Abstract
The Valsalva maneuver (VM) produces large and abrupt increases in mean arterial pressure (MAP) at the onset of strain (Phase I), however, hypotension, sufficient to induce syncope, occurs upon VM release (phase III). We examined the effect of VM intensity and duration on middle cerebral artery blood velocity (MCAv) responses. Healthy men (n = 10; mean +/- SD: 26 +/- 4 years) completed 30%, 60%, and 90% of their maximal VM mouth pressure, for 5 and 10 sec (order randomized) while standing. Beat-to-beat MCAv and MAP during phase I (peak), at nadir (phase III), and recovery are reported as the change from standing baseline. During phase I, MCAv rose 15 +/- 6 cm +/- s +/- 1 (P < 0.001), which was not reliably different between intensities (P = 0.11), despite graded increases in MAP (P < 0.001; e.g., +12 +/- 9 mmHg vs. +35 +/- 14 for 5 sec 30% and 90% VM, respectively). During Phase III, the MCAv response was duration-(P = 0.045) and intensity dependent (P < 0.001), with the largest decrease observed following the 90% VM (e.g., +/- 19 +/- 13 and +/- 15 +/- 11 cm +/- s +/- 1 for 5 and 10 sec VM, respectively) with a concomitant decrease in MAP (P < 0.001, - 23 +/- 11 and - 23 +/- 9 mmHg). This asymmetric response may be attributable to the differential modulators of MCAv throughout the VM. The mechanical effects of the elevated intrathoracic pressure during phase I may restrain increases in cerebral perfusion via related increases in intracranial pressure; however, during phase III the decrease in MCAv arises from an abrupt hypotension, the extent of which is dependent upon both the duration and intensity of the VM.