Effects of hydration state on hormonal and renal responses during moderate exercise in the heat

The effects of hydromineral hormones and catecholamines on renal concentrating ability at different hydration states were examined in five male volunteers while they performed three trials. Each of these trials comprised a 60-min exercise bout on a treadmill (at 50% of maximal oxygen uptake) in a warm environment (dry bulb temperature, 35°C; relative humidity, 20–30%). In one session, subjects were euhydrated before exercise (C). In the two other sessions, after thermal dehydration (loss of 3% body mass) which markedly reduced plasma volume (PV) and increased plasma osmolality (osm_pl), the subjects exercised either not rehydrated (Dh) or rehydrated (Rh) by drinking 600 ml of mineral water before and 40 min after the onset of exercise. During exercise in the Dh compared to C state, plasma renin, aldosterone, arginine vasopressin (AVP), noradrenaline and adrenaline concentrations were increased (P < 0.05). A reduction in creatinine clearance and urine flow was also observed (P < 0.05) together with a decrease in urine osmolality, osmolar clearance and sodium excretion, while free water clearance increased (P < 0.05). However, compared to Dh, Rh partially restored PV and osm_pl and induced a marked reduction in the time courses of both the plasma AVP and catecholamine responses (P < 0.05). Values for renal water and electrolyte excretion were intermediate between those of Dh and C. Plasma atrial natriuretic peptide presented similar changes whatever the hydration state. These results demonstrate that during moderate exercise in the heat, renal concentrating ability is paradoxically reduced by prior dehydration in spite of high plasma AVP levels, and might be the result of marked activation of the sympatho-adrenal system. Rehydration, by reducing this activation, could partially restore the renal concentrating ability despite the lowered plasma AVP. Accepted: 23 April 1997     

Plasma vasopressin and aldosterone responses to oral and intravenous saline rehydration.

This investigation examined plasma arginine vasopressin (AVP) and aldosterone (Ald) responses to 1) oral and intravenous (IV) methods of rehydration (Rh) and 2) different IV Rh osmotic loads. We hypothesized that AVP and Ald responses would be similar between IV and oral Rh and that the greater osmolality and sodium concentration of a 0.9% IV saline treatment would stimulate a greater AVP response compared with a 0.45% IV saline treatment. On four occasions, eight men (age: 22.1 +/- 0.8 yr; height: 179.6 +/- 1.5 cm; weight: 73.6 +/- 2.5 kg; maximum O(2) consumption: 57.9 +/- 1.6 ml. kg(-1). min(-1), body fat: 7.7 +/- 0.9%) performed a dehydration (Dh) protocol (33 degrees C) to establish a 4-5% reduction in body weight. After Dh, subjects underwent each of three randomly assigned Rh (back to -2% body wt) treatments (0.9 and 0.45% IV saline, 0.45% oral saline) and a no Rh treatment during the first 45 min of a 100-min rest period. Blood samples were obtained pre-Dh, immediately post-Dh, and at 15, 35, and 55 min post-Rh. Before Dh, plasma AVP and Ald were not different among treatments but were significantly elevated post-Dh. In general, at 15, 35, and 55 min post-Rh, AVP, Ald, osmolality, and plasma volume shifts did not differ between IV and oral fluid replacement. These results demonstrated that the manner in which plasma AVP and Ald responded to oral and IV Rh or to different sodium concentrations (0.9 vs. 0.45%) was not different given the degree of Dh (-4.5% body wt) and Rh and amount of time after Rh (55 min).     

