This study sought to determine whether the temperature of water ingested before exercise alters the onset threshold and subsequent thermosensitivity of local vasomotor and sudomotor responses after exercise begins. Twenty men [24 (SD 4) yr of age, 75.8 (SD 8.1) (V˙kg body mass, 52.3 (SD 7.7) ml·min^-1·kg^-1 peak O₂ consumption_O2peak)] ingested 1.5°C, 37°C, orV˙ 50°C water (3.2 ml/kg), rested for 5 min, and then cycled at 50%_O2peak for 15 min at 23.0 (SD 0.9) °C and 32 (SD 10) % relative humidity. Mean body temperature (T_b), local sweat rate (LSR), and skin blood flow (SBF) were measured. In a subset of eight men [25 (SD^-1·kg^-15) yrV˙ of age, 78.6 (SD 8.3) kg body mass, 48.9 (SD 11.1) ml·min_O2peak], blood pressure was measured and cutaneous vascular conductance (CVC) was determined. The change in T_b was greater at the onset of LSR measurement with ingestion of 1.5°C than 50°C water [ΔT_b = 0.19 (SD 0.15) vs. 0.11 (SD 0.12) °C, P = 0.04], but not 37°C water [ΔT_b = 0.14 (SD 0.14) °C, P = 0.23], but did not differ between trials for SBF measurement [ΔT_b = 0.18 (SD 0.15) °C, 0.11 (SD 0.13) °C, and 0.09 (SD 0.09) °C with 1.5°C, 37°C, and 50°C water, respectively, P = 0.07]. Conversely, the thermosensitivity of LSR and SBF was not different [LSR = 1.11 (SD 0.75), 1.11 (SD 0.75), and 1.34 (SD 1.11) mg·min^-1·cm^-2·°C^-1 with 1.5°C, 37°C, and 50°C ingested water, respectively (P = 0.46); SBF = 717 (SD 882), 517 (SD 606), and 857 (SD 904) %baseline arbitrary units (AU)/°C with 1.5°C, 37°C, and 50°C ingested water, respectively (P = 0.95)]. After 15 min of exercise, LSR and SBF were greater with ingestion of 50°C than 1.5°C water [LSR = 0.40 (SD 0.17) vs. 0.31 (SD 0.19) mg·min^-1·cm^-2 (P = 0.02); SBF = 407 (SD 149) vs. 279 (SD 117) %baseline AU (P < 0.001)], but not 37°C water [LSR = 0.50 (SD 0.22) mg·min^-1·cm^-2; SBF = 324 (SD 169) %baseline AU]. CVC was statistically unaffected [275 (SD 81), 340 (SD 114), and 384 (SD 160) %baseline CVC with 1.5°C, 37°C, and 50°C ingested water, respectively, P = 0.30]. Collectively, these results support the concept that visceral thermoreceptors modify the central drive for thermoeffector responses.