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)     

The influence of the initial state of hydration on endocrine responses to exercise in the heat

This study examines the effect of the initial state of hydration on hormone responses to prolonged exercise in the heat. Five subjects at two initial hydration levels (hypohydrated and hyperhydrated) were exposed to a 36 degrees C environment for 3 h of intermittent exercise. During exercise, the subjects were either fluid-deprived, or rehydrated with water or an isotonic electrolyte sucrose solution (ISO). Both the stress hormones, adrenocorticotropic hormone and cortisol, and the main fluid regulatory hormones, aldosterone, renin activity (PRA) and arginine vasopressin (AVP), were measured in blood samples taken every hour. Prior hyperhydration significantly reduced initial AVP, aldosterone and PRA levels. However, except for AVP, which responded to exercise significantly less in previously hyperhydrated subjects (p less than 0.05), the initial hydration state did not influence the subsequent vascular and hormonal responses when the subjects were fluid-deprived while exercising. Concurrent rehydration, either with water or with ISO, reduced or even abolished the hormonal responses. There were no significant differences according to the initial hydration state, except for PRA responses, which were significantly lower (p less than 0.01) in previously hyperhydrated subjects who also received water during exercise. These results indicate that prior hydration levels influence only slightly the hormonal responses to prolonged exercise in the heat. Progressive rehydration during exercise, especially when extra electrolytes are given, is more efficient in maintaining plasma volume and osmolarity and in reducing the hormonal responses.     

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.     

Influence of body temperature on the development of fatigue during prolonged exercise in the heat.

We investigated whether fatigue during prolonged exercise in uncompensable hot environments occurred at the same critical level of hyperthermia when the initial value and the rate of increase in body temperature are altered. To examine the effect of initial body temperature [esophageal temperature (Tes) = 35.9 +/- 0.2, 37.4 +/- 0. 1, or 38.2 +/- 0.1 (SE) degrees C induced by 30 min of water immersion], seven cyclists (maximal O2 uptake = 5.1 +/- 0.1 l/min) performed three randomly assigned bouts of cycle ergometer exercise (60% maximal O2 uptake) in the heat (40 degrees C) until volitional exhaustion. To determine the influence of rate of heat storage (0.10 vs. 0.05 degrees C/min induced by a water-perfused jacket), four cyclists performed two additional exercise bouts, starting with Tes of 37.0 degrees C. Despite different initial temperatures, all subjects fatigued at an identical level of hyperthermia (Tes = 40. 1-40.2 degrees C, muscle temperature = 40.7-40.9 degrees C, skin temperature = 37.0-37.2 degrees C) and cardiovascular strain (heart rate = 196-198 beats/min, cardiac output = 19.9-20.8 l/min). Time to exhaustion was inversely related to the initial body temperature: 63 +/- 3, 46 +/- 3, and 28 +/- 2 min with initial Tes of approximately 36, 37, and 38 degrees C, respectively (all P < 0.05). Similarly, with different rates of heat storage, all subjects reached exhaustion at similar Tes and muscle temperature (40.1-40.3 and 40. 7-40.9 degrees C, respectively), but with significantly different skin temperature (38.4 +/- 0.4 vs. 35.6 +/- 0.2 degrees C during high vs. low rate of heat storage, respectively, P < 0.05). Time to exhaustion was significantly shorter at the high than at the lower rate of heat storage (31 +/- 4 vs. 56 +/- 11 min, respectively, P < 0.05). Increases in heart rate and reductions in stroke volume paralleled the rise in core temperature (36-40 degrees C), with skin blood flow plateauing at Tes of approximately 38 degrees C. These results demonstrate that high internal body temperature per se causes fatigue in trained subjects during prolonged exercise in uncompensable hot environments. Furthermore, time to exhaustion in hot environments is inversely related to the initial temperature and directly related to the rate of heat storage.     

