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.

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.

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.

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.

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.

General and local cold responses in humans after 2 weeks at high altitude.

To investigate the effects of a short-term high altitude residence (2 weeks between 4150 m and 6885 m in the Andes) on the general and local cold responses after descent, 11 subjects were submitted both to a whole body standard cold air test (SCAT, dry bulb temperature = 1 degree C, 2 h, nude, at rest) and to a local cold water test of the right upper limb (CWT, 5 degrees C, 5 min) both before and after the expedition. Compared to before the expedition, a lower systolic blood pressure was observed after the high altitude residence [130.00 (SEM 3.35) mm Hg vs 140.40 (SEM 4.74) mm Hg at the end of CWT, P < 0.05] whereas no significant change either in diastolic blood pressure or in heart rate was found. All skin temperatures of the right upper limb were lowered (P < 0.05). During SCAT, body temperatures were unchanged (rectal and mean skin temperature, Tsk) but metabolic heat production was slightly but significantly diminished [110 (SEM 4) W.m-2 vs 125 (SEM 3) W.m-2, P < 0.05] and heat debt increased [11.37 (SEM 1.11) kJ.kg-1 vs 9.30 (SEM 2.30) kJ.kg-1, P < 0.05]. Moreover, the time of onset of continuous shivering (d) was shortened [8.20 (SEM 1.90) min vs 17.30 (SEM 3.60) min, P < 0.05] and the level of Tsk observed at (d) was higher [25.70 (SEM 0.80) degrees C vs 23.57 (SEM 0.78) degrees C, P < 0.05] suggesting an increase in the sensitivity of the thermoregulatory system despite the slight decreased shivering activity observed. It was concluded that general and local cold tolerance were modified by a short-term residence at altitude and that the changes observed were not in accordance with general or (and) local cold adaptation. In contrast, high altitude sojourn could be a risk factor for frostbite of the extremities.

Pre-adaptation, adaptation and de-adaptation to high altitude in humans: cardio-ventilatory and haematological changes.

The aim of this study was first to investigate cardio-ventilatory and haematological responses induced by intermittent acclimation and second to study de-adaptation from high altitude observed after descent. To achieve these objectives nine subjects were submitted to intermittent acclimation in a low barometric chamber (8 h daily for 5 days, day 1 at 4500 m, day 5 at 8500 m) before an expedition to the Himalayas. Cardio-ventilatory changes were measured during a hypobaric poikilocapnic hypoxic test (4500 m, barometric pressure = 589 hPa) and haematological changes were studied at sea level. These measurements were performed before and after acclimation, after return to sea level, but also 1 and 2 months after the expedition. In addition, partial pressures of oxygen and carbon dioxide in arterial blood (PaO2, PaCO2) and arterial erythropoietin concentration [EPO] were measured at rest during the hypoxic test. Results suggested the pre-adaptation protocol was efficient since an increased PaO2 (+12%, P < 0.05), a smaller difference in alveolo-arterial PO2 ( -63%, P < 0.05) and a lower PaCO2 ( -11%, P < 0.05), subsequent to ventilatory changes, were observed after acclimation with a significant increase in reticulocytes and in sea level [EPO] (+44% and +62% respectively, P < 0.05). De-adaptation was characterized by a loss of these cardio-ventilatory changes 1 month after descent, whereas the haematological changes (increased red blood cells and packed cell volume, P < 0.05) persisted for 1 month before disappearing 2 months after descent. This study would also suggest that acute hypoxia performed after a sojourn at high altitude could induce significantly depressed EPO responses (P < 0.05).

Evaluation of the Lake Louise acute mountain sickness scoring system in a hypobaric chamber.

This study evaluated the relevance of the Lake Louise acute mountain sickness (AMS) scoring system in comparison with other AMS scoring systems. To achieve this objective nine subjects were submitted to a 9-hr exposure to hypoxia in a hypobaric chamber (altitude 4500-5500 m) that led to the development of AMS. AMS was scored at the end of this exposure period both by questionnaires (Hackett AMS questionnaire, Lake Louise AMS self-report questionnaire, Environmental Symptoms Questionnaire ESQ II and ESQ IV) and by a clinical investigation following the Lake Louise AMS clinical and functional AMS assessment. The AMS scores were between 0 and 9 for the Hackett AMS score, 0 and 38 for the ESQ II AMS score, 0 and 13.7 for the ESQ IV AMS score, 0 and 10 for the Lake Louise AMS self-report, 0 and 2 for the Lake Louise AMS clinical assessment score, and between 0 and 2 for the Lake Louise functional score. All the AMS questionnaire scores were related to the clinical AMS assessment score (p < 0.05) without significant differences between them. The Lake Louise AMS self-report score appeared highly correlated to other AMS scoring systems (Hackett, ESQ II and ESQ IV) (p < 0.05). Suggestions were proposed to improve the sensitivity and the specificity of the Lake Louise AMS scoring questionnaire but also the Lake Louise AMS clinical assessment. In conclusion, this study suggests the relevance of the Lake Louise AMS self-report questionnaire to assess and score AMS with simplicity and rapidity.

Physiological changes induced by pre-adaptation to high altitude.

To study the physiological effects of pre-adaptation to high altitude, seven subjects were submitted to acclimatization at 4350 m followed by intermittent acclimation in a low barometric pressure chamber (5000 m to 8500 m). The subjects then spent 25 days in the Himalayas. Ventilatory and cardiac responses were studied during a hypobaric poikilocapnic hypoxic test performed both at rest and during exercise (100 W) in normoxia and in hypoxia (barometric pressure: 589 hPa, altitude: 4500 m). Haemoglobin, erythrocytes, reticulocytes, packed cell volume, 2,3-diphosphoglycerate (2,3-DPG) and erythropoietin (EPO) were measured. All variables were studied before pre-adaptation to high altitude (A), after the acclimatization period (B), after the acclimation period (C) and after the expedition (D). The ventilatory and cardiac responses were characterized by an increased tidal volume in hypoxia (+33% during exercise in B, P < 0.05; +100% at rest and +33% during exercise in C, P < 0.05) without any change in respiratory frequency, whereas an increased systolic blood pressure was only observed in C during exercise in hypoxia [+23 mmHg (3.07 kPa), P < 0.01]. Arterial O2 saturation was higher in hypoxia in C and D, both at rest (+8.2% and +4.7%, P < 0.01, respectively), and during exercise (+6.3% and +6.3%, P < 0.01, respectively). Erythrocytes, haemoglobin and packed cell volume did not vary significantly. The number of reticulocytes was higher in B (+172%, P < 0.05) and in C (+249%, P < 0.05). EPO and 2,3-DPG increased only in C (+770%, P < 0.01 and +23%, P < 0.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)