Exercise-induced Dehydration Research Articles

Effects of fluid ingestion on cognitive function after heat stress or exercise-induced dehydration

This study investigated the effects of heat exposure, exercise-induced dehydration and fluid ingestion on cognitive performance. Seven healthy men, unacclimatized to heat, were kept euhydrated or were dehydrated by controlled passive exposure to heat (H, two sessions) or by treadmill exercise (E, two sessions) up to a weight loss of 2.8%. On completion of a 1-h recovery period, the subjects drank a solution containing 50 g l −1 glucose and 1.34 g l −1 NaCl in a volume of water corresponding to 100% of his body weight loss induced by dehydration. (H1 and E1) or levels of fluid deficit were maintained (H0, E0). In the E0, H0 and control conditions, the subject drank a solution containing the same quantity of glucose diluted in 100 ml of water. Psychological tests were administered 30 min after the dehydration phase and 2 h after fluid ingestion. Both dehydration conditions impaired cognitive abilities (i.e. perceptive discrimination, short-term memory), as well as subjective estimates of fatigue, without any relevant differences between the methods. By 3.5 h after fluid deficit, dehydration (H0 and E0) no longer had any adverse effect, although the subjects felt increasingly tired. Thus, there was no beneficial effect of fluid ingestion (H1 and E1) on the cognitive variables. However, long-term memory retrieval was impaired in both control and dehydration situations, whereas there was no decrement in performance in the fluid ingestion condition (H1, E1).

Combined effect of heat stress, dehydration and exercise on neuromuscular function in humans.

This study examined the combined effect of exercise induced hyperthermia and dehydration on neuromuscular function in human subjects. Six trained male runners ran for 40 min on a treadmill at 65% of their maximal aerobic velocity while wearing a tracksuit covered with an impermeable jacket and pants to impair the evaporation of sweat. These stressful experimental running conditions led the runners to a physiological status close to exhaustion. On average, the 40 min run ended at a heart rate of 196 (SD 8) beats.min-1, a tympanic temperature of 40 (SD 0.3) degrees C and with a loss of body mass of 2 (SD 0.5)%. Pre- and post-running strength tests included measurements of maximal knee extension and flexion torques in both isometric and isokinetic (at 60 and 240 degrees.s-1) conditions. A 20 s endurance test at 240 degrees.s-1 was also performed. Surface electromyographic (EMG) activity was recorded from six knee extensor and flexor muscles during the entire protocol. The treadmill run led to clear decrements in maximal extension torque and EMG activity both in isometric and at the slowest isokinetic velocity (60 degrees.s-1). However, no differences in these parameters were observed at 240 degrees.s-1. Furthermore, the EMG patterns of the major knee extensor and flexor muscles remained remarkably stable during the treadmill run. These results demonstrate that the exercise-induced hyperthermia and dehydration in the present experiments had only minor effects on the neuromuscular performance. However, it is also suggested that high internal body temperature per se could limit the production of high force levels.

The effects in humans of rapid loss of body mass on a boxing-related task.

The physiological effects of strategies for a rapid loss of body mass immediately before weighing-in for competition in weight-governed sports are unclear. This study examined the effects of a 3%-4% loss in body mass on a boxing-related task. Seven novice amateur boxers completed three 3 min rounds of simulated boxing on a prototype boxing ergometer in an euhydrated state (E-trial) and after exercise-induced thermal dehydration (D-trial). All subjects lost body mass following dehydration-mean body mass fell 3.8 (SD +/- 0.3)% [77.3 (SD +/- 11.3) to 74.4 (SD +/- 10.7) kg, P<0.001] - but changes in plasma volume (PV) were inconsistent. Four subjects suffered reductions in PV between 15% and 30%, one subject maintained his E-trial value and two recorded an increase. The D-trial mean PV value was 8.0 (SD +/- 17.2)% lower but this fall was not statistically significant (P>0.05). Analysis of D-trial boxing performance showed one subject maintained his performance over the two trials and a second improved 17.8%. A two-way ANOVA (condition x time) with repeated measures on both factors showed no significant main effect differences for condition (F1,6 = 3.93 P>0.05), time (F1.83,48 = 1.12, P>0.05) or interaction between them (F1.93,48, P>0.05). Furthermore, neither heart rate nor blood lactate responses in the boxing task differed between trials. These data were affected by the small sample. Power and effect size analysis using eta(2) procedure and removing the outlier data produced a mean fall in boxing performance of 26.8%. However, some subjects appeared able to resist the deleterious effects of a rapid loss of body mass prior to competition and further research is needed to explain the mechanisms under-pinning this ability.

