The purpose of this study was to measure the in vivo Na(+) secretion and Na(+) reabsorption rates of the human eccrine sweat gland with increases in sweat rate. Such data should help to elucidate the physiological mechanism responsible for the previously reported linear relationship between increases in sweat rate and Na(+) concentration in sweat. On 5 days, each subject (n = 10) completed a 30-min exercise bout in an environmental chamber set at 35 degrees C and 40% relative humidity. The intensity for the five exercise bouts in the heat was set to approximate 50, 60, 70, 80, and 90% of age-predicted maximum heart rate. Forearm sweat samples and capillary blood samples were collected during each of the five 30-min exercise bouts. The sweat and blood samples were analyzed for Na(+) concentration in sweat and serum, which were used to calculate the rate of Na(+) secretion and Na(+) reabsorption. The mean correlation between sweat rate and Na(+) concentration in sweat was found to be r = 0.73. Within the sweat rate range of the present study, both Na(+) secretion rate and Na(+) reabsorption rate increased linearly; however, the Na(+) secretion rate increased almost twice as fast (slope = 141 vs. 80). Thus the rate at which Na(+) escaped reabsorption increased with increases in sweat rate and was significantly (P < 0.05) correlated to the Na(+) concentration in sweat (mean r = 0.90). Such results strongly suggest that the physiological mechanism responsible for the previously reported linear increase in Na(+) concentration in sweat seen with increases in sweat rate is that the Na(+) secretion rate increases proportionally more than the Na(+) reabsorption rate.

We investigated whether the eccrine sweat glands must actively produce sweat during heat acclimation if they are to adapt and increase their capacity to sweat. Eight volunteers received intradermal injections of BOTOX, to prevent neural stimulation and sweat production of the sweat glands during heat acclimation, and saline injections as a control in the contralateral forearm. Subjects performed 90 min of moderate-intensity exercise in the heat (35 degrees C, 40% relative humidity) on 10 consecutive days. Heat acclimation decreased end-exercise heart rate (156 +/- 22 vs. 138 +/- 17 beats/min; P = 0.0001) and rectal temperature (38.2 +/- 0.3 vs. 37.9 +/- 0.3 degrees C; P = 0.0003) and increased whole body sweat rate (0.70 +/- 0.29 vs. 1.06 +/- 0.50 l/h; P = 0.030). During heat acclimation, there was no measurable sweating in the BOTOX-treated forearm, but the control forearm sweat rate during exercise increased 40% over the 10 days (P = 0.040). Peripheral sweat gland function was assessed using pilocarpine iontophoresis before and after heat acclimation. Before heat acclimation, the pilocarpine-induced sweat rate of the control and BOTOX-injected forearms did not differ (0.65 +/- 0.20 vs. 0.66 +/- 0.22 mg x cm(-2) x min(-1)). However, following heat acclimation, the pilocarpine-induced sweat rate in the control arm increased 18% to 0.77 +/- 0.21 mg x cm(-2) x min(-1) (P = 0.021) but decreased 52% to 0.32 +/- 0.18 mg x cm(-2) x min(-1) (P < 0.001) in the BOTOX-treated arm. Using complete chemodenervation of the sweat glands, coupled with direct cholinergic stimulation via pilocarpine iontophoresis, we demonstrated that sweat glands must be active during heat acclimation if they are to adapt and increase their capacity to sweat.