Intense exercise stimulates albumin synthesis in the upright posture.

We tested the hypothesis that an elevation in albumin synthetic rate contributes to increased plasma albumin content during exercise-induced hypervolemia. Albumin synthetic rate was measured in seven healthy subjects at 1-5 and 21-22 h after 72 min of intense (85% peak oxygen consumption rate) intermittent exercise and after 5 h recovery in either upright (Up) or supine (Sup) postures. Deuterated phenylalanine (d(5)-Phe) was administrated by a primed-constant infusion method, and fractional synthetic rate (FSR) and absolute synthetic rate (ASR) of albumin were calculated from the enrichment of d(5)-Phe in plasma albumin, determined by gas chromatography-mass spectrometry. FSR of albumin in Up increased significantly (P < 0.05) from 4.9 +/- 0.9%/day at control to 7.3 +/- 0.9%/day at 22 h of recovery. ASR of albumin increased from 87.9 +/- 17.0 to 141.1 +/- 16.6 mg albumin. kg body wt(-1). day(-1). In contrast, FSR and ASR of albumin were unchanged in Sup (3.9 +/- 0.4 to 4.0 +/- 1.4%/day and 74.2 +/- 8.9 to 85.3 +/- 23.9 mg albumin. kg body wt(-1). day(-1) at control and 22 h of recovery, respectively). Increased albumin synthesis after upright intense exercise contributes to the expansion of greater albumin content and its maintenance. We conclude that stimuli related to posture are critical in modulating the drive for albumin synthesis after intense exercise.

Human cardiovascular and humoral responses to moderate muscle activation during dynamic exercise.

We examined the hypothesis that activation of the muscle metaboreflex during dynamic exercise would augment influences tending to cause a rise in arginine vasopressin, plasma renin activity, and catecholamines during dynamic exercise in humans. Ten healthy adults performed 30 min of supine cycle ergometer exercise at approximately 50% of peak oxygen consumption with or without moderate muscle metaboreflex activation by application of 35 mmHg lower body positive pressure (LBPP). Application of LBPP during the first 15 or last 15 min of exercise increased mean arterial blood pressure, plasma lactate concentration, and minute ventilation, indicating an activation of the muscle metaboreflex. These changes were rapidly reversed when LBPP was removed. During exercise at this intensity, LBPP augmented the release of arginine vasopressin and catecholamines but not of plasma renin activity. These results suggest that, although in humans hormonal responses are induced by moderate activation of the muscle metaboreflex during dynamic exercise, the thresholds for these responses may not be uniform among the various glands and hormones.

Effects of oral contraceptives on body fluid regulation.

To test the hypothesis that estrogen reduces the operating point for osmoregulation of arginine vasopressin (AVP), thirst, and body water balance, we studied nine women (25 +/- 1 yr) during 150 min of dehydrating exercise followed by 180 min of ad libitum rehydration. Subjects were tested six different times, during the early-follicular (twice) and midluteal (twice) menstrual phases and after 4 wk of combined [estradiol-norethindrone (progestin), OC E + P] and 4 wk of norethindrone (progestin only, OC P) oral contraceptive administration, in a randomized crossover design. Basal plasma osmolality (P(osm)) was lower in the luteal phase (281 +/- 1 mosmol/kgH(2)O, combined means, P < 0.05), OC E + P (281 +/- 1 mosmol/kgH(2)O, P < 0.05), and OC P (282 +/- 1 mosmol/kgH(2)O, P < 0. 05) than in the follicular phase (286 +/- 1 mosmol/kgH(2)O, combined means). High plasma estradiol concentration lowered the P(osm) threshold for AVP release during the luteal phase and during OC E + P [x-intercepts, 282 +/- 2, 278 +/- 2, 276 +/- 2, and 280 +/- 2 mosmol/kgH(2)O, for follicular, luteal (combined means), OC E + P, and OC P, respectively; P < 0.05, luteal phase and OC E + P vs. follicular phase] during exercise dehydration, and 17beta-estradiol administration lowered the P(osm) threshold for thirst stimulation [x-intercepts, 280 +/- 2, 279 +/- 2, 276 +/- 2, and 280 +/- 2 mosmol/kgH(2)O for follicular, luteal, OC E + P, and OC P, respectively; P < 0.05, OC E + P vs. follicular phase], without affecting body fluid balance. When plasma 17beta-estradiol concentration was high, P(osm) was low throughout rest, exercise, and rehydration, but plasma arginine vasopressin concentration, thirst, and body fluid retention were unchanged, indicating a lowering of the osmotic operating point for body fluid regulation.

