Water is the most essential constituent of the human body, undergoing continuous recycling. Body water functions as a solvent, a means for heat balance, and a regulator of cell volume and overall functioning.1 Its balance in humans has been regulated to a large extent by the sensation of thirst, a key survival instinct in body fluid homeostasis. The Merriam-Webster Dictionary defines thirst as “a sensation of dryness in the mouth and throat associated with a desire for liquid, also: the bodily condition (as of dehydration) that induces this sensation.” In fact, the sensation of thirst is well recognized as a very potent reminder of fluid consumption, thus making human survival possible.
The regulation of drinking is related to the physiological stimulation of thirst (ie, osmolality), as well as many other nonhomeostatic factors (ie, oropharyngeal cues). Other factors influencing drinking include palatability,2 availability, and behavior. The main physiological signal of thirst and arginine vasopressin (AVP) secretion is an increase in plasma osmolality (hyperosmolality). Even though AVP has a lower osmotic threshold of secretion than thirst, a relatively small increase of 1% to 3% in plasma osmolality results in a dipsogenic (thirst-inducing) effect.3 A decrease in plasma volume can also stimulate thirst, but osmoreceptor activation seems to be a more sensitive signal during progressive dehydration, because hypovolemia requires a 10% reduction in the absence of any changes in osmolality.4 A substantial decrease in plasma volume (ie, hemorrhage) can also be a very strong signal, both for thirst elevation and AVP secretion. Interestingly, loading in baroreceptors by head-out water immersion reduces thirst and drinking in dehydrated subjects.5 Thirst in older adults seems to be less intense in comparison to younger counterparts when it is a response to water deprivation6 and osmotic stimulation via hypertonic saline infusion.7 Researchers from the John B. Pierce Laboratory at Yale University have suggested that the decrease in thirst among older adults is linked to the diminished effectiveness of baroreceptors.8
Factors other than osmolality and plasma volume seem to affect thirst and drinking. In 1950, Adolph and Northrop9 showed in several experimental animals that an increase in stomach volume decreased thirst before any fluid absorption in the circulation took place. Mouth receptors are also involved in thirst signaling during mouth dryness, food consumption (especially dry), and in efforts to relieve discomfort due to spicy food consumption.10 Additionally, mouth wetness has been shown to rapidly decrease thirst after maximally induced thirst.11 Noteworthy is that humans stop drinking following dehydration-induced thirst well before body fluid restoration is achieved. In 1997, Figaro and Mack12 studied thirst and fluid-regulating hormone regulation in 6 dehydrated, healthy adults following rehydration. They noticed that both thirst and AVP returned almost to euhydrated values not only within 5 minutes from the onset of ad libitum drinking, but also before any change in plasma osmolality or volume occurred. They hypothesized that this finding was the result of the drinking act itself, possibly driven by oropharyngeal receptor stimulation. To ensure that this decrease in AVP and thirst was the result of drinking, and not water absorption, they repeated the experiment. This time, they extracted water from the stomach during ingestion via a nasal-gastric tube. They found that the subjects’ thirst also returned to baseline values even though no water was absorbed, thus concluding that the oropharyngeal receptors had a clear role in the dehydration-induced dipsogenic drive. The oropharyngeal receptors seem to influence thirst and drinking, fluid balance, thermoregulation, and possibly exercise performance. According to Takamata et al,13 the drinking act has a reflex effect on the osmotic regulation of sweating and AVP in dehydrated subjects. Recently, Arnaoutis and his colleagues14 studied the effect of mouth rinsing or drinking a very small amount of water every 5 minutes during cycling exercise to exhaustion in the heat. They concluded that ingestion of a small amount of water, but not mouth rinsing, increased exercise time in dehydrated subjects, possibly through the activation of oropharyngeal receptors.14
Clearly, hyperosmolality and/or hypovolemia stimulate thirst. Nevertheless, it is not clear whether drinking is a response of changes in osmolality or plasma volume during normal daily conditions. Phillips et al studied human behavior during ad libitum drinking.15 They concluded that humans consume fluid well before any water deficit, mostly during food consumption and possibly in response to oropharyngeal cues. These data are in agreement with other studies indicating that fluids are consumed mainly during food consumption.10,16
Fluid intake and thirst stimulation seem to be altered during exercise. In 1944, Pitts and his colleagues17 studied subjects’ drinking responses during exercise in the heat. They concluded that drinking during exercise rarely exceeded the two-thirds of net water losses due to sweating. Later on, Greenleaf18 identified that phenomenon as involuntary dehydration: “the delay in rehydration by spontaneous drinking after dehydration induced by exercise, fuid restriction, environmental heat and cold.” Interestingly, this involuntary dehydration takes place while athletes are exposed to 2 well-known thirst triggers, hyperosmolality, and hypovolemia. More recently, Passe et al studied runners’ drinking behavior during an 8-mile run in 20°C, whereas subjects had access to a carbohdyrate-electrolyte solution for rehydration every 2 miles.19 They observed that subjects replaced only 30% of their sweat loss, while underestimating their sweat loss by 40%. The data indicated that even under favorable conditions, runners were unable to maintain optimal hydration.
It is well known that a significant number of both recreational and professional athletes often start their training or competition hypohydrated (ie, increased urine specific gravity).20–22 In this regard, Arnaoutis et al23 showed that around 90% of young volleyball and basketball players participating in a summer camp were hypohydrated, as indicated by their high urine osmolality values (>700 mOsm/kg). Surprisingly, when athletes were asked to score their effort on staying hydrated, they reported they were doing a very good job. More recently, Arnaoutis et al23 also found that 90% of 107 young, male soccer players (aged 11–16 years) participating in a summer camp were hypohydrated. They hypothesized that the hypohydrated athletes would get thirsty faster and drink more during subsequent exercise, thus preventing further dehydration. In contrast, drinking ad libitum during practice did not prevent further dehydration in the already hypohydrated players. These results clearly indicated that thirst was not effective in maintaining optimal hydration, not even when subjects were starting exercise hypohydrated.
In summary, even though thirst has played a key survival role, it might not be an effective signal in maintaining day-to-day optimal hydration.
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