Effects of 29-h total sleep deprivation on local cold tolerance in humans.

To study the effects of a 29-h total sleep deprivation (TSD) on local cold tolerance, 10 healthy men immersed their right hand for 30 min in a 5°C water bath (CWI) after a 30-min rest period in a thermoneutral environment (Control), after a normal night (NN) and after a 29-h TSD. CWI was followed by a 30-min passive rewarming (Recovery). Finger 2 and 4 skin temperatures (Tfi2, Tfi4) and finger 2 cutaneous vascular conductance (CVC) were monitored to study cold-induced vasodilation (CIVD). Rectal temperature (Tre), mean skin temperature ([Formula: see text]), heart rate (HR) and blood pressure (BP) were also measured. Blood samples were collected at the end of the Control, at the lower and at the first maximal Tfi2 values during CWI and at Recovery. Tfi2, Tfi4 and CVC did not differ after TSD at Control, whereas they were reduced during CWI (-2.6 ± 0.7°C for Tfi2; -2 ± 0.8°C for Tfi4, -79 ± 25% for relative CVC, P < 0.05) as during Recovery (-4.9 ± 1.9°C for Tfi2, -2.6 ± 1.8°C for Tfi4, -70 ± 22% for relative CVC, P < 0.05). After TSD, the lower CVC values appeared earlier during CWI (-59 ± 19.6 s, P < 0.05). After TSD at Control and CWI, plasma endothelin levels were higher and negatively correlated with Tfi2, Tfi4 and CVC. However, no effect of TSD was found on the number and amplitude of CIVD and in Tre, HR, BP and catecholamines, for all periods. We concluded that TSD induced thermal and vascular changes in the hand which impair the local cold tolerance, suggesting that TSD increases the risk of local cold injuries.

Substrate utilization during prolonged exercise with ingestion of (13)C-glucose in acute hypobaric hypoxia (4,300 m).

Energy substrate oxidation was measured using indirect respiratory calorimetry combined with tracer technique in five healthy young male subjects, during a 80-min exercise period on ergocycle with ingestion of 140 g of (13)C-labelled glucose, in normoxia and acute hypobaric hypoxia (445 mmHg or 4,300 m), at the same relative [77% V(.-)((O)(2)(max))] and absolute workload (161+/-8 W, corresponding to 77 and 54% V(.-)((O)(2)(max)) in hypoxia and normoxia). The oxidation rate of exogenous glucose was not significantly different in the three experimental situations: 21.4+/-2.9, 20.2+/-1.2 and 17.2+/-0.6 g over the last 40 min of exercise at approximately 77 and approximately 54% V(.-)((O)(2)(max)) in normoxia and in hypoxia, respectively, providing 12.5+/-1.5, 16.8+/-1.1 and 14.9+/-1.1% of the energy yield, although ingestion of glucose during exercise resulted in a higher plasma glucose concentration in hypoxia than normoxia. The contribution of carbohydrate (CHO) oxidation to the energy yield was significantly higher in hypoxia (92.0+/-2.1%) than in normoxia for both a given absolute (75.3+/-5.2%) and relative workload (78.1+/-1.8%). This greater reliance on CHO oxidation in hypoxia was entirely due to the significantly larger contribution of endogenous glucose oxidation to the energy yield: 75.9+/-1.7% versus 66.6+/-3.3 and 55.2+/-3.7% in normoxia at the same relative and absolute workload.

Comparison of passive heat or exercise-induced dehydration on renal water and electrolyte excretion: the hormonal involvement.