Excess abdominal adiposity remains correlated with altered lipid concentrations in healthy older women.

OBJECTIVE: To determine associations between overall adiposity, absolute and relative abdominal adiposity, and lipid concentrations in healthy older women. DESIGN: Cross-sectional analysis of baseline data. SUBJECTS: Subjects were 21 healthy, untrained older women (71 +/- 1 y) entering a randomized, controlled aerobic training program. MEASUREMENTS: Overall adiposity was assessed by anthropometry and the body mass index (BMI=kg/m2). Absolute and relative abdominal adiposity was determined by computed tomography (CT) and circumference measures. Fasting serum lipid concentrations of total-, high density lipoprotein (HDL)-, and low density lipoprotein (LDL)-cholesterol (C) and triglycerides (TGs) were determined by standard enzymatic procedures. RESULTS: Compared to the measures of overall adiposity, we observed much stronger correlations between measures more specific to absolute or relative abdominal adiposity and lipid concentrations. Visceral fat area was the strongest correlate of HDL-C (r = -0.75; P < 0.001) and the total-/HDL-C ratio (r = 0.86; P < 0.001). The abdomen-to-hip circumference ratio (AHR) was strongly correlated with TGs (r = 0.54; P < 0.01), HDL-C (r= -0.69; P < 0.001), and the total-/HDL-C ratio (r = 0.75; P < 0.001). CONCLUSION: Excess abdominal adiposity remains an important correlate of lipid metabolism, even in healthy older women of normal weight. Thus, overall obesity is not a necessary condition for the correlation between excess abdominal fat and metabolic risk among postmenopausal women.

Mechanism for the posture-specific plasma volume increase after a single intense exercise protocol.

To test the hypothesis that exercise-induced hypervolemia is a posture-dependent process, we measured plasma volume, plasma albumin content, and renal function in seven healthy subjects for 22 h after single upright (Up) or supine (Sup) intense (85% peak oxygen consumption rate) exercise. This posture was maintained for 5 h after exercise. Plasma volume decreased during exercise but returned to control levels by 5 h of recovery in both postures. By 22 h of recovery, plasma volume increased 2.4 +/- 0.8 ml/kg in Up but decreased 2.1 +/- 0.8 ml/kg in Sup. The plasma volume expansion in Up was accompanied by an increase in plasma albumin content (0.11 +/- 0.04 g/kg; P < 0.05). Plasma albumin content was unchanged in Sup. Urine volume and sodium clearance were lower in Up than Sup (P < 0.05) by 5 h of recovery. These data suggest that increased plasma albumin content contributes to the acute phase of exercise-induced hypervolemia. More importantly, the mechanism by which exercise influences the distribution of albumin between extra- and intravascular stores after exercise is altered by posture and is unknown. We speculate that factors associated with postural changes (e.g., central venous pressure) modify the increase in plasma albumin content and the plasma volume expansion after exercise.

Physiological variability of fluid-regulation hormones in young women.

We tested the physiological reliability of plasma renin activity (PRA) and plasma concentrations of arginine vasopressin (P[AVP]), aldosterone (P[ALD]), and atrial natriuretic peptide (P[ANP]) in the early follicular phase and midluteal phases over the course of two menstrual cycles (n = 9 women, ages 25 +/- 1 yr). The reliability (Cronbach's alpha >/=0.80) of these hormones within a given phase of the cycle was tested 1) at rest, 2) after 2.5 h of dehydrating exercise, and 3) during a rehydration period. The mean hormone concentrations were similar within both the early follicular and midluteal phase tests; and the mean concentrations of P[ALD] and PRA for the three test conditions were significantly greater during the midluteal compared with the early follicular phase. Although Cronbach's alpha for resting and recovery P[ANP] were high (0.80 and 0.87, respectively), the resting and rehydration values for P[AVP], P[ALD], and PRA were variable between trials for the follicular (alpha from 0.49 to 0.55) and the luteal phase (alpha from 0.25 to 0. 66). Physiological reliability was better after dehydration for P[AVP] and PRA but remained low for P[ALD]. Although resting and recovery P[AVP], P[ALD], and PRA were not consistent within a given menstrual phase, the differences in the concentrations of these hormones between the different menstrual phases far exceeded the variability within the phases, indicating that the low within-phase reliability does not prevent the detection of menstrual phase-related differences in these hormonal variables.