Pre-exercise hyperhydration delays dehydration and improves endurance capacity during 2 h of cycling in a temperate climate

Whether the use of pre-exercise hyperhydration could improve the performance of athletes who do not hydrate sufficiently during prolonged exercise is still unknown. We therefore compared the effects of pre-exercise hyperhydration and pre-exercise euhydration on endurance capacity, peak power output and selected components of the cardiovascular and thermoregulatory systems during prolonged cycling. Using a randomized, crossover experimental design, 6 endurance-trained subjects underwent a pre-exercise hyperhydration (26 ml of water x kg body mass(-1) with 1.2 g glycerol x kg body mass(-1)) or pre-exercise euhydration period of 80 min, followed by 2 h of cycling at 65% maximal oxygen consumption (VO(.)2max) (26-27 degrees C) that were interspersed by 5, 2-min intervals performed at 80% V(.)O2max. Following the 2 h cycling exercise, subjects underwent an incremental cycling test to exhaustion. Pre-exercise hyperhydration increased body water by 16.1+/-2.2 ml.kg body mass(-1). During exercise, subjects received 12.5 ml of sports drink x kg body mass(-1). With pre-exercise hyperhydration and pre-exercise euhydration, respectively, fluid ingestion during exercise replaced 31.0+/-2.9% and 37.1+/-6.8% of sweat losses (p>0.05). Body mass loss at the end of exercise reached 1.7+/-0.3% with pre-exercise hyperhydration and 3.3+/-0.4% with pre-exercise euhydration (p<0.05). During the 2 h of cycling, pre-exercise hyperhydration significantly decreased heart rate and perceived thirst, but rectal temperature, sweat rate, perceived exertion and perceived heat-stress did not differ between conditions. Pre-exercise hyperhydration significantly increased time to exhaustion and peak power output, compared with pre-exercise euhydration. We conclude that pre-exercise hyperhydration improves endurance capacity and peak power output and decreases heart rate and thirst sensation, but does not reduce rectal temperature during 2 h of moderate to intense cycling in a moderate environment when fluid consumption is 33% of sweat losses.     

Water temperature and intensity of exercise in maintenance of thermal equilibrium

This study examined the thermal and metabolic responses of six men during exercise in water at critical temperature (Tcw, 31.2 +/- 0.5 degrees C), below Tcw (BTcw, 28.8 +/- 0.6 degrees C), at thermoneutrality (Ttn, 34 degrees C), and above Ttn (ATtn, 36 degrees C). At each water temperature (Tw) male volunteers wearing only swimming trunks completed four 1-h experiments while immersed up to the neck. During one experiment, subjects remained at rest (R), and the other three performed leg exercise (LE) at three different intensities (LE-1, 2 MET; LE-2, 3 MET; LE-3, 4 MET). In water warmer than Tcw, there was no difference in metabolic rate (M) during R. The M for each work load was independent of Tw. Esophageal temperature (Tes) remained unchanged during R in water of ATtn (36 degrees C). However, Tes significantly (P less than 0.05) declined over 1 h during R at Ttn (delta Tes = -0.39 degrees C), Tcw (delta Tes = -0.54 degrees C), and BTcw (delta Tes = -0.61 degrees C). All levels of underwater exercise elevated Tes and M compared with R at all Tw. In water colder than Tcw, the ratio of heat loss from limbs compared with the trunk became greater as LE intensity increased, indicating a preferential increase in heat loss from the limbs in cool water. Tissue insulation (Itissue) was lower during LE than at R and was inversely proportional to the increase in LE intensity. A linearly inverse relationship was established between Tw and M in maintaining thermal equilibrium.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thermoregulation in hyperhydrated men during physical exercise

The influence of hyperhydration on thermoregulatory function was tested in 8 male volunteers. The subjects performed cycle exercise in the upright position at 52% Vo2max for 45 min in a thermoneutral (Ta = 23 degrees C) environment. The day after the control exercise the subjects were hyperhydrated with tap water (35 ml X kg-1 of body weight) and then performed the same physical exercise as before. Total body weight loss was lower after hyperhydration (329 +/- 85 g) than during the control exercise (442 +/- 132 g), p less than 0.05. The decrease in weight loss after hyperhydration was probably due to a decrease in dripped sweat (58 +/- 64 and 157 +/- 101 g, p less than 0.05). With hyperhydration delay in onset of sweating was reduced from 5.8 +/- 3.2 to 3.7 +/- 2.0 min (p less than 0.05), and rectal temperature increased less (0.80 +/- 0.20 and 0.60 +/- 0.10 degrees C, p less than 0.01). The efficiency of sweating was higher in hyperhydrated (81.4%) than in euhydrated subjects (57.1%), p less than 0.01. It is concluded that hyperhydration influences thermoregulatory function in exercising men by shortening the delay in onset of sweating and by decreasing the quantity of dripped sweat. As a result, the increases in body temperature in hyperhydrated exercising men are lower than in normally hydrated individuals.     

