muscle ischaemia or hypoxaemia. The present study investigated whether progressive increases in perception of exertion and relative oxygen uptake %VO2peak which occur during prolonged steady-load exercise as a result of progressively increased peripheral fatigue, might also affect the regulation of heat loss responses and hence the exercise-induced increase in mean body temperature. Ten male subjects first performed a ramp-test to exhaustion on a cycle ergometer to evaluate their initial peak oxygen uptake (Control VO2peak). On a separate day, 120 min of cycling at constant power output corresponding to 60% of Control VO2peak was performed in thermoneutral environment (Ta = 23 degrees C, RH = 50%, wind speed = 5 m s(-1)). This was immediately followed by another maximal performance test (Fatigue VO2peak). During prolonged exercise, median (range) rating of perceived exertion for whole-body (RPEwb) increased (P < 0.01) from initial 3.5 (1-5) to 5.5 (5-9) at the end of exercise. Fatigue VO2peak and peak power output were 9 (5) and 10 (5)% lower (P < 0.01) when compared to control values. At the onset of exercise, heat production, mechanical efficiency, heat loss and mean body temperature increased towards asymptotic values, thereafter remained constant throughout the 120 min exercise, despite the concomitant progressive increase in relative work rate, as reflected in increased RPEwb and relative oxygen uptake. It is thus concluded that the increase in relative work rate induced predominantly by peripheral muscle fatigue affects neither the level of increase in mean body temperature nor the regulation of heat loss responses during prolonged steady-load exercise.

The effect of acute and 23 days of intermittent exposures to normobaric hypoxia on the forehead sweating response during steady-state exercise was investigated. Eight endurance athletes slept in a normobaric hypoxic room for a minimum of 8 h per day at a simulated altitude equivalent to 2,700 m for 23 days (sleep high-train low regimen). Peak oxygen uptake (VO2(peak)) and peak work rate (WR(peak)) were determined under normoxic (20.9%O(2)) and hypoxic (13.5%O(2)) conditions prior to (pre-IHE), and immediately after (post-IHE) the intermittent hypoxic exposures (IHE). Also, each subject performed three 30-min cycle-ergometry bouts: (1) normoxic exercise at 50% WR(peak) attained in normoxia (control trial; CT); (2) hypoxic exercise at 50% WR(peak) attained in hypoxia (hypoxic relative trial; HRT) and (3) hypoxic exercise at the same absolute work rate as in CT (hypoxic absolute trial; HAT). Exposure to hypoxia induced a 33 and 37% decrease (P < 0.001) in (VO2(peak)) pre-IHE and post-IHE, respectively. Despite similar relative oxygen uptake during HAT pre-IHE and post-IHE, the ratings of perceived whole-body exertion decreased substantially (P < 0.05) post-IHE. Pre-IHE the sweat secretion on the forehead (m(sw)f) was greater (P < 0.01) in the HAT (2.60 (0.80) mg cm(-2) min(-1)) compared to the other two trials (CT = 1.87 (1.09) mg cm(-2) min(-1); HRT = 1.57 (0.82) mg cm(-2) min(-1)) despite a similar exercise-induced elevation in body temperatures, resulting in an augmented (P < 0.01) gain of the sweating response (m(sw)f/Delta T(re)). The augmented (m(sw)f) and m(sw)f/Delta T(re) during the HAT were no longer evident post-IHE. Thus, it appears that exercise sweating on the forehead is potentiated by acute exposure to hypoxia, an effect which can be abolished by 23 days of intermittent hypoxic exposures.

