Key points Humans are unique in controlling body temperature in a hot environment by a large amount of skin blood flow; however, the decrease in total peripheral resistance due to systemic cutaneous vasodilatation and the reduction of venous return to the heart due to blood pooling in the cutaneous vein threatens blood pressure maintenance in the upright position, and occasionally causes heat syncope. Against this condition, cutaneous vasodilatation is reportedly suppressed to maintain arterial pressure; however, the nerve activity responsible for this phenomenon has not been identified. In the present study, we found that the skin sympathetic nerve activity component that was synchronised with the cardiac cycle increased in hyperthermia, but the increase was suppressed when the posture was changed from supine to head‐up tilt. The profile of the component agreed with that of cutaneous vasodilatation. Thus, the component might contribute to the prevention of heat syncope in humans. Abstract In humans, the cutaneous vasodilatation response to hyperthermia has been suggested to be suppressed by baroreflexes to maintain arterial pressure when the posture is changed from supine to upright, and if the reflexes do not function sufficiently, it can cause heat syncope. However, the efferent signals of the reflexes have not been identified. To identify the signals, we continuously measured skin sympathetic nerve activity (SSNA; microneurography), right atrial volume (RAV; echocardiography, the baroreceptors for the reflexes are reportedly located in the right atrium), cutaneous vascular conductance on the chest (CVCchest; laser Doppler flowmetry), and oesophageal temperature (Toes; thermocouple) in young men before and after passive warming with a perfusion suit, during which periods the posture was changed from supine to 30 deg head‐up tilt positions. During these periods, we also simultaneously measured muscle sympathetic nerve activity (MSNA) to distinguish the SSNA from MSNA. We found that an increase in Toes by ∼0.7°C (P < 0.0001) increased the total SSNA (P < 0.005); however, the head‐up tilt in hyperthermia did not change the total SSNA (P > 0.26) although an increase in CVCchest (P < 0.019) was suppressed and RAV was reduced (P < 0.008). In contrast, the SSNA component synchronised with the cardiac cycle increased in hyperthermia (P < 0.015), but decreased with the postural change (P < 0.017). The SSNA component during the postural change before and after warming was highly correlated with the CVCchest (r = 0.817, P < 0.0001), but the MSNA component was not (r = 0.359, P = 0.085). Thus, the SSNA component synchronised with the cardiac cycle appeared to be involved in suppressing cutaneous vasodilatation during postural changes.