Plasma hypoxanthine and ammonia in humans during prolonged exercise

In this study we examined the time course of changes in the plasma concentration of oxypurines [hypoxanthine (Hx), xanthine and urate] during prolonged cycling to fatigue. Ten subjects with an estimated maximum oxygen uptake (VO2(max)) of 54 (range 47-67) ml x kg(-1) x min(-1) cycled at [mean (SEM)] 74 (2)% of VO2(max) until fatigue [79 (8) min]. Plasma levels of oxypurines increased during exercise, but the magnitude and the time course varied considerably between subjects. The plasma concentration of Hx ([Hx]) was 1.3 (0.3) micromol/l at rest and increased eight fold at fatigue. After 60 min of exercise plasma [Hx] was >10 micromol/l in four subjects, whereas in the remaining five subjects it was <5 micromol/l. The muscle contents of total adenine nucleotides (TAN = ATP+ADP+AMP) and inosine monophosphate (IMP) were measured before and after exercise in five subjects. Subjects with a high plasma [Hx] at fatigue also demonstrated a pronounced decrease in muscle TAN and increase in IMP. Plasma [Hx] after 60 min of exercise correlated significantly with plasma concentration of ammonia ([NH(3)], r = 0.90) and blood lactate (r = 0.66). Endurance, measured as time to fatigue, was inversely correlated to plasma [Hx] at 60 min (r = -0.68, P < 0.05) but not to either plasma [NH(3)] or blood lactate. It is concluded that during moderate-intensity exercise, plasma [Hx] increases, but to a variable extent between subjects. The present data suggest that plasma [Hx] is a marker of adenine nucleotide degradation and energetic stress during exercise. The potential use of plasma [Hx] to assess training status and to identify overtraining deserves further attention.     

Atrial natriuretic peptide during and after maximal and submaximal exercise under normoxic and hypoxic conditions

The present study was designed to investigate the influence of exercise intensity and duration as well as of inspiratory oxygen content on plasma atrial natriuretic peptide concentration [( ANP]) and furthermore to compare ANP with the effect on aldosterone concentration [( Aldo]). Ten untrained male subjects performed a maximal exercise test (ME) on a cycle ergometer and a submaximal test of 60-min duration at 60% of maximal performance (SE) under normoxia (N) and normobaric hypoxia (H) (partial pressure of oxygen: 12.3 kPa). Five subjects were exposed to hypoxia at rest for 90 min. The [ANP] was mostly affected by exercise intensity (5 min after ME-N, +298.1%, SEM 39.1%) and less by exercise duration (at the end of SE-N: +229.5%, SEM 33.2%). Hypoxia had no effect at rest and reduced the exercise response (ME-H, +184.3%, SEM 27.2%; SE-H, +172.4%, SEM 15.7%). In contrast to ANP, the Aldo response was affected more by duration at submaximal level (+290.1%, SEM 34.0%) than by short maximal exercise (+235.7%, SEM 22.2%). Exposure to hypoxia rapidly decreased [Aldo] (-28.5%, SEM 3.7% after 30 min, P less than 0.01), but did not influence the exercise effects (ME-H, +206.2%, SEM 26.4%; SE-H, +321.6%, SEM 51.6%). The [ANP] increase was faster than that of [Aldo] during the maximal tests and there was no difference during submaximal exercise. Changes in plasma volume (PV), sodium concentration, and osmolality (Osm) were most pronounced during maximal exercise (for ME-N: PV -13.1%, SD 3.6%, sodium +6.2 mmol.l-1, SD 2.7, Osm +18.4 mosmol.kg H2O-1, SD 6.5). Regression analysis showed high correlations between changes in [ANP] and in Osm during and after maximal exercise and between changes in [ANP] and heart rate for submaximal exercise. It is concluded that besides other mechanisms increased Osm might be involved in the exercise-dependent increase of plasma [ANP].     