Thermoregulation during cold exposure: effects of prior exercise.

This study examined whether acute exercise would impair the body's capability to maintain thermal balance during a subsequent cold exposure. Ten men rested for 2 h during a standardized cold-air test (4.6 degrees C) after two treatments: 1) 60 min of cycle exercise (Ex) at 55% peak O(2) uptake and 2) passive heating (Heat). Ex was performed during a 35 degrees C water immersion (WI), and Heat was conducted during a 38.2 degrees C WI. The duration of Heat was individually adjusted (mean = 53 min) so that rectal temperature was similar at the end of WI in both Ex (38.2 degrees C) and Heat (38.1 degrees C). During the cold-air test after Ex, relative to Heat 1) rectal temperature was lower (P < 0.05) from minutes 40-120, 2) mean weighted heat flow was higher (P < 0.05), 3) insulation was lower (P < 0.05), and 4) metabolic heat production was not different. These results suggest that prior physical exercise may predispose a person to greater heat loss and to experience a larger decline in core temperature when subsequently exposed to cold air. The combination of exercise intensity and duration studied in these experiments did not fatigue the shivering response to cold exposure.     

Glycerol hyperhydration: physiological responses during cold-air exposure.

Hypohydration occurs during cold-air exposure (CAE) through combined effects of reduced fluid intake and increased fluid losses. Because hypohydration is associated with reduced physical performance, strategies for maintaining hydration during CAE are important. Glycerol ingestion (GI) can induce hyperhydration in hot and temperate environments, resulting in greater fluid retention compared with water (WI) alone, but it is not effective during cold-water immersion. Water immersion induces a greater natriuresis and diuresis than cold exposure; therefore, whether GI might be effective for hyperhydration during CAE remains unknown. This study examined physiological responses, i.e., thermoregulatory, cardiovascular, renal, vascular fluid, and fluid-regulating hormonal responses, to GI in seven men during 4 h CAE (15 degrees C, 30% relative humidity). Subjects completed three separate, double-blind, and counterbalanced trials including WI (37 ml water/l total body water), GI (37 ml water/l total body water plus 1.5 g glycerol/l total body water), and no fluid. Fluids were ingested 30 min before CAE. Thermoregulatory responses to cold were similar during each trial. Urine flow rates were higher (P = 0.0001) with WI (peak 11.8 ml/min, SD 1.9) than GI (5.0 ml/min, SD 1.8), and fluid retention was greater (P = 0.0001) with GI (34%, SD 7) than WI (18%, SD 5) at the end of CAE. Differences in urine flow rate and fluid retention were the result of a greater free water clearance with WI. These data indicate glycerol can be an effective hyperhydrating agent during CAE.     

Nutritional needs for exercise in the heat

Although hot conditions are not typically conducive to optimal sports performance, nutritional strategies play an important role in assisting an athlete to perform as well as possible in a hot environment. A key issue is the prevention of hypohydration during an exercise session. Fluid intake strategies should be undertaken in a cyclical sequence: hydrate well prior to the workout, drink as much as is comfortable and practical during the session, and rehydrate aggressively afterwards in preparation for future exercise bouts. There is some interest in hyperhydration strategies, such as hyperhydration with glycerol, to prepare the athlete for a situation where there is little opportunity for fluid intake to match large sweat losses. Recovery of significant fluid losses after exercise is assisted by the simultaneous replacement of electrolyte losses. Carbohydrate (CHO) requirements for exercise are increased in the heat, due to a shift in substrate utilization towards CHO oxidation. Daily food patterns should focus on replacing glycogen stores after exercise, and competition strategies should include activities to enhance CHO availability, such as CHO loading for endurance events, pre-event CHO intake, and intake of sports drinks in events lasting longer than 60 min. Although CHO ingestion may not enhance the performance of all events undertaken in hot weather, there are no disadvantages to the consumption of beverages containing 4-8% CHO and electrolytes. In fact, the palatability of these drinks may enhance the voluntary intake of fluid. Although there is some evidence of increased protein catabolism and cellular damage due to production of oxygen radicals during exercise in the heat, there is insufficient evidence to make specific dietary recommendations to account for these issues.     

