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First page of Do transdermal administration of α1  and α2 adrenergic receptor antagonists modulate sweating in exercising young females in the heat?

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 minutes at 32°C and 40% relative humidity. Sweat rates (ventilated capsule technique) on both forearms were assessed following pre-treatment with terazosin (α1-adrenergic receptor antagonist), rauwolscine (α2-antagonist), or control (NaCl) using transdermal iontophoresis procedure. The efficacy of α1-blockade was confirmed post-exercise 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 males and females, 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 post-exercise (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.

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