The hypothesis that the magnitude of the postexercise onset threshold for sweating is increased by the intensity of exercise was tested in eight subjects. Esophageal temperature was monitored as an index of core temperature while sweat rate was measured by using a ventilated capsule placed on the upper back. Subjects remained seated resting for 15 min (no exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption (V O2 peak) followed by a 20-min seated recovery. Subjects then donned a liquid-conditioned suit used to regulate mean skin temperature. The suit was first perfused with 20°C water to control and stabilize skin and core temperature before whole body heating. Subsequently, the skin was heated (ϳ4.0°C/h) until sweating occurred. Exercise resulted in an increase in the onset threshold for sweating of 0.11 Ϯ 0.02, 0.23 Ϯ 0.01, and 0.33 Ϯ 0.02°C above that measured for the no-exercise resting values (P Ͻ 0.05) for the 55, 70, and 85% of V O2 peak exercise conditions, respectively. We did note that there was a greater postexercise hypotension as a function of exercise intensity as measured at the end of the 20-min exercise recovery. Thus it is plausible that the increase in postexercise threshold may be related to postexercise hypotension. It is concluded that the sweating response during upright recovery is significantly modified by exercise intensity and may likely be influenced by the nonthermal baroreceptor reflex adjustments postexercise. sudomotor activity; baroreceptor reflexes; heat loss; thermoregulation RECENT STUDIES INDICATE THAT exercise induces a residual effect on thermal control, resulting in an increase in the postexercise esophageal temperature at which sweating occurs (11,13). Although the mechanism(s) for thermoregulatory control of sweating before and during exercise has been evaluated, there remains a lack of information on its nature and role during postexercise temperature regulation. Various studies have shown that the sweating response during exercise not only involves changes in thermal factors, such as core and skin temperatures (4, 23, 24), but also nonthermal factors, including central command, baroreceptors, mechanoreceptors, and metaboreceptors (15,24,30). This is in contrast to passive heating at rest, in which the primary stimuli for sweating is thought to be a factor of thermal origin (25).More recently, it has been shown that the postexercise sweating response is to some degree influenced by nonthermal baroreflex control (10). Specifically, the modification of postexercise venous pooling by lower body positive pressure results in a lowering of the resting postexercise elevation in the onset threshold for sweating. However, the mechanism of control is still unknown. Dynamic exercise is known to result in postexercise hypotension in the upright position (3,6,7,14,18,26,27). During postexercise hypotension, mean arterial pressure (MAP) is reduced subsequent to both neural and vascular activity (6-8). This postexercise hypotension is ...