Osmotic and nonosmotic regulation of arginine vasopressin during prolonged endurance exercise.
BACKGROUND
Although the primary cause of exercise-associated hyponatremia (EAH) is relative overconsumption of fluids beyond the kidneys' ability to excrete excess fluid, the mechanisms limiting maximum renal excretory ability during exercise remain to be elucidated.


OBJECTIVE
The objective of the study was to: 1) perform a comprehensive evaluation of the endocrine secretion of pituitary, natriuretic and adrenal steroid hormones, and cytokines immediately before and after running an ultramarathon; and 2) evaluate the relationship between osmotic and nonosmotic stimuli to arginine vasopressin (AVP) secretion within the overall context of assessing the hormonal regulation of fluid balance during prolonged endurance exercise.


METHODS
This was an observational study.


METHODS
The study setting was a 56-km ultramarathon.


METHODS
Eighty-two runners participated in the study.


METHODS
There were no interventions.


METHODS
Plasma sodium concentration [Na(+)] and plasma volume [(AVP)(p)] were measured.


RESULTS
Fluid homeostasis during exercise (356 +/- 4 min) was maintained with ad libitum fluid intakes. [Na(+)] was maintained from before the race (139.3 +/- 0.3 mmol/liter) to after the race (138.1 +/- 0.4 mmol/liter) with a significant decrease in plasma volume (-8.5 +/- 0.1%, P < 0.01). Increases in the plasma (AVP)(p) (3.9-fold), oxytocin (1.9-fold), brain natriuretic peptide (4.5-fold), and IL-6 (12.5-fold) were highly significant (P < 0.0001). Changes in brain natriuretic peptide, oxytocin, and corticosterone were associated with 47% of the variance noted in (AVP)(p) and 13% of the variance in plasma [Na(+)] in pathway analyses.


CONCLUSIONS
(AVP)(p) was markedly elevated after the ultramarathon despite unchanged plasma [Na(+)](.) Therefore, an inability to maximally suppress (AVP)(P) during exercise as a result of nonosmotic stimulation of AVP secretion may contribute to the pathogenesis of exercise-associated hyponatremia if voluntary fluid intake were to exceed fluid output.
Hew-Butler
Tamara
T
Department of Human Biology, University of Cape Town, Cape Town, South Africa. tamara.hew@chw.edu
Jordaan
Esme
E
Stuempfle
Kristin J
KJ
Speedy
Dale B
DB
Siegel
Arthur J
AJ
Noakes
Timothy D
TD
Soldin
Steven J
SJ
Verbalis
Joseph G
JG
D001127:Arginine Vasopressin / Q000097:blood / Q000378:metabolism / Q000493:pharmacokinetics*; D001835:Body Weight; D015444:Exercise / Q000502:physiology*; D005260:Female; D006728:Hormones / Q000097:blood; D006801:Humans; D007010:Hyponatremia / Q000097:blood / Q000209:etiology; D008297:Male; D008954:Models, Biological; D009995:Osmosis; D010121:Oxytocin / Q000097:blood; D010807:Physical Endurance / Q000502:physiology*; D013997:Time Factors; D014882:Water-Electrolyte Balance / Q000502:physiology*
D006728:Hormones; D001127:Arginine Vasopressin; D010121:Oxytocin