BACKGROUND Human thermal responses during prolonged whole-body immersion in cold water are of interest for the military, especially French SEALS. This study aims at describing the thermo-physiological responses. METHODS There were 10 male military divers who were randomly assigned to a full immersion in neutral (34 degrees C), moderately cold (18 degrees C), and cold (10 degrees C) water wearing their operational protective devices (5.5 mm wetsuit with 3.0 mm thick underwear) for 6 h in a static position. Rectal temperature (T(re)) and 14 skin temperatures (T(sk)), blood analysis (stress biomarkers, metabolic substrates), and oxygen consumption (Vo2) were collected. RESULTS At 34 degrees C, there were no significant modifications of the thermo-physiological responses over time. The most interesting result was that rates of rectal temperature decrease (0.15 +/- 0.02 degrees C x min(-1)) were the same between the two cold stress experimental conditions (at 18 degrees C and 10 degrees C). At the final experiment, rectal temperature was not significantly different between the two cold stress experimental conditions. Mean T(sk) decreased significantly during the first 3 h of immersion and then stabilized at a lower level at 10 degrees C (25.6 +/- 0.8 degrees C) than at 18 degrees C (29.3 +/- 0.9 degrees C). Other results demonstrate that the well-trained subjects developed effective physiological reactions. However, these reactions are consistently too low to counterbalance the heat losses induced by cold temperature conditions and long-duration immersion. CONCLUSION This study shows that providing divers with thermal protection is efficient for a long-duration immersion from a medical point of view, but not from an operational one when skin extremities were taken into account.

INTRODUCTION:Wearing protective clothing can have deleterious effects on operational capacities and can cause non-compensable thermal stress. We studied the effects of moderate exercise on orthostatic tolerance while wearing protective clothing in eight healthy subjects tolerant to orthostatism.METHODS:Subjects performed a 60-min moderate exercise on a treadmill followed by a 45-min head-up tilt test. Subjects performed the moderate exercise either in a comfortable condition (control, CON) or wearing protective clothing (PRO) in a random order.RESULTS:Compared with the CON trial, exercise in the PRO trial induced higher body dehydration, heart rate, and rectal temperature and a decrease in plasma volume. Orthostatic tolerance was significantly reduced in the PRO trial (23.7 +/- 0.2 min) compared with the CON trial (40.7 +/- 1.0 min). Transition from supine to head-up position caused a significant decrease in blood pressure in the PRO compared with the CON. RR interval was smaller in the PRO trial compared with CON in both the supine and head-up positions. Spontaneous baroreflex sensitivity was decreased in the PRO, either supine or standing, compared to CON (4.6 +/- 0.5 ms x mmHg(-1) and 14.5 +/- 4.2 ms x mmHg(-1) in supine, and 3.3 +/- 0.6 ms x mmHg(-1) and 7.0 +/- 0.6 ms x mmHg(-1) in standing, for PRO and CON, respectively).DISCUSSION:These results suggest that the large decrease in the tolerance to orthostatism after exercise while wearing protective clothing was due to the impossibility of maintaining an adapted blood pressure induced by a conflict between the needs of peripherical vasoconstriction linked to the standing posture, the needs of vasodilatation linked to thermoregulation, and a drop in the sensibility of the spontaneous baroreflex.

This experiment was designed to assess the effects of prolonged whole body immersion (WBI) in thermoneutral and cold conditions on plasma volume and hydromineral homeostasis.10 navy “combat swimmers” performed three static 6-h immersions at 34°C (T34), 18°C (T18) and 10°C (T10). Rectal temperature, plasma volume (PV) changes, plasma proteins, plasma and urine ions, plasma osmolality, renin, aldosterone and antidiuretic hormone (ADH) were measured. Results show that compared to pre-immersion levels, PV decreased throughout WBI sessions, the changes being markedly accentuated in cold conditions. At the end of WBI, maximal PV variations were −6.9% at T34, −14.3% at T18, and −16.3% at T10. Plasma osmolality did not change during and after T34 immersion, while hyperosmolality was present at the end of T18 immersion and began after only 1 h of T10 immersion. In the three temperature conditions, significant losses of water (1.6–1.7 l) and salt (6–8 g) occurred and were associated with similar increases in osmolar and free water clearances. Furthermore, T18 and T10 immersions increased the glomerular filtration rate. There was little or no change in plasma renin and ADH, while the plasma level of aldosterone decreased equally in the three temperature conditions. In conclusion, our data indicate that cold water hastened PV changes induced by immersion, and increased the glomerular filtration rate, causing larger accumulated water losses. The iso-osmotic hypovolemia may impede the resumption of baseline fluid balance. Results are very similar to those repeatedly described by various authors during head-out water immersion.