Evaluation of renal function and fluid homeostasis during recovery from exercise-induced hyponatremia

Renal function including fluid and electrolyte balance was studied during recovery in eight subjects who developed symptomatic hyponatremia (HN; plasma sodium concentration less than 130 mM) during an 88-km ultramarathon footrace and compared with results for normonatremic runners [NN; n = 18, mean postrace plasma sodium concentration, 138.2 +/- 1.2 (SE) mM]. Estimated fluid intake during the race for HN was 12.5 +/- 1.6 (SE) liters over 9 h 41 min (+/- 28 min). HN excreted a net fluid excess of 2.95 +/- 0.56 (range 1.2-5.9) liters compared with a fluid deficit of 2.7 +/- 0.3% body weight in NN. The sodium deficit was 153 +/- 35 mmol in HN and 187 +/- 37 mmol in NN. Despite the fluid overload, plasma volume was decreased by 24.1 +/- 5.0% in HN compared with 8.2 +/- 2.6% in NN. Serum renin activity (5.1 +/- 2.0 ng.ml-1.h-1), aldosterone concentrations (410 +/- 34 ng/l), creatinine clearances (174.8 +/- 28.2 ml/min), and urine output (6.4 +/- 1.0 ml/min) were markedly elevated in HN during recovery. Thus the hyponatremia of exercise results from fluid retention in subjects who ingest abnormally large fluid volumes during prolonged exercise.     

Physiological changes and gastro-intestinal symptoms as a result of ultra-endurance running

One hundred and seventy-two competitors of the Swiss Alpine Marathon, Davos, Switzerland, 1988, volunteered for this research project. Of these volunteers 170 (158 men, 12 women) finished the race (99%). The race length was 67 km with an altitude difference of 1,900 m between the highest and lowest points. Mean age was 39 (SEM 0.8) years. Average finishing times were 8 h 18 min (men) and 8 h 56 min (women). Loss of body mass averaged 3.4% body mass [mean 3.3 (SEM 0.2)%; 4.0 (SEM 0.4)%; men and women, respectively]. Blood samples from a subgroup of 89 subjects (6 women and 83 men) were taken prior to and immediately after completion of the race. Changes in haemoglobin (9.3 mmol.l-1 pre-race, 9.7 mmol.l-1 post-race) and packed cell volume (0.44 pre, 0.48 post-race) were in line with the moderate level of dehydration displayed by changes in body mass. Mean plasma volume decreased by 8.3%. No significant changes in plasma osmolality, sodium, or chloride were observed but plasma potassium did increase by 5% (4.2 mmol.l-1 pre-race, 4.4 mmol.l-1 post-race). Mean fluid consumption was 3290 (SEM 103) ml. Forty-three percent of all subjects, and 33% of those who gave blood samples, complained of gastro-intestinal (GI) distress during the race. No direct relationship was found between the quantity or quality of beverage consumed and the prevalence of GI symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasma volume changes during and after acute variations of body hydration level in humans

This study examined plasma volume changes (deltaPV) in humans during periods with or without changes in body hydration: exercise-induced dehydration, heat-induced dehydration and glycerol hyperhydration. Repeated measurements of plasma volume were made after two injections of Evans blue. Results were compared to deltaPV calculated from haematocrit (Hct) and blood haemoglobin concentration ([Hb]). Eight well-trained men completed four trials in randomized order: euhydration (control test C), 2.8% dehydration of body mass by passive controlled hyperthermia (D) and by treadmill exercise (60% of their maximal oxygen uptake, VO2max) (E), and hyperhydration (H) by glycerol ingestion. The Hct, [Hb], plasma protein concentrations and plasma osmolality were measured before, during and after the changes in body hydration. Different Hct and [Hb] reference values were obtained to allow for posture-induced variations between and during trials. The deltaPV values calculated after two Evans blue injections were in good agreement with deltaPV calculated from Hct and [Hb]. Compared to the control test, mean plasma volume declined markedly during heat-induced dehydration [-11.4 (SEM 1.7)%] and slightly during exercise-induced dehydration [-4.2 (SEM 0.9)%] (P < 0.001 compared to D), although hyperosmolality was similar in these two trials. Conversely, glycerol hyperhydration induced an increase in plasma volume [+7.5 (SEM 1.0)%]. These results would indicate that, for a given level of dehydration, plasma volume is dramatically decreased during and after heat exposure, while it is better maintained during and after exercise.     

