Effect of hydration status on thirst, drinking, and related hormonal responses during low-intensity exercise in the heat.

During exercise-heat stress, ad libitum drinking frequently fails to match sweat output, resulting in deleterious changes in hormonal, circulatory, thermoregulatory, and psychological status. This condition, known as voluntary dehydration, is largely based on perceived thirst. To examine the role of preexercise dehydration on thirst and drinking during exercise-heat stress, 10 healthy men (21 +/- 1 yr, 57 +/- 1 ml x kg(-1) x min(-1) maximal aerobic power) performed four randomized walking trials (90 min, 5.6 km/h, 5% grade) in the heat (33 degrees C, 56% relative humidity). Trials differed in preexercise hydration status [euhydrated (Eu) or hypohydrated to -3.8 +/- 0.2% baseline body weight (Hy)] and water intake during exercise [no water (NW) or water ad libitum (W)]. Blood samples taken preexercise and immediately postexercise were analyzed for hematocrit, hemoglobin, serum aldosterone, plasma osmolality (P(osm)), plasma vasopressin (P(AVP)), and plasma renin activity (PRA). Thirst was evaluated at similar times using a subjective nine-point scale. Subjects were thirstier before (6.65 +/- 0.65) and drank more during Hy+W (1.65 +/- 0.18 liters) than Eu+W (1.59 +/- 0.41 and 0.31 +/- 0.11 liters, respectively). Postexercise measures of P(osm) and P(AVP) were significantly greater during Hy+NW and plasma volume lower [Hy+NW = -5.5 +/- 1.4% vs. Hy+W = +1.0 +/- 2.5% (P = 0.059), Eu+NW = -0.7 +/- 0.6% (P < 0.05), Eu+W = +0.5 +/- 1.6% (P < 0.05)] than all other trials. Except for thirst and drinking, however, no Hy+W values differed from Eu+NW or Eu+W values. In conclusion, dehydration preceding low-intensity exercise in the heat magnifies thirst-driven drinking during exercise-heat stress. Such changes result in similar fluid regulatory hormonal responses and comparable modifications in plasma volume regardless of preexercise hydration state.     

Cortical activation and lamina terminalis functional connectivity during thirst and drinking in humans

The pattern of regional brain activation in humans during thirst associated with dehydration, increased blood osmolality, and decreased blood volume is not known. Furthermore, there is little information available about associations between activation in osmoreceptive brain regions such as the organum vasculosum of the lamina terminalis and the brain regions implicated in thirst and its satiation in humans. With the objective of investigating the neuroanatomical correlates of dehydration and activation in the ventral lamina terminalis, this study involved exercise-induced sweating in 15 people and measures of regional cerebral blood flow (rCBF) using a functional magnetic resonance imaging technique called pulsed arterial spin labeling. Regional brain activations during dehydration, thirst, and postdrinking were consistent with the network previously identified during systemic hypertonic infusions, thus providing further evidence that the network is involved in monitoring body fluid and the experience of thirst. rCBF measurements in the ventral lamina terminalis were correlated with whole brain rCBF measures to identify regions that correlated with the osmoreceptive region. Regions implicated in the experience of thirst were identified including cingulate cortex, prefrontal cortex, striatum, parahippocampus, and cerebellum. Furthermore, the correlation of rCBF between the ventral lamina terminalis and the cingulate cortex and insula was different for the states of thirst and recent drinking, suggesting that functional connectivity of the ventral lamina terminalis is a dynamic process influenced by hydration status and ingestive behavior.     

Early fluid and protein shifts in men during water immersion

High precision blood and plasma densitometry was used to measure transvascular fluid shifts during water immersion to the neck. Six men (28-49 years) undertook 30 min of standing immersion in water at 35.0 +/- 0.2 degrees C; immersion was preceded by 30 min control standing in air at 28 +/- 1 degrees C. Blood was sampled from an antecubital catheter for determination of blood density (BD), plasma density (PD), haematocrit (Ht), total plasma protein concentration (PPC), and plasma albumin concentration (PAC). Compared to control, significant decreases (p less than 0.01) in all these measures were observed after 20 min immersion. At 30 min, plasma volume had increased by 11.0 +/- 2.8%; the average density of the fluid shifted from extravascular fluid into the vascular compartment was 1006.3 g.l-1; albumin moved with the fluid and its albumin concentration was about one-third of the plasma protein concentration during early immersion. These calculations are based on the assumption that the F-cell ratio remained unchanged. No changes in erythrocyte water content during immersion were found. Thus, immersion-induced haemodilution is probably accompanied by protein (mainly albumin) augmentation which accompanies the intravascular fluid shift.     