Climatic Heat Stress and the Exercising Child and Adolescent

This Policy Statement was revised. See https://doi.org/10.1542/peds.2011-1664. For morphologic and physiologic reasons, exercising children do not adapt as effectively as adults when exposed to a high climatic heat stress. This may affect their performance and well-being, as well as increase the risk for heat-related illness. This policy statement summarizes approaches for the prevention of the detrimental effects of children's activity in hot or humid climates, including the prevention of exercise-induced dehydration.

Use of bioelectrical impedance analysis to estimate body fluid compartments after acute variations of the body hydration level.

Physiological measurements including body mass, plasma osmolality, natremia, plasma volume measured by Evans Blue dilution, and total body water (TBW) and extracellular water (ECW) volumes estimated by bioelectrical impedance analysis (BIA) were recorded in eight healthy young Caucasian subjects before and after acute variations of their body hydration state on four separate occasions: 1) euhydration or control trial (C); 2) heat-induced dehydration of 2.8% body mass (D); 3) exercise-induced dehydration of 2.8% body mass (E); and 4) glycerol-hyperhydration (H). Heart rate, rectal and mean skin temperatures were also recorded throughout the experiment. The main result of the study is that BIA only half predicted the body water loss after exercise, although conditions were standardized (electrode placement, side of the body, limb position, posture, and ambient temperature). Differences in body temperatures cannot explain such an unexpected result, nor did the study of plasma osmolality and sodium concentration. If BIA appears to adequately predict changes in TBW after heat-induced dehydration and glycerol hyperhydration, further studies including measures of TBW and ECW by dilution tracer methods would be necessary to establish the validity of using the BIA method to measure such changes and to interpret ECW variations.

Acute Pancreatitis Secondary to Dehydration: Case Report and Review of the Literature

Recent reports have documented the potentially catastrophic consequences of dehydration induced by vigorous exercise in otherwise healthy individuals. A case of acute pancreatitis secondary to exercise-induced dehydration is presented, and the literature of dehydration-induced syndromes, both research and clinical, is reviewed. The goal of this case report is to heighten awareness of dehydration as a potential cause of acute pancreatitis.

Metabolic and thermodynamic responses to dehydration-induced reductions in muscle blood flow in exercising humans.