Hydration and vascular fluid shifts during exercise in the heat

This study examined the effects of hypohydration on plasma volume and red cell volume during rest in a comfortable (20 degrees C, 40% relative humidity) and exercise in a hot-dry (49 degrees C, 20% relative humidity) environment. A group of six male and six female volunteers [matched for maximal O2 uptake (VO2 max)] completed two test sessions following a 10-day heat acclimation program. One test session was completed when subjects were euhydrated and the other when subjects were hypohydrated (-5% from base-line body wt). The test sessions consisted of rest for 30 min in a 20 degrees C antechamber, followed by two 25-min bouts of treadmill walking (approximately 30% of VO2 max) in the heat, interspersed by 10 min of rest. No significant differences were found between the genders for the examined variables. At rest, hypohydration elicited a 5% decrease in plasma volume with less than 1% change in red cell volume. During exercise, plasma volume increased by 4% when subjects were euhydrated and decreased by 4% when subjects were hypohydrated. These percent changes in plasma volume values were significantly (P less than 0.01) different between the euhydration and hypohydration tests. Although red cell volume remained fairly constant during the euhydration test, these values were significantly (P less than 0.01) lower when hypohydrated during exercise. We conclude that hydration level alters vascular fluid shifts during exercise in a hot environment; hemodilution occurs when euhydrated and hemoconcentration when hypohydrated during light intensity exercise for this group of fit men and women.     

Effects of prolonged exercise at a similar percentage of maximal oxygen consumption in trained and untrained subjects

Six trained male cyclists and six untrained but physically active men participated in this study to test the hypothesis that the use of percentage maximal oxygen consumption (%VO2max) as a normalising independent variable is valid despite significant differences in the absolute VO2max of trained and untrained subjects. The subjects underwent an exercise test to exhaustion on a cycle ergometer to determine VO2max and lactate threshold. The subjects were grouped as trained (T) if their VO2max exceeded 60 ml.kg-1.min-1, and untrained (UT) if their VO2max was less than 50 ml.kg-1.min-1. The subjects were required to exercise on the ergometer for up to 40 min at power outputs that corresponded to approximately 50% and 70% VO2max. The allocation of each exercise session (50% or 70% VO2max) was random and each session was separated by at least 5 days. During these tests venous blood was taken 10 min before exercise (- 10 min), just prior to the commencement of exercise (0 min), after 20 min of exercise (20 min), at the end of exercise and 10 min postexercise (+ 10 min) and analysed for concentrations of cortisol, [Na+], [K+], [Cl-], glucose, free fatty acid, lactate [la-], [NH3], haemoglobin [Hb] and for packed cell volume. The oxygen consumption (VO2) and related variables were measured at two time intervals (14-15 and 34-35 min) during the prolonged exercise tests. Rectal temperature was measured throughout both exercise sessions. There was a significant interaction effect between the level of training and exercise time at 50% VO2max for heart rate (fc) and venous [la-].(ABSTRACT TRUNCATED AT 250 WORDS)     

Endocrine responses during exercise-heat stress: effects of prior isotonic and hypotonic intravenous rehydration

