We studied the effects of graded hypohydration levels on thermoregulatory and blood responses during exercise in the heat. Eight heat-acclimated male subjects attempted four heat-stress tests (HSTs). One HST was attempted during euhydration, and three HSTs were attempted while the subjects were hypohydrated by 3, 5, and 7% of their body weight. Hypohydration was achieved by an exercise-heat regimen on the day prior to each HST. After 30 min of rest in a 20 degrees C antechamber the HST consisted of a 140-min exposure (4 repeats of 10 min rest and 25 min treadmill walking) in a hot-dry (49 degrees C, 20% relative humidity) environment. The following observations were made: 1) a low-to-moderate hypohydration level primarily reduced plasma volume with little effect on plasma osmolality, whereas a more severe hypohydration level resulted in no further plasma volume reduction but a large increment in plasma osmolality; 2) core temperature and heart rate responses increased with severity of hypohydration; 3) sweating rate responses for a given rectal temperature were systematically decreased with severity of hypohydration; and 4) the reduction in sweating rate was more strongly associated with plasma hyperosmolality than hypovolemia. In conclusion, an individual's thermal strain increases linearly with the severity of hypohydration during exercise in the heat, and plasma hyperosmolality influences the reduction in sweating more profoundly than hypovolemia.

Glycerol ingestion has been shown to mediate hyperhydration; however, the mechanism(s) responsible for this improved fluid retention is not well understood. This study examined the hormonal, renal, and vascular fluid responses to glycerol hyperhydration in 11 resting male volunteers who ingested one of two experimental solutions and then a water bolus. The volume of fluid ingested was determined from the subjects' measured total body water (TBW; total volume = 37 ml/l TBW, 1,765 +/- 162 ml). Experimental solutions (5.0 ml/l TBW) were matched for color and taste and differed only in that one contained 1.5 g glycerol/l TBW (total osmolar load = 777 +/- 24 mosmol). Nine of the 11 subjects also completed a control trial during which no fluid was ingested. Glycerol ingestion (GI) resulted in greater fluid retention than the ingestion of water alone (WI; 60 vs. 32% 3-h posthyperhydration, P < 0.01). This improved fluid retention with GI resulted from lower urine flow rates (peak 6.2 vs. 10.5 ml/min, P < 0.01) associated with lower free water clearance rates (peak = 1.2 vs. 8.2 ml/min, P < 0.01). Hyperhydration had no effect on plasma atrial natriuretic peptide concentrations. Changes in plasma aldosterone were unrelated to differences in fluid retention. Antidiuretic hormone concentrations (ADH) were significantly reduced from prehyperhydration levels during both hyperhydration trials but tended (P = 0.07) to rise during GI compared with WI at the very time urine flow and free water clearance differences were also evident. This suggests that ADH may, in part, be responsible for glycerol's effectiveness, although differences in ADH concentrations were small and near the assay's sensitivity limits. Alternatively, glycerol's effectiveness may result from its directly increasing the kidneys' medullary concentration gradient and, hence, water reabsorption.

Bioelectrical impedance analysis (BIA) has been suggested as a simple, rapid method to assess changes in hydration status. BIA measures the electrical impedance to a low amperage current that is affected by both water and electrolyte content of the body. While BIA can reliably estimate total body water and body density in euhydrated individuals under standardized clinical conditions, changes in fluid and electrolyte content can independently alter bioimpedance measurements. Because hydration changes typically involve concomitant changes in fluid and electrolyte content, the interpretation of a change in bioimpedance will often be confounded. This paper examines the assumptions underlying estimations of total body water from BIA and addresses the factors known to influence bioimpedance independently from actual change in total body water. The results indicate that current BIA methodology may not provide valid estimates of total body water when hydration state is altered.

We studied sea-level residents during 13 days of altitude acclimatization to determine 1) altitude acclimatization effects on erythrocyte volume and plasma volume, 2) if exogenous erythrocyte volume expansion alters subsequent erythrocyte volume and plasma volume adaptations, 3) if an increased blood oxygen content alters erythropoietin responses during altitude acclimatization, and 4) mechanisms responsible for plasma loss at altitude. Sixteen healthy men had a series of hematologic measurements made at sea level, on the first and ninth days of altitude (4,300 m) residence, and after returning to sea level. Twenty-four hours before the ascent to altitude, one group received a 700-ml infusion of autologous erythrocytes (42% hematocrit), whereas the other group received only a saline infusion. Erythrocyte infusion increased erythrocyte volume by approximately 10%, whereas saline infusion had no effect; in addition, initially at altitude, blood oxygen content was 8% higher in erythrocyte-infused than in saline-infused subjects. The new findings regarding altitude acclimatization are summarized as follows: 1) erythrocyte volume does not change during the first 13 days and is not affected by prior exogenous expansion, 2) a modest increase in blood oxygen content does not modify erythropoietin responses, 3) plasma losses are related to vascular protein losses, and 4) exogenous erythrocyte volume expansion coincides with transient increases in plasma loss, vascular protein loss, and mean arterial pressure elevation. These findings better define human blood volume responses during altitude acclimatization.

The effects of graded levels of hypohydration (3, 5, and 7% of body weight) on hormonal responses to exercise in the heat were examined in six heat-acclimated male volunteers. On the day following dehydration, subjects performed light (approximately 25% maximal O2 consumption, 1.03 1 X min-1) exercise in a hot (49 degrees C, 20% relative humidity) environment for four consecutive 25-min intervals interspaced by 10-min rests; blood was obtained before exercise and at approximately 10 min before completion of each exercise period. During euhydration, plasma cortisol (PC) levels manifested significant decrements over time (e.g., time 0, 14.2 micrograms X 100 ml-1 vs. time 2, 8.9 micrograms X 100 ml-1), probably related to its diurnal periodicity. However, during hypohydration, levels of PC were increased and correlated with hypohydration intensity (e.g., time 0, 0, 3, 5, and 7% hypohydration, 14.2, 16.5, 19.8, and 36.2 micrograms X 100 ml-1, respectively). Plasma renin activity (PRA) was increased significantly by hypohydration (e.g., time 0, euhydrated vs. 3%, 3.7 vs. 6.2 units) but was unaffected by exercise in the heat. Plasma aldosterone (ALD) levels were generally increased by exercise in the heat (e.g., time 0 vs. time 4, 3% hypohydration, 12.1 vs. 18.7 ng X 100 ml-1). Regression analysis illustrated that graded intensities of hypohydration were correlated with incremented PRA and ALD through 5% hypohydration. Conversely, PC was incrementally elevated through 7% hypohydration.(ABSTRACT TRUNCATED AT 250 WORDS)