Thermoregulatory responses during exercise are reduced following thermal dehydration. If individuals do not rehydrate adequately, it could lead to heat exhaustion or stroke with the worst case scenario being death. Plasma volume loss during dehydration has been suggested to suppress cutaneous vasodilatation in response to hyperthermia via a baroreflex–mediated reduction in active vasodilator activity rather than enhanced active vasoconstrictor activity. However, no changes in the electrical signals of the efferent neural pathway have ever been identified. In the present study, we found a component of efferent skin sympathetic nerve activity that was synchronized with the cardiac cycle in thermally stressed individuals. This nerve activity increased with an increase in oesophageal temperature and the increase was significantly suppressed by hypovolaemia. Thus, this component of skin sympathetic nerve activity might represent the active vasodilator signals that regulate skin blood flow during hyperthermia in humans.
Although cutaneous vasodilatation in hyperthermia was suppressed during hypovolaemia, the efferent neural pathway mediating this suppression has not been identified. To determine the electrical nerve signals which account for the suppression of cutaneous vasodilatation during hypovolaemia, skin sympathetic nerve activity (SSNA; microneurography) from the peroneal nerve, laser–Doppler blood flow (LDF) on the ipsilateral dorsal foot, mean arterial pressure (MAP; sonometry) and oesophageal temperature (Toes) were measured before and during 45 min of passive warming in 20 healthy subjects during normovolaemia (n= 10) or hypovolaemia (n= 10) conditions. Hypovolaemia was achieved by diuretic administration. Cutaneous vascular conductance (CVC = LDF/MAP), SSNA burst frequency and total SSNA obtained from rectified and filtered SSNA signal increased as Toes increased by ˜0.5°C by the end of warming in both groups. The increase in CVC was significantly lower in hypovolaemia than normovolaemia (P < 0.0001), but with no significant difference in the increase in burst frequency and total SSNA between groups (P > 0.32). However, using an alternative analysis that constructed spike incidence histograms from the original signal using 0.05 s bins during the 5 s following a given R–wave, we found a SSNA component synchronized with the cardiac cycle with a 1.1–1.3 s latency. This component increased with an increase in Toes and the increase was significantly suppressed by hypovolaemia (P < 0.0001). In conclusion, hypovolaemic suppression of cutaneous vasodilatation during hyperthermia might be caused by a reduction in the SSNA component synchronized with cardiac cycle.