Exercise following exercise-induced dehydration (EID) has been shown to elevate concentrations of plasma norepinephrine (NE) and hypothalamic-pituitary-adrenal axis hormones. However, it is not known how intravenous (i.v.) rehydration (Rh) with isotonic (ISO) or hypotonic (HYPO) saline affects these hormone concentrations. It was hypothesized that HYPO, versus ISO, would lead to lower plasma NE and cortisol concentrations ([CORT]) during subsequent exercise following EID due to a decrease in plasma sodium concentration [Na⁺]. Eight non-heat acclimated men completed three experimental treatments (counterbalanced design) immediately following EID (33°C) to −4% body mass loss. The Rh treatments were i.v. 0.9% NaCl (ISO, 25 ml · kg⁻¹), i.v. 0.45% NaCl (HYPO, 25 ml · kg⁻¹), and no fluid (NF). After Rh and rest (2 h total), the subjects walked at 53–54 percent of maximal O₂ uptake for 45 min at 36°C. After Rh, the following observations were made before/during exercise: percentage change in plasma volume (PV) was lower in NF compared to ISO and HYPO but similar between ISO and HYPO; Δ[Na⁺] was similar between ISO and NF and higher in ISO compared to HYPO; Δ plasma NE was higher in NF compared to ISO and HYPO, but similar between ISO and HYPO; Δ plasma [CORT] was higher in NF compared to ISO and HYPO and higher in ISO compared to HYPO; rectal temperature was higher in NF compared to ISO and HYPO. These data would suggest that sympathetic nervous activity and [CORT] during exercise, subsequent to EID and Rh, was affected by lower PV (probably through cardiopulmonary baroreflexes) as well as core temperature. Furthermore, [CORT] was affected by Δ[Na⁺] after Rh through an unknown mechanism. Accepted: 16 July 1997     

The effects of body position and exercise on plasma volume dynamics

We examined the plasma volume changes associated with a protocol of either exercise or controlled rest under identical positional and ambient conditions. Nine healthy adult males rode (E) and on another occasion sat quietly (C) on a cycle ergometer for 30 min. Ten minutes of cycle exercise immediately followed the resting C protocol. Ambient temperature was 30 degrees C (rh = 35%) and exercise load was equal to 50% of peak VO2. Venous blood samples were obtained with subjects both in the supine and seated positions prior to all experiments. Additional blood was drawn during minutes 1, 5, 10, and 30 in both experimental conditions. A final sample was taken during C after the 10 min exercise. Moving from the supine to a seated position resulted in an average loss of 162 ml of plasma across all experiments. During the E condition a further reduction in plasma volume (76 ml) occurred by one minute of exercise. Plasma volume stabilized by 5 min of exercise under the E protocol. During the C condition, subsequent fluid loss (98 ml) was not apparent until 10 min after the first seated sample and totalled 176 ml at the end of 30 min of rest. Ten minutes of cycling at the end of the C experiment resulted in a further plasma volume reduction of 137 ml. Plasma protein and albumin contents decreased by 5 min of exercise in E and by 30 min of rest in C. [Na+] and [Cl-] did not change in either condition but a rapid increase in [K+] during exercise indicated an addition of potassium to the vascular volume.(ABSTRACT TRUNCATED AT 250 WORDS)     

Local sweating responses of different body areas in dehydration-hydration experiments

Five subjects performed intermittent exercise on a bicycle ergometer (25 min work, 5 min rest cycles for 2 hours, and 20 min work, 10 min rest cycles for a further hour) in a hot environment (air and wall temperatures = 36 degrees C; dew-point temperature = 10 degrees C; air velocity = 0.6 m.s-1). The relative mechanical work load was of 70 W (30% of the maximal aerobic capacity). Seven experimental tests were carried out in order to induce a plasma hypovolemia associated with either a plasma hypo- or hyperosmolarity. The preexercise level of body hydration was also manipulated by giving a diuretic, or by ingestion of 500 ml of isotonic electrolyte sucrose solution before the start of exercise. Continuous measurements were made of rectal and mean skin temperatures. The sweating responses of the chest and of the thigh (over the active muscles of the leg) were monitored from 4 sweat collection capsules highly ventilated. On each of these body areas, the local skin temperatures under one of the 2 capsules was kept at a constant level (37 degrees C). The effects of the level of body hydration on the sweating response only appear when a high local thermal clamp is imposed beneath the capsule. This local effect is particularly strong over the active muscles of the thigh. The influence of the preexercise hydration appears during dehydration tests. This effect is not significant when fluid is given to the subject during the exercise. The change in the sensitivity of the thermoregulatory system is more strongly associated with plasma osmolarity than hypovolemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of repeated bouts of short-term exercise on plasma free and sulphoconjugated catecholamines in humans

