A proposed method for assessing plasma hypertonicity in vivo.

Indices of plasma hypertonicity, elevated plasma concentrations of solutes that draw fluid out of cells by osmosis, are needed to pursue hypertonicity as a possible risk factor for obesity and chronic disease. This paper proposes a new index that may be more sensitive to mild hypertonicity in vivo at a point in time than traditional measures. The index compares mean corpuscular volume (MCV) estimates from diluted (in solution by automated cell counter) and nondiluted blood (calculated from manual hematocrit, MCV=Hct/RBC*10(6)). A larger Auto vs Manual MCV (>2 fl) in vitro indicates hypertonicity in vivo if the cell counter diluent is isotonic with the threshold for plasma vasopressin (PVP) release and PVP is detectable in plasma (>0.5 pg/ml). To evaluate this principle of concept, hypertonicity was induced by 24-h fluid restriction after a 20 ml/kg water load in four healthy men (20-46 years). Unlike serum and urine indices, the MCV difference-&-PVP index detected hypertonicity in all participants.

Exercise training and 3-day head down bed rest deconditioning: exercise thermoregulation.

UNLABELLED: Bed rest (BR) deconditioning causes excessive increase of exercise core body tempera-ture, while aerobic training improves exercise thermoregulation. The study was designed to determine whether 3 days of 6 degrees head-down bed rest (HDBR) affects body temperature and sweating dynamics during exercise and, if so, whether endurance training before HDBR modifies these responses. Twelve healthy men (20.7+/-0.9 yrs, VO2max: 46+/-4 ml x kg(-1) x min(-1) ) underwent HDBR twice: before and after 6 weeks of endurance training. Before and after HDBR, the subjects performed 45 min sitting cycle exercise at the same workload equal to 60% of VO2max determined before training. During exercise the VO2, HR, tympanic (Ttymp) and skin (Tsk) temperatures were recorded; sweating dynamics was assayed from a ventilated capsule on chest. Training increased VO2max by 12.1% (p<0.001). Resting Ttymp increased only after first HDBR (by 0.22 +/- 0.08 degrees C, p<0.05), while exercise equilibrium levels of Ttymp were increased (p<0.05) by 0.21 +/- 0.07 and 0.26 +/- 0.08 degrees C after first and second HDBR, respectively. Exercise mean Tsk tended to be lower after both HDBR periods. Total sweat loss and time-course of sweating responses were similar in all exercise tests. The sweating threshold related to Ttymp was elevated (p<0.05) only after first HDBR. IN CONCLUSION: six-week training regimen prevents HDBR-induced elevation of core temperature (Ttymp) at rest but not during ex-ercise. The post-HDBR increases of Ttymp without changes in sweating rate and the tendency for lower Tsk suggest an early (<3d) influence of BR on skin blood flow.

Intensive exercise training suppresses testosterone during bed rest.

Spaceflight and prolonged bed rest (BR) alter plasma hormone levels inconsistently. This may be due, in part, to prescription of heavy exercise as a countermeasure for ameliorating the adverse effects of disuse. The initial project was to assess exercise programs to maintain aerobic performance and leg strength during BR. The present study evaluates the effect of BR and the performance of the prescribed exercise countermeasures on plasma steroid levels. In a 30-day BR study of male subjects, the efficacy of isotonic (ITE, n = 7) or isokinetic exercise (IKE, n = 7) training was evaluated in contrast to no exercise (n = 5). These exercise countermeasures protected aerobic performance and leg strength successfully. BR alone (no-exercise group) did not change steroidogenesis, as assessed by the plasma concentrations of cortisol, progesterone, aldosterone, and free (FT) and total testosterone (TT). In the exercise groups, both FT and TT were decreased (P < 0.05): FT during IKE from 24 +/- 1.7 to 18 +/- 2.0 pg/ml and during ITE from 21 +/- 1.5 to 18 +/- 1 pg/ml, and TT during IKE from 748 +/- 68 to 534 +/- 46 ng/dl and during ITE from 565 +/- 36 to 496 +/- 38 ng/dl. The effect of intensive exercise countermeasures on plasma testosterone was not associated with indexes of overtraining. The reduction in plasma testosterone associated with both the IKE and ITE countermeasures during BR supports our hypothesis that intensive exercise countermeasures may, in part, contribute to changes in plasma steroid concentrations during spaceflight.

Catecholamine responses to environmental stressors in trained and untrained men after 3-day bed rest.

