Journal of Applied Physiology  AJP: Regulatory, Integrative and Comparative Physiology
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J Appl Physiol 98: 1740-1744, 2005. First published January 7, 2005; doi:10.1152/japplphysiol.00860.2004
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Pilocarpine-induced sweat gland function in individuals with multiple sclerosis

Scott L. Davis,1 Thad E. Wilson,2 Jamie M. Vener,1 Craig G. Crandall,3,4 Jack H. Petajan,5 and Andrea T. White1

1Department of Exercise and Sport Science, University of Utah, Salt Lake City, Utah; 2Department of Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania; 3Institute for Exercise and Environmental Medicine, Presbyterian Hospital, Dallas, Texas; 4Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; and 5Department of Neurology, University of Utah School of Medicine, Salt Lake City, Utah

Submitted 8 August 2004 ; accepted in final form 27 December 2004

This investigation tested the hypothesis that cholinergic sweat function of individuals with multiple sclerosis (MS) (MS-Con; n = 10) is diminished relative to matched healthy control subjects (Con; n = 10). In addition, cholinergic sweat function was determined before and after 15 wk of aerobic training in a subgroup of individuals with MS (MS-Ex; n = 7). Cholinergic sweating responses were assessed via pilocarpine iontophoresis on ventral forearm skin. A collection disk placed over the stimulated area collected sweat for 15 min. Sweat rate (SR) was calculated by dividing sweat collector volume by collection area and time. Iodine-treated paper was applied to the stimulated area to measure number of activated sweat glands (ASG). Sweat gland output (SGO) was calculated by dividing SR by density of glands under the collector. Sweat gland function was determined in MS-Ex to test the hypothesis that exercise training would increase sweating responses. No differences in ASG were observed between MS-Con and Con. SR and SGO in MS-Con [0.18 mg·cm–2·min–1 (SD 0.08); 1.74 µg·gland–1·min–1 (SD 0.79), respectively] were significantly lower (P ≤ 0.05) than in Con [0.27 mg·cm–2·min–1 (SD 0.10); 2.43 µg·gland–1·min–1 (SD 0.69)]. Aerobic exercise training significantly (P ≤ 0.05) increased peak aerobic capacity in MS-Ex [1.86 (SD 0.75) vs. 2.10 (SD 0.67) l/min] with no changes in ASG, SR, and SGO. Sweat gland function in individuals with MS is impaired relative to healthy controls. Fifteen weeks of aerobic training did not increase stimulated sweating responses in individuals with MS. Diminished peripheral sweating responses may be a consequence of impairments in autonomic control of sudomotor function.

sweat rate; sweat gland density; demyelination; sudomotor



Address for reprint requests and other correspondence: A. T. White, Dept. of Exercise and Sport Science, Univ. of Utah, 250 South 1850 East, Rm. 257, Salt Lake City, UT 84112-0920 (E-mail: Andrea.White{at}health.utah.edu)







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