We tested the hypothesis that measurement of plasma catecholamine sulphate concentration after exercise reflects the overall activation of the sympathoadrenergic system during the whole period of repeated bouts of short-term exercise. A group of 11 male athletes performed two exercise tests at similar average power outputs consisting of three sets each. The tests either started with one set of three very intense sprints (95% of maximal running speed) followed by two sets of three less intense sprints (85% of maximal running speed; HLX) or vice versa (LHX). Similar mean areas under the curve of free noradrenaline (NA) during HLX and LHX [622 (SEM 13) v.s. 611 (SEM 14) nmol x l(-1) min) as well as similar mean heart rates [143 (SEM 9) v.s. 143 (SEM 8) beats x min(-1)] indicated comparable sympathetic activation during both exercise tests. Even so, plasma concentration of free NA was still significantly higher at the end of LHX than of HLX [35.7 (SEM 3.5) v.s. 22.5 (SEM 2.1) nmol x l(-1), respectively], i.e. when exercise ended with the more intense set of sprints. Plasma noradrenaline sulphate (NA-S) increased with exercise intensity showing higher mean increments after the first set of HLX compared to LHX [1.83 (SEM 0.42) v.s. 1.18 (SEM 0.29) nmol x l(-1); P<0.05]. However, after the end of HLX and LHX, increments in plasma NA-S were similar [4.52 (SEM 0.76) v.s. 4.06 (SEM 0.79) nmol x l(-1)], suggesting that NA-S response changed in parallel with the overall activation of the sympathetic nervous system during repeated bouts of short-term exercise. The results supported the hypothesis that measurement of plasma NA-S immediately after repeated bouts of short-term exercise reflects overall activation of the sympathetic nervous system during prolonged periods of this type of exercise.     

High-sweat Na+ in cystic fibrosis and healthy individuals does not diminish thirst during exercise in the heat

Sweat Na(+) concentration ([Na(+)]) varies greatly among individuals and is particularly high in cystic fibrosis (CF). The purpose of this study was to determine whether excess sweat [Na(+)] differentially impacts thirst drive and other physiological responses during progressive dehydration via exercise in the heat. Healthy subjects with high-sweat [Na(+)] (SS) (91.0 ± 17.3 mmol/l), Controls with average sweat [Na(+)] (43.7 ± 9.9 mmol/l), and physically active CF patients with very high sweat [Na(+)] (132.6 ± 6.4 mmol/l) cycled in the heat without drinking until 3% dehydration. Serum osmolality increased less (P < 0.05) in CF (6.1 ± 4.3 mosmol/kgH(2)O) and SS (8.4 ± 3.0 mosmol/kgH(2)O) compared with Control (14.8 ± 3.5 mosmol/kgH(2)O). Relative change in plasma volume was greater (P < 0.05) in CF (-19.3 ± 4.5%) and SS (-18.8 ± 3.1%) compared with Control (-14.3 ± 2.3%). Thirst during exercise and changes in plasma levels of vasopressin, angiotensin II, and aldosterone relative to percent dehydration were not different among groups. However, ad libitum fluid replacement was 40% less, and serum NaCl concentration was lower for CF compared with SS and Control during recovery. Despite large variability in sweat electrolyte loss, thirst appears to be appropriately maintained during exercise in the heat as a linear function of dehydration, with relative contributions from hyperosmotic and hypovolemic stimuli dependent upon the magnitude of salt lost in sweat. CF exhibit lower ad libitum fluid restoration following dehydration, which may reflect physiological cues directed at preservation of salt balance over volume restoration.     

