Dehydration is associated with a decrement in endurance performance (6,13,23,27,33,39) which has been linked to reductions in plasma volume and an increased plasma osmolality. The physiological consequences of dehydration are thought to lead to a reduction in cardiac output which in turn can alter V̇O2max and reduce the ability to regulate core body temperature. Additionally, alterations in muscle metabolism (glycogen utilization and lactate production) have also been reported during prolonged submaximal exercise (14) and high-intense short-term exercise (6) without fluid ingestion. However, a recent study by Mountain et al. (27) found that moderate hypohydration (4% body weight) which elicited a reduction in muscle endurance was not associated with changes in H+ or Pi levels. Differences between studies may reflect experimental conditions (level of dehydration, type and duration of exercise, thermal environment, etc.). Thus, it is of interest to know to what extent dehydration can influence muscle metabolism as well as the possible mechanisms regulating this response.
While V̇O2max has been considered a strong indicator of endurance performance, short to medium distances lasting from 5 to 10 min rely heavily on both endurance capabilities and anaerobic sprints. The lactate threshold has been found to be a more reliable indicator for such events (1,4,26,42) as well as for short, high intensity events. However, few studies look at how dehydration affects lactate concentrations and the lactate threshold (10,40), and these studies found confounding results. England et al. (10) reported that the onset of blood lactate accumulation occurred at a lower V̇O2 during exercise while Webster et al. (40) found no change in the V̇O2 at which the lactate threshold occurred but did find a decrease in velocity at the lactate threshold. Neither of these studies measured any factors that could possibly elucidate a mechanism for the changes observed, however.
Physical stress induced by exercise and potentiated by dehydration stimulates increased secretion of catecholamines via the hypothalamic-adrenal neural pathways (13,15,25). It has been found that dehydration alone can cause an increase in catecholamine production (25,31,37). This increase is attributed to stimulation of the hypothalamus by osmoreceptors (29), atrial stretch receptors (17), and the temperature-regulating center of the brain (17). During an acute bout of exercise catecholamines enhance the rate of muscle glycogenolysis via β-adrenergic mechanisms resulting in an increase rate of lactate production (12,19,24,35,38,41). Elevated rates of muscle glycogen utilization lead to glycogen depletion and can contribute to fatigue. Thus, one possible mechanism whereby dehydration could alter muscle metabolism during exercise is via an exaggerated catecholamine response (14).
Past research has focused on dehydration and endurance exercise lasting longer then 60 min. However, as athletes use dehydration as a means for weight loss to compete in lower weight classes, events associated with these activities are generally of shorter duration and higher intensity. Thus, there is a need to examine influences of dehydration on this form of exercise. Athletes exercising under temperate conditions, as well as for short-term durations, are less likely to be concerned about water balance. However, even low levels of dehydration associated with such activities have been shown to have an adverse effect on performance (6).
The purpose of this study is to determine whether exercise-induced dehydration in women shifts the lactate threshold to a lower absolute V̇O2, to determine whether dehydration shifts the lactate threshold to a lower percent of V̇O2max, and to elucidate possible mechanisms that may cause the shift in the lactate threshold during dehydration. It was hypothesized that there would be shift in the lactate threshold to a lower intensity of exercise caused by dehydration and that this shift would relate to an increased production of catecholamines.
Seven healthy female subjects volunteered for the study. They were recruited from the University of Colorado at Boulder. The subjects were between the ages of 18–31 yr (23.6 ± 1.6 yr) and were considered to be in a moderate to high fitness range based on V̇O2max measurements. All were members of the University of Colorado rowing team and were active on a regular basis. The subjects supplied written informed consent and the study was approved by the Human Research Committee of the University of Colorado at Boulder.
