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Paper |
1 Systemic Inflammation Lab, United States
2 University of Illinois at Chicago, United States
3 University of Cape Town, South Africa
4 Georgetown University Medical Center, United States
* To whom correspondence should be addressed. E-mail: tamara.hew{at}chw.edu.
Accepted 1 July 2008
| Abstract |
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Objective: To evaluate the osmotic and non-osmotic regulation of arginine vasopressin (AVP) during endurance cycling
Design: observational study
Setting: 109 km cycle race
Participants: 33 cyclists
Interventions: none
Main Outcome Measurements: plasma sodium concentration ([Na+]), plasma volume (PV) and plasma AVP concentration ([AVP]p)
Results: A 4-fold increase in [AVP]p occurred despite a 2 mmol/L decrease in plasma [Na+] combined with only modest (5%) plasma volume contraction. A significant inverse correlation was noted between [AVP]p Ä versus urine osmolality Ä (r=-0.41; p<0.05) while non-significant inverse correlations were noted between [AVP]p versus both plasma [Na+] Ä and % PV Ä. Four cyclists finished the race with asymptomatic hyponatraemia. The only significant difference between the entire cohort with this subset of athletes was post-race plasma [Na+] (137.7 vs. 133.5 mmol/L; p<0.001) and plasma [Na+] Ä (-1.9 vs. -5.1 mmol/L; p<0.05). The mean pre-race [AVP]p of these four cyclists was just below the minimum detectable limit (0.3 pg/mL) and increased marginally (0.4 pg/mL) despite the decline in plasma [Na+].
Conclusions: Non-osmotic AVP secretion overshadowed the osmotic regulation of [AVP]p during competitive cycling. The modest decrease in plasma volume was not the primary non-osmotic stimulus to AVP. Partial suppression of AVP occurred in four (12%) cyclists who developed hyponatraemia during five hours of riding. Therefore, these results confirm that non-osmotic AVP secretion and EAH does, in fact, occur in cyclists participating in a 109 km cycle race. However, the stimuli to AVP is likely different between cycling versus running.
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