INTRODUCTION: The effect of decreased physical activity with reduced gravitational stress on activity, sensitivity, and reactivity of the sympathetic nervous system (SNS) is not fully recognized. We hypothesized that the effect is most pronounced in physically active subjects. Thus, basal plasma norepinephrine [NE] and epinephrine [E], and catecholamine responses to physiological stimuli were determined after 3 d of horizontal bed rest (BR) in subjects differing in level and kind of habitual activity. METHODS: Before and after BR, 11 untrained students, 8 endurance athletes, and 10 power/strength athletes were submitted to oral glucose tolerance test (OGTT) and orthostatic stand test (OST). Another 32 men (12 untrained, 10 endurance athletes, and 10 power/strength athletes) underwent cold pressor test (CPT) and graded exercise test (GET) performed until volitional exhaustion. RESULTS: After BR, basal [NE] was decreased only in athletes (p < 0.01). Increases in both catecholamines during OGTT were diminished (p < 0.05), particularly in endurance athletes. Plasma [NE] response to standing was not affected by BR in individual groups, but it was diminished in the whole group (p < 0.05). Bed rest did not affect the increases in catecholamines induced by CPT and GET. Heart rate response to OST, and BP responses to OST, CPT, and glucose ingestion were enhanced. CONCLUSIONS: Basal sympathetic activity is diminished after 3 d of BR in physically active men. Although catecholamine responses to glucose load and standing were reduced, the general reactivity and sensitivity of SNS were not attenuated since catecholamine responses to the most (exercise) and least (CPT) powerful stimuli were unchanged.

Plasma sodium-osmotic dissociation and hormonal interaction with drinking-induced hypervolemia at 2800 m altitude.

PURPOSE: To study hormonal factors that may account for the dissociation between beverage-induced plasma sodium p[Na+] and osmotic p[Osm] concentrations that appear to refute the high theoretical correlation between p[Na+] and p[Osm]. METHODS: Ten men (24 +/- SD 3 yr of age) sat reclining (head up) for 12 h in a chamber (21-23 degrees C dry bulb, 25-33% relative humidity) at 2800 m (9184 ft, 539 mm Hg) altitude (ALT), and at 321 m (1053 ft, 732 mm Hg) on the ground (GND). During 1000-1030 hours they consumed 3 fluids (12 ml x kg(-1),X = 948 ml x d(-1)) with large differences in sodium and osmotic contents: AstroAde (AA) with 185 mEq x L(-1) Na+ and 283 mOsm x kg(-1), Performance 1 (Shaklee) (P1) with 22 mEq x L(-1) Na+ and 365 mOsm kg(-1), or H2O at ALT; and only H2O on the GND. RESULTS: After drinking: plasma volume (PV) increased at 1200 hours by 8.3% (p < 0.05) with AA but was not significantly (NS) changed in the other sessions (Xdelta = +0.9%, range -0.9 to 2.8%); p[Na+] and p[Osm] were unchanged. Urinary rates and free-water clearances were attenuated with AA and P1 vs. those with H2O. Correlations between and among p[Na+] and p[Osm] suggest that the pNa+ ion is more tightly controlled than pOsm; and that there was no clear hormonal response that could account for this dissociation from theoretical considerations. CONCLUSIONS: There is significant dissociation between plasma sodium and osmotic concentrations after fluid intake. Induction and maintenance of hypervolemia requires increased (near isotonic) drink Na+ osmols rather than increased non-ionic osmols.

Effects of 3-day bed rest on physiological responses to graded exercise in athletes and sedentary men.

To test the hypotheses that short-term bed-rest (BR) deconditioning influences metabolic, cardiorespiratory, and neurohormonal responses to exercise and that these effects depend on the subjects' training status, 12 sedentary men and 10 endurance- and 10 strength-trained athletes were submitted to 3-day BR. Before and after BR they performed incremental exercise test until volitional exhaustion. Respiratory gas exchange and heart rate (HR) were recorded continuously, and stroke volume (SV) was measured at submaximal loads. Blood was taken for lactate concentration ([LA]), epinephrine concentration ([Epi]), norepinephrine concentration ([NE]), plasma renin activity (PRA), human growth hormone concentration ([hGH]), testosterone, and cortisol determination. Reduction of peak oxygen uptake (VO(2 peak)) after BR was greater in the endurance athletes than in the remaining groups (17 vs. 10%). Decrements in VO(2 peak) correlated positively with the initial values (r = 0.73, P < 0.001). Resting and exercise respiratory exchange ratios were increased in athletes. Cardiac output was unchanged by BR in all groups, but exercise HR was increased and SV diminished in the sedentary subjects. The submaximal [LA] and [LA] thresholds were decreased in the endurance athletes from 71 to 60% VO(2 peak) (P < 0.001); they also had an earlier increase in [NE], an attenuated increase in [hGH], and accentuated PRA and cortisol elevations during exercise. These effects were insignificant in the remaining subjects. In conclusion, reduction of exercise performance and modifications in neurohormonal response to exercise after BR depend on the previous level and mode of physical training, being the most pronounced in the endurance athletes.

Low LBNP tolerance in men is associated with attenuated activation of the renin-angiotensin system.