The effects of hydromineral hormones and catecholamines on renal water and electrolyte excretion were examined during and after dehydration induced by either passive heat or exercise. Eight healthy young Caucasian subjects participated in three separate trials, each including three consecutive phases. Phases 1 and 3 involved a 90-min period at rest in a thermoneutral environment, while phase 2 involved a 120-min period designed to provide: (1) euhydration (control trial), (2) passive heat-induced dehydration of 2.8% body mass, or (3) exercise-induced dehydration of 2.8% body mass. During the two dehydration procedures, the decreases in urine flow and sodium excretion were more marked during exercise (P < 0.05). An increase in plasma catecholamines occurred only during exercise, together with a reduction in creatinine clearance and more marked increases in plasma renin and aldosterone than during passive heat exposure (P < 0.05). Although plasma vasopressin was elevated during the two dehydration procedures, urine osmolality did not change and, moreover, free water clearance increased during exercise (P < 0.05). Plasma levels of atrial natriuretic peptide increased markedly only during exercise compared to the other trials (P < 0.05). After the dehydration procedures, urine flow decreased again and urine osmolality increased markedly (P < 0.05), while plasma vasopressin remained elevated. These results suggest that sympathoadrenal activation during exercise plays a major role in the more marked reduction in diuresis and natriuresis than during passive heat exposure. Despite high plasma vasopressin concentrations during the two dehydrating events, the observed antidiuresis was not due to an increased renal concentrating ability, and the vasopressin was more effective after the dehydration procedures.

[Sports and extreme conditions. Cardiovascular incidence in long term exertion and extreme temperatures (heat, cold)]. / Sports et conditions extrêmes. Incidence cardiovasculaire des efforts de longue durée et des températures extrêmes (chaleur, froid).

During ultra-endurance exercise, both increase in body temperature and dehydration due to sweat losses, lead to a decrease in central blood volume. The heart rate drift allows maintaining appropriate cardiac output, in order to satisfy both muscle perfusion and heat transfer requirements by increasing skin blood flow. The resulting dehydration can impair thermal regulation and increase the risks of serious accidents as heat stroke. Endurance events, lasting more than 8 hours, result in large sweat sodium chloride losses. Thus, ingestion of large amounts of water with poor salt intake can induce symptomatic hyponatremia (plasma sodium < 130 mEq/L) which is also a serious accident. Heat environment increases the thermal constraint and when the air humidity is high, evaporation of sweat is compromise. Thus, thermal stress becomes uncompensable which increases the risk of cardiovascular collapse. Cold exposure induces physiological responses to maintain internal temperature by both limiting thermal losses and increasing metabolic heat production. Cold can induce accidental hypothermia and local frost-bites; moreover, it increases the risk of arrhythmia during exercise. Some guidelines (cardiovascular fitness, water and electrolyte intakes, protective clothing) are given for each extreme condition.

Positive end expiratory pressure (PEEP) slightly modifies ventilatory response during incremental exercise.

To clarify the ventilatory effects of a 5-cm H2O positive end expiratory pressure (PEEP) in healthy men during incremental exercise in normoxic conditions, 22 subjects were subjected to a constant workload (0 W, 50 W, 100 W, 150 W and 200 W) on a cycle ergometer for periods of 8 min each, both with and without 5-cm H2O PEEP. Results show that PEEP increases inspiratory (TI) and expiratory (TE) duration and tidal volume (VT) and decreases breathing frequency (fB) at rest (p < 0.05). During exercise, TI is higher at 50 W and 100 W (p < 0.05), but not at 150 and 200 W. TE only increases at 50 W (p < 0.05). An increased VT (p < 0.05 at 50, 100 and 150 W) and a decreased fB (p < 0.05 throughout the experiment) were observed. However, mean inspiratory flow (VT/T1) and duty cycle (TI/TT) were unaffected by PEEP. In conclusion, this study shows that a 5-cm H2O PEEP slightly modifies the ventilatory parameters in healthy subjects during incremental exercise in normoxic conditions.

Diagnosis of heat stroke in forensic medicine. Contribution of thermophysiology.

The diagnosis of heat stroke is difficult to establish in forensic medicine due to the absence of observations made on the victims whilst alive. A recent case, concerning the death of two children in a vehicle, was restudied by taking into account calculations of thermophysiology. The results obtained allowed some assumptions of the investigation to be checked, and adds to the data provided previously in literature on the subject.

Positive expiratory pressure as a method for preventing the impairment of attentional processes by hypoxia.