Body temperature and plasma prolactin and norepinephrine relationships during exercise in a warm environment: effect of dehydration

The effects of euhydration (Eh) and light (Dh1) and moderate (Dh2) dehydrations on plasma prolactin (PRL) levels were studied in 5 young male volunteers at rest and during exercise to exhaustion (50% of VO2max) in a warm environment (Tdb = 35 degrees C, rh = 20-30%). Light and moderate dehydrations (loss of 1.1 and 1.8% body respectively) were obtained before exercise by controlled hyperthermia. Compared to Eh, time for exhaustion was reduced in Dh1 and Dh2 (p less than 0.01) and rectal temperature (Tre) rose faster in Dh2 (p less than 0.05). Both venous plasma PRL and norepinephrine (NE) increased during exercise at any hydration level (p less than 0.05). Plasma PRL reached higher values after 40 and 60 min in Dh2 and Dh1 (p less than 0.05). Plasma NE values were higher in Dh2 at rest and at the 40th min during exercise (p less than 0.05). Plasma PRL was linearly correlated to Tre and plasma NE (p less than 0.001) but unrelated to plasma volume variation and osmolality. Our results provide further evidence for the major effect of body temperature in exercise-induced PRL changes. Moreover, the plasma PRL-NE relationship suggests that these changes may result from central noradrenergic activation.     

Fluid replacement following dehydration reduces oxidative stress during recovery

To investigate the effects of hydration status on oxidative DNA damage and exercise performance, 10 subjects ran on a treadmill until exhaustion at 80% VO_2max during four different trials [control (C), 3% dehydration (D), 3% dehydration + water (W) or 3% dehydration + sports drink (S)]. Dehydration significantly decreased exercise time to exhaustion (D < C and S). Plasma MDA levels were significantly higher at pre-exercise in D than C. Plasma TAS was significantly lower at pre-exercise in C and S than in D, and was significantly lower in S than D at 60 min of recovery. Dehydration significantly increased oxidative DNA damage during exercise, but fluid replacement with water or sports drink alleviated it equally. These results suggest that (1) dehydration impairs exercise performance and increases DNA damage during exercise to exhaustion; and (2) fluid replacement prolongs exercise endurance and attenuates DNA damage.     

Effect of moderate physical activity on plasma leptin concentration in humans

In subjects who maintain a constant body mass, the increased energy expenditure induced by exercise must be compensated by a similar increase in energy intake. Since leptin has been shown to decrease food intake in animals, it can be expected that physical exercise would increase energy intake by lowering plasma leptin concentrations. This effect may be secondary either to exercise-induced negative energy balance or to other effects of exercise. To delineate the effects of moderate physical activity on plasma leptin concentrations, 11 healthy lean subjects (4 men, 7 women) were studied on three occasions over 3 days; in study 1 they consumed an isoenergetic diet (1.3 times resting energy expenditure) over 3 days with no physical activity; in study 2 the subjects received the same diet as in study 1, but they exercised twice daily during the 3 days (cycling at 60 W for 30 min); in study 3 the subjects exercised twice daily during the 3 days, and their energy intake was increased by 18% to cover the extra energy expenditure induced by the physical activity. Fasting plasma leptin concentration (measured on the morning of day 4) was unaltered by exercise [8.64 (SEM 2.22) 7.17 (SEM 1.66), 7.33 (SEM 1.72) 1 microg x l(-1) in studies 1, 2 and 3, respectively]. It was concluded that a moderate physical activity performed over a 3-day period does not alter plasma leptin concentrations, even when energy balance is slightly negative. This argues against a direct effect of physical exercise on plasma leptin concentrations, when body composition is unaltered.     