1. The present study examined whether reductions in muscle blood flow with exercise-induced dehydration would reduce substrate delivery and metabolite and heat removal to and from active skeletal muscles during prolonged exercise in the heat. A second aim was to examine the effects of dehydration on fuel utilisation across the exercising leg and identify factors related to fatigue. 2. Seven cyclists performed two cycle ergometer exercise trials in the heat (35 C; 61 +/- 2 % of maximal oxygen consumption rate, VO2,max), separated by 1 week. During the first trial (dehydration, DE), they cycled until volitional exhaustion (135 +/- 4 min, mean +/- s.e.m.), while developing progressive DE and hyperthermia (3.9 +/- 0.3 % body weight loss and 39.7 +/- 0.2 C oesophageal temperature, Toes). On the second trial (control), they cycled for the same period of time maintaining euhydration by ingesting fluids and stabilising Toes at 38.2 +/- 0.1 degrees C. 3. After 20 min of exercise in both trials, leg blood flow (LBF) and leg exchange of lactate, glucose, free fatty acids (FFA) and glycerol were similar. During the 20 to 135 +/- 4 min period of exercise, LBF declined significantly in DE but tended to increase in control. Therefore, after 120 and 135 +/- 4 min of DE, LBF was 0.6 +/- 0.2 and 1.0 +/- 0.3 l min-1 lower (P < 0.05), respectively, compared with control. 4. The lower LBF after 2 h in DE did not alter glucose or FFA delivery compared with control. However, DE resulted in lower (P < 0.05) net FFA uptake and higher (P < 0.05) muscle glycogen utilisation (45 %), muscle lactate accumulation (4.6-fold) and net lactate release (52 %), without altering net glycerol release or net glucose uptake. 5. In both trials, the mean convective heat transfer from the exercising legs to the body core ranged from 6.3 +/- 1.7 to 7.2 +/- 1.3 kJ min-1, thereby accounting for 35-40 % of the estimated rate of heat production ( approximately 18 kJ min-1). 6. At exhaustion in DE, blood lactate values were low whereas blood glucose and muscle glycogen levels were still high. Exhaustion coincided with high body temperature ( approximately 40 C). 7. In conclusion, the present results demonstrate that reductions in exercising muscle blood flow with dehydration do not impair either the delivery of glucose and FFA or the removal of lactate during moderately intense prolonged exercise in the heat. However, dehydration during exercise in the heat elevates carbohydrate oxidation and lactate production. A major finding is that more than one-half of the metabolic heat liberated in the contracting leg muscles is dissipated directly to the surrounding environment. The present results indicate that hyperthermia, rather than altered metabolism, is the main factor underlying the early fatigue with dehydration during prolonged exercise in the heat.

EFFECTS OF REHYDRATION WITH I.V. AND ORAL FLUIDS ON POSTURAL HYPOTENSION AFTER - 4% DEHYDRATION

1792 Although intravenous (i.v.) infusion effectively relieves the symptoms of heat syncope, the specific influences of rehydration (RE) on postural hypotension (H) are not well documented. This investigation examined the effects of three RE modes (∼2L) on cardiovascular responses in supine (S) and erect (E) postures, after exercise-induced dehydration (D). Eight fit males (22 ± 2 yr, 57.9 ± 4.6 ml/kg/min VO2max) underwent D to −4% of body mass (2-4 h, 50% VO2max) four times in a hot environment (33°C, 43%rh), then were exposed to one of four treatments: either oral 0.45% NaCl (OR), intravenous NaCl (0.45% and 0.9%), or no fluid (CON). Heart rate (HR), systolic (SYS) and diastolic blood pressures were automatically measured (S and E) before D (euhydrated), after D, and 45 min after each treatment (POST). Upon standing, the absolute SYS value in all tests exhibited a similar decrease after D (mean range 9-17 mmHg), absolute SYS was higher (P<.05) at POST (vs. D) in all tests, but was greater in the three RE modes (mean range 20-27 mmHg) than in CON (6 mmHg). The change in SYS due to standing was smaller at POST (P<.05) than after D, in all experiments. In moving from S to E, HR were lower at POST (P<.05, vs. D) in the OR, .45% and CON trials. We concluded that cardiovascular responses changed in a similar pattern in all trials, but OR and i.v. solutions reduced H (i.e., the decrease in SYS) and the rise in mean HR, resulting in more effective cardiovascular control during standing.

Effects of dehydration on exercise performance.

Dehydration refers both to hypohydration (dehydration induced prior to exercise) and to exercise-induced dehydration (dehydration that develops during exercise). The latter reduces aerobic endurance performance and results in increased body temperature, heart rate, perceived exertion, and possibly increased reliance on carbohydrate as a fuel source. Although the negative effects of exercise-induced dehydration on exercise performance were clearly demonstrated in the 1940s, athletes continued to believe for years thereafter that fluid intake was not beneficial. More recently, negative effects on performance have been demonstrated with modest (<2%) dehydration, and these effects are exacerbated when the exercise is performed in a hot environment. The effects of hypohydration may vary, depending on whether it is induced through diuretics or sauna exposure, which substantially reduce plasma volume, or prior exercise, which has much less impact on plasma volume. Hypohydration reduces aerobic endurance, but its effects on muscle strength and endurance are not consistent and require further study.