This study investigated the effects of hypoxia on parallel/preattentional and serial/attentional processes in early vision, and the use of a positive-end-expiratory-pressure (PEEP) to prevent the impairment in performance. Twenty-one subjects were submitted to an 8-h hypoxia exposure in a hypobaric chamber (4500 m, 589 hPa, 22 degrees C), both with and without a 5-cm H2O PEEP. Subjects carried out a visual search task consisting of detecting a target among distractors in normoxia, in acute and in prolonged hypoxia. Conjointly their sensitivity to acute mountain sickness (AMS) was scored through the Lake Louise AMS scoring system. Results showed that prolonged hypoxia slowed serial/attentional processing whereas parallel/preattentional processes were not impaired either by acute or by prolonged hypoxia. PEEP prevented serial/attentional processes from slowing and those effects were more clearly observed in the AMS sensitive subjects with respect to the AMS insensitive subjects. These results suggest that the slowing induced by prolonged hypoxia is specific to an early visual process that pilots the scanning of an attentional spotlight throughout the visual field.

Use of bioelectrical impedance analysis to estimate body fluid compartments after acute variations of the body hydration level.

Physiological measurements including body mass, plasma osmolality, natremia, plasma volume measured by Evans Blue dilution, and total body water (TBW) and extracellular water (ECW) volumes estimated by bioelectrical impedance analysis (BIA) were recorded in eight healthy young Caucasian subjects before and after acute variations of their body hydration state on four separate occasions: 1) euhydration or control trial (C); 2) heat-induced dehydration of 2.8% body mass (D); 3) exercise-induced dehydration of 2.8% body mass (E); and 4) glycerol-hyperhydration (H). Heart rate, rectal and mean skin temperatures were also recorded throughout the experiment. The main result of the study is that BIA only half predicted the body water loss after exercise, although conditions were standardized (electrode placement, side of the body, limb position, posture, and ambient temperature). Differences in body temperatures cannot explain such an unexpected result, nor did the study of plasma osmolality and sodium concentration. If BIA appears to adequately predict changes in TBW after heat-induced dehydration and glycerol hyperhydration, further studies including measures of TBW and ECW by dilution tracer methods would be necessary to establish the validity of using the BIA method to measure such changes and to interpret ECW variations.

Sympathetic stimulation induced by hand cooling alters cold-induced vasodilatation in humans.

Hand cooling is a cold pressor test, which induces general sympathetic stimulation. This cooling procedure is often performed to investigate cold induced vasodilatation (CIVD) in one finger. To investigate the effects of this sympathetic stimulation on local CIVD, 12 subjects immersed either the right index finger (T1), right hand (T2) or left hand and right index finger (T3) for 30 min in water at 5 degrees C followed by 15-min recovery. Skin temperature and skin blood flow (Q(sk)) measured by laser Doppler flowmetry on the right index finger, as well as heart rate (f(c)) and mean arterial blood pressure (BP(a)), were continuously monitored during the three tests. Cutaneous vascular conductance was calculated as Q(sk)/(BP(a)). Concentrations of plasma noradrenaline (NA) and adrenaline (AD) were measured at different times during the tests. The results showed no cardiovascular change in T1, whereas f(c) and (BP(a)) increased significantly at the beginning of both T2 and T3. Similarly, sympathetic stimulation was reflected in the NA concentrations, which increased significantly (P < 0.01) during T2 and T3 after 5 min of immersion, and remained elevated until the recovery period. The AD concentration did not change during the three tests. During T2, the CIVD appeared later and slower in comparison with T1 [CIVD onset: 12.81 (SEM 2.30) min in T2 and 5.62 (SEM 0.33) min in T1]. During T3, the CIVD onset was not delayed compared to T1 [6.38 (SEM 0.67) min], but the rewarming was lower [+5.40 (SEM 0.86) degrees C in T3 and +9.10 (SEM 1.31) degrees C in T1]. These results showed that CIVD could be altered by sympathetic stimulation but it also appeared that the onset of CIVD could be influenced by local cooling, independently of the general sympathetic stimulation.

Short hypobaric hypoxia and breathing pattern: effect of positive end expiratory pressure.

