To examine the baroreflex response in humans during acute high-altitude exposure, the carotid baroreflex cardiac responsiveness was studied using a neck chamber in seven unacclimatized male subjects. Measurements were made in a high-altitude chamber on separate days at sea level and during 1-h exposure at two different altitudes of 3,800 m [partial pressure of oxygen in inspired air (Pi O2 ) = 90 mmHg] and 4,300 m (Pi O2  = 82 mmHg). R-R intervals were plotted against neck chamber pressures, and the baroreceptor response was analyzed by applying a four-parameter sigmoidal logistic function. The baroreceptor response curve shifted downward in either altitude, reflecting a tachycardic response at high altitude, and the magnitude of the shift was greater at 4,300 m than at 3,800 m. There was no change in the sigmoidal parameters at 3,800 m compared with sea level except for a reduction ( P < 0.05) of the minimum R-R interval. At 4,300 m the maximal R-R range, slope coefficient, minimum R-R interval, and maximal gain of the curve decreased significantly ( P < 0.05) compared with sea level values, whereas the centering point of the curve remained unchanged. These results suggest that hypoxia (Pi O2  = 82 mmHg) reduces the sensitivity of carotid baroreflex cardiac response.

The purpose of this study was to examine the effect of hyperthermia on the carotid baroreceptor-cardiac reflexes in humans. Nine healthy males underwent acute hyperthermia (esophageal temperature -38.0 degrees C) produced by hot water-perfused suits. Beat-to-beat heart rate (HR) responses were determined during positive and negative R-were-triggered neck pressure steps from +40 to -65 mm Hg during normothermia and hyperthermia. The carotid baroreceptor-cardiac reflex sensitivity was evaluated from the maximum slope of the HR response to changes in carotid distending pressure. Buffering capacity of the HR response to carotid distending pressure was evaluated in % from a reference point calculated as (HR at 0 mm Hg neck pressure-minimum HR)/HR range x 100. An upward shift of the curve was evident in hyperthermia because HR increased from 57.7 +/- 2.4 beats/min in normothermia to 88.7 +/- 4.1 beats/min in hyperthermia (P < 0.05) without changes in mean arterial pressure. The maximum slope of the curve in hyperthermia was similar to that in normothermia. The reference point was increased (P < 0.05) during hyperthermia. These results suggest that the sensitivity of the carotid baroreflex of HR remains unchanged in hyperthermia. However, the capacity for tachycardia response to rapid onset of hypotension is reduced and the capacity for bradycardia response to sudden hypertension is increased during acute hyperthermia.

To investigate precisely the fluid shifts associated with water drinking in humans, we measured continuously blood density and plasma electrolyte concentrations using the mechanical oscillator technique and ion-selective electrodes, respectively, in healthy young volunteers before (10 min) and after (48 min) water drinking for a period of 2 min. Beat-by-beat blood pressure was also monitored throughout the experiment. Drinking 1 l tap water caused a transient increase in blood density immediately after the drinking episode (from 1051.1+/-0.5 g/l before drinking to 1051.8+/-0.5 g/l 4 min after the start of drinking, P<0.05), followed by a gradual reduction (1050.1+/-0.5 g/l at 31 min). This drinking-induced change paralleled those of haematocrit, plasma density and plasma volume. Plasma [Na+] and [Cl-] and osmolality decreased after drinking without transient increases and reached minima at about 30 min. A transient increase in mean arterial blood pressure was observed prior to the increase in blood density. These findings suggest that water drinking causes a biphasic change in plasma volume: initial haemoconcentration, probably due to sympathetic acceleration, followed by haemodilution due to the post-absorptive effect, and further suggest that the fluid shift associated with the initial haemoconcentration is isosmotic.

We conclude that exercise-trained females have a high incidence of orthostatic intolerance during LBNP, with a greater reduction of SV independent of changes in baroreflex and neurohumoral function. A lower incidence of LBNP intolerance in UT may be accounted for by a lower reduction of SV during LBNP. An increase in leg compliance in the exercise-trained females may play an important role in inducing pronounced reduction of SV and hence the intolerance to LBNP.

Plasma arginine vasopressin (AVP) concentration is reduced in human subjects during prolonged saturation dive exposures of 4 atmospheres absolute (atm abs) and greater. The objectives of the present study were to determine if AVP would be reduced in eight male subjects during a 1-h exposure of 3 atm abs air and, if so, to determine the mechanisms responsible for the AVP response. Assessments of transmural central venous pressure (central venous pressure-esophageal pressure) and cardiac volume measurements were made to evaluate the possible role of cardiopulmonary receptors on the AVP response. Also, plasma osmolality (P(osmol)), venous blood gases, and mean corpuscular volume (MCV) were determined to evaluate potential effects of osmoreceptor and other fluid shifts on AVP release. AVP decreased (P < 0.05) by 0.5 microU/ml at 3 atm abs, whereas the transmural central venous pressure and cardiac volume remained unchanged throughout the experimental periods. A significant reduction (P < 0.05) in P(osmol) (by approximately 3 mosmol/kgH2O) was detected at 3 atm abs. Therefore, we conclude that the reduction in P(osmol) may cause the reduction in AVP during exposure to 3 atm abs pressure. The reduction in P(osmol) without water intake requires the postulation of an internal source of water. We propose that the threefold increase (P < 0.01) in venous PO2 and concomitant decrease (P < 0.05) in venous MCV suggest that the red blood cell may contribute to hypotonicity at 3 atm abs.