Rehydration following exercise: effects of administration of water versus an isotonic oral rehydration solution (ORS)

The effects of administering (1) 6L isotonic oral rehydration solution (ORS), similar in composition to plasma (except for an elevated potassium concentration) and with an osmotic skeleton and (2) 6L water (no osmotic skeleton), were evaluated in five thoroughbred horses following exercise-induced dehydration. The horses were exercised on a treadmill for 10 min at walk (1.7 m.s-1; approximately 15% VO2max), 40 min at trot (3.7 m.s-1; approximately 25% VO2max) and 10 min at walk (1.7 m.s-1; approximately 15% VO2max). Exercise was undertaken on a 3 degrees incline at 30 degrees C/80% RH. Solutions of water or ORS at 20 degrees C were administered by nasogastric tube over 60s 5 min following exercise. Mean weight loss following exercise was 9.2 +/- 1.7 kg (2.0 +/- 0.4% body weight; mean +/- SEM) with water and 9.2 +/- 1.1 kg (2.0 +/- 0.2% body weight) with ORS and was not different between treatments (P > 0.05). Water treatment resulted in a fall in plasma [Na+] (approximately 3 mmol.L-1) and C1- (1-2 mmol.L-1) concentrations by 30 min after administration and the effect persisted until the end of the study (300 min post fluids). There was little change in plasma total protein (TP) from that at the end of exercise, suggesting a failure of water to restore or maintain PV. In contrast, ORS administration resulted in a small increase in plasma [Na+] (1-2 mmol.L-1) and [Cl-] (2-3 mmol.L-1) with a corresponding decrease in plasma TP. By 120 min post ORS, plasma TP and PV were no longer significantly different from rest or pre-exercise (P > 0.05), whilst with water, TP was elevated (approximately 3-4 g.L-1) and PV reduced (approximately 4-5 mL.kg-1). Total urine output was not significantly different between water (1096 +/- 135 mL) and ORS (750 +/- 215 mL, P > 0.05). Estimates of expected plasma volume and electrolyte concentration changes as a result of either treatment compared well with measured changes of TP and PV. On the basis of calculated or measured changes, it was estimated that only 1L of water contributed to rehydration following exercise compared to 4L isotonic, plasma-like ORS. The administration of 6L ORS restored the PV deficit induced by exercise with minimal or no disturbance of plasma electrolyte concentrations. In contrast, water alone resulted in minimal improvement in PV. When fluid intake after periods of fluid loss, such as induced by exercise or transport, is not accompanied by food intake, the present study has clearly demonstrated that water alone is ineffective in promoting rehydration compared with an isotonic, plasma-like ORS.

Hydration effects on physiological strain of horses during exercise-heat stress.

This study examined the effects of hyperhydration, exercise-induced dehydration, and oral fluid replacement on physiological strain of horses during exercise-heat stress. On three occasions, six horses completed a 90-min exercise protocol (50% maximal O2 uptake, 34.5 degrees C, 48% relative humidity) divided into two 45-min periods (exercise I and exercise II) with a 15-min recovery between exercise bouts. In random order, horses received no fluid (NF), 10 liters of water (W), or a carbohydrate-electrolyte solution (CE) 2 h before exercise and between exercise bouts. Compared with NF, preexercise hyperhydration (W and CE) did not alter heart rate, cardiac output (Q), stroke volume (SV), core body temperature, sweating rate (SR), or sweating sensitivity during exercise I. In contrast, after exercise II, exercise-induced dehydration in NF (decrease in body mass: NF, 5.6 +/- 0.8%; W, 1.1 +/- 0.4%; CE, 1.0 +/- 0.2%) resulted in greater heat storage, with core body temperature approximately 1. 0 degrees C higher compared with W and CE. In exercise II, the greater thermal strain in NF was associated with significant (P < 0. 05) decreases in Q (10 +/- 2%), SV (9 +/- 3%), SR, and sweating sensitivity. We concluded that 1) preexercise hyperhydration provided no thermoregulatory advantage; 2) maintenance of euhydration by oral fluid replacement ( approximately 85% of sweat fluid loss) during exercise in the heat was reflected in higher Q, SV, and SR with decreased heat storage; and 3) W or an isotonic CE solution was equally effective in reducing physiological strain associated with exercise-induced dehydration and heat stress.