Effect of carbohydrate ingestion on glucose kinetics during exercise in the heat.

Six endurance-trained men [peak oxygen uptake (V(O(2))) = 4.58 +/- 0.50 (SE) l/min] completed 60 min of exercise at a workload requiring 68 +/- 2% peak V(O(2)) in an environmental chamber maintained at 35 degrees C (<50% relative humidity) on two occasions, separated by at least 1 wk. Subjects ingested either a 6% glucose solution containing 1 microCi [3-(3)H]glucose/g glucose (CHO trial) or a sweet placebo (Con trial) during the trials. Rates of hepatic glucose production [HGP = glucose rate of appearance (R(a)) in Con trial] and glucose disappearance (R(d)), were measured using a primed, continuous infusion of [6,6-(2)H]glucose, corrected for gut-derived glucose (gut R(a)) in the CHO trial. No differences in heart rate, V(O(2)), respiratory exchange ratio, or rectal temperature were observed between trials. Plasma glucose concentrations were similar at rest but increased (P < 0.05) to a greater extent in the CHO trial compared with the Con trial. This was due to the absorption of ingested glucose in the CHO trial, because gut R(a) after 30 and 50 min (16 +/- 5 micromol. kg(-1). min(-1)) was higher (P < 0.05) compared with rest, whereas HGP during exercise was not different between trials. Glucose R(d) was higher (P < 0.05) in the CHO trial after 30 and 50 min (48.0 +/- 6.3 vs 34.6 +/- 3.8 micromol. kg(-1). min(-1), CHO vs. Con, respectively). These results indicate that ingestion of carbohydrate, at a rate of approximately 1.0 g/min, increases glucose R(d) but does not blunt the rise in HGP during exercise in the heat.     

Stroke volume during exercise: interaction of environment and hydration

Euhydrated and dehydrated subjects exercised in a hot and a cold environment with our aim to identify factors that relate to reductions in stroke volume (SV). We hypothesized that reductions in SV with heat stress are related to the interaction of several factors rather than the effect of elevated skin blood flow. Eight male endurance-trained cyclists [maximal O(2) consumption (VO(2 max)) 4.5 +/- 0.1 l/min; means +/- SE] cycled for 30 min (72% VO(2 max)) in the heat (H; 35 degrees C) or the cold (C; 8 degrees C) when euhydrated or dehydrated by 1.5, 3.0, or 4.2% of their body weight. When euhydrated, SV and esophageal temperature (T(es) 38. 2-38.3 degrees C) were similar in H and C, whereas skin blood flow was much higher in H vs. C (365 +/- 64% higher; P < 0.05). With each 1% body weight loss, SV declined 6.4 +/- 1.3 ml (4.8%) in H and 3.4 +/- 0.4 ml (2.5%) in C, whereas T(es) increased 0.21 +/- 0.02 and 0. 10 +/- 0.02 degrees C in H and C, respectively (P < 0.05). However, reductions in SV were not associated with increases in skin blood flow. The reduced SV was highly associated with increased heart rate and reduced blood volume in both H (R = 0.96; P < 0.01) and C (R = 0. 85; P < 0.01). In conclusion, these results suggest that SV is maintained in trained subjects during exercise in euhydrated conditions despite large differences in skin blood flow. Furthermore, the lowering of SV with dehydration appears largely related to increases in heart rate and reductions in blood volume.     

Exogenous carbohydrate oxidation rates are elevated after combined ingestion of glucose and fructose during exercise in the heat.