Plasma vasoactive hormone concentrations [epinephrine (p(Epi)), norepinephrine (p(NE)), ANG II (p(ANG II)), vasopressin (p(VP)), endothelin-1 (p(ET-1))] and plasma renin activity (p(RA)) were measured periodically and compared during lower body negative pressure (LBNP) to test the hypothesis that responsiveness of the renin-angiotensin system, the latter being one of the most powerful vasoconstrictors in the body, is of major importance for LBNP tolerance. Healthy men on a controlled diet (2,822 cal/day, 2 mmol. kg(-1). day(-1) Na(+)) were exposed to 30 min of LBNP from -15 to -50 mmHg. LBNP was uneventful for seven men [25 +/- 2 yr, high-tolerance (HiTol) group], but eight men (26 +/- 3 yr) reached presyncope after 11 +/- 1 min [P < 0.001, low-tolerance (LoTol) group]. Mean arterial pressure (MAP) did not change measurably, but central venous pressure and left atrial diameter decreased similarly in both groups (5-6 mmHg, by approximately 30%, P < 0.05). Control (0 mmHg LBNP) hormone concentrations were similar between groups, however, p(RA) differed between them (LoTol 0.6 +/- 0.1, HiTol 1.2 +/- 0.1 ng ANG I. ml(-1). h(-1), P < 0.05). LBNP increased (P < 0. 05) p(RA) and p(ANG II), respectively, more in the HiTol group (9.9 +/- 2.2 ng ANG I. ml(-1). h(-1) and 58 +/- 12 pg/ml) than in LoTol subjects (4.3 +/- 0.9 ng ANG I. ml(-1). h(-1) and 28 +/- 6 pg/ml). In contrast, the increase in p(VP) was higher (P < 0.05) in the LoTol than in the HiTol group. The increases (P < 0.05) for p(NE) were nonsignificant between groups, and p(ET-1) remained unchanged. Thus there may be a causal relationship between attenuated activation of p(RA) and p(ANG II) and presyncope, with p(VP) being a possible cofactor. Measurement of resting p(RA) may be of predictive value for those with lower hypotensive tolerance.

Effects of three-day bed rest on metabolic, hormonal and circulatory responses to an oral glucose load in endurance or strength trained athletes and untrained subjects.

The study was designed to find out (1) whether the effect of 3-day bed rest on blood glucose (BG) and plasma insulin (IRI) responses to glucose ingestion depends on preceding physical activity and (2) whether plasma adrenaline (A), noradrenaline (NA) and cardiovascular changes following a glucose load are modified by bed rest. Eleven sedentary students (22.5+/-0.3 yrs), 8 long distance runners (18.6+/-0.3 yrs) and 10 strength trained athletes (21.2+/-2.1 yrs) were examined before and after bed rest. Plasma IRI, BG, NA, A, heart rate (HR), and blood pressure (BP) were measured during 2 hrs following glucose (75 g) ingestion. The responses of BG and IRI to glucose load were calculated as incremental areas under the curves (auc). Both in athletes and untrained subjects bed rest markedly increased IRIauc, while BGauc was elevated only in sedentary subjects (p<0.05). The greatest increases in IRIauc and IRI/BG ratios were found in the endurance athletes. The data from all subjects (n = 29) revealed that the initial plasma NA and glucose-induced increases in NA and A were lowered after bed rest (p < 0.01). These effects were most pronounced in the endurance athletes. Bed rest did not influence HR or BP in any group. It is concluded that (1) the athletes have more adequate compensation for the bed-rest-induced decrement in insulin sensitivity than sedentary men; (2) three-day bed rest diminishes basal sympathetic activity and attenuates sympathoadrenal response to oral glucose; (3) endurance athletes have greater sympathetic inhibition than strength athletes or sedentary men.

Exercise thermoregulation in men after 1 and 24-hours of 6 degrees head-down tilt.

BACKGROUND: Exercise thermoregulation is dependent on heat loss by increased skin blood flow (convective and conductive heat loss) and through enhanced sweating (evaporative heat loss). Reduction of plasma volume (PV), increased plasma osmolality, physical deconditioning, and duration of exposure to simulated and actual microgravity reduces the ability to thermoregulate during exercise. HYPOTHESIS: We hypothesized that 24 h of head down tilt (HDT24) would alter thermoregulatory responses to a submaximal exercise test and result in a higher exercise rectal temperature (Tre) when compared with exercise Tre after 1 h of head down tilt (HDT1). METHODS: Seven men (31+/-SD 6 yr, peak oxygen uptake (VpO2peak) of 44+/-6 ml x kg(-1) x min(-1)) were studied during 70 min of supine cycling at 58+/-SE 1.5% VO2peak at 22.0 degrees C Tdb and 47% rh. RESULTS: Relative to pre-tilt sitting chair rest data, HDT1 resulted in a 6.1+/-0.9% increase and HDT24 in a 4.3+/-2.3% decrease in PV (delta = 10.4% between experiments, p<0.05) while plasma osmolality remained unchanged (NS). Pre-exercise Tre was elevated after HDT24 (36.71 degrees C +/-0.06 HDT1 vs. 36.93 degrees C+/-0.11 HDT24, p<0.05). The 70 min of exercise did not alter this relationship (p<0.05) with respective end exercise increases in Tre to 38.01 degrees C and 38.26 degrees C (degrees = 1.30 degrees C (HDT1) and 1.33 degrees C (HDT24)). While there were no pre-exercise differences in mean skin temperature (Tsk), a significant (p<0.05) time x treatment interaction occurred during exercise: after min 30 in HDT24 the Tsk leveled off at 31.1 degrees C, while it continued to increase reaching 31.5 degrees C at min 70 in HDT1. A similar response (NS) occurred in skin blood velocity. Neither local sweating rates nor changes in body weight during exercise of -1.63+/-0.24 kg (HDT1) or - 1.33+/-0.09 kg (HDT24) were different (NS) between experiments. CONCLUSION: While HDT24 resulted in elevated pre-exercise Tre, reduced PV, attenuation of Tsk and skin blood velocity during exercise, the absolute increase in exercise Tre was not altered. But if sweat rate and cutaneous vascular responses were similar at different core temperatures (unchanged thermoregulation), the Tre offset could have been caused by the HDT-induced hypovolemia.