The influence of exercise and dehydration on postural stability

The aim of this study was to investigate the effects of exercise-induced and thermal dehydration on postural.balance. Eight male subjects cycled for 2 h at a power output equal to 57 - 63% V O on two different occasions: once without 2 max drinking (NF) and once with intake of 1.9 1 of a carbohydrate-electrolyte solution (FR). Before and after the exercise test, the velocity of the centre of pressure (COP) excursion was measured on a force platform during 30-s bipedal standing in normal position, feet side by side, and tandem position, feet heel to toe. On another occasion, eight subjects underwent seven consecutive sauna sessions (85 C, 50% rh) of 15 min duration with no fluid replacement (S) to induce thermal dehydration. Mean fluid loss was 2.7 (0.4)%, 0.5 (0.5)% and 3.0 (0.6)% of body mass after NF, FR and S, respectively. Mean velocity of COP excursion after the exercise test was significantly higher in the NF than in the FR trial (p < 0.05). Postural stability was not influenced by S. In conclusion, prolonged exercise without fluid ingestion seems to negatively affect postural stability, whereas no effect is observed after exercise with fluid replacement or after thermal dehydration.

Treatment of Exercise-Induced Dehydration

One of the most common consequences of prolonged exercise is fluid and electrolyte depletion. Fluid and electrolyte losses during exercise may limit the horse's performance and, in extreme cases, jeopardize its health. To avoid or treat the deleterious effects of dehydration, fluid and electrolyte supplementation is essential. This article provides recommendations for fluid and electrolyte supplementation for horses involved in endurance-related events.

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 degrees C) to -4% body mass loss. The Rh treatments were i.v. 0.9% NaCl (ISO, 25 ml x kg[-1]), i.v. 0.45% NaCl (HYPO, 25 ml x 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 degrees 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; delta[Na+] was similar between ISO and NF and higher in ISO compared to HYPO; delta plasma NE was higher in NF compared to ISO and HYPO, but similar between ISO and HYPO; delta 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 delta[Na+] after Rh through an unknown mechanism.

Salt Preference in Adolescence Is Predicted by Common Prenatal and Infantile Mineralofluid Loss

Leshem, M. Salt preference in adolescence is predicted by common prenatal or infantile mineralofluid loss. Physiol Behav 63(4) 699–704, 1998. We investigated early determinants of salt preference in humans. In animals, physiological events, among them perinatal mineralofluid loss, contribute to long-term salt intake. Recent findings suggest that in humans prenatal mineralofluid loss (high levels of maternal vomiting) may increase the lifelong avidity for salt in offspring. Here we report that commonly occurring events that cause mild fluid loss and electrolyte imbalance in infancy, as well as prenatally, predict the avidity for salt in adolescents. Using questionnaires, 50 mothers recalled incidence and severity of infantile diarrhea and vomiting in their adolescent offspring. The adolescents’ avidity for salt was determined by testing the preferred concentration of salt in soup, voluntary consumption of salty snack items, and by self report of salt use habits, and a dietary questionnaire. A reported history of mineralofluid loss including maternal vomiting and infantile vomiting and diarrhea increases the avidity for salt but not for sweet. Thus, commonly occurring early mineralofluid loss may contribute to lifelong salt intake. The findings raise the possibility that other causes of mineralofluid loss such as hemorrhage, exercise-induced dehydration, or neonatal diuretic therapy may also increase the avidity for salt, and its attendant health risks.