The first purpose of this study was to investigate whether a glucose (GLU)+fructose (FRUC) beverage would result in a higher exogenous carbohydrate (CHO) oxidation rate and a higher fluid availability during exercise in the heat compared with an isoenergetic GLU beverage. A second aim of the study was to examine whether ingestion of GLU at a rate of 1.5 g/min during exercise in the heat would lead to a reduced muscle glycogen oxidation rate compared with ingestion of water (WAT). Eight trained male cyclists (maximal oxygen uptake: 64+/-1 ml.kg-1.min-1) cycled on three different occasions for 120 min at 50% maximum power output at an ambient temperature of 31.9+/-0.1 degrees C. Subjects received, in random order, a solution providing either 1.5 g/min of GLU, 1.0 g/min of GLU+0.5 g/min of FRUC, or WAT. Exogenous CHO oxidation during the last hour of exercise was approximately 36% higher (P<0.05) in GLU+FRUC compared with GLU, and peak oxidation rates were 1.14+/-0.05 and 0.77+/-0.08 g/min, respectively. Endogenous CHO oxidation was significantly lower (P<0.05) in GLU+FRUC compared with WAT. Muscle glycogen oxidation was not different after ingestion of GLU or WAT. Plasma deuterium enrichments were significantly higher (P<0.05) in WAT and GLU+FRUC compared with GLU. Furthermore, at 60 and 75 min of exercise, plasma deuterium enrichments were higher (P<0.05) in WAT compared with GLU+FRUC. Ingestion of GLU+FRUC during exercise in the heat resulted in higher exogenous CHO oxidation rates and fluid availability compared with ingestion of GLU and reduced endogenous CHO oxidation compared with ingestion of WAT.     

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.     

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

This study examined the effects ofhyperhydration, exercise-induced dehydration, and oral fluidreplacement on physiological strain of horses during exercise-heatstress. On three occasions, six horses completed a 90-min exerciseprotocol (50% maximal O₂ uptake,34.5°C, 48% relative humidity) divided into two 45-min periods(exercise I andexercise II) with a 15-min recoverybetween exercise bouts. In random order, horses receivedno fluid (NF), 10 liters of water (W), or a carbohydrate-electrolytesolution (CE) 2 h before exercise and between exercise bouts. Compared with NF, preexercise hyperhydration (W and CE) did not alter heart rate, cardiac output (), stroke volume (SV), corebody temperature, sweating rate (SR), or sweating sensitivity duringexercise I. In contrast, afterexercise II, exercise-induceddehydration 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 ~1.0°C higher compared with W and CE.In exercise II, the greater thermalstrain in NF was associated with significant(P < 0.05) decreases in (10 ± 2%), SV (9 ± 3%), SR, and sweatingsensitivity. We concluded that 1)preexercise hyperhydration provided no thermoregulatory advantage;2) maintenance of euhydration byoral fluid replacement (~85% of sweat fluid loss) during exercise inthe heat was reflected in higher , SV, and SR withdecreased heat storage; and 3) W oran isotonic CE solution was equally effective in reducing physiological strain associated with exercise-induced dehydration and heat stress.

     

Effect of carbohydrate ingestion and ambient temperature on muscle fatigue development in endurance-trained male cyclists.

The aim of the present study was to determine the effect of carbohydrate (CHO; sucrose) ingestion and environmental heat on the development of fatigue and the distribution of power output during a 16.1-km cycling time trial. Ten male cyclists (Vo(2max) = 61.7 +/- 5.0 ml.kg(-1).min(-1), mean +/- SD) performed four 90-min constant-pace cycling trials at 80% of second ventilatory threshold (220 +/- 12 W). Trials were conducted in temperate (18.1 +/- 0.4 degrees C) or hot (32.2 +/- 0.7 degrees C) conditions during which subjects ingested either CHO (0.96 g.kg(-1).h(-1)) or placebo (PLA) gels. All trials were followed by a 16.1-km time trial. Before and immediately after exercise, percent muscle activation was determined using superimposed electrical stimulation. Power output, integrated electromyography (iEMG) of vastus lateralis, rectal temperature, and skin temperature were recorded throughout the trial. Percent muscle activation significantly declined during the CHO and PLA trials in hot (6.0 and 6.9%, respectively) but not temperate conditions (1.9 and 2.2%, respectively). The decline in power output during the first 6 km was significantly greater during exercise in the heat. iEMG correlated significantly with power output during the CHO trials in hot and temperate conditions (r = 0.93 and 0.73; P < 0.05) but not during either PLA trial. In conclusion, cyclists tended to self-select an aggressive pacing strategy (initial high intensity) in the heat.     

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.     