Each subject performed two graded exercise tests (hydrated and dehydrated state) to maximal volition on an electronically braked cycle ergometer (Quinton, Bethell, WA) in the morning following an overnight fast. The night preceding each graded exercise test, the subjects were weighed in the clothes they would be wearing the next morning to determine baseline body weight and they were asked to sit in a chair for 5 min before blood samples were taken. Blood was then taken from a finger prick for determination of baseline hemoglobin (Hb) concentration and hematocrit (Hct). All subjects then performed 45 min of submaximal exercise that elicited a heart rate of 130–150 beats·min−1. For the hydrated trial, unlimited access to fluid was allowed, whereas for the dehydrated trial subjects exercised in a full sweat suit and were not allowed fluid intake until after the graded exercise test the following morning. Dehydration was considered obtained if the subject had lost at least 2% of her body weight. Subjects were instructed not to eat the following morning before the test.
On the morning of the graded exercise test (between 8 and 10 a.m.) the subjects were weighed in the same clothes they had been weighed in the night before to determine changes in body weight. The dehydrated subjects did not wear the sweat suits for the graded exercise tests. An indwelling catheter was placed in a forearm vein. After a 20-min resting period in the supine position, a baseline blood sample of 7 mL was drawn for later analysis. The subject was positioned on the bike and baseline measurements were recorded. The two graded exercise tests occurred within a 2-wk period during the same phase of the menstrual cycle for a given subject. The order of testing (trials) was randomized to ensure that no learning effect was introduced.
The graded exercise test began at 50 W with 25 W increments every 2 min. Heart rate, oxygen consumption (V̇O2), carbon dioxide production (V̇CO2), ventilation rate (V̇E), and respiratory quotient (R values) were monitored throughout the test and recorded during the last 30 s of each workload. Seven milliliters of blood were drawn during the last 30 s of each workload and were aliquoted as described below into prelabeled tubes for plasma catecholamine and lactate concentration determinations.
V̇O2, V̇O2max, V̇E, and R value determination.
Oxygen consumption (V̇O2) and carbon dioxide production (V̇CO2) were measured every 30 s using standard computer assisted, open circuit, indirect calorimetry system (Perkin-Elmer, 1100, Norwalk, CT). Gas volumes were calibrated using a 3-L volumeter (Calibringe, Vacumed, Ventura, CA) at four different volumes. V̇E was measured breath-by-breath analysis. V̇O2max was considered achieved when R-values exceeded 1.15 and there was a plateau in V̇O2 over two workloads.
Heart rate was monitored using a 5-lead ECG (Schiller, Tustin, CA). Heart rate was recorded at baseline and again during the last 30 s of each workload.
Hb and Hct determination.
Hct was measured in duplicate with a microHct centrifuge. Hb was measured in duplicate using a B-Hb photometer (HemoCue). The photometer was calibrated by the standardized Hbexyanide (HiCN) method to approximately 14 ± 0.3 g·dL−1. The calibration was checked daily using a control cuvette supplied by the manufacturer. Percent changes in blood volume (BV), red cell volume (CV), and plasma volume (PV) were calculated from the values of Hb and Hct using the equations as described by Dill and Costill (9).
Colloid osmotic pressure determination.
Plasma osmolality was calculated from a formula derived from the Landis-Pappenheimer cubic equation as described by Navar and Navar (28). π = 2.1C + 0.16C2 + 0.009C3 where π represents colloid osmotic pressure and C represents the plasma protein concentration. Plasma protein concentration was determined by the Bradford protein assay.
Lactate concentration and lactate threshold determination.
One milliliter of blood was used to determine plasma lactate concentrations via spectrophotometric method of Hohorst (16). Lactate threshold was determined using the log-log transformation described by Beaver et al. (2). The log (lactate concentration) was plotted against the log (V̇O2) at each workload. Using this method, two distinct phases of lactate concentration as a function of workload are observed. The intersection of the lines of best fit for the two phases is the lactate threshold point.
Catecholamine concentration determination.