Short-arm (1.9 m) +2.2 Gz acceleration: isotonic exercise load-O2 uptake relationship.

BACKGROUND: The deconditioning syndrome from prolonged bed rest (BR) or spaceflight includes decreases in maximal oxygen uptake (VO2max), muscular strength and endurance, and orthostatic tolerance. In addition to exercise training as a countermeasure, +Gz (head-to-foot) acceleration training on 1.8-2.0 m centrifuges can ameliorate the orthostatic and acceleration intolerances induced by BR and immersion deconditioning. PURPOSE: Study A was designed to determine the magnitude and linearity of the heart rate (HR) response to human-powered centrifuge (HPC) acceleration with supine exercise vs. passive (no exercise) acceleration. Study B was designed to test the hypothesis that moderate +Gz acceleration during exercise will not affect the respective normal linear relationships between exercise load and VO2max, HR, and pulmonary ventilation (VEBTPS). Study C: To determine if these physiological responses from the HPC runs (exercise + on-platform acceleration) will be similar to those from the exercise + off-platform acceleration responses. METHODS: In Study A, four men and two women (31-62 yr) were tested supine during exercise + acceleration and only passive acceleration at 100% [maximal acceleration (rpm) = Amax] and at 25%, 50%, and 75% of Amax. In Studies B and C, seven men (33+/-SD 7 yr) exercised supine on the HPC that has two opposing on-platform exercise stations. A VO2max test and submaximal exercise runs occurred under three conditions: (EX) exercise (on-platform cycle at 42%, 61%, 89% and 100% VO2max) with no acceleration; (HPC) exercise + acceleration via the chain drive at 25%,50%, and 100% Gzmax (35%, 72% and 100% VO2max); and (EXA) exercise (on-platform cycle at 42%, 61%, 89%, and 100% VO2max) with acceleration performed via the off-platform cycle operator at +2.2+/-0.2 Gz [50% of max (rpm) G]. RESULTS: Study A: Mean (+/-SE) Amax was 43.7+/-1.3 rpm (mean = +3.9+/-0.2, range = 3.3 to 4.9 Gz). Amax run time for exercise +acceleration was 50-70 s, and 40-70 s for passive acceleration. Regression of X HR on Gz levels indicated explained variances (r2) of 0.88 (exercise) and 0.96 (passive). The mean exercise HR of 107+/-4 (25%), to 189+/-13 (100%) bpm were 43-50 bpm higher (p < 0.05) than comparable passive HR of 64+/-2 to 142+/-22 bpm, respectively. Study B: There were no significant differences in VO2, HR or VEBTPS at the submaximal or maximal levels between the EX and EXA runs. Mean (+/-SE) VO2max for EX was 2.86+/-0.12 L x min(-1)(35+/-2 ml x min(-1) x kg(-1)) and for EXA was 3.09+/-0.14 L x min(-1) (37+/-2 ml-min(-1) x kg(-1)). Study C: There were no significant differences in the essentially linear relationships between the HPC and EXA data for VO2 (p = 0.45), HR (p < 0.08), VEBTPS (p = 0.28), or the RE (p = 0.15) when the exercise load was % VO2max. CONCLUSION: Addition of + 2.2 Gz acceleration does not significantly influence levels of oxygen uptake, heart rate, or pulmonary ventilation during submaximal or maximal cycle ergometer leg exercise on a short-arm centrifuge.

Is the Gauer-Henry reflex important for immersion diuresis in men?