Motion sickness (MS) has been found to increase body-core cooling during immersion in 28 degrees C water, an effect ascribed to attenuation of the cold-induced peripheral vasoconstriction (Mekjavic et al. in J Physiol 535(2):619-623, 2001). The present study tested the hypothesis that a more profound cold stimulus would override the MS effect on peripheral vasoconstriction and hence on the core cooling rate. Eleven healthy subjects underwent two separate head-out immersions in 15 degrees C water. In the control trial (CN), subjects were immersed after baseline measurements. In the MS-trial, subjects were rendered motion sick prior to immersion, by using a rotating chair in combination with a regimen of standardized head movements. During immersion in the MS-trial, subjects were exposed to an optokinetic stimulus (rotating drum). At 5-min intervals subjects rated their temperature perception, thermal comfort and MS discomfort. During immersion mean skin temperature, rectal temperature, the difference in temperature between the non-immersed right forearm and 3rd finger of the right hand (DeltaTff), oxygen uptake and heart rate were recorded. In the MS-trial, rectal temperature decreased substantially faster (33%, P < 0.01). Also, the DeltaTff response, an index of peripheral vasomotor tone, as well as the oxygen uptake, indicative of the shivering response, were significantly attenuated (P < 0.01 and P < 0.001, respectively) by MS. Thus, MS may predispose individuals to hypothermia by enhancing heat loss and attenuating heat production. This might have significant implications for survival in maritime accidents.

The set point has been used to define the regulated level of body temperature, suggesting that displacements of core temperature from the set point initiate heat production (HP) and heat loss (HL) responses. Human and animal experiments have demonstrated that the responses of sweating and shivering do not coincide at a set point but rather establish a thermoeffector threshold zone. Neurophysiological studies have demonstrated that the sensor-to-effector pathways for HP and HL overlap and, in fact, mutually inhibit each other. This reciprocal inhibition theory, presumably reflecting the manner in which thermal factors contribute to homeothermy in humans, does not incorporate the effect of nonthermal factors on temperature regulation. The present review examines the actions of these nonthermal factors within the context of neuronal models of temperature regulation, suggesting that examination of these factors may provide further insights into the nature of temperature regulation. It is concluded that, although there is no evidence to doubt the existence of the HP and HL pathways reciprocally inhibiting one another, it appears that such a mechanism is of little consequence when comparing the effects of nonthermal factors on the thermoregulatory system, since most of these factors seem to exert their influence in the region after the reciprocal cross-inhibition. At any given moment, both thermal and several nonthermal factors will be acting on the thermoregulatory system. It may, therefore, not be appropriate to dismiss the contribution of either when discussing the regulation of body temperature in humans.

The effect of graded ischaemia in the legs on the regulation of body temperature during steady-state exercise was investigated in seven healthy males. It was hypothesised that graded ischaemia in the working muscles increases heat storage within the muscles, which in turn potentiates sweat secretion during exercise. Blood perfusion in the working muscles was reduced by applying a supra-atmospheric pressure (+6.6 kPa) around the legs, which reduced maximal working capacity by 29%. Each subject conducted three separate test trials comprising 30 min of steady-state cycling in a supine position. Exercise with unrestricted blood flow (Control trial) was compared to ischaemic exercise conducted at an identical relative work rate (Relative trial), as well as at an identical absolute work rate (Absolute trial); the latter corresponding to a 20% increase in relative workload. The average (SD) increases in both the rectal and oesophageal temperatures during steady-state cycling was 0.3 (0.2) degrees C and did not significantly differ between the three trials. The increase in muscle temperature was similar in the Control (2.7 (0.3) degrees C) and Absolute (2.4 (0.7) degrees C) trials, but was substantially lower (P < 0.01) in the Relative trial (1.4 (0.8) degrees C). Ischaemia potentiated (P < 0.01) sweating on the forehead in the Absolute trial (24.2 (7.3) g m(-2) min(-1)) compared to the Control trial (13.4 (6.2) g m(-2) min(-1)), concomitant with an attenuated (P < 0.05) vasodilatation in the skin during exercise. It is concluded that graded ischaemia in working muscles potentiates the exercise sweating response and attenuates vasodilatation in the skin initiated by increased core temperature, effects which may be attributed to an augmented muscle metaboreflex.