Plasma catecholamine concentrations were determined by means of high performance liquid chromatography (HPLC, BioRad, model 1330, Hercules, CA) with electrochemical determination (BioRad, model 1340) as previously described (24). Four milliliters of blood were placed in a tube containing reduced glutathione to prevent the oxidation of the catecholamines. The samples were vortexed and the plasma was removed and frozen at −70°C. DHBA was used as an internal standard. To all samples and standards, 25 mg of acid washed alumina, 1 mL of Tris buffer (pH 8.6), and 25 μL of DHBA was added. The samples were then vortexed for 10 min, aspirated, washed with 3 mL of distilled H2O and vortexed for 5 min and aspirated. One hundred microliters of 0.1 M HClO4 was added to extract the catecholamines from the alumina. The acid extract was vortexed for 10 min. Each sample was injected into the HPLC column (Reverse phase, Bio Sil ODS-5S, BioRad) and eluted with an ion pair mobile phase. The chromatograph was analyzed by computer integration (Shimanzu C-R3A chromatopac, Lillehammer, Norway). Samples were compared with the known concentrations of norepinephrine and epinephrine standards.
Data are presented as means ± SE. Statistical differences for all physiological parameters, as well as epinephrine, norepinephrine, and lactate data between the hydration states at rest and at maximum were determined by using paired t-tests (P < 0.05). Single factor ANOVA was used to determine significant difference between hydrated and dehydrated trials across workloads. Pearson product correlations were used to determine the relationships between heart rate, R-values, and V̇O2 as well as relationships between lactate, norepinephrine, and epinephrine.
Body weights, plasma volume, and plasma osmolality.
Absolute weight loss from night to morning measurements averaged 0.8 ± 0.2 kg for the hydrated trial and 1.8 ± 0.2 kg for the dehydrated trial. The decrease in body weight for the dehydrated trial was significantly greater then seen in the hydrated trial (P = 0.0001). This represented a 1.5 ± 0.2% (range: 0.8%–2.2%) decrease in body weight for the dehydrated trial when compared with that for the hydrated trial. This 1.5% difference in body weight for the dehydrated trial was associated with a 3.5 ± 2.6% decrease in plasma volume when compared with that for the hydrated trial (P = 0.04). There was no significant difference measured in plasma osmolality between the hydrated trial (28.6 ± 0.8 ng·mL−1) and the dehydrated trial (29.5 ± 1.2 ng·mL−1).
There were no significant differences found at rest or at maximum effort between the hydrated trial and the dehydrated trial for V̇O2, V̇CO2, V̇E, or R-values (Table 1). Heart rate values at rest were significantly higher for the dehydrated trial (80.0 ± 3.2 beats·min−1; hydrated and 92.9 ± 2.6 beats·min−1; dehydrated, P = 0.03), but at maximum effort there no significant differences were found. The maximum workload obtained was significantly lower for the dehydrated (236 ± 9.2 W) when compared with that for the hydrated trial (250 ± 7.7 W).
Lactate concentrations and lactate threshold.
Blood lactate levels as a function of workload for the hydrated and dehydrated trials are presented in Figure 1. There was a significant shift of the lactate threshold to a lower percent of V̇O2max with dehydration (72.2 ± 1.1 and 65.5 ± 1.9% for hydrated and dehydrated trials, respectively;P = 0.03). Absolute V̇O2 at the lactate threshold was significantly lower in the dehydrated trial (31.5 ± 1.3 mL·kg−1·min−1 and 28.4 ± 1.7 mL·kg−1·min−1 for the hydrated and dehydrated trials, respectively;P = 0.006) as was the workload at the lactate threshold (146 ± 4.9 and 128 ± 6.5 W for hydrated and dehydrated trials, respectively;P = 0.02). Table 2). presents data for baseline and maximum values for blood lactate concentrations. There were no significant differences found at baseline or at maximal exercise for plasma lactate concentrations.
Catecholamine concentrations and thresholds.
Table 2 presents data for plasma norepinephrine and epinephrine concentrations at baseline and at maximum exercise for both the hydrated and dehydrated trials. There were no significant differences found at baseline or at maximal exercise for either plasma norepinephrine or plasma epinephrine concentrations. Plasma epinephrine concentrations were higher during the dehydrated trial at submaximal workloads with no differences between trials found at maximal workloads (Fig. 2). No significant differences were observed for norepinephrine at any workload between hydrated and dehydrated trials (Fig. 3). Norepinephrine and epinephrine thresholds are presented in Table 3 and followed a pattern similar to that found for the lactate threshold.
