This is the hormone your BF was talking about. It can unfortunately sometimes cause fluid overload when it gets out of whack. This is a portion of the article "Drinking Too Much" by Lulu Weschler, from the ultramarathon cycling website.

PS, I believe I've heard Karl King, developer of Succeed Electrolyte Caps, say that if you take one before starting to exercise, it will make you not have to pee right away.




Water retention caused by inappropriately high concentrations of AVP
Normal kidneys can excrete about 0.8 to 1.0 liters of water per hour in urine at rest (Noakes 2001). It is therefore easy to understand the development of EAH when hourly rates of fluid ingestion far exceed these limits. However it is not clear why some athletes accumulate a fluid overload while consuming fluid at rates equal to or considerably lower than this. An emerging culprit is the hormone arginine vasopressin (AVP). AVP is the only human antidiuretic hormone (ADH), so when you see 'ADH', think 'AVP', at least for humans. About a week's worth of AVP is stored in the brain (posterior pituitary) and is ready to be released in time of need (Verbalis 2003). As an antidiuretic, AVP's job is to protect against dehydration by stimulating water reabsorption by the kidneys. Thus, it is appropriately released into the blood stream in response to an increase in plasma osmolality (to which it is very sensitive) or a decrease in body water volume (to which it is considerably less sensitive) both situations in which the body needs to conserve fluid. There are, however, 'non-need' and hence inappropriate triggers for AVP's release. The most potent of all is nausea; other stimuli include various drugs, too little oxygen or too much carbon dioxide in blood, pain, and hypoglycemia (Verbalis 2003). Any of these conditions can be present during exercise. Some drugs, such as NSAIDs, do not stimulate release of AVP, but they increase the antidiuretic response to any AVP that is already circulating.

AVP acts primarily in the kidney (and does not appear to have an effect on sweat glands). Kidneys filter a certain fraction of blood (the filtrate), which is destined to be urine unless it is re-absorbed. AVP facilitates re-absorption of the water part of the filtrate. AVP does not, however, directly stimulate sodium re-absorption, with the result that sodium continues on into what will be a decreased volume of urine. Under conditions of volume expansion, an inappropriately high level of AVP can cause a dumping of sodium and re-absorption of water so extreme that an infusion of Isotonic Saline (NS, 0.9% or 154 mEq sodium/liter) ultimately has the same effect as infusing an extremely dilute, hypotonic fluid. This particlar phenomenon was key to elucidating the Syndrome of Inappropriate AntiDiuretic Hormone Secretion (SIADH), or in more modern terminology, Syndrome of Inappropriate Antidiuresis (SIAD) (Schwartz 1957 with Schwartz and Verbalis commentaries).

To date, only a few cases of inappropriately high levels of AVP have been documented in EAH (Verbalis 2005). There are two problems with assaying AVP levels during exercise. First, AVP has a half-life of just 6 to 10 minutes, and is rapidly degraded if samples are not handled correctly. Secondly, in EAH, the basal levels from which AVP increases can be very low, and the increases can also be relatively small. AVP operates in a 'leveraged' range where relatively small increases from low baseline values have a large effect on water reabsorption of urine water. Nonetheless, it should be noted that the original diagnostic criteria for SIAD, established before AVP assay techniques were available, remain valid. Thus, it has been possible to implicate inappropriately high levels of AVP as the culprit in EAH where sufficient data (e.g.,plasma osmolality, urine osmolality and urine sodium concentration) are available (Verbalis 2005).