Relationship between increase in intracellular Ca 2+ concentration during global ischemia and delayed ischemic damage

The effects of administering (1) 6L isotonic oral rehydration solution (ORS), similar in composition toplasma (except for an elevated potassium concentration) and with an osmotic skeleton and (2) 6L water (no osmotic skeleton), were evaluated in five thoroughbred horses following exercise-induced dehydration. The horses were exercised on a treadmill for 10min at walk (1.7m.−1; ∼15% VO2max), 40min at trot (3.7m.−1; 25% VO2max) and l0min at walk (1.7m.rl; ∼15% VO2max). Exercise was undertaken on a 3* incline at 3°C/80% RH. Solutions of water or ORS at 20°C were administered by nasogastric tube over 60s 5 min following exercise. Mean weight loss following exercise was 9.2±l.7kg (2.010.4% body weight; meant±sem) with water and 9.2±1.1 kg (2.0±0.2% body weight) with ORS and was not different between treatments (P>0.05). Water treatment resulted in a fall in plasma [Na+] (∼3mmol.Lt) and Cl− (1–2mmol.L−1) concentrations by 30min after administration and the effect persisted until the end of the study (300min post fluids). There was little change in plasma total protein (TP) from that at the end of exercise, suggesting a failure of water to restore or maintain PV. In contrast, ORS administration resulted in a small increase in plasma [Na+] (1–2mmol.L−1) and [Cl−] (2-3mmol.L−1) with a corresponding decrease in plasma TP. By 120min post ORS, plasma TP and PV were no longer significantly different from rest or pre-exercise (P>0.05), whilst with water, TP was elevated (∼3–4g.L−1) and PV reduced (∼4–5mL.kg−1). Total urine output was not significantly different between water (1096±135mL) and ORS (750±215mL, P>0.05). Estimates of expected plasma volume and electrolyte concentration changes as a result of either treatment compared well with measured changes of TP and PV. On the basis of calculated or measured changes, it was estimated that only 1 L of water contributed to rehydration following exercise compared to 4 L isotonic, plasma-like ORS. The administration of 6 L ORS restored the PV deficit induced by exercise with minimal or no disturbance of plasma electrolyte concentrations. In contrast, water alone resulted in minimal improvement in PV. When fluid intake after periods of fluid loss, such as induced by exercise or transport, is not accompanied by food intake, the present study has clearly demonstrated that water alone is ineffective in promoting rehydration compared with an isotonic, plasma-like ORS.

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Thermal and circulatory responses during exercise: effects of hypohydration, dehydration, and water intake.

This investigation examined the distinct and interactive effects of initial hydration state, exercise-induced dehydration, and water rehydration in a hot environment. On four occasions, 10 men performed a 90-min heat stress test (treadmill walking at 5.6 km/h, 5% grade, 33 degrees C, 56% relative humidity). These heat stress tests differed in pretest hydration [2 euhydrated (EU) and 2 hypohydrated (HY) trials] and water intake during exercise [2 water ad libitum (W) and 2 no water (NW) trials]. HY+NW indicated greater physiological strain than all other trials (P < 0.05-0.001) in heart rate, plasma osmolality (Posm), sweat sensitivity (g/degrees C.min), and rectal temperature. Unexpectedly, final HY+W and EU+W responses for rectal temperature, heart rate, and Posm were similar, despite the initial 3.9 +/- 0.2% hypohydration in HY+W. We concluded that differences in pretest Posm (295 +/- 7 and 287 +/- 5 mosmol/kg for HY+W and EU+W, respectively) resulted in greater water consumption (1.65 and 0.31 liter for HY+W and EU+W, respectively), no voluntary dehydration (0.9% body mass increase), and attenuated thermal and circulatory strain during HY+W.

Intravenous vs. oral rehydration: effects on subsequent exercise-heat stress.

