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</script>doi: 10.1007/bf02941143 , 10.1097/01.csmr.0000305608.60177.2a , 10.1097/01.csmr.0000306456.47810.72 , 10.1007/s11932-007-0017-8 , 10.1097/01.csmr.0000306548.96216.52 , 10.1097/01.csmr.0000306486.30777.66 , 10.1007/s11932-007-0047-2 , 10.1007/s11932-007-0001-3 , 10.1097/01.csmr.0000306471.57219.68 , 10.1007/s11932-007-0032-9 , 10.1097/01.csmr.0000306442.48703.52 , 10.1007/s11932-007-0060-5
doi: 10.1007/bf02941143 , 10.1097/01.csmr.0000305608.60177.2a , 10.1097/01.csmr.0000306456.47810.72 , 10.1007/s11932-007-0017-8 , 10.1097/01.csmr.0000306548.96216.52 , 10.1097/01.csmr.0000306486.30777.66 , 10.1007/s11932-007-0047-2 , 10.1007/s11932-007-0001-3 , 10.1097/01.csmr.0000306471.57219.68 , 10.1007/s11932-007-0032-9 , 10.1097/01.csmr.0000306442.48703.52 , 10.1007/s11932-007-0060-5
An Ultracyclist with Pulmonary Edema During the Bicycle Race Across America A recently published case report in the January 2007 issue of Medicine & Science in Sports & Exercise, the official journal of the ACSM, highlights the pitfalls of overly aggressive sodium intake during an endurance race at altitude. It is well known that multiday ultra-endurance athletic events tax the body’s ability to maintain sodium and water homeostasis. Much focus has been placed on the danger associated with excessive water intake without sodium repletion, namely hyponatremia. This case study presents the risk associated with aggressive sodium intake coupled with heavy exertion at a high altitude. The subject presented is an extremely fit 38-year-old male participant in the Bicycle Race Across America who developed severe pulmonary edema while cycling at an altitude of 2380 meters on the fourth day of his race. His daily sodium intake over the course of the race averaged between 1000 and 1100 mEq and his weight on the day of hospitalization was 2.7 kg greater than his prerace weight. The athlete responded appropriately to standard support for pulmonary edema while in the hospital and he made a full recovery. Later, he underwent testing for cardiopulmonary disease or susceptibility to high-altitude pulmonary edema. The results of the entire work-up were negative. The authors hypothesize that the excessive sodium intake led to an expanded extracellular volume, increased hydrostatic pressure, and decreased oncotic pressure. Racing at high altitudes, where a hypoxia-induced rise in pulmonary artery pressures already exists, may have exaggerated the effects of the changes in hydrostatic and oncotic pressures seen with extracellular volume expansion. This, coupled with ambient hypoxia, elevated cardiac output, and reduced renal perfusion associated with sustained highlevel exercise seems to lead to the development of acute pulmonary edema.
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