BACKGROUND: This study examines the relationship between the threshold for plasma vasopressin concentration [PVP] responses and diuresis (Gauer-Henry reflex), and tests the hypothesis that water intake would not influence diuresis. METHODS: Eight men (19-25 yr) underwent four treatments: euhydration in air (Eu-air), euhydration in water immersion (Eu-H2O), and with prior 3.6% hypohydration in air (Hypo-air), and hypohydration in immersion (Hypo-H2O). Ad libitum drinking was allowed during the 3-h experimental and 1-h recovery periods. RESULTS: Drinking was greatest during the first 10 min: 3.5 ml x kg(-1) with Hypo-air (450 ml x 3 h(-1)) and only 1.7 ml x kg(-1) (p < 0.05) with Hypo-H2O (235 ml x 3 h(-1)). At 1 h, concomitant [PVP] decreased from a control level of 6.6+/-1.5 to 4.0+/-1 .0 pg x ml(-1) (delta = 2.6 pg x ml(-1), p < 0.05) with Hypo-air, and from 5.9+/-0.6 to 2.3+/-0.2 pg x ml(-1) (delta = 3.6 pg x ml(-1), p < 0.05) with Hypo-H2O. Urine flow was unchanged from control level (<1.0 ml x min(-1)) with Hypo-air, Hypo-H2O, and Eu-air, but increased to 4-5 ml x min(-1) with Eu-H2O. Neither water intake volume nor urine flow was related to the magnitude of [PVP] depression. Regression of Uosm/Posm ratio on [PVP] and urine flow indicated that [PVP] above 2 pg x ml(-1) did not affect urine flow. Thus, ad libitum water intake in previously hypohydrated subjects did not affect urine flow or the decrease in [PVP]. The threshold [PVP] to initiate significant diuresis was about 2 pg x ml(-1), and significant diuresis can occur with no change in [PVP] maintained at about 1 pg x ml(-1) during immersion in euhydrated subjects. CONCLUSIONS: Thus, it appears that the Gauer-Henry reflex is not the major mechanism for immersion-induced diuresis. Clearly, other diuretic factors are also involved.

Effect of an exercise-heat acclimation program on body fluid regulatory responses to dehydration in older men.

We examined if an exercise-heat acclimation program improves body fluid regulatory function in older subjects, as has been reported in younger subjects. Nine older (Old; 70 +/- 3 yr) and six younger (Young; 25 +/- 3 yr) male subjects participated in the study. Body fluid regulatory responses to an acute thermal dehydration challenge were examined before and after the 6-day acclimation session. Acute dehydration was produced by intermittent light exercise [4 bouts of 20-min exercise at 40% peak rate of oxygen consumption (VO(2 peak)) separated by 10 min rest] in the heat (36 degrees C; 40% relative humidity) followed by 30 min of recovery without fluid intake at 25 degrees C. During the 2-h rehydration period the subjects drank a carbohydrate-electrolyte solution ad libitum. In the preacclimation test, the Old lost approximately 0.8 kg during dehydration and recovered 31 +/- 4% of that loss during rehydration, whereas the Young lost approximately 1.2 kg and recovered 56 +/- 8% (P < 0.05, Young vs. Old). During the 6-day heat acclimation period all subjects performed the same exercise-heat exposure as in the dehydration period. Exercise-heat acclimation increased plasma volume by approximately 5% (P < 0.05) in Young subjects but not in Old. The body fluid loss during dehydration in the postacclimation test was similar to that in the preacclimation in Young and Old. The fractional recovery of lost fluid volume during rehydration increased in Young (by 80 +/- 9%; P < 0.05) but not in Old (by only 34 +/- 5%; NS). The improved recovery from dehydration in Young was mainly due to increased fluid intake with a small increase in the fluid retention fraction. The greater involuntary dehydration (greater fluid deficit) in Old was accompanied by reduced plasma vasopressin and aldosterone concentrations, renin activity, and subjective thirst rating (P < 0.05, Young vs. Old). Thus older people have reduced ability to facilitate body fluid regulatory function by exercise-heat acclimation, which might be involved in attenuation of the acclimation-induced increase in body fluid volume.

Leucocytosis, thrombocytosis, and plasma osmolality during rest and exercise: an hypothesis.

The mechanism for inducing leucocytosis (increase in white blood cells) and thrombocytosis (increase in platelets) during exercise is unclear. Because plasma osmolality (Osm) may influence T-cell proliferation, Osm and the number of leucocytes (WBC) and platelets in blood were measured periodically during a 90 min rest period, and were compared with those during upright sitting ergometer exercise in six untrained, healthy men who cycled for 70 min at 71% of their maximal oxygen uptake (VO2max). There were 6 experiments in which the subjects drank different fluid formulations (10 ml x kg(-1) of various ionic and osmotic concentrations intermittently during 60 min of the rest period and during the exercise period. Osmolality, and WBC and platelet counts increased significantly (p < 0.05) within the first 10 min of exercise, but the additional 60 min of exercise did not significantly change the leucocytosis or thrombocytosis. There were low but significant correlations between individual values of total WBC and total Osm during exercise (r0.001(2),284 = 0.39) and during rest plus exercise (r0.001(2),499 = 0.43). With combined data from the six experiments, mean Osm correlated highly and significantly with both mean WBC (r0.001(2),6 = 0.95, p < 0.001) and mean platelets (r0.001(2),6 = 0.94, p < 0.01) during the exercise phase. These data indicate that increases in leucocytes, thrombocytes, and osmolality occur primarily within the first 10 min of high-intensity exercise, but neither hypovolemia nor hyperthermia during exercise contributed to the leucocytosis, thrombocytosis, or hyperosmolality. The high correlations between plasma Osm and WBC or platelet counts suggest changes in osmolality may contribute to the mechanism of leucocytosis and thrombocytosis induced by exercise.

