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This thesis sought to evaluate whether the impairments in nitric oxide (NO)-dependent cutaneous vasodilation and sweating observed in older adults during exercise in the heat stem from age-related increases in oxidative stress and/or arginase activity. Furthermore, we assessed whether changes in the sensitivity to NO at the level of the end-organ (i.e., cutaneous vasculature and sweat gland) also contribute. A total of 20 young (age, 23 ± 3 yrs) and 28 older (age, 63 ± 7 yrs) males completed one of two intermittent exercise protocols that consisted of two 30-min bouts of semi-recumbent cycling in the heat (35˚C) at a rate of metabolic heat production of 500 (protocol I; 11 young, 19 older) or 400 (protocol II; 9 young, 9 older) W. Each exercise bout was followed by a 20-min recovery period. During each protocol, local cutaneous vascular conductance (CVC; laser-Doppler flowmetry/mean arterial pressure) and sweat rate (SR, ventilated capsule) were continuously measured at four forearm skin sites. In protocol I, each forearm skin site was continuously perfused via intradermal microdialysis with either: 1) lactated Ringer’s serving as a control (Control); 2) 10 mM NG-nitro-L-arginine methyl ester (L-NAME), a non-selective NO synthase inhibitor; 3) 10 mM ascorbate (Ascorbate), a non-selective antioxidant or 4) a combination of 10 mM ascorbate and 10 mM L-NAME (L-NAME + Ascorbate). In protocol II, the Ascorbate and L-NAME + Ascorbate skin sites were replaced with 5 mM Nω-hydroxy-nor-Arginine + 5 mM S-(2-boronoethyl)-L-cysteine to inhibit arginase activity (Nor-NOHA+BEC) and 1 µM sodium nitroprusside, a nitric oxide donor (SNP). In the …