Albumin infusion in humans does not model exercise induced hypervolaemia after 24 hours.

We rapidly infused 234 +/- 3 mL of 5% human serum albumin in eight men while measuring haematocrit, haemoglobin concentration, plasma volume (PV), albumin concentration, total protein concentration, osmolality, sodium concentration, renin activity, aldosterone concentration, and atrial natriuretic peptide concentration to test the hypotheses that plasma volume expansion and plasma albumin content expansion will not persist for 24 h. Plasma volume and albumin content were expanded for the first 6 h after infusion (44.3 +/- 1.9-47.2 +/- 2.0 mL kg-1 and 1.9 +/- 0.1-2.1 +/- 0.1 g kg-1 at pre-infusion and 1 h, respectively, P < 0.05), but by 24 h plasma volume and albumin content decreased significantly from 1 h post-infusion and were not different from pre-infusion (44.8 +/- 1.9 mL kg-1 and 1.9 +/- 0.1 g kg-1, respectively). Plasma aldosterone concentration showed a significant effect of time over the 24 h after infusion (P < 0.05), and showed a trend to decrease at 2 h after infusion (167.6 +/- 32.5(-1) 06.2 +/- 13.4 pg mL-1, P = 0.07). These data demonstrate that a 6.8% expansion of plasma volume and 10.5% expansion of plasma albumin content by infusion does not remain in the vascular space for 24 h and suggest a redistribution occurs between the intravascular space and interstitial fluid space.

Effects of posture on cardiovascular responses to lower body positive pressure at rest and during dynamic exercise.

We tested the hypothesis that cardiovascular responses to lower body positive pressure (LBPP) would be dependent on the posture of the subject and also on the background condition (rest or exercise). We measured heart rate (HR), mean arterial blood pressure (MAP), and cardiac stroke volume in eight subjects at rest and during cycle ergometer exercise (76 +/- 3 W) with and without LBPP (25, 50, and 75 mmHg) in the supine and upright positions. At rest, the increase in MAP was proportional to the increase in LBPP and was greater in the supine (6 +/- 2, 15 +/- 3, and 26 +/- 3 mmHg) than in the upright (2 +/- 3, 9 +/- 3, and 17 +/- 3 mmHg) position. During dynamic exercise, the increases in MAP evoked by 25, 50, and 75 mmHg LBPP were greater in the supine (13 +/- 2, 28 +/- 3, and 40 +/- 3 mmHg) than in the upright (7 +/- 3, 12 +/- 3, and 25 +/- 3 mmHg) position. We conclude that the systemic pressure response to LBPP is clearly dependent on the body position, with the larger pressure responses being associated with the supine position both at rest and during dynamic leg exercise.

Moderate-intensity aerobic training improves glucose tolerance in aging independent of abdominal adiposity.

OBJECTIVE: To test the hypothesis that training-related improvements in glucose and insulin responses to an oral glucose tolerance test (OGTT) are independent of changes in abdominal adiposity. DESIGN: Adiposity and responses to an OGTT were measured before and after a 4-month randomized, controlled aerobic training program. SETTING: An academic medical institution. PARTICIPANTS: Sixteen healthy older (73+/-1 year) men and women. INTERVENTION: Both the training (T) (n=9) and control (C) (n=7) groups exercised 4 times a week for 60-minute sessions. T exercised on mini-trampolines at 55 to 65% of HRmax (determined from a graded treadmill test) for 1 month and then at 75% for 3 months; C engaged in supervised stretching and yoga. MEASUREMENTS: At baseline and follow-up, we estimated abdominal fat (from computed tomography and anthropometry), plasma glucose, and serum insulin responses to the OGTT and fasting concentrations of free fatty acids (FFA). RESULTS: Aerobic training resulted in a 16% increase in VO2 peak and a 24% decrease in FFA in the T group (P < .05), but training had no effect on abdominal fat. In the T group, the glucose response curve shifted to the left, and the incremental area under the glucose curve decreased by 25% (P < .05). This improvement in glucose response occurred, however, only in those with impaired glucose tolerance at baseline and without any observed change in insulin response. No change in any variables occurred in the C group. CONCLUSIONS: Our data suggest that moderate-intensity aerobic training has a favorable effect on glucose tolerance in older people, independent of changes in abdominal adiposity.

