Obstructive apnea and voluntary breath holding are associated with transien
t increases in muscle sympathetic nerve activity (MSNA) and arterial pressu
re. The contribution of changes in blood flow relative to the contribution
of changes in vascular resistance to the apnea-induced transient rise in ar
terial pressure is unclear. We measured heart rate, mean arterial blood pre
ssure (MAP), MSNA (peroneal microneurography), and femoral artery blood vel
ocity (V-FA, Doppler) in humans during voluntary end-expiratory apnea while
they were exposed to room air, hypoxia (10.5% inspiratory fraction of O-2)
, and hyperoxia (100% inspiratory fraction of O-2). Changes from baseline o
f leg blood flow ((Q) over dot) and vascular resistance (R) were estimated
from the following relationships: (Q) over dot infinity V-FA, corrected for
the heart rate, and R infinity MAP/(Q) over dot . During apnea, MSNA rose;
this rise in MSNA was followed by a rise in MAP, which peaked a few second
s after resumption of breathing. Responses of MSNA and MAP to apnea were gr
eatest during hypoxia and smallest during hyperoxia (P < 0.05 for both comp
ared with room air breathing). Similarly, apnea was associated with a decre
ase in Q and an increase in R. The decrease in Q was greatest during hypoxi
a and smallest during hyperoxia (-25 +/- 3 vs. -6 +/- 4%, P < 0.05), and th
e increase in R was the greatest during hypoxia and the least during hypero
xia (60 +/- 8 vs. 21 +/- 6%, P < 0.05). Thus voluntary apnea is associated
with vasoconstriction, which is in part mediated by the sympathetic nervous
system. Because apnea induced vasoconstriction is most intense during hypo
xia and attenuated during hyperoxia, it appears to depend at least in part
on stimulation of arterial chemoreceptors.