Acute (~2 min) baroreceptor unloading was reported to modulate metaboreflex control of postexercise cutaneous blood flow, but not sweating. We examined whether sustained changes in baroreceptor loading status during prolonged postexercise recovery can alter the metaboreceptors’ influence on heat loss. Thirteen young males performed a 1-min isometric handgrip exercise (IHG) at 60% maximal voluntary contraction followed by 2-min of forearm ischemia (to activate metaboreceptors) before and 15, 30, 45 and 60-min after a 15-min intense treadmill running exercise (>90% maximal heart rate) in the heat (35°C). This procedure was repeated on three separate days with the application of lower-body positive (LBPP, +40 mmHg), negative (LBNP, -20 mmHg), or no pressure (Control) postexercise. Sweat rate (ventilated capsule; forearm, chest, upper back) and cutaneous vascular conductance (CVC; forearm, upper back) were measured. Relative to pre-IHG levels, sweating at all sites increased during IHG and remained elevated during ischemia at baseline and similarly at 30, 45, and 60-min postexercise (site average sweat rate increase during ischemia: Control, 0.13±0.02; LBPP, 0.12±0.02; LBNP, 0.15±0.02 mg·min-1·cm-2; all P<0.01), but not at 15-min (all P>0.10). LBPP and LBNP application did not modulate the pattern of sweating to IHG and ischemia (all P>0.05). At 15-min postexercise, forearm CVC was reduced from pre-IHG levels during both IHG and ischemia under LBNP only (ischemia: 3.9±0.8 %CVCmax; P<0.02). Therefore, we show metaboreceptors modulate postexercise sweating in the mid-to-late stages (30-60 min) of recovery, independent of baroreceptor loading status and similarly between skin sites. In contrast, metaboreflex modulation of forearm but not upper back CVC occurs only in the early stages of recovery (15 min) and depends upon baroreceptor unloading.