The ventilatory effects of a 5-cm H2O positive end expiratory pressure (PEEP) and its influence on the breathing pattern during short hypoxic exposure both at rest and during physical exercise were studied. There were 22 healthy subjects who were submitted to normoxia and to 4-h of hypoxia in a hypobaric chamber (4500 m, PB = 589 hPa) both at rest and during an 8-min cycle ergometer exercise (100 W) without and with a 5 cm H2O PEEP. The results show that hypoxia compared with normoxia induces increases in tidal volume (VT) (+28.5%, p < 0.05 at rest; and +19.4%, p < 0.01 at 100 W) and in respiratory frequency (f) at 100 W (p < 0.05), and significant decreases in inspiratory (tI) (p < 0.05 at rest and at 100 W), and expiratory (tE) durations (p < 0.05 at 100 W). However, the breathing pattern expressed as duty cycle (tI/tt) is unchanged, whereas an increased mean inspiratory flow (VT/tI) is observed (p < 0.01 at rest and at 100 W). This study also demonstrates that PEEP during a 4-h hypobaric hypoxia significantly increases VT (+22.2% p < 0.01 at rest, +8.9% p < 0.05 at 100 W), tI, and tE at rest (p < 0.05), but not during exercise and tends to decrease f (p = 0.06 at rest and at 100 W). However, PEEP does not alter the breathing pattern in hypoxia since VT/tI and tI/tt are unchanged. Heart rate and arterial O2 saturation are also unaffected by PEEP. In conclusion, this study shows that a 4-h hypoxia modifies ventilatory parameters and mean inspiratory flow (VT/tI) at rest and during exercise (100 W), whereas a 5-cm H2O PEEP does not alter the breathing pattern despite changes in ventilatory parameters are observed.

Plasma volume changes during and after acute variations of body hydration level in humans.

This study examined plasma volume changes (deltaPV) in humans during periods with or without changes in body hydration: exercise-induced dehydration, heat-induced dehydration and glycerol hyperhydration. Repeated measurements of plasma volume were made after two injections of Evans blue. Results were compared to deltaPV calculated from haematocrit (Hct) and blood haemoglobin concentration ([Hb]). Eight well-trained men completed four trials in randomized order: euhydration (control test C), 2.8% dehydration of body mass by passive controlled hyperthermia (D) and by treadmill exercise (60% of their maximal oxygen uptake, VO2max) (E), and hyperhydration (H) by glycerol ingestion. The Hct, [Hb], plasma protein concentrations and plasma osmolality were measured before, during and after the changes in body hydration. Different Hct and [Hb] reference values were obtained to allow for posture-induced variations between and during trials. The deltaPV values calculated after two Evans blue injections were in good agreement with deltaPV calculated from Hct and [Hb]. Compared to the control test, mean plasma volume declined markedly during heat-induced dehydration [-11.4 (SEM 1.7)%] and slightly during exercise-induced dehydration [-4.2 (SEM 0.9)%] (P < 0.001 compared to D), although hyperosmolality was similar in these two trials. Conversely, glycerol hyperhydration induced an increase in plasma volume [+7.5 (SEM 1.0)%]. These results would indicate that, for a given level of dehydration, plasma volume is dramatically decreased during and after heat exposure, while it is better maintained during and after exercise.

Effects of acute hypobaric hypoxia on the appearance of ingested deuterium from a deuterium oxide-labelled carbohydrate beverage in body fluids of humans during prolonged cycling exercise.