Regulation of blood volume during training in post-menopausal women.

UNLABELLED: In younger people the increase in aerobic capacity following training is related, in part, to blood volume (BV) expansion and the consequent improvements in maximal cardiac output. This training-induced hypervolemia is associated with a decrease in cardiopulmonary baroreflex (CPBR) control of peripheral vascular tone. PURPOSE: To test the hypothesis that improvement in peak oxygen consumption (VO2peak) during training in older women is associated with specific central adaptations, such as BV expansion and a reduction in CPBR control of vascular tone. METHODS: Seventeen healthy older women were randomized into training (N = 9, 71 +/- 2 yr) and control (N = 8, 73 +/- 3 yr) groups. The training group exercised three to four times per wk for 30 min at 60% peak heart rate for 12 wk and then 40-50 min at 75% peak heart rate for 12 wk. The control group participated in yoga exercises over the same time period. We measured resting BV (Evans blue dye), VO2peak, and the forearm vascular resistance response to unloading low pressure mechanoreceptors during low levels of lower body negative pressure (through -20 mm Hg) before and after aerobic training. The slope of the increase in forearm vascular resistance (response) per unit decrease in central venous pressure (stimulus) was used to assess CPBR responsiveness. RESULTS: Aerobic training increased VO2peak 14.2% from 24.2 mL x kg(-1) x min(-1) to 27.7 mL x kg(-1) x min(-1) (P < 0.05), a smaller improvement than typically seen in younger subjects. Blood volume (59.9 +/- 1.9 and 60.9 +/- 1.9 mL x kg[-1]) and CPBR function (-3.98 +/- 0.92 and -3.46 +/- 0.94 units x mm(-1) Hg) were similar before and after training. CONCLUSIONS: These data indicate that the inability to induce adaptations in CPBR function may limit BV expansion during training in older women. In addition, the absence of these specific adaptations may contribute to the relatively poor improvements in VO2peak in older women during short (10-12 wk) periods of training.

Albumin synthesis after intense intermittent exercise in human subjects.

We measured hepatic albumin synthesis in five volunteers (4 men and 1 woman) at 3 and 6 h after recovery from intense exercise. A primed-constant infusion of a stable isotopic tracer of phenylalanine was used to determine hepatic fractional synthetic rate (FSR) and absolute synthetic rate (ASR) of albumin from the enrichment of phenylalanine in albumin. The infusion of the stable isotope tracer began 2 h after upright exercise or upright rest. Albumin FSR and ASR were 6.39 +/- 0.48%/day and 120 +/- 9 mg.kg body wt-1.day-1, respectively, 3-6 h after recovery from exercise; the FSR and ASR on the time control study day were 5.94 +/- 0.47%/day and 104 +/- 9 mg.kg body wt-1.day-1, respectively. The 6 and 16% increases (P < 0.05) in FSR and ASR after exercise were associated with an elevated plasma albumin content at 5 and 6 h of recovery (P < 0.05), an increased total protein content throughout recovery (P < 0.05), and a negative free water clearance (P < 0.05) at 2, 3, and 6.5 h of recovery compared with baseline values; these variables were unchanged from their baselines on the time control study day. Increased albumin content and reduced free water clearance contribute to a retention of fluid within the circulation after intense exercise. The measured increase in albumin synthesis could not account for the entire increase in albumin content at 6 h of recovery from exercise. However, we estimate that if the increased activity was maintained for the next 18 h, it could account for the expected increase in albumin content at 24 h of recovery.

Estrogen influences osmotic secretion of AVP and body water balance in postmenopausal women.