Effect of glucose-water ingestion on exercise thermoregulation in men dehydrated after water immersion.

BACKGROUND: The influence of non-ionic osmols on thermoregulation is unclear. HYPOTHESIS: Hyperglycemia will attenuate the rise in exercise core temperature. METHODS: Dehydrated by 4-h of water immersion (34.5 degrees C) to the neck, 6 men, (35+/-SD 7 yr) participated in each of three trials where 2.0 g x kg(-1) body wt of oral glucose (33.8% weight per volume) was consumed followed by 80 min supine rest (Glu/Rest), or 70 min supine cycle exercise at 62.8%+/-SE 0.5% (1.97+/-0.02 L x min(-1)) peak O2 uptake, followed by 10 min supine recovery with prior (Glu/Ex) or without glucose (No Glu/Ex) ingestion. Blood samples were taken periodically for measurement of Hb, Hct, Na+, K+, Osm, and glucose; mean skin (Tsk) and rectal (Tre) temperatures, and sweating rate (resistance hygrometry) and skin blood velocity (laser Doppler) were measured intermittently. RESULTS: Mean percent changes in plasma volume (p<0.05) for the exercise trials were not different: -12.3+/-2.2% (No Glu/Ex) and -12.1+/-2.1% (Glu/Ex). Mean (+/-SE) pre-exercise plasma [glucose] for Glu/Ex was higher than that of No Glu/Ex (108.4+/-3.9 vs. 85.6+/-1.6 mg x dL(-1), respectively, p<0.05). Glu/Ex vs. No Glu/Ex data, respectively, at the end of exercise indicated that: Tre was lower by 0.4 degrees C (38.2+/-0.2 vs. 38.6+/-0.1 degrees C, p<0.05), Tsk was lower (32.0+/-0.3 vs. 32.4+/-0.2 degrees C, p<0.05), forearm sweating rate was lower (0.94+/-0.09 vs. 1.05+/-0.07 mg x cm(-2) x min(-1), p<0.05); and head (temporal) skin blood velocity was not different (1.67+/-0.21 vs. 1.51+/-0.24 Hz x 10(3), NS). CONCLUSIONS: Elevation of plasma [glucose] prior to supine submaximal exercise in dehydrated men attenuates the increase of Tre without alteration of heat production, total body sweating, serum electrolytes and osmolality, or exercise-induced hypoglycemia: the mechanism may be enhanced peripheral blood flow that could enhance body heat loss.

Thermoregulatory effects of caffeine ingestion during submaximal exercise in men.

BACKGROUND: The exclusive effect of caffeine ingestion on exercise thermoregulation is unclear; data indicate that caffeine may have a positive effect, a negative effect, or no effect. METHODS: Rectal (TRE) and mean skin (TSK) temperatures, skin heat conductance (HSK), and sweat rate (MSW) were measured during 30 min of rest and subsequent 70 min of submaximal cycle-ergometer exercise (67% VO2PEAK) in 11 aerobically conditioned men (mean +/- SD 29 +/- 6 yr, 49 +/- 6 mL x min(-1) x kg(-1) VO2PEAK) under two conditions: a caffeine (10 mg x kg(-1) ingestion (CI) session and a noncaffeine ingestion (NCI) control session. RESULTS: There were no significant differences in physiological or thermoregulatory parameters during exercise: X (+/-SE) end exercise levels for the NCI and CI sessions, respectively, were VO2 = 2.50 +/- 0.09 vs. 2.55 +/- 0.09 L x min(-1); heart rate = 145 +/- 7 vs. 145 +/- 5 bpm; HSK = 30 +/- 3 vs. 28 +/- 3 kcal x m(-2) x h(-1) x degrees C(-1); MSW = 393 +/- 35 vs. 378 +/- 36 g x m(-2) x h(-1); and TRE = 38.3 +/- 0.2 vs. 38.4 +/- 0.1 degrees C. Control TSK was lower than that for CI by 0.4 to 0.5 degrees C at rest and during exercise. CONCLUSION: Ingestion of a high level (10 mg x kg(-1) of caffeine has no effect on skin heat conductance, sweating, or the rate of increase and final level of rectal temperature during moderate, submaximal leg exercise.

Sodium chloride-citrate beverages attenuate hypovolemia in men resting 12 h at 2800 m altitude.