To determine whether or not acute hypobaric hypoxia alters the rate of water absorption from a carbohydrate beverage ingested during exercise, six men cycled for 80 min on three randomly assigned different occasions. In one trial, exercise was performed in hypoxia (barometric pressure, P(B) = 594 hPa, altitude 4,400 m) at an exercise intensity selected to elicit 75% of the individual's maximal oxygen uptake (VO2max) previously determined in such conditions. In the two other experiments, the subjects cycled in normoxia (P(B) = 992 hPa) at the same absolute and the same relative intensities as in hypoxia, which corresponded to 55% and 75%, respectively, of their VO2max determined in normoxia. The subjects consumed 400 ml of a 12.5% glucose beverage just prior to exercise, and 250 ml of the same drink at 20, 40 and 60 min from the beginning of exercise. The first drink contained 20 ml of deuterium oxide to serve as a tracer for the entry of water into body fluids. The heart rate (HR) during exercise was higher in hypoxia than in normoxia at the same absolute exercise intensity, whereas it was similar to HR measured in normoxia at the same relative exercise intensity. Both in normoxia and hypoxia, plasma noradrenaline concentrations were related to the relative exercise intensity up to 40 min of exercise. Beyond that duration, when exercise was performed at the highest absolute power in normoxia, the noradrenaline response was higher than in hypoxia at the same relative exercise intensity. No significant differences were observed among experimental conditions, either in temporal profiles of plasma D accumulation or in elimination of water ingested in sweat. Conversely, elimination in urine of the water ingested appeared to be related to the severity of exercise, either high absolute power or the same relative power combined with hypoxia. We concluded that water absorption into blood after drinking a 12.5% glucose beverage is not altered during cycling exercise in acute hypobaric hypoxia. It is suggested that the elimination of water ingested in sweat and urine may be dependent on local circulatory adjustments during exercise.

Thermoregulatory changes in the cold induced by physical training in humans.

It has previously been demonstrated that metabolic heat production (M) during cold exposure at rest was related to maximal oxygen uptake (VO2max). Consequently, an increase in VO2max could allow an increase M in the cold. The aim of the present study was therefore to test this hypothesis. Eight male volunteers undertook interval training (periods of 25% VO2max of 30-s duration and 110% VO2max of 60-s duration until exhaustion, five times a week over 8 weeks) to increase VO2max. Both before and after this physical training, they were subjected to a 10 degrees, 5 degrees and 1 degrees C 2-h cold air test in a climatic chamber. During the cold exposure, rectal temperature (Tre), tympanic temperature (Tty) mean skin temperature (Tsk) and M were measured as well as the time to onset of shivering (t) and body temperatures (Tre, Try and Tsk) at t. The results showed that physical training involved an increase in VO2max (14%-15%, P < 0.05). During the cold exposure, Tre was higher after training both at 10 degrees, 5 degrees and 1 degree C (P < 0.05) whereas Tty, TSk and M were not significantly changed. However, an increase in the sensitivity of the thermoregulatory system was attested by a decreased t at higher Tsk. These slight physiological changes found after training were not related to the increases in VO2max. In conclusion, this study demonstrated that interval training induced slight thermoregulatory changes unrelated to changes in VO2max and it suggested that M during cold exposure could be related mainly to the level of VO2max observed before training, since increases in VO2max did not modify M.

Positive end expiratory pressure as a method for preventing acute mountain sickness.

In order to study the use of positive end expiratory pressure (PEEP) to prevent acute mountain sickness (AMS), 22 subjects were exposed randomly to 8-h hypobaric hypoxia in a hypobaric chamber (4500 m, 589 hPa, 22 degrees C) once being administered 5-cm H2O PEEP and once without. The prevention of AMS by PEEP was evaluated by scoring AMS according to the Lake Louise system (self-report questionnaire and clinical assessment) throughout the experiment with O2 saturation (SO2) and heart rate measurements being made. Arterial blood analyses (partial pressures of arterial O2 and CO2, PaO2, PaCO2, and pH) were made at the end of the exposure. Results showed decreased AMS scores with PEEP at the end of the 8-h hypoxia [1.50 (SEM 1.32) vs 3.23 (SEM 2.07), P < 0.01 for self-report plus clinical assessment scores] with a lower prevalence (23% vs 55%, P < 0.01). The SO2, PaO2, PaCO2 and HCO3- did not change significantly. However, a smaller increase in arterial pH [7.47 (SEM 0.02) vs 7.50 (SEM 0.02), P < 0.05] was observed with PEEP, attesting a lesser alkalosis. Moreover, heart rate increased with PEEP (P < 0.05). In conclusion, this study would suggest that a 5-cm H2O PEEP may help decrease AMS scores at the end of an 8-h exposure to hypoxia in a hypobaric chamber. Such a method could be used to prevent AMS in such experimental conditions without adverse effects.