To determine if estrogen upregulates osmotic secretion of arginine vasopressin (AVP) and alters body water balance, we infused hypertonic (3% NaCl) saline in 6 women (68 +/- 3 yr) after 14 days of 17 beta-estradiol (transdermal patch, approximately 0.1 mg/day, E2) and placebo (control) administration. Hypertonic saline was infused at 0.1 ml.kg-1.min-1 for 120 min, and after a 30-min equilibration period, the subjects drank water ad libitum for 180 min. E2 increased basal plasma estradiol concentration from < or = 12 to 80 +/- 12 pg/ml and plasma AVP concentration (P[AVP]) from 2.1 +/- 0.7 to 3.1 +/- 0.8 pg/ml (P < 0.05), but not plasma osmolality (Posm, 288 +/- 1 and 287 +/- 1, for control and E2, respectively). Hypertonic saline infusion increased Posm by 18 +/- 1 and 17 +/- 1 mosmol/kgH2O and P[AVP] by 5.2 +/- 0.5 and 4.9 +/- 0.4 pg/ml for control and E2 treatments, respectively. The P[AVP]-Posm relationship shifted upward after E2, with no change in sensitivity (slope, 0.36 +/- 0.02 and 0.33 +/- 0.03 pg.ml-1.mosmol-1 for control and E2, respectively). Water intake was similar between control and E2 (24 vs. 22 ml/kg), but by 180 min of drinking, urine output and free water clearance (CH2O) were reduced by 5.6 +/- 2.3 ml/kg and 2.6 +/- 2.0 ml/min, respectively (P < 0.05) after E2. Plasma aldosterone concentration was unaffected by E2, but fractional sodium excretion was reduced from 2.7 +/- 0.5 to 1.7 +/- 0.4% (P < 0.05) at 180 min of drinking. Our data suggest that E2 augments osmotic AVP secretion, thereby implicating elevated AVP as a contributor to water retention in high E2 states; however, an increase in renal sodium reabsorption was a major component of the enhanced fluid retention.

Transcapillary escape rate of albumin in humans during exercise-induced hypervolemia.

To test the hypotheses that plasma volume (PV) expansion 24 h after intense exercise is associated with reduced transcapillary escape rate of albumin (TERalb) and that local changes in transcapillary forces in the previously active tissues favor retention of protein in the vascular space, we measured PV, TERalb, plasma colloid osmotic pressure (COPp), interstitial fluid hydrostatic pressure (Pi), and colloid osmotic pressure in leg muscle and skin and capillary filtration coefficient (CFC) in the arm and leg in seven men and women before and 24 h after intense upright cycle ergometer exercise. Exercise expanded PV by 6.4% at 24 h (43.9 +/- 0.8 to 46.8 +/- 1.2 ml/kg, P < 0.05) and decreased total protein concentration (6.5 +/- 0.1 to 6.3 +/- 0.1 g/dl, P < 0.05) and COPp (26.1 +/- 0.8 to 24.3 +/- 0.9 mmHg, P < 0.05), although plasma albumin concentration was unchanged. TERalb tended to decline (8.4 +/- 0.5 to 6.5 +/- 0.7%/h, P = 0.11) and was correlated with the increase in PV (r = -0.69, P < 0.05). CFC increased in the leg (3.2 +/- 0.2 to 4.3 +/- 0.5 microl . 100 g-1 . min-1 . mmHg-1, P < 0. 05), and Pi showed a trend to increase in the leg muscle (2.8 +/- 0. 7 to 3.8 +/- 0.3 mmHg, P = 0.08). These data demonstrate that TERalb is associated with PV regulation and that local transcapillary forces in the leg muscle may favor retention of albumin in the vascular space after exercise.

Venous and arterial reflex responses to positive-pressure breathing and lower body negative pressure.

We examined the relative importance of arteriolar and venous reflex responses during reductions in cardiac output provoked by conditions that increase [positive end-expiratory pressure (PEEP)] or decrease [lower body negative pressure (LBNP)] peripheral venous filling. Five healthy subjects were exposed to PEEP (10, 15, 20, and 25 cmH2O) and LBNP (-10, -15, -20, and -25 mmHg) to induce progressive but comparable reductions in right atrial transmural pressure (control to minimum): from 5.9 +/- 0.4 to 1.8 +/- 0.7 and from 6.5 +/- 0.6 to 2.0 +/- 0.2 mmHg with PEEP and LBNP, respectively. Cardiac output (impedance cardiography) fell less during PEEP than during LBNP (from 3.64 +/- 0.21 to 2.81 +/- 0.21 and from 3.39 +/- 0.21 to 2.14 +/- 0.24 l.min-1.m-2 with PEEP and LBNP, respectively), and mean arterial pressure increased. We observed sustained increases in forearm vascular resistance (i.e., forearm blood flow by venous occlusion plethysmography) and systemic vascular resistance that were greater during LBNP: from 19.7 +/- 2.91 to 27.97 +/- 5.46 and from 20.56 +/- 2.48 to 50.25 +/- 5.86 mmHg.ml-1.100 ml tissue-1.min (P < 0.05) during PEEP and LBNP, respectively. Venomotor responses (venous pressure in the hemodynamically isolated limb) were always transient, significant only with the greatest reduction in right atrial transmural pressure, and were similar for LBNP and PEEP. Thus arteriolar rather than venous responses are predominant in blood volume mobilization from skin and muscle, and venoconstriction is not intensified with venous engorgement during PEEP.

