The study was undertaken to determine the changes in skin circulation in response to systemic hypoxia. Transient hypoxia was induced in 24 healthy subjects by breathing 8% O2 in N2 for 90 s. Arterial oxygen tension was measured transcutaneously (tcpO2), photoplethysmography was employed to monitor changes in cutaneous vessel tone, and respiratory tidal volumes were measured by a Fleisch pneumotachograph. End tidal CO2 concentration, ECG, heart rate, finger skin resistance, and finger skin temperature were monitored continuously as well. Multi-unit skin sympathetic activity was recorded in the median nerve at wrist level by using Tungsten microelectrodes. By the end of the 90 s hypoxic test period tcpO2 was reduced from the control value of 95 +/- 1.8 mm Hg to 51.7 +/- 2.8 mm Hg; respiratory tidal volume increased from the resting value of 585 +/- 22 ml to 746 +/- 38 ml, while photoplethysmographic pulse amplitude decreased to 60% of control, together with a 0.22 +/- 0.03 degree C drop in skin temperature. The values are +/- S.E. In half of the cases skin resistance was reduced as well. Skin sympathetic activity increased during hypoxia and each major burst was followed by a reduction in pulse amplitude. The respiratory and photoplethysmographic responses exhibited similar time courses, with corresponding peaks. Voluntary hyperventilation for 90 s with room air also produced an initial reduction in pulse amplitude; however, it recovered within 60 s. It is concluded that in conscious human subjects, transient systemic hypoxia leads to constriction of cutaneous vessels in the hand, and that the vasoconstriction is the result of increased traffic in sympathetic efferent fibers. Skin vasoconstriction can develop independently of respiratory changes; usually the concomitant hyperventilation facilitates the cutaneous response.