Crystalline beta-cyclodextrin.12H2O reversibly dehydrates to beta-cyclodextrin.10.5 H2O under ambient conditions.

In contact with mother liquor, crystalline beta-cyclodextrin (beta-CD) hydrate has composition approximately beta-CD.12H2O. If crystals are dried at ambient conditions (18 degrees C, approximately 50% humidity), the unit cell volume diminishes approximately 30 to 50 A3. X-ray structure analysis of a dry crystal (0.89 A resolution, 4617 data, R = 0.059) showed the composition beta-CD.10.5 H2O, with approximately 5.5 water molecules in the beta-CD cavity (7 partially and 2 fully occupied sites) and approximately 5.0 between the beta-CD molecules. The positions of the beta-CD host and of most of the hydration waters are conserved during dehydration, but the occupancies of the waters in the beta-CD cavity diminish. Dry crystals put into solvent re-hydrate to the original form. The mechanism of de- and re-hydration is not evident.     

Hypohydration adversely affects lactate threshold in endurance athletes

The purpose of this investigation was to observe the effect of hypohydration (-4% body mass) on lactate threshold (LAT) in 14 collegiate athletes (8 men and 6 women; age, 20.9 +/- 0.5 years; height, 171.1 +/- 2.4 cm; weight, 64.8 +/- 2.3 kg; V(O)2 max, 62.8 +/- 1.9 ml x kg(-1) x min(-1); percentage of fat, 11.4 +/- 1.5%). Subjects performed 2 randomized, discontinuous treadmill bouts at a dry bulb temperature (T(db)) of 22 degrees C to volitional exhaustion in 2 states of hydration, euhydrated and hypohydrated. The hypohydrated condition was achieved in a thermally neutral environment (T(db), 22 degrees C; humidity, 45%), with exercise conducted at a moderate intensity as defined by rating of perceived exertion (RPE, approximately 12) 12-16 hours before testing. On average, subjects decreased 3.9% of their body mass before the hypohydration test. Blood lactate, hematocrit, V(O)2, minute ventilation (VE), R value, heart rate (HR), and RPE were measured during each 4-minute stage of testing. In the hypohydrated condition, LAT occurred significantly earlier during exercise and at a lower absolute V(O)2, VE, respiratory exchange ratio, RPE, and blood lactate concentration. Also, the blood lactate concentration was significantly lower in the hypohydrated condition (6.7 +/- 0.8 mmol) compared with the euhydrated condition (10.2 +/- 0.9 mmol) at peak exercise. There were no differences in HR or percentage of maximum HR at LAT nor did plots of V(CO2):V(O)2 reveal differences in bicarbonate buffering during exercise between the 2 conditions. From these results, we speculate that hypohydration did not significantly alter cardiovascular function or buffering capacity but did cause LAT to occur at a lower absolute exercise intensity.     

Effects of exercise detraining and deacclimation to the heat on plasma volume dynamics

The effects of the discontinuation (DET) of an endurance training/heat acclimation (T/A) program on vascular volumes were studied in 16 adult males. Resting and exercise blood volume dynamics were examined prior to and during an exercise task performed after completion of T/A (CT1) and again at the end of DET (CT2). T/A consisted of cycling at 60% of peak VO2 for 90 min per day, 6 days per week, for 4 weeks. Ambient temperature was 20 degrees C for the first 3 weeks and 40 degrees C for the last week (rh = 30-35%). Subjects were randomly assigned to one of the following DET conditions: 1) cycling one day per week at 40 degrees C, 2) cycling one day per week at 20 degrees C, 3) resting one day per week at 40 degrees C, 4) control. The exercise tasks consisted of 60 min of continuous cycle ergometer exercise at 50% of peak VO2 (Ta = 30 degrees C, rh = 35%). Although significant differences were found between CT1 and CT2, there were no interactions between the various DET conditions. Resting red cell volume decreased 98 ml and plasma volume decreased 248 ml following DET. A reduction in plasma protein content accounted for 97% of the decrease in plasma volume. Hemoconcentration occurred during exercise in both CT1 and CT2, while there were slight increases in plasma [Na+] and [Cl-] and a rapid rise in [K+]. It appears that a single exercise and/or heat exposure per week was not different from complete cessation of endurance exercise in the heat with regard to maintenance of the various vascular volumes.