Hypercapnia elicits differential vascular and blood flow responses in the cerebral circulation and active skeletal muscles in exercising humans.

The purpose of this study was to investigate the effects of a rise in arterial carbon dioxide pressure (PaCO 2 ) on vascular and blood flow responses in the cerebral circulation and active skeletal muscles during dynamic exercise in humans. Thirteen healthy young adults (three women) participated in hypercapnia and normocapnia trials. In both trials, participants performed a two-legged dynamic knee extension exercise at a constant workload that increased heart rate to roughly 100 beats min -1 . In the hypercapnia trial, participants performed the exercise with spontaneous breathing while end-tidal carbon dioxide pressure (P ET CO 2 ), an index of PaCO 2 , was held at 60 mmHg by inhaling hypercapnic gas (O 2 : 20.3 ± 0.1%; CO 2 : 6.0 ± 0.5%). In the normocapnia trial, minute ventilation during exercise was matched to the value in the hypercapnia trial by performing voluntary hyperventilation with P ET CO 2 clamped at baseline level (i.e., 40-45 mmHg) through inhalation of mildly hypercapnic gas (O 2 : 20.6 ± 0.1%; CO 2 : 2.7 ± 1.0%). Middle cerebral artery mean blood velocity and the cerebral vascular conductance index were higher in the hypercapnia trial than in the normocapnia trial. By contrast, vascular conductance in the exercising leg was lower in the hypercapnia trial than in the normocapnia trial. Blood flow to the exercising leg did not differ between the two trials. These results demonstrate that hypercapnia-induced vasomotion in active skeletal muscles is opposite to that in the cerebral circulation. These differential vascular responses may cause a preferential rise in cerebral blood flow.