BACKGROUND: The mechanism for reduction and restoration of total body water and plasma volume (PV) during initial exposure to acute altitude (ALT) is not clear but may involve involuntary dehydration; i.e., delayed voluntary fluid intake. METHOD: Ten men (24 +/- SD 3 yr, 180.8 +/- 8.1 cm height, 78.8 +/- 12.8 kg weight, 1.99 +/- 0.19 m2 surface area, and 12.2 +/- 4.0% body fat) were in a semi-reclining position for 12 h in a chamber at 2800 m (539 mmHg) ALT or at 321 m (732 mmHg; ground). They ate a controlled breakfast (450 kcal + 3 ml x kg(-1) H2O) on the ground, and lunch and dinner at ALT (or on the ground) for a total daily intake of 2850 kcal (14% PRO, 67% CHO, 16% fat, 2.6g NaCl). At hour 10 they consumed fluid-electrolyte beverages or water (12 ml x kg(-1), 948 ml x d(-1)) in 4 sessions at weekly intervals. Beverage compositions were: a) 185 mEq x L(-1) Na+, 283 mOsm x kg(-1); b) 21.6 mEq x L(-1) Na+, 365 mOsm x kg(-1); c) water at ALT; and d) water on the ground. RESULTS: After 10 h at ALT % deltaPV (Hb-Hct) decreased (p < 0.05) by: a) 9.0 +/- SE 1.5%; b) 6.2 +/- 1.7%; c) 7.4 +/- 2.2%; and d) by 9.0 +/- 2.4%, respectively. After drinking from 1000-1030 h, PV at 1200 h changed by: a) +8.3 +/- SE 2.0% (p < 0.05); b) +2.8 +/- 2.7% (NS); c) -0.9 +/- 1.5% (NS); and d) by +0.8 +/- 3.5% (NS), respectively. The similar ground-induced hypovolemia suggests a response to confinement rather than an ALT effect and involuntary dehydration does not appear to be implicated. CONCLUSION: The significant increase in PV after consuming the (a) NaCl-NaCitrate beverage indicates that drink ionic composition appears to be more important than its osmolality for restoring PV in these conditions. Practical considerations: Because this hypovolemia was probably due to the confinement rather that reduced ambient pressure, appropriate countermeasures could be consumption of isotonic beverages, elastic stockings, leg exercise, and leg elevation.

Plasma volume expansion with oral fluids in hypohydrated men at rest and during exercise.

BACKGROUND: The purpose for this study was to evaluate various carbohydrate (CHO)-electrolyte fluid formulations for consumption by astronauts to maintain or restore their plasma volume (PV) and total body water (TBW) during and after extravehicular activity (exercise experiment, EE) and for a few hours before reentry and immediately after landing (rest experiment RE). HYPOTHESIS: That fluid formulation electrolyte content would be more important than osmotic (Osm) content for increasing or maintaining PV during the RE and EE. METHODS: In the RE, 5 healthy men (23-44 yr), previously dehydrated for 24 h, drank 6 fluid formulations (Water, 19.6 Na, 157 Na, 19.6 Na + glucose, and the prepared drinks Performances and Power)--one each at weekly intervals, and then sat for 70 min. In the EE, four healthy 24-h dehydrated men (30-46 yr) exercised for 70 min supine on a cycle ergometer (load = 71 +/- 1% peak VO2). RESULTS: Rest: Subjects who consumed formulations with total Osm concentrations nearer the normal range (157 Na - 270 mOsm x kg(-1), Performance with 19.6 mEq x L(-1) Na - 380 mOsm, and to some extent Power with 23.5 mEq x L(-1) Na - 390 mOsm) had the greater increases in PV; intake of drink 157 Na, with the largest Na content, induced the greatest hypervolemia of 7.6% (p < 0.05). The various additional ions, in addition to 19.6 Na, probably contributed to the 4.6% (p < 0.05) hypervolemia with Performance. Water was not effective. Exercise: Stabilization of PV between 15-70 min was not related to drink total CHO, Na or Osm content. Performance and 157 Na were no more effective than 19.6 Na or 19.6 Na + glu for PV stabilization. Water was the least effective. Regulatory mechanisms controlling PV during exercise appear to be independent of oral fluid formulation Osm-electrolyte content. CONCLUSIONS: Drink cation (sodium) content is more important that its total osmotic content for increasing plasma volume at rest. Fluid formulations with greater hypervolemic action in resting subjects may not be as effective during exercise; therefore different formulations for use during exercise appear to be necessary.

Hypervolemia in men from fluid ingestion at rest and during exercise.