Thermoneutral water immersion increases cardiac preload and changes the neuroendocrine settings of blood volume regulation. The resulting marked diuresis may lead to significant haemodynamic changes after the end of a prolonged water immersion. Ten volunteers underwent 6 h of complete thermoneutral water immersion. Changes in cardiovascular status were assessed 1 h and 16 h after water immersion. Haemodynamic changes were assessed by Doppler echocardiography. Arterial wall distensibility was estimated by pulse wave velocity analysis. One hour after water immersion, mean weight loss was 1.78 kg and urine volume amounted to 1.5 litres. Echocardiographic measurements evidenced a significant decrease in dimensions of the left cardiac chambers and inferior vena cava. The decreased cardiac preload was paralleled by a lower stroke volume and cardiac output. A peripheral vasoconstriction associated with a relative decrease in the lower limb blood flow was evidenced by an increase in carotid-pedal pulse wave velocity and by a decrease in ankle brachial index. Sixteen hours after water immersion, cardiac preload and cardiac output remained below baseline values and peripheral vascular tone was still higher than at baseline. Marked haemodynamic changes had not returned to baseline 16 h after water immersion. There is a need to design fluid-replacement protocols to improve this recovery.

We hypothesized that the changes in muscle temperature and interstitial pressure during thermoneutral immersion may affect the reflex adaptation of the motor drive during static contraction, assessed by the decrease in median frequency (MF) of electromyogram (EMG) power spectrum. Ten subjects were totally immerged for 6 h at 35°C and repeated maximal voluntary contraction (MVC) and submaximal (60% MVC) leg extensions sustained until exhaustion. In vastus lateralis (VL) and soleus (SOL) muscles, the compound muscle potential evoked by muscle stimulation with single shocks (M-wave) was recorded at rest, and MF of surface EMG was calculated during 60% MVCs. We measured lactic acid and potassium venous blood concentrations and calculated plasma volume changes. Data were compared to those obtained in the same individuals exercising at 35°C under dry conditions where the MF decrease during 60% MVCs was modest (−4 to−5%). During immersion, the rectal temperature remained stable, but the thigh and calf surface temperatures significantly increased. Lactic acid and potassium concentrations did not vary, but plasma volume decreased from the 180th min of immersion. The M-wave did not vary in VL but was prolonged in SOL from the 30th min of immersion. From the 220th min of immersion, the maximal MF decrease was majored in both muscles (−18 to −22%). Thus, compared to the dry condition, total body thermoneutral immersion enhances fatigue-induced EMG changes in leg muscles, perhaps through the activation of warm-sensitive muscle endings and/or the changes in interstitial pressure because of vasodilatation.

INTRODUCTION:As exercise while wearing protective clothing exacerbates body heat storage compared to exercise in the heat, and as exercise alters immune responses, it appeared worthwhile to examine immune and stress responses while wearing protective clothing during moderate exercise.METHODS:Eight subjects completed two bouts of exercise at 45% Vo2(max) in a thermoneutral environment: once while wearing shorts only (Control trial, CON) and again while wearing protective clothing (PRO). Venous blood samples were taken to analyze TNF-alpha mRNA by RT-PCR in LPS stimulated blood, plasma catecholamines, and cortisol. Blood cell count was analyzed by flow cytometry. Rectal temperature (T(re)) was monitored continuously.RESULTS:Exercise with PRO resulted in significantly greater increases in T(re) (39.2 +/- 0.2 degrees C in PRO vs. 38.0 +/- 0.1 degrees C in CON) and plasma epinephrine and norepinephrine (+70% and 150%, respectively). Plasma cortisol increased only at the end of PRO exercise (+33%). Leukocyte and lymphocyte cell count was 14% and 18% higher, respectively, but there were no significant changes in T cytotoxic and NK cell counts compared to the CON trial. Only T helper lymphocyte count was lower (-29%). During both exercise trials, T helper lymphocytes were significantly decreased at the end of exercise and recovery. With or without protective clothing, exercise was associated with an inhibition of TNF- alpha expression in stimulated monocytes (approximately -50% at min 20 and 40, and approximately -30% at min 60).DISCUSSION:Protective clothing wearing induces significant thermal challenge during exercise. The inhibition of TNF-alpha appears to be mediated primarily by exercise and not the added thermal load associated with protective clothing.