This study compared the influence of intravenous vs. oral rehydration after exercise-induced dehydration during a subsequent 90-min exercise bout. It was hypothesized that cardiovascular, thermoregulatory, and hormonal variables would be the same between intravenous and oral rehydration because of similar restoration of plasma volume (PV) and osmolality (Osmo). Eight non-heat-acclimated men received three experimental treatments (counterbalanced design) immediately after exercise-induced dehydration (33 degrees C) to -4% body weight loss. Treatments were intravenous 0.45% NaCl (iv; 25 ml/kg), no fluid (NF), and oral saline (Oral; 25 ml/kg). After rehydration and rest (2 h total), subjects walked at 50% maximal O2 consumption for up to 90 min at 36 degrees C. The following observations were made: 1) heart rate was higher (P < 0.05) in Oral vs. iv at minutes 45, 60, and 75 of exercise; 2) rectal temperature, sweat rate, percent change in PV, and change in plasma Osmo were similar between iv and Oral; 3) change in plasma norepinephrine decreased less (P < 0.05) in Oral compared with iv at minute 45; 4) changes in plasma adrenocorticotropic hormone and cortisol were similar between iv and Oral after exercise was initiated; and 5) exercise time was similar between iv (77.4 +/- 5.4 min) and Oral (84.2 +/- 2.3 min). These data suggest that after exercise-induced dehydration, iv and Oral were equally effective as rehydration treatments. Thermoregulation, change in adrenocorticotropic hormone, and change in cortisol were not different between iv and Oral after exercise began; this is likely due to similar percent change in PV and change in Osmo.

Restoration of fluid balance after exercise-induced dehydration: effects of food and fluid intake.

This study investigated the effects of post-exercise rehydration with fluid alone or with a meal plus fluid. Eight healthy volunteers (five men, three women) were dehydrated by a mean of 2.1 (SEM 0.0)% of body mass by intermittent cycle exercise in a warm [34 (SEM 0) degrees C], humid [55 (SEM 1)% relative humidity] environment. Over 60 min beginning 30 min after exercise, the subjects ingested a commercially-available sports drink (21 mmol.l-1 Na+, 3.4 mmol.l-1 K+, 12 mmol.l-1 Cl-) on trials A and B: on trial C a standard meal [63 kJ.kg-1 body mass (53% CHO, 28% fat, 19% protein; 0.118 mmol.kJ-1 Na+, 0.061 mmol.kJ-1 K+)] plus drink (1 mmol.l-1 Na+, 0.4 mmol.l-1 K+, 1 mmol.l-1 Cl-) were consumed. Water intake (in millilitres) was 150% of the mass loss (in grams). The trials took place after an overnight fast and were separated by 7 days. Blood and urine samples were collected at intervals throughout the study. Blood was analysed for haematocrit, haemoglobin concentration, serum osmolality, Na+, K+ and Cl- concentrations and plasma angiotensin II concentration. Urine volume, osmolality and electrolyte concentrations were measured. Dehydration resulted in a mean 5.2 (SEM 1.3)% reduction in plasma volume. With the exception of serum osmolality, which was higher on trial B than A at the end of the rehydration period, no differences were recorded for any of the measured parameters between trials A and B. Cumulative urine output following rehydration was lower (P < 0.01) on trial C [median 665 (range 396-1190)ml] than on trial B [median 934 (range 550-1403)ml] which was not different (P = 0.44) from trial A [median 954 (range 474-1501)ml]. Less urine was produced over the 1-h period ending 2 h after rehydration on trial C than on B (P = 0.01). On trials A and B the subjects were in net negative fluid balance by 337 (range 779-minus 306) ml and 373 (range 680-minus 173)ml, respectively (P < 0.01): on trial C the subjects were no different from their initial euhydrated state [median minus 29 (range minus 421-137)ml] 6 h after the end of rehydration (P = 1.00). A larger fraction of total water intake was retained when the standard meal plus drink was consumed. This may have been due to the larger quantities of Na+ and K+ ingested with the meal [mean 63 (SEM 4) mmol Na+, 21.3 (SEM 1.3)mmol K+] than with the drink [mean 42(SEM 2)mmol Na+, 6.8 (SEM 0.4)mmol K+]. There was no difference between trials B and C in any of the measured blood parameters, but urinary Na+ and K+ excretion were both higher on trial C and B. These results suggest that post-exercise fluid replacement can be achieved by ingestion of water if consumed in sufficient volume together with a meal providing significant amounts of electrolytes.