Mechanisms and implications of sodium loss in sweat during exercise in the heat for patients with cystic fibrosis and healthy individuals

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Brown, Mary Beth
Millard-Stafford, Mindy L.
McCarty, Nael A.
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Our aim was to understand mechanisms responsible for excessive electrolyte loss in the sweat gland and the potential impact on fluid balance during exercise in heat stress conditions. Human physiological testing under exercise/heat stress and immunofluorescence staining of sweat glands from skin biopsies were compared between healthy individuals (with normal and high sweat sodium chloride concentration, [NaCl]) and with cystic fibrosis patients (CF), who exhibit excessively salty sweat due to a defect of Cl- channel cystic fibrosis transmembrane conductance regulator (CFTR). Three novel findings are presented. First, excessively salty sweat may be associated with reduced expression of CFTR in the sweat gland reabsorptive duct of healthy individuals in addition to in those with CF; however, although a link to a CF gene mutation in healthy individuals with high sweat [NaCl] was not demonstrated, the possibility of an undetected CFTR mutation or polymorphism remains to be investigated as an underlying mechanism. Two, CF and healthy individuals with excessively salty sweat respond to moderate dehydration (3% body weight loss during exercise) with an attenuated rise in serum osmolality, greater relative loss in plasma volume, but similar perceived thirst compared to healthy individuals with "normal" sweat [NaCl]. However, individuals with CF respond to rehydration with hypotonic beverage by drinking less ad libitum in response to reduced serum [NaCl], suggesting that thirst-guided fluid replacement may be more appropriate for this population rather than restoring 100% of sweat loss following dehydration as is often recommended in healthy individuals.
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