Mechanism of attenuated thirst in aging: role of central volume receptors.

To test the hypothesis that the inhibitory action of central blood volume expansion on thirst and renal fluid regulation is attenuated with aging, we monitored the drinking and renal responses of dehydrated older (70 +/- 2 yr, n = 6) and younger (24 +/- 1 yr, n = 6) subjects during 195 min of head-out water immersion (HOI), which shifts blood centrally and increases plasma volume (PV). Subjects dehydrated by exercising for 2 h at 36 degrees C in the evening and refraining from fluids overnight before HOI in 34 degrees C water or a seated control in water perfusion suit [time control (TC)] the next morning. Ad libitum water intake was allowed after 15 min of HOI. Dehydration decreased PV by 10.6 +/- 1 and 7.3 +/- 1.8% (P < 0.05) and increased plasma osmolality by 6 +/- 2 and 7 +/- 1 mosmol/kg H2O (P < 0.05) in older and younger subjects, respectively. Thirst ratings increased in both groups, but pre-HOI thirst perception on a line rating scale was lower in older (69 +/- 8 mm) than younger (94 +/- 6 mm, P < 0.05) subjects. Fifteen minutes of HOI restored PV by 7.8 +/- 1.0 and 5.7 +/- 1.0% in older and younger subjects, respectively, but suppressed thirst rating in younger subjects only (P < 0.05). Fluid intake was reduced in HOI compared with TC in younger (6.3 +/- 0.5 vs. 14.3 +/- 2.2 ml/kg, P < 0.05) but not in older (6.7 +/- 2.1 vs. 8.4 +/- 3.3 ml/kg) subjects. During HOI, older subjects had smaller suppression of plasma renin activity and aldosterone concentration but a greater increase in the plasma atrial natriuretic peptide concentration (P[ANP], P < 0.05). HOI increased fractional sodium excretion in both groups, but mean arterial pressure increased only in the older subjects (P < 0.05). We conclude that the inhibitory influence of central volume expansion on thirst and drinking behavior is diminished with aging. Furthermore, in contrast to younger people, HOI natriuresis is associated with exaggerated increases in P[ANP] and arterial blood pressure in older people, suggesting arterial baroreceptors may be involved in the fluid regulatory response to central blood volume expansion in older people.

Thirst and fluid regulatory responses to hypertonicity in older adults.

To assess the fluid regulatory responses in aging adults, we measured thirst perception and osmoregulation during and after infusion of hypertonic NaCl) saline in older (72 +/- 2 yr, n = 6) and younger (26 +/- n = 6) subjects. Hypertonic saline was infused at 0.1 min-1.kg-1 for 120 min. On a separate day, the same subjects were infused identically with isotonic saline as a control. After infusion and a 30-min equilibration period, the drank water ad libitum for 180 min. Hypertonic infusion led to graded increases in plasma osmolality (Posm; 18 +/- 2 and 20 +/- 2 mosmol/kgH2O) and percent changes plasma volume (16.2 +/- 1.9 and 18.0 +/- 1.2%) that were in older and younger subjects. Osmotically stimulated increases in thirst (94.8 +/- 18.9 and 88.3 +/- 25.6 mm), assessed on a line rating scale, and plasma arginine vasopressin concentration (6.08 +/- 1.50 and 4.51 +/- 1.37 pg/ml, for older younger, respectively) were also unaffected by age. subsequent hypervolemia, both groups of subjects sufficient water to restore preinfusion levels of Posm. Renal handling of free water and sodium was also unaffected by age during recovery from hypertonic saline infusion, but was significantly lower in older subjects during recovery from saline infusion, resulting in net fluid retention and a significant fall in Posm (6 mosmol/kgH2O). In contrast to earlier reports of a blunted thirst response to dehydration hypertonicity, we found that osmotically stimulated thirst and renal osmoregulation were intact in older adults after hypertonic saline infusion.

Body temperature modification of osmotically induced vasopressin secretion and thirst in humans.

