Tracing oral Na+ and K+ in sweat during exercise and recovery in horses.

In two series of experiments, this study used radioactive sodium (Na+ ) and potassium (K+ ) to trace the net flux, and calculate the unidirectional fluxes, of these ions from extracellular fluid into sweat of horses during exercise and recovery. The effect of an oral electrolyte supplement (PNW) on the sweating responses and ion fluxes was also examined. Compared to 8 litres of water (controls), provision of 8 litres of PNW resulted in significantly increased sweating duration (P < 0.001). Two hours before exercise, 99 Tc-labelled diethylene-triamine-pentaacetate (DTPA) was administered i.v. to determine if there was paracellular flux of this molecule in sweat glands during the period of sweating. One hour before beginning moderate-intensity exercise, horses were nasogastrically administered either 24 Na (1-3 litres) or 42 K (8 litres) with water (control) or an electrolyte supplement. Both radiotracers appeared in sweat within 10 min of exercise onset, and the sweat specific activity of both ions increased during exercise (P < 0.001), approaching plasma specific activities. There was no appearance of 99 Tc-DTPA in sweat. The activities of 24 Na and 42 K, together with the concentrations Na+ , K+ and Cl- , argued against significant paracellular flux of these ions into the lumen of sweat glands. The flux analysis for 24 Na indicated a small intracellular pool within sweat gland cells, and no evidence for an active transport component. The flux analysis for 42 K indicated a relatively large intracellular equilibration pool within sweat gland cells, with evidence for an active transport component. The results are discussed with respect to the current understanding of sweat gland epithelial cell ion transport mechanisms at both the basal and the apical membranes. It appears likely that the majority of ions appearing in sweat pass through sweat gland epithelial cells by transcellular mechanisms that include ion transporting pathways as well as apical vesicular exocytosis.