Acute effects of sodium ingestion on thirst and cardiovascular function.

Sweating during exercise, especially during exercise in the heat, leads to sodium and water losses, and the quantity of these losses depends upon the intensity and duration of the activity, genetic predisposition and conditioning of the individual, and environmental factors. In athletes, adequate sodium intake is necessary to maintain fluid balance during training and competition. To ensure the precise regulation of volume and osmolality of body fluids, a number of integrated neural and hormonal systems have evolved to control thirst and sodium appetite. These systems respond to stimuli that arise from a deficit of fluid arising in both the intracellular and extracellular fluid compartments or to systemic hypertonicity. Thirst is highly sensitive to increases in plasma sodium concentration and osmolality, requiring only a 2%-3% increase to induce feelings of thirst. A larger change in plasma volume (10%) is required to induce thirst if there is no concomitant change in plasma sodium concentration. If plain water is used to replenish body water, plasma volume is preferentially restored over the interstitial and intracellular fluid space, suppressing plasma sodium concentration and removing the dipsogenic drive long before total body fluid has been restored. During or after dehydrating exercise, sodium ingestion helps to maintain and restore plasma volume and osmolality by continuing thirst sensation (thus drinking) and also by increasing body fluid retention. A high sodium meal or intravascular hypertonic saline infusion may cause transient osmotically mediated blood pressure increases, but in healthy people, acute sodium ingestion does not cause sustained hypertension. The purpose of this review is to provide evidence that acute increases in sodium are an intrinsic part of the thirst response during and after exercise, and that blood pressure increases associated with hypertonicity appear to be short lived.