Role of osmolality and plasma volume during rehydration in humans

To determine how the sodium content of ingested fluids affects drinking and the restoration of the body fluid compartments after dehydration, we studied six subjects during 4 h of recovery from 90-110 min of a heat [36 degrees C, less than 30% relative humidity (rh)] and exercise (40% maximal aerobic power) exposure, which caused body weight to decrease by 2.3%. During the 1st h, subjects rested seated without any fluids in a thermoneutral environment (28 degrees C, less than 30% rh) to allow the body fluid compartments to stabilize. Over the next 3 h, subjects rehydrated ad libitum using tap water and capsules containing either placebo (H2O-R) or 0.45 g NaCl (Na-R) per 100 ml water. During the 3-h rehydration period, subjects restored 68% of the lost water during H2O-R, whereas they restored 82% during Na-R (P less than 0.05). Urine volume was greater in H2O-R than in Na-R; thus only 51% of the lost water was retained during H2O-R, whereas 71% was retained during Na-R (P less than 0.05). Plasma osmolality was elevated throughout the rehydration period in Na-R, whereas it returned to the control level by 30 min in H2O-R (P less than 0.05). Changes in free water clearance followed changes in plasma osmolality. The restoration of plasma volume during Na-R was 174% of that lost. During H2O-R it was 78%, which seemed to be sufficient to diminish volume-dependent dipsogenic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rehydration with fluid of varying tonicities: effects on fluid regulatory hormones and exercise performance in the heat.

This study examined the effects of rehydration (Rehy) with fluids of varying tonicities and routes of administration after exercise-induced hypohydration on exercise performance, fluid regulatory hormone responses, and cardiovascular and thermoregulatory strain during subsequent exercise in the heat. On four occasions, eight men performed an exercise-dehydration protocol of approximately 185 min (33 degrees C) to establish a 4% reduction in body weight. Following dehydration, 2% of the fluid lost was replaced during the first 45 min of a 100-min rest period by one of three random Rehy treatments (0.9% saline intravenous; 0.45% saline intravenous; 0.45% saline oral) or no Rehy (no fluid) treatment. Subjects then stood for 20 min at 36 degrees C and then walked at 50% maximal oxygen consumption for 90 min. Subsequent to dehydration, plasma Na(+), osmolality, aldosterone, and arginine vasopressin concentrations were elevated (P < 0.05) in each trial, accompanied by a -4% hemoconcentration. Following Rehy, there were no differences (P > 0.05) in fluid volume restored, post-rehydration (Post-Rehy) body weight, or urine volume. Percent change in plasma volume was 5% above pre-Rehy values, and plasma Na(+), osmolality, and fluid regulatory hormones were lower compared with no fluid. During exercise, skin and core temperatures, heart rate, and exercise time were not different (P > 0.05) among the Rehy treatments. Plasma osmolality, Na(+), percent change in plasma volume, and fluid regulatory hormones responded similarly among all Rehy treatments. Neither a fluid of greater tonicity nor the route of administration resulted in a more rapid or greater fluid retention, nor did it enhance heat tolerance or diminish physiological strain during subsequent exercise in the heat.     

Fluid balance in exercise dehydration and rehydration with different glucose-electrolyte drinks

After exercise dehydration (3% of body weight) the restoration of water and electrolyte balance was followed in 6 male subjects. During a 2 h rest period after exercise, a drink of one of four solutions was given as 9 X 300 ml portions at 15 min intervals: control (C-drink), high potassium (K-drink), high sodium (Na-drink) or high sugar (S-drink). An exercise test (submaximal and supramaximal work) was performed before dehydration and after rehydration. Dehydration reduced plasma volume by 16%, a process reversed on resting even before fluid ingestion began, due to release of water accumulated in the muscles during exercise. After 2 h rehydration, plasma volume was above the initial resting value with all 4 drinks. The final plasma volumes after the Na-drink (+14%) and C-drink (+9%) were significantly higher than after the K- and S-drinks. The Na-drink favoured filling of the extracellular compartment, whereas the K- and S-drinks favoured intracellular rehydration. In spite of the higher than normal plasma volume after rehydration, mean heart rate during the submaximal test was 10 bpm higher after rest and rehydration than in the initial test, and was not different between the drinks. The amount of work which could be performed in the supramaximal test (105% VO2max) was 20% less after exercise dehydration and subsequent rest and rehydration than before. This reduction was similar for all drinks, and may be due to a decreased muscle glycogen content (70% of initial) at the time of the second test.