MOQUIN, A. and ROBERT S. MAZZEO. Effect of mild dehydration on the lactate threshold in women. Med. Sci. Sports Exerc., Vol. 32, No. 2, pp. 396–402, 2000.
Purpose: The purpose of this investigation was to examine the effects of dehydration on the lactate threshold and performance time to exhaustion in women.
Methods: Seven moderately trained women (age = 23.6 ± 1.6 yr) performed two graded exercise tests on separate occasions, once in a normally hydrated state (HY) and once in a dehydrated state (DE). Dehydration was achieved by a 45-min submaximal exercise the evening before testing, followed by a 12-h period of fluid restriction. V̇O2, V̇CO2, V̇E, R-values, blood lactate, and catecholamine concentrations were measured at baseline and during each workload. Plasma volume and plasma osmolality were also determined. Body weight dropped significantly for the dehydrated trial (2.6 ± 0.7%).
Results: There was a corresponding decrease in plasma volume measured (3.5 ± 2.6%). The V̇O2max (3.1 ± 0.3 L·min−1 HY; 3.0 ± 0.1 L·min−1 DE) obtained was not significantly different between the hydration and dehydration trial. Plasma norepinephrine, epinephrine, and lactate concentrations were not significantly different at baseline or maximum intensity although epinephrine concentrations were higher for the dehydrated trial during submaximal workloads. Lactate concentrations were highly correlated with epinephrine (r = 0.95 HY; r = 0.97 DE). The lactate threshold occurred at a significantly lower relative percent of V̇O2max for the dehydrated trial (72.2 ± 1.1% HY; 65.5 ± 1.8% DE) as well as a lower absolute power output when compared with that in the hydrated trial. There was a significant decrease in time to exhaustion for the dehydrated trial (17.3 ± 0.7 min HY; 16.3+0.7 min DE). Time to exhaustion for the dehydrated trial was correlated with the % V̇O2max at which the lactate threshold occurred (r = 0.74).
Conclusions: These data indicate that low levels of dehydration induced a shift in the lactate threshold, in part because of elevated epinephrine concentrations. This shift may have been one cause for the decrease in time to exhaustion for the dehydrated trial.
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.