Menu Menu

News Archive

Sunday, May 15, 2011 - Why does running 100 miles cause you to lower your sodium concentration?
Runners can suffer from a decrease in the sodium ion concentration in their blood (hyponatremia). A possible mechanism for the loss of sodium is through the hormone vasopressin, which causes the kidneys to retain water. In order to study this hypothesis, one needs to measure this hormone, or some marker for the hormone, in runners. This is precisely what Assistant Prof Tamara Hew-Butler, of the School of Health Sciences, and her colleagues describe in their paper Changes in Copeptin and Bioactive Vasopressin in Runners With and Without Hyponatremia published in the May issue of the Clinical Journal of Sport Medicine (Volume 21, Pages 211-217). They took blood samples of athletes after 100-mile runs, and analyzed hormone levels. Their paper begins:
Exercise-associated hyponatremia (EAH) is thought to be a variant of the syndrome of inappropriate antidiuretic hormone secretion (SIADH), but direct evidence supporting nonosmotic arginine vasopressin (AVP) secretion as a primary pathophysiological mechanism in individuals with EAH is limited and somewhat equivocal. A major scientific hurdle to defining a clear relation between EAH and SIADH is the inherent difficulty in measuring circulating levels of bioactive AVP in the blood. The short half-life (10-20 minutes) and moderate amount of plasma (0.5-1.0 mL) required to measure bioactive AVP makes appropriate blood collection and processing difficult, particularly in field settings. Additionally, the technical difficulties and labor intensive process of accurately quantifying AVP within physiologically meaningful ranges (0-5 pg/mL) makes both the cost and the availability of AVP measurement prohibitive to many scientists performing research at athletic events…

To critically evaluate exercise-induced changes in AVP secretion, we simultaneously measured both copeptin [a fragment of the hormone] and bioactive AVP prospectively in runners competing at extreme distances (approximately 160 km) because the incidence of EAH in finishers of races of this distance has previously been documented to be as high as 44% to 51%. Three separate study trials were performed in 2 different approximately 160-km races to evaluate copeptin and AVP levels in runners with and without EAH. Due to the differential stability of the short-peptide (AVP) and long-peptide (copeptin) fragments of provasopressin in plasma, we hypothesized that copeptin would be a better surrogate measure of chronic AVP secretion during prolonged endurance running, whereas bioactive AVP would better reflect more acute changes in plasma osmolality."
They concluded that
"Simultaneous measurement of both the N-terminal nonpeptide AVP and the C-terminal 39-amino acid copeptin products of the vasopressin prohormone suggests that exercise-induced nonosmotic stimuli to AVP secretion commonly override osmotic regulation during competitive long-distance running events. Furthermore, these studies suggest the possible utility of using [copeptin]p and bioactive [AVP]p differentially to delineate predominant stimuli to AVP secretion during non-steady-state conditions, although these data are limited in size and strength. The opportunity to choose either a long-term measure (copeptin) and/or a short-term measure (AVP) may offer a more flexible approach toward differentially studying and monitoring disorders of AVP secretion, including treatment and surveillance, in clinical care and exercise settings."