Do Transdermal Administration of α1- and α2-Adrenergic Receptor Antagonists Modulate Sweating in Exercising Young Females in the Heat?

Abstract

Introduction: Adrenergic modulation of sweating remains equivocal in females. We investigated whether α1- and α2-adrenergic receptors can modulate sweating during active heat stress in healthy female participants.

Methods: Thirty young adults (15 females) cycled at 50% peak oxygen uptake for 30 min at 32°C and 40% relative humidity. Sweat rates (ventilated capsule technique) on both forearms were assessed following pretreatment with terazosin (α1-adrenergic receptor antagonist), rauwolscine (α2 antagonist), or control (NaCl) using transdermal iontophoresis procedure. The efficacy of α1 blockade was confirmed postexercise with phenylephrine (α1-adrenergic agonist)-induced sweating, while α2 antagonist efficacy was verified in a separate follow-up study assessing clonidine (α2 agonist)-induced cutaneous vasoconstriction.

Results: Participants sweated by 0.32 ± 0.13 and 0.54 ± 0.26 mg∙cm-2∙min-1 at the end of exercise for females and males, respectively. Neither terazosin nor rauwolscine affected sweating during exercise in males (p ≥ 0.125, interaction and treatment effect) or females (p ≥ 0.277) as compared to control sites. However, the reduction in sweat rate at the terazosin-treated site was negatively correlated with sweat rate at control sites in both sexes (all p ≤ 0.050, r ≤ -0.514), while no such correlation was observed for rauwolscine. Successful α1-blockade was confirmed by attenuated phenylephrine-induced sweating during postexercise (p ≤ 0.025). Rauwolscine effectively abolished clonidine-induced cutaneous vasoconstriction in a follow-up study, verifying successful transdermal delivery.

Conclusion: The α1- and α2-adrenergic receptors do not alter sweating during moderate-intensity exercise in males and females, at least among individuals with relatively low sweat production.