UNLABELLED:Different stress hormones are released during prolonged exercise and passive hyperthermia. We hypothesized that these different hormonal responses could contribute to the different changes in the immune response during these two challenges.METHODS:Eight subjects completed three trials in a randomized order. In the control trial (C), the subjects remained in a sitting posture for three hours in thermoneutral conditions. In the exercise hyperthermia trial (E), they exercised for two hours on a treadmill at 65% max in thermoneutral conditions, followed by 1-h recovery in thermoneutral conditions; in the passive hyperthermia trial (PH), the subjects remained in a semi-recumbent position in a climatic chamber for two hours in hot conditions, followed by 1-h recovery in thermoneutral conditions. During the E and PH trials, wind speed and thermal conditions were modulated to reach a rectal temperature (Tre) of 38.5 degrees C at 60 min and 39 degrees C at 120 min. The subjects did not drink during the experiments. Blood samples (10 mL) were taken at 0, 60, 120 and 180 min of each trial. The total white cell count and its subsets were measured; plasma catecholamines, cortisol and prolactin were assayed. In a whole blood assay, blood leukocytes were stimulated by lipopolysaccharide (LPS) or phytohemagglutinin (PHA) for 24 and 48 hours, respectively. Cytokines, such as TNF-alpha, IL-10 and INF-gamma were measured in the culture supernatant.RESULTS:The plasma levels of catecholamines were increased only during E, prolactin was increased only during PH, and cortisol was increased in both E and PH. Only the exercise caused a mobilization of blood leukocytes and leukocyte subsets. The INF-gamma and TNF-alpha production by PHA- and LPS-stimulated blood, respectively, were inhibited in a substantial way in both E and PH compared to control when Tre reached 39 degrees C. Only LPS-induced IL-10 production was enhanced during the exercise. The effects of the challenges were increased with 39 degrees C compared to 38.5 degrees C.CONCLUSIONS:Catecholamines play a major role in the mobilization of immunocompetent cells and the production of IL-10 during exercise. Prolactin and catecholamines have adverse role on the immune response, whereas cortisol exerts similar effects during both trials. The consequence could be a protection against inflammatory overshooting.

The consequences of a prolonged total body immersion in cold water on the muscle function have not been documented yet, and they are the object of this French Navy research program. Ten elite divers were totally immerged and stayed immobile during 6 h in cold (18 and 10 degrees C) water. We measured the maximal voluntary leg extension (maximal voluntary contraction, MVC) and evoked compound muscle potential (M wave) in vastus lateralis and soleus muscles at rest, after a submaximal (60% MVC) isometric extension allowing the measurement of the endurance time (Tlim). The power spectrum of surface electromyograms (EMG) was computed during 60% MVCs. MVCs and 60% MVC maneuvers were repeated four times during the immersion. Data were compared with those obtained in a control group studied in dry air condition during a 6-h session. Total body cooling did not affect MVC nor Tlim. The M wave duration increased in the coolest muscle (soleus), but only at 10 degrees C at rest. There were no further fatigue-induced M wave alterations in both muscles. During 60% the MVCs, a time-dependant increase in the leftward shift of the EMG spectrum occurred at the two temperatures. These EMG changes were absent in the control group of subjects studied in dry air. The plasma lactate concentration was elevated throughout the 18 and mostly the 10 degrees C immersion conditions. Throughout the 18 degrees C immersion study, the resting potassium level did not significantly vary, whereas at 10 degrees C, a significant potassium increase occurred soon and persisted throughout the study. Thus, total body immersion in cold water did not affect the global contractile properties of leg muscles during static efforts but elicited significant alterations in electromyographic events which may be related to the variations of interstitial fluid composition.

PURPOSE:This study was designed to describe the responses of fluid-regulating hormones during exercise in acute hypobaric hypoxia and to test the hypothesis that they would be dependent on the relative intensity of exercise rather than the absolute workload. METHODS:Thirteen men cycled for 60 min on four occasions in the same individual hydration status: in normoxia at 55% and 75% of normoxia maximal aerobic power (N55 and N75, respectively), in hypoxia (PB = 594 hPa) at the same absolute workload and at the same relative intensity as N55 (H75 and H55, respectively). VO2, heart rate, and rectal and mean skin temperatures were recorded during exercise. The total water loss was measured by the difference in nude body mass adjusted for metabolic losses. Venous blood samples were drawn before and 15, 30, 45, and 60 min after the beginning of exercise to measure variations in plasma volume, osmolality, and concentrations in arginine vasopressin (AVP), atrial natriuretic factor (ANF), plasma renin activity (ARP), aldosterone (Aldo), and noradrenaline (NA). RESULTS:During N55 and H55, AVP, Aldo and ARP did not change, whereas ANF increased slightly. Increases in AVP, Aldo, ARP, and NA were greater during N75 than during H75, whereas the increase in ANF was greater during H75 than N75. CONCLUSION:Plasma levels of AVP, Aldo, and ARP increase during exercise when a threshold is reached and thereafter are dependent on the absolute workload, without any specific effect of hypoxia. The time course of ANF appears to be different from that of the other hormones.