Effect of voluntary dehydration on thermoregulatory responses to heat in men and women

The effects of dehydration prior to heat exposure on sweating and body temperature were tested in 8 men and 8 women, dehydration being 1.3 and 1.0% of body weight, respectively. The subjects were exposed to 40 degrees C for 60 min. Compared with controls (C), in the dehydrated men (D) there was a longer delay in the onset of sweating (C, 7.8, D, 11.6 min, p less than 0.05), a lower total sweat loss (C, 153, D, 127 g X m-2 X h-1, p less than 0.001), and a greater increase in Tre (C, 0.31, D, 0.43 degree C, p less than 0.002). In women, dehydration did not influence the control time course of sweating significantly, nor were these significant body temperature increases during heat exposure. Delay in the onset of sweating in women (C, 18.1, D, 18.7 min) was generally longer than in men (C, 7.8, D, 11.6 min), [F(1,14) = 7.41, p less than 0.05]. A significant correlation was found between the inertia time of sweating and delta Tre in both control and dehydration conditions in the men (r = 0.81, p less than 0.01). The rectal temperature increases in men were also related to the inertia time of electrical skin resistance (r = 0.83, p less than 0.01). It is concluded that dehydration affects sweating and body temperature in men more severely than in women.     

Effects of dehydration on the vasopressin response to immersion

Nine healthy volunteers underwent three experimental procedures in random order. The protocols were 4 h of thermal dehydration followed by 2 h of head-out water immersion, 4 h of thermal dehydration followed by 2 h of chair rest, and 6 h of rest in the supine position. Four hours of heat exposure (50 degrees C) resulted in a body weight loss of approximately 3.5%. Plasma osmolality rose by approximately 5 mosmol/kg, mean arterial pressure (MAP) decreased from 85 to 78 mmHg, and body temperature increased from 36.8 to 38.6 degrees C. As a consequence of the combined action of hypertonicity, hypovolemia, hypotension, and hyperthermia, plasma arginine vasopressin (AVP) increased from 2.1 to 8.1 pg/ml after 4 h thermal dehydration. Changes in body weight, plasma osmolality, body temperature, and MAP were similar after either a subsequent 2 h of water immersion or 2 h of chair rest. However, during chair rest plasma AVP remained elevated (8.4 pg/ml), whereas during immersion plasma AVP decreased from 8.1 to 4.7 pg/ml. This was probably due to the central hypervolemia induced by immersion. Our results support the hypothesis that central hypervolemia rather than hypotonicity is the primary stimulus for AVP suppression during water immersion in dehydrated subjects. During the early immersion period hypoosmolality might contribute to the AVP suppression.     

Thermal responses of men and women during cold-water immersion: influence of exercise intensity

The influence of exercise intensity on thermoregulation was studied in 8 men and 8 women volunteers during three levels of arm-leg exercise (level I: 700 ml oxygen (O2).min-1; level II: 1250 ml O2.min-1; level III: 1700 ml O2.min-1) for 1 h in water at 20 and 28 degrees C (Tw). For the men in Tw 28 degrees C the rectal temperature (Tre) fell 0.79 degree C (P less than 0.05) during immersion in both rest and level-I exercise. With level-II exercise a drop in Tre of 0.54 degree C (P less than 0.05) was noted, while at level-III exercise Tre did not change from the pre-immersion value. At Tw of 20 degrees C, Tre fell throughout immersion with no significant difference in final Tre observed between rest and any exercise level. For the women at rest at Tw 28 degrees C, Tre fell 0.80 degree C (P less than 0.05) below the pre-immersion value. With the two more intense levels of exercise Tre did not decrease during immersion. In Tw 20 degrees C, the women maintained higher Tre (P less than 0.05) during level-II and level-III exercise compared to rest and exercise at level I. The Tre responses were related to changes in tissue insulation (I(t)) between rest and exercise with the largest reductions in I(t) noted between rest and level-I exercise across Tw and gender. For mean and women of similar percentage body fat, decreases in Tre were greater for the women at rest and level-I exercise in Tw 20 degrees C (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of nifedipine on core cooling in rats during tail cold water immersion