Pre-adaptation, adaptation and de-adaptation to high altitude in humans: hormonal and biochemical changes at sea level.

High altitude residence is known to modify body biochemistry and hormone status. However, the effects of such a sojourn on these status observed at sea level both immediately and later after return are not as well established as are the effects of an intermittent acclimation. The aim of this study was therefore to investigate these changes. To achieve our objectives, nine subjects received intermittent acclimation at low pressure in a barometric chamber (8 h daily for 5 days, day 1 at 4500 m, day 5 at 8500 m) before an expedition to the Himalayas. Hormonal and biochemical changes were studied using samples of venous blood taken at sea level before and after acclimation, after return from the expedition and 1 and 2 months after descent. Concentrations of thyroid hormones, adrenaline, noradrenaline (NA), hormones of hydromineral metabolism (aldosterone, renin, arginine vasopressin, atrial natriuretic peptide) as well as prolactin, cortisol, insulin and endothelin 1 were measured. Biochemical measurements made were plasma osmolality, and concentrations of glucose, total cholesterol, total proteins, pre-albumin, transferrin, complement 3C, apolipoproteins A1 and B and serum iron. Acclimation induced no alteration in hormone (except for NA with increases of about 1.5, fold P < 0.05) and biochemistry data. After the expedition, hormone responses were characterized by a higher total triidothyronine concentration (+18%, P < 0.05) while other hormones did not vary. A linear relationship was found between thyroid-stimulating-hormone and body mass changes after the expedition (r = 0.67, P < 0.05). The observed increased concentrations of plasma proteins and total cholesterol (P < 0.05) could be related to the restoration of lean body mass. At 1 and 2 months after return, no changes in hormones were observed but a significant decrease in transferrin concentration was noticed. The higher serum iron concentration reported after 1 month (P < 0.05) could have been the result of a physiological haemolysis. It was concluded that both acclimation and the expedition in the Himalayas affected hormone status and body biochemistry status even though the observed changes were slight and rapidly reversed.

Cognitive performance during short acclimation to severe hypoxia.

BACKGROUND: Exposure to high altitudes requires acclimation or acclimatization, to prevent the negative effects of severe hypoxia. Among several methods, short acclimation with intermittent exposure to severe hypoxia in a hypobaric chamber triggers efficient physiological pre-adaptation mechanisms (11-13). However, we have little knowledge about the cognitive repercussions of such an acclimation protocol. METHODS: Four mountaineers were tested daily in the course of a short acclimation protocol (5 d). After their SaO2 (arterial oxyhemoglogin saturation) were recorded, they carried out a choice reaction time task (Manikin test) twice every day; first at ground level (250 m, control sessions), second at the highest altitude of the day (D1 = 5000 m, D2 = 5500 m, D3 = 6000 m, D4 = 6500 m, D5 = 7000 m). RESULTS: High altitude SaO2 level decreased during the first 3 d, then stabilized around 72-73%. Despite a slight and transient increase at the highest altitude relative to the ground level in D4, the error rate remained low throughout the protocol. Further, response time to the Manikin task did not show significant changes among the days during the acute stage of hypoxia relative to ground level up to 7000 m. CONCLUSIONS: On the whole, it seems that a short acclimation protocol based on intermittent exposure to simulated high altitudes triggered adaptive processes without major impairment in a choice reaction time task during the acute stages of severe hypoxia.

Are the laboratory and field conditions observations of acute mountain sickness related?