Lors des exercices de longue duree (ultra-endurance), l'elevation de la temperature corporelle et la deshydratation due aux pertes sudorales, entrainent une baisse du volume sanguin central. La derive de frequence cardiaque permet de maintenir un debit cardiaque adapte aux besoins locaux des muscles actifs ainsi qu'au transfert de chaleur par l'augmentation du debit sanguin cutane. La deshydratation est defavorable a la regulation thermique et favorise l'apparition d'accidents graves comme le coup de chaleur d'exercice. Les exercices tres prolonges, superieurs a 8 h, s'accompagnent d'importantes pertes de chlorure de sodium par la sueur. Si l'apport de sel est trop faible par rapport a la quantite d'eau ingeree, une hyponatremie symptomatique (natremie < 13 m qlL), accident egalement gravissime, peut se produire. L'environnement chaud majore la contrainte thermique et, si l'humidite de l'air est elevee, l'evaporation de la sueur est compromise. Dans ces conditions, le stress thermique devient non compensable, ce qui favorise l'apparition d'un collapsus cardiovasculaire. L'exposition au froid induit des reactions physiologiques visant a maintenir la temperature interne en limitant les pertes thermiques ou en augmentant la production de chaleur metabolique. Le froid expose a l'hypothermie accidente le et aux gelures des extremites; il favorise egalement les arythmies cardiaques en cours d'exercice. Des recommandations (aptitude cardiovasculaire, apports hydromineraux et energetiques, protection vestimentaire) sont proposees pour chaque condition extreme.

. 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 sympatho-adrenal 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.

The theoretical velocity associated with VO2max (vVO2max) defined by Daniels (1985) is extrapolated from the submaximal VO2-velocity relationship. VO2 is generally determined by assuming that the aerobic response reacts like a linear first-order system at the beginning of square-wave exercise with a steady-state reached by the 4th minute. However, at supra-ventilatory threshold work rates, the steady state in VO2 is delayed or not attained.The present study was carried out to compare three values for vVO2max determined with Daniels' method, but with VO2 either measured at the 4th minute (vVO2max4), the 6th minute (vVO2max6), or after the attainment of the true steady-state (vVO2maxSS). The metabolic response during square-wave exercise at each of the three vVO2max were also assessed.These velocities were significantly different (P < 0.05), but vVOmaxSS and vVO2max6 were highly correlated (r = 0.98; P < 0.05). Blood lactate concentrations measured after exercise at velocities very close to the three vVO2max were similar and the end-exercise VO2 were not different from VO2max, but the time required to elicit 95% VO2max during these three square-wave tests were significantly different.Therefore, when vVO2max is determined by extrapolation from the submaximal VO2-velocity relationships, submaximal VO2 should be measured beyond the 6th minute of square-wave exercise (at least if it takes 30 s to reach the desired velocity) to ensure that all vVO2max reported in future studies describe a similar quantitative index.

During high-intensity running, the oxygen uptake ( V˙ O 2 ) kinetics is characterised by a slow component which delays the attainment of the steady-state beyond the 3rd min of exercise. To assess if the aerobic energy cost of running measured at the 3rd min ( C 3 ) adequately reflects the variability of the true aerobic energy cost measured during the steady-state ( C ss ), 13 highly-trained runners completed sessions of square-wave running at intensities above 80% maximal oxygen uptake ( V˙ O 2max ) on a level treadmill. To evaluate the time at which the steady-state V˙ O 2 was attained ( t ss ), the V˙ O 2 responses were described using a general double-exponential equation and t ss was defined as the time at which V˙ O 2 was less than 1% below the asymptotic value given by the model. All the subjects achieved a steady state for intensities equal to or greater than 92% V˙ O 2max , and 8 out of 13 achieved it at 99% V˙ O 2max . In all cases, t ss was less than 13 min. For intensities greater than 85% V˙ O 2max , C ss was significantly higher than C 3 and was positively related to % V˙ O 2max ( r = 0.44; P < 0.001) while C 3 remained constant. The C 3 only explained moderately the variability of C ss (0.39 < r 2 < 0.72, depending on the velocity or the (relative intensity at which the relationship was calculated). Moreover, the excess aerobic energy cost of running the (difference between C ss and C 3 ) was well predicted by age (0.90 < r 2 < 0.93). Therefore, when the aerobic profile of runners is evaluated, it is recommended that their running efficiencies at velocities which reflect their race intensities should be determined, with V˙ O 2 data being measured at the true steady-state.