BACKGROUND: Plasma osmolality (Osm) is important for controlling and maintaining plasma volume (PV) and body water. The effect of oral rehydration fluids for ameliorating dehydration is well-established; but optimal composition and Osm of fluids for hyperhydrating normally hydrated subjects is less clear. METHODS: Six treatments were used without and with oral fluids of varying ionic and constituent concentrations for hyperhydrating six previously euhydrated men (30 +/- SD 8 yr, 76.84 +/- 16.19 kg, 73 +/- 12 ml.kg-1 PV, 40 +/- 10 ml.min-1.kg-1 peak VO2) sitting at rest for 90 min (VO2 = 0.39 +/- SE 0.02 L.min-1) and during subsequent 70 min of submaximal exercise (VO2 = 2.08 +/- SE 0.33 L.min-1, 70 +/- 7% peak VO2). The hypothesis was that the fluid composition is more important than plasma Osm for increasing PV in euhydrated subjects at rest and maintaining it during exercise. Drink formulation compositions, given at 10 ml.kg-1 body wt, (mean = 768 ml), for the sitting period were: Performance 1 (P1; 55 mEq Na+, 365 mOsm.kg H2O-1), P2 (97 mEq Na+, 791 mOsm.kg-1), P2G (113 mEq Na+, 4% glycerol, 1382 mOsm.kg-1), AstroAde (AA; 164 mEq Na+, 253 mOsm.kg-1), and 01 and 02 (no drinking). The exercise drink (10 ml.kg-1, 768 ml) was P1 for all treatments except 02 (no drinking); thus, drink designations were: P1/P1, P2/P1, P2G/P1, AA/P1, 0/P1, and 0/0. RESULTS: PV at rest increased (p < 0.05) by 4.7% with P1 and by 7.9% with AA. Percent change in PV during exercise was +1% to +3% (NS) with AA/P1; -6% to 0% (NS) with P1/P1, P2/P1, P2G/P1, and 0/P1; and -8% to -5% (p < 0.05) with 0/0. AA, with the lowest Osm of 253 mOsm.kg-1, increased PV at rest (as did P1) and maintained it during exercise, whereas the other drinks with lower Na+ and higher Osm of 365-1382 mOsm.kg-1 did not. CONCLUSION: Drink composition appears to be more important than its Osm for increasing PV at rest and for maintaining it during exercise in previously euhydrated subjects.

Beta-adrenergic blockade does not prevent polycythemia or decrease in plasma volume in men at 4300 m altitude.

When humans ascend to high altitude (ALT) their plasma volume (PV) and total blood volume (BV) decrease during the first few days. With continued residence over several weeks, the hypoxia-induced stimulation of erythropoietin increases red cell production which tends to restore BV. Because hypoxia also activates the beta-adrenergic system, which stimulates red blood cell production, we investigated the effect of adrenergic beta-receptor inhibition with propranolol on fluid volumes and the polycythemic response in 11 healthy unacclimatized men (21-33 years old exposed to an ALT of 4300 m (barometric pressure 460 Torr) for 3 weeks on Pikes Peak, Colorado. PV was determined by the Evans blue dye method (PVEB), BV by the carbon monoxide method (BVCO), red cell volume (RCV) was calculated from hematocrit (Hct) and BVCO, and serum erythropoietin concentration ([EPO]) and reticulocyte count, were also determined. All determinations were made at sea level and after 9-11 (ALT-10) and 19-20 (ALT-20) days at ALT. At sea level and ALT, six men received propranolol (pro, 240 mg x day[-1]), and five received a placebo (pla). Effective beta-blockade did not modify the mean (SE) maximal values of [EPO] [pla: 24.9 (3.5) vs pro: 24.5 (1.5) mU x ml(-1)] or reticulocyte count [pla: 2.7 (0.7) vs pro: 2.2 (0.5)%]; nor changes in PVEB [pla: -15.8 (3.8) vs pro: -19.9 (2.8)%], RCVCO [pla: +7.0 (6.7) vs pro: + 10.1 (6.1)%], or BVCO [pla: -7.3 (2.3) vs pro: -7.1 (3.9)%]. In the absence of weight loss, a redistribution of body water with no net loss is implied. Hence, activation of the beta-adrenergic system did not appear to affect the hypovolemic or polycythemic responses that occurred during 3 weeks at 4300 m ALT in these subjects.

Body temperature and thermoregulation during submaximal exercise after 115-day spaceflight.

BACKGROUND: Altered thermoregulation has been reported following spaceflight simulations (bed rest and water immersion) but has never been examined after actual spaceflight. HYPOTHESIS: We tested the null hypothesis that body temperatures and heat loss responses during exercise would be similar before and after spaceflight. METHODS: Two male crewmembers of the 115-d Mir 18 mission performed supine submaximal cycle exercise (20 min at 40% and 20 min at 65% of preflight VO2peak) once at 145-146 d preflight and once at 5 d postflight (R + 5). RESULTS: After flight neither crewmember could complete the exercise protocol, stopping after 28-29 min. The core temperature (Tin, ingestible telemetry pill) at test termination was similar (37.8 degrees C for both subjects) pre- and postflight despite shorter postflight test duration. The slopes of the skin blood flow (laser Doppler)/Tin relationship (subject 1: 396 vs. 214; subject 2: 704 vs. 143% change Perfusion Unit/degree C), and the sweating rate (dew point hygrometry)/Tin relationship (subject 1: 6.3 vs. 2.0; subject 2: 4.6 vs. 0.7 mg.min-1.cm-2.degree C-1), were both reduced postflight without appreciable change in the Tin thresholds for sweating or skin blood flow. CONCLUSION: In this preliminary report for two crewmembers, the sensitivity of the heat loss responses were reduced after long-duration spaceflight, resulting in a faster rate of rise in core temperature.