In order to study relationships between acute mountain sickness (AMS) observations done both during a short-term hypoxic exposure in a hypobaric chamber, and in field conditions during a high altitude expedition, nine subjects were submitted to a 9-h hypoxic exposure in a hypobaric chamber. Then, they experienced a high altitude expedition in the Himalayas. The Lake Louise AMS scoring system was used to assess AMS in both conditions, especially the self report questionnaire. During the expedition, the mean self report score of each subject, defined as the ratio between the sum of daily self report scores and the duration of the expedition, appears to be correlated not only to the maximal self report score observed in altitude (r = +0.77, p < 0.05) but also to the self report and self report+clinical assessment scores observed at the end of the hypobaric chamber sojourn (r = +0.81, p < 0.01 and r = +0.75, p < 0.05, respectively). In conclusion, the Lake Louise AMS scoring system, especially the self report questionnaire, is relevant to assess AMS with simplicity and rapidity both in laboratory and in field conditions. Our study also suggests that AMS induced by a short term sojourn in a hypobaric chamber is related to AMS observed in field conditions.

Cold induced vasodilatation and cardiovascular responses in humans during cold water immersion of various upper limb areas.

To study the physiological responses induced by immersing in cold water various areas of the upper limb, 20 subjects immersed either the index finger (T1), hand (T2) or forearm and hand (T3) for 30 min in 5 degrees C water followed by a 15-min recovery period. Skin temperature of the index finger, skin blood flow (Qsk) measured by laser Doppler flowmetry, as well as heart rate (HR) and mean arterial blood pressure (BPa) were all monitored during the test. Cutaneous vascular conductance (CVC) was calculated as Qak/BPa. Cold induced vasodilatation (CIVD) indices were calculated from index finger skin temperature and CVC time courses. The results showed that no differences in temperature, CVC or cardiovascular changes were observed between T2 and T3. During T1, CIVD appeared earlier compared to T2 and T3 [5.90 (SEM 0.32) min in T1 vs 7.95 (SEM 0.86) min in T2 and 9.26 (SEM 0.78) min in T3, P < 0.01]. The HR was unchanged in T1 whereas it increased significantly at the beginning of T2 and T3 [+13 (SEM 2) beats.min-1 in T2 and +15 (SEM 3) beats.min-1 in T3, P < 0.01] and then decreased at the end of the immersion [-12 (SEM 3) beats.min-1 in T2, and -15 (SEM 3) beats.min-1 in T3, P < 0.01]. Moreover, BPa increased at the beginning of T1 but was lower than in T2 and T3 [+9.3 (SEM 2.5) mmHg in T1, P < 0.05; +20.6 (SEM 2.6) mmHg and 26.5 (SEM 2.8) mmHg in T2 and T3, respectively, P < 0.01]. The rewarming during recovery was faster and higher in T1 compared to T2 and T3. These results showed that general and local physiological responses observed during an upper limb cold water test differed according to the area immersed. Index finger cooling led to earlier and faster CIVD without significant cardiovascular changes, whereas hand or forearm immersion led to a delayed and slower CIVD with a bradycardia at the end of the test.

Effects of different carbohydrate-electrolyte beverages on the appearance of ingested deuterium in body fluids during moderate exercise by humans in the heat.

To determine whether different forms of glucose (free and polymer) associated with sodium chloride influence the rate of water absorption during exercise in the heat, six men took part in five trials. Each trial included a passive heating session which resulted in a 2% loss of body mass, followed by 1h of treadmill exercise (at 50% of maximal oxygen uptake) in warm conditions (dry bulb temperature 35 degrees C, relative humidity 20%-30%). Immediately before exercise, the subjects were given either no fluid or a volume equal to 50% of the fluid previously lost (about 650 ml), chosen from among four D2O-labelled beverages: mineral water, a 6% glucose-electrolyte solution (GS), a 6% maltodextrin solution and a 6% maltodextrin-electrolyte solution. No significant differences were observed among these various beverages so far as temporal accumulation of deuterium in plasma, sweat and urine was concerned. During GS, the plasma volume was completely restored and the drifts of heart rate and rectal temperature were less marked than during other trials. These results would suggest that rehydration with GS was more efficient, probably because of an internal redistribution of water. The proportion of ingested water was twice as high in sweat as it was in urine. These findings may reflect the essential part played by circulatory adjustments in the transfer of plasma water into sweat and urine.