Lactate concentrations correlated highly with norepinephrine (r = 0.92, hydrated) and (r = 0.90, dehydrated) and epinephrine concentrations (r = 0.95, hydrated) and (r = 0.97, dehydrated).
Time to exhaustion for the graded exercise test was significantly lower for the dehydrated trial when compared with the hydrated trial (17.3 ± 0.3 and 16.3 ± 0.4 min for the hydrated and dehydrated trials, respectively, P = 0.02).
The major finding of the present study was that mild dehydration associated with a net 1.5 ± 0.2% drop in body weight and a 3.5 ± 2.6% decrease in plasma volume was sufficient to cause a shift in the lactate threshold to a lower percent of V̇O2max. Despite finding no differences in V̇O2max measured between trials, the workload and absolute V̇O2 at which the lactate threshold occurred were significantly lower for the dehydrated trial. A significant decrease in time to exhaustion for the dehydrated trial was also observed. Currently the few studies that have examined the influence of dehydration on high intensity, short-term exercise have yielded equivocal results (6,11,21,40).
Research has demonstrated that glycogen depletion before a graded-exercise test is one experimental manipulation known to cause a shift in the lactate threshold to an earlier workload (5,18,30). However, several lines of evidence suggest that glycogen depletion most likely did not contribute to the shift in the lactate threshold observed for the dehydrated trial in the present study. The exercise protocol the night before experimental testing was identical for both the hydrated and dehydrated trials. Additionally, studies employing glycogen depletion techniques consistently report a reduction in RER values as well as in lactate levels for a given workload (18,30). No differences in RER values or absolute lactate concentrations were found between the two experimental conditions in the present study, suggesting that muscle glycogen availability was sufficient. Finally, mild dehydration, as reported here, has been shown to have no effect on muscle glycogen levels (7).
It has been well documented that catecholamines regulate lactate production by increasing glycogenolysis and glycolysis in the muscle, consequently influencing the lactate threshold (8,22,24,30). The catecholamines bind to the β-adrenergic receptors initiating a series of cascading reactions which lead to the activation of phosphorylase a, the regulating enzyme for glycogenolysis. During muscular contraction, epinephrine is known to be the major regulator of glycogenolysis in muscle (12,32,35). As muscle glycogenolysis is elevated, the rate of lactate production is increased with its subsequent release into the circulation. Stainsby et al. (35) have provided direct evidence that infusions of epinephrine in the contracting gastrocnemius muscle produce increases in lactate output from that muscle. Studies employing β-blockade have shown a reduction in both the rate of muscle glycogen breakdown as well as lactate turnover during exercise in humans and animals (12,19). The present study found high correlations between blood lactate levels and epinephrine concentrations for both the hydrated (r = 0.95) and dehydrated (r = 0.97) trials. Additionally, a modest increase in plasma epinephrine levels were found during the dehydrated trial compared with that in the hydrated trial, and this may have contributed to the modest shift in the lactate threshold to an earlier workload. This is in agreement with Hargreaves et al. (14) who found that dehydration associated with 2 h of submaximal exercise resulted in a greater rate of muscle glycogen utilization compared with that in the rehydrated condition. It was concluded that elevations in circulating epinephrine levels contributed to the increase in muscle glycogenolysis which resulted in greater lactate production during dehydration.
A similar relationship between epinephrine and the lactate threshold has been observed in previous investigations (8,22,24). Langfort et al. (18) looked at the effects of prolonged elevation of epinephrine on performance and the lactate threshold. They found that when epinephrine was elevated for 6–12 h there was a decrease in performance time, an increase in blood lactate, and a shift of the lactate threshold to a lower exercise intensity. Mazzeo et al. (24) found high correlations with lactate responses similar to results found in this study. These investigators (24) also reported that the inflection point for epinephrine during a graded exercise test occurred simultaneously with that found for the lactate threshold. Using training specificity to manipulate the lactate threshold, they concluded that the lactate threshold could be shifted as a function of changes in epinephrine levels during graded exercise. Results from the present investigation are consistent with this hypothesis.