We examined the effect of increased body core temperature (Tes) on the plasma arginine vasopressin concentration ([AVP]p) and thirst responses to increased plasma osmolality (Posm) induced by 3% NaCl infusion for 120 min in seven healthy humans. Tes was increased by immersion of the lower legs in 41 degrees C water in a 28 degrees C room (passive heating; HT). Immersion of the lower legs in 34.5 degrees C water on a separate day served as the control (thermoneutral; NT). The 120-min hypertonic saline infusion was initiated 30 min after the onset of leg immersion and was followed by a 30-min rehydration period. Tes in HT increased by 0.21 +/- 0.04 degree C before infusion and by 0.86 +/- 0.08 degree C at the end of infusion. The change in Tes in NT before and after the infusion was negligible. Posm was increased by 15.0 +/- 1.0 mosmol/kgH2O by infusion in both NT and HT. [AVP]p increased by 3.48 +/- 0.72 pg/ml in NT and by 7.59 +/- 1.02 pg/ml in HT. Thus the increase in [AVP]p at a given increase in Posm was markedly higher in HT than in NT. The plasma renin activity response to hypertonic saline infusion in both conditions was similar. Subjective thirst rating and cumulative water intake during rehydration were higher in HT than in NT.(ABSTRACT TRUNCATED AT 250 WORDS)

Osmoregulatory modulation of thermal sweating in humans: reflex effects of drinking.

To gain better insight into the interaction between thermoregulation and osmoregulation, we examined the thermal sweating response to drinking in cell-dehydrated humans. Cell dehydration (CDH) was induced by infusion of a 3% NaCl solution, at 1.2 ml/kg, for 2 h; infusion of a 0.9% NaCl solution in a separate experiment served as a control (euhydrated condition, EH). After infusion, subjects were heated by immersion of the lower legs in 42 degrees C water at an ambient temperature of 28 degrees C for 90 min. Subjects drank 4.3 ml/kg of H2O (approximately 38 degrees C) at 60 min of heating. The 3% NaCl infusion increased plasma osmolality by 13.6 +/- 0.8 mosmol/kgH2O and plasma arginine vasopressin concentration ([AVP]) by 3.3 +/- 0.7 pg/ml. Neither variable was altered with 0.9% NaCl infusion. Before drinking, esophageal temperature (Tes) had increased by 0.91 +/- 0.08 degrees C in CDH and by 0.40 +/- 0.11 degrees C in EH. Local chest sweating rate (SRch) had increased by 0.67 +/- 0.08 and 0.63 +/- 0.07 mg.min-1.cm-2 in CDH and EH, respectively. Thus the change in SRch per unit rise in Tes was much lower in CDH than in EH. Drinking immediately increased SRch and reduced Tes in CDH, with a reduction in plasma [AVP] and thirst rating. Drinking did not change thermoregulatory and osmoregulatory responses in EH. These results suggest that the act of drinking itself eliminates, at least partially, an osmotic inhibitory input to the thermoregulatory center, as well as osmotic AVP secretion and thirst.

Cardiovascular and renal function during exercise-induced blood volume expansion in men.

To test the hypothesis that reduced baroreflex sensitivity is a direct result of exercise, we measured forearm vascular conductance (FVC) responses to graded lower body negative pressure (LBNP) 2, 20, and 44 h after intense exercise. Eight 4-min bouts of exercise at 85% of maximum oxygen uptake produced 3.5 +/- 0.7 and 3.9 +/- 1.0% blood volume (BV) expansions at 20 and 44 h of recovery, respectively. BV was unchanged from control values 2 h after exercise. The reduction in FVC was significantly less than control values during 30 and 40 mmHg of LBNP at 2 and 20 h of recovery, respectively, whereas heart rate and cardiac stroke volume responses were unchanged. Thus, a reduced FVC response to LBNP preceded BV expansion, demonstrating that exercise itself can elicit an attenuation of baroreflex function. To test the hypothesis that volume sensitivity of renal function is attenuated by intense exercise, we measured cardiovascular variables, plasma hormone concentrations, and renal output. At 20 h of recovery, resting mean arterial blood pressure and cardiac output were increased by 6 +/- 1 mmHg and 0.6 +/- 0.2 l/min, respectively, but resting plasma aldosterone and overnight Na+ excretion rate were unchanged. At 44 h of recovery, plasma aldosterone was decreased by 26 +/- 9% and overnight Na+ excretion rate was increased by 51 +/- 26%. Thus, appropriate endocrine and renal responses to increased BV were delayed until 44 h of recovery. Our findings suggest that a postexercise attenuation of baroreflex function participates in the induction of BV expansion by intense exercise.