We examined osmotic control of thirst and free water clearance in healthy older (65+, n = 10) and younger (Y, n = 6) subjects during a 3-h rehydration period after an approximately 2.4% decrease in body weight. Plasma volume (PV), plasma osmolality (Posm), renal function, and thirst were measured before and after dehydration and during rehydration. In 65+, baseline PV was lower (43.1 +/- 1.6 vs. 48.1 +/- 2.5 ml/kg), Posm was higher (287 +/- 1 vs. 281 +/- 2 mosmol/kgH2O), and perceived thirst was lower than in Y. During dehydration, the osmotic threshold for increased thirst was shifted to a higher Posm in 65+. Total fluid intake was greater in Y than in 65+ (16.6 +/- 4.1 vs. 8.9 +/- 2.0 ml/kg); however, the relation between thirst and the rate of fluid intake was identical. Thus the blunted rehydration in 65+ is related to a lower overall sensation of thirst. The stimulus-response characteristics of osmotic control of free water clearance was similar in 65+ and Y; however, 65+ operated around a higher Posm and on a less-steep portion of the stimulus-response curve. These data support the hypothesis that the hyperosmotic hypovolemic state of healthy older individuals is not a result of a simple water deficit but represents a shift in the operating point for control of body fluid volume and composition.

This study was designed to determine the extent to which changes in the evaporative power of the environment (Emax) affect sweating and evaporative rates. Six male subjects undertook four 60-min bouts of cycle ergometer exercise at 56% maximal O2 uptake (VO2max).Emax was varied by differences in ambient temperature and airflow; two exercise bouts took place at 24 degrees C and two at 35 degrees C, with air velocity at < 0.2 and 3.0 m/s in both. Total sweat production was estimated from body weight loss, whereas whole body evaporative rate was measured continuously from a Potter beam balance. Body core temperature was measured continuously from a thermocouple in the esophagus (T(es)), with mean skin temperature (Tsk) computed each minute from thermocouples at eight sites. Total body sweat loss was significantly greater (P < 0.05) in the 0.2- than in the 3.0-m/s condition at both 24 and 35 degrees C. Tsk was higher (P < 0.05) in the still-air conditions at both temperatures, but final T(es) was significantly higher (P < 0.05) in still air only in the 35 degrees C environment. Thus the reduced Emax in still air caused a greater heat storage, thereby stimulating a greater total sweat loss. However, in part because of reduced skin wettedness, the slope of the sweat rate-to-T(es) relation at 35 degrees C in the 3.0-m/s condition was 118% that at 0.2 m/s (P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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