The present study evaluated the effect of 35 days of experimental horizontal bed-rest on exercise and immersion thermoregulatory function. Fifteen healthy male volunteers were assigned to either a Control (n = 5) or Bed-rest (n = 10) group. Thermoregulatory function was evaluated during a 30-min bout of submaximal exercise on a cycle ergometer, followed immediately by a 100-min immersion in 28 degrees C water. For the Bed-rest group, exercise and immersion thermoregulatory responses observed post-bed-rest were compared with those after a 5 week supervised active recovery period. In both trials, the absolute work load during the exercise portion of the test was identical. During the exercise and immersion, we recorded skin temperature, rectal temperature, the difference in temperature between the forearm and third digit of the right hand (DeltaT(forearm-fingertip))--an index of skin blood flow, sweating rate from the forehead, oxygen uptake and heart rate at minute intervals. Subjects provided ratings of temperature perception and thermal comfort at 5-min intervals. Exercise thermoregulatory responses after bed-rest and recovery were similar. Subjective ratings of temperature perception and thermal comfort during immersion indicated that subjects perceived similar combinations of Tsk and Tre to be warmer and thermally less uncomfortable after bed-rest. The average (SD) exercise-induced increase in Tre relative to resting values was not significantly different between the Post-bed-rest (0.4 (0.2) degrees C) and Recovery (0.5 (0.2) degrees C) trials. During the post-exercise immersion, the decrease in Tre, relative to resting values, was significantly (P < 0.05) greater in the Post-bed-rest trial (0.9 (0.5) degrees C) than after recovery (0.4 (0.3) degrees C). DeltaT(forearm-fingertip) was 5.2 (0.9) degrees C and 5.8 (1.0) degrees C at the end of the post-bed-rest and recovery immersions, respectively. The gain of the shivering response (increase in VO(2) relative to the decrease in Tre; VO(2)/Tre) was 1.19 l min(-1) degrees C(-1) in the Recovery trial, and was significantly attenuated to 0.51 l min(-1) degrees C(-1) in the Post-bed-rest trial. The greater cooling rate observed in the post-bed-rest trial is attributed to the greater heat loss and reduced heat production. The former is the result of attenuated cold-induced vasoconstriction and enhanced sweating rate, and the latter a result of a lower shivering VO(2) response.

New Findings: What is the central question of this study?Does a 35‐day horizontal bedrest impair thermoeffector responses during whole‐body submaximal exercise performed in temperate conditions?What is the main finding and its importance?Cardiovascular and muscular deconditioning ensuing from prolonged recumbency seems to augment, at least to a degree, exercise‐induced increase in body core temperature, most likely due to an impairment in non‐evaporative heat loss. The response is a function of the absolute exercise intensity imposed. We examined the effects of a 35‐day horizontal bedrest on thermoregulation during whole‐body exercise. Fifteen healthy men were randomly assigned to either a bedrest (BR; n = 10) or a control (CON; n = 5) group. Prior to bedrest, both groups performed 40‐min constant‐load upright cycling at 30% of their peak workload (Wpeak; PRE). One and 2 days after bedrest, the BR group performed, in a randomised counterbalanced order, two 40‐min trials at 30% of (i) the pre‐bedrest Wpeak (i.e., at a fixed absolute intensity; POST‐A) and (ii) the post‐bedrest Wpeak (i.e., at a fixed relative intensity; POST‐R). The CON group conducted only the POST‐A trial, at the same time intervals. During the trials, rectal (Trec) and skin (T¯sk) temperatures, and the forehead sweating rate (SwR) were monitored. In the CON group, no differences were observed between the trials. Bedrest potentiated moderately the Trec elevation during the latter part of POST‐A (∼0.10°C; P ≤ 0.05), but not of POST‐R (∼0.04°C; P = 0.11). In both post‐bedrest trials, T¯sk was attenuated by ∼1.5–2.0°C throughout (P < 0.01), whereas the forehead SwR was not modulated. Trec and T¯sk were similar in POST‐A and POST‐R, yet the forehead SwR was more dependent on the relative workload imposed (P = 0.04). The present findings therefore suggest that the cardiovascular and muscular deconditioning ensuing from a 35‐day bedrest may aggravate the exercise‐induced increase in body core temperature when working at a given absolute intensity, most likely due to an impairment in non‐evaporative heat loss. [ABSTRACT FROM AUTHOR]