Both cyclooxygenase (COX) and nitric oxide synthase (NOS) contribute to sweating, whereas NOS alone contributes to cutaneous vasodilation during exercise in the heat. Here, we evaluated if type 1 diabetes mellitus (T1DM) modulates these responses. Adults with (n=11, 25±5 years) and without (n=12, 24±4 years) T1DM performed two bouts of 30-min cycling at a fixed rate of heat production of 400W in the heat (35°C); each followed by a 20- and 40-min recovery period respectively. Sweat rate and cutaneous vascular conductance (CVC) were measured at four intradermal microdialysis sites treated with either 1) lactated Ringer (vehicle control site), 2) 10mM ketorolac (non-selective COX inhibitor), 3) 10mM N^G-nitro-_L-arginine methyl ester (non-selective NOS inhibitor), or 4) a combination of both inhibitors. In non-diabetic adults, separate and combined inhibition of COX and NOS reduced exercise sweat rate (P≤0.05) and the magnitude of reductions were similar across sites. In individuals with T1DM, inhibition of COX resulted in an increase in sweat rate of 0.10±0.09 and 0.09±0.08 mg.min^-1.cm^-2 for the first and second exercise bouts respectively relative to vehicle control site (P≤0.05), while NOS inhibition had no effect on sweating. In both groups, NOS inhibition reduced CVC during exercise (P≤0.05) although the magnitude of reduction did not differ between the non-diabetic and T1DM groups (Exercise 1: -28±10 vs. -23±8%max, P=0.51; Exercise 2: -31±12 vs. -24±10%max, P=0.38). We show that in individuals with T1DM performing moderate intensity exercise in the heat, NOS-dependent sweating but not cutaneous vasodilation is attenuated, whereas COX inhibition increases sweating.