Male rats (450 g, n=11/group) were heated at an ambient temperature of 42°C until a rectal temperature of 42.8°C was attained. Rats, then received either saline (30°C)+tail ice water immersion (F+I) or saline (30°C)+tail ice water immersion+Nifedipine, a peripheral vasodilator, (F+I+N) to determine cooling rate effectiveness and survivability. The time to reach a rectal temperature of 42.8°C averaged 172 min in both groups resulting in similar heating rates (0.029°C/min). The cooling rates in group F+I and F+I+N were not significantly different from each other. We conclude that since Nifedipine did not improve cooling rates when combined with fluid+tail ice water immersion, its use as a cooling adjunct does not seem warranted.     

Investigating the role of angiotensin II in thirst: interactions between arterial pressure and the control of drinking.

Several lines of evidence suggest that angiotensin II plays a physiological role in the control of thirst. Establishing that, however, has been surprisingly difficult, given our current knowledge about the renin-angiotensin systems in the circulation and the brain and the variety of techniques available to measure and manipulate them. A major problem is that stimulating or blocking the renin-angiotensin system affects several physiological variables simultaneously. Since several of these variables also influence the controls of water intake directly or indirectly, the interpretation of the effect on drinking becomes more difficult. To illustrate the problem and recent developments, this paper describes some of the interactions between the effects of angiotensin II on arterial pressure and thirst, and it shows how they have contributed to the controversy over the physiological role of the peptide.     

Effect of hyperosmotic solutions on salt excretion and thirst in rats

We investigated urinary changes and thirst induced by infusion of hyperosmotic solutions in freely moving rats. Intracarotid infusions of 0.3 M NaCl (4 ml/20 min, split between both internal carotid arteries) caused a larger increase in excretion of Na(+) and K(+) than intravenous infusions, indicating that cephalic sensors were involved in the response to intracarotid infusions. Intravenous and intracarotid infusions of hyperosmotic glycerol or urea (300 mM in 150 mM NaCl) had little or no effect, suggesting the sensors were outside the blood-brain barrier (BBB). Intracarotid infusion of hypertonic mannitol (300 mM in 150 mM NaCl) was more effective than intravenous infusion, suggesting that cell volume rather than Na(+) concentration of the blood was critical. Similarly, intracarotid infusion (2 ml/20 min, split between both sides), but not intravenous infusion of hypertonic NaCl or mannitol caused thirst. Hyperosmotic glycerol, infused intravenously or into the carotid arteries, did not cause thirst. We conclude that both thirst and electrolyte excretion depend on a cell volume sensor that is located in the head, but outside the BBB.     

Effect of occluded venous return on core temperature during cold water immersion

Recent studies using inanimate and animal models suggest that the afterdrop observed upon rewarming from hypothermia is based entirely on physical laws of heat flow without involvement of the returning cooled blood from the limbs. During the investigation of thermoregulatory responses to cold water immersion (15 degrees C), blood flow to the limbs (minimized by the effects of hydrostatic pressure and vasoconstriction) was occluded in 17 male subjects (age, 29.0 +/- 3.3 yr). Comparisons of rectal (Tre) and esophageal temperature (Tes) responses were made during the 5 min before occlusion, during the 10-min occlusion period, and for 5 min immediately after the release of the cuffs (postocclusion). In the preocclusion phase, Tre and Tes showed similar cooling rates. The occlusion of blood flow to the extremities significantly arrested the cooling of Tes (P less than 0.05) with little effect on Tre. Upon release of the pressure cuffs, the returning extremity blood flow resulted in an increased rate of cooling, that was three times greater at the esophageal site (-0:149 +/- 0.052 vs. -0.050 +/- 0.026 degrees C.min-1). These results suggest that the cooled peripheral circulation, minimized during cold water immersion, may dramatically affect esophageal temperature and the complete neglect of the circulatory component to the afterdrop phenomenon is not warranted.