Low levels of dehydration witnessed in this study did not augment the increase in norepinephrine response to exercise. In investigations by Melin et al. (25) and Powers et al.(31) it was found that norepinephrine was elevated by dehydration. In both of those studies, however, there was a combination of dehydration and exercise in the heat that elicited the increased concentration of norepinephrine. In contrast, Turlejski et al. (37) found that dehydration alone caused an increase in epinephrine concentration and that during 1 h of running both epinephrine and norepinephrine were elevated. No studies have looked at the effects of dehydration and catecholamines during short intense exercise.
Previously England et al. (10) reported that the lactate threshold occurred at a lower V̇O2 (as in the present study) but that the blood lactate concentrations were significantly greater with dehydration (unlike the present study where lactate levels are similar). It was suggested that the increase in blood lactate concentrations found in their study could have resulted from a decreased muscle blood flow in favor of increased skin blood flow. England et al. (10) reported finding a significant decline in plasma volume of 5.8 ± 0.5% for the dehydrated group corresponding to a 5.0 ± 0.05% decrease in body weight as compared with that for the hydrated group. The extent of dehydration was significantly greater than that elicited in the present investigation which may account for their elevation in blood lactate. Further, their method for inducing dehydration was different; they used sauna-induced dehydration techniques and achieved dehydration on the day of the exercise test. According to Caldwell et al. (7) the method used to induce dehydration may influence the results seen in the changes in plasma volume and plasma osmolality. These authors found that dehydration through exercise alone resulted in a drop in weight without a decrease in plasma volume, but dehydration associated with sauna resulted in a drop in body weight as well as a decrease in plasma volume.
Finally, Webster et al. (40) found that running velocity at lactate threshold was significantly reduced as was peak blood lactate concentrations with dehydration. Our finding that both the workload and V̇O2 associated with the lactate threshold were reduced with dehydration is consistent with their findings.
We observed that dehydration was associated with a decrease in performance time to exhaustion. Others have reported a reduction in muscle endurance and overall performance with moderate dehydration during shot-term exercise (6,27,36,40). The exact mechanisms responsible for this observation are unknown and beyond the scope of the present study. However, as described above, differences in muscle glycogen content are not likely to have been a factor. Further, alterations in V̇O2max were not a contributing factor as values were similar between the two trials. This was an expected finding since it is generally reported that more severe dehydration (5% or greater reduction in body weight) than induced in the present study is necessary to elicit reductions in V̇O2max, cardiac output, and stroke volume (3,7,20). It is possible that the earlier inflection of blood lactate during the dehydration trial was associated with a greater acid-base disturbance locally in the exercising muscle. The decrease in time to exhaustion was correlated with the lactate threshold for the dehydrated group. A decrease in muscle pH is known to contribute to fatigue during high intense, short-term exercise. However, the observation that peak lactate levels did not differ between groups casts some doubt on this hypothesis. Further, a recent study by Montain et al. (27), using whole body magnetic resonance spectroscopy, concluded that moderate hypohydration (4% body wt) which elicited a reduction in muscle endurance was not associated with changes in H+, pH, or Pi levels in skeletal muscles recruited. The exact mechanisms responsible for the decrease in performance time with dehydration during a graded exercise test remain to be determined. It should be noted, however, that others have observed similar responses to ours such that a decrease in time to exhaustion to a standardized maximal exercise load is found with dehydration even when no changes in V̇O2max are present (34).
In summary, a mild dehydration in the women of the present study was associated with a shift in the lactate threshold, which occurred at a lower percent of V̇O2max, as well as at a lower workload and absolute V̇O2. The high correlation between lactate and epinephrine concentrations suggests that the shift in the lactate threshold can in part be attributed to increases in epinephrine concentrations. This study did find that performance, defined as a decrease in time to exhaustion, was highly correlated with the lactate threshold for the dehydrated group and that there was a significant decrease in time to exhaustion. Mechanisms for this response remain to be determined.
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Keywords:©2000The American College of Sports Medicine
CATECHOLAMINES; EPINEPHRINE; NOREPINEPHRINE; PERFORMANCE; HYPOHYDRATION; FEMALES