Dynamic blood pressure control and middle cerebral artery mean blood velocity variability at rest and during exercise in humans.

AIMS: Cardiac failure and ischaemic heart disease patients receive standard of care cardiac beta(1)-adrenergic blockade medication. Such medication reduces cardiac output and cerebral blood flow. It is unknown whether the beta(1)-adrenergic blockade-induced reduction of cardiac output in the presence of an exercise-induced reduction in cardiac-arterial baroreflex gain affects cerebral blood flow variability. This study evaluated the influence of cardiac output variability on beat-to-beat middle cerebral artery mean blood velocity (MCA V(mean)) during exercise with and without cardiac beta(1)-adrenergic blockade. METHODS: Eight men (22 +/- 1 years; mean +/- SE) performed 15 min bouts of moderate (105 +/- 11 W) and heavy (162 +/- 8 W) intensity cycling before and after cardio-selective beta(1)-adrenergic blockade (0.15 mg kg(-1) metoprolol). The relationship between changes in cardiac output or mean arterial pressure (MAP) and MCA V(mean) as well as cardiac-arterial baroreflex gain were evaluated using transfer function analysis. RESULTS: Both exercise intensities decreased the low frequency (LF) transfer function gain between cardiac output and MCA V(mean) (P < 0.05) with no significant influence of beta(1)-blockade. In contrast, the LF transfer function gain between MAP and MCA V(mean) remained stable also with no significant influence of metoprolol (P > 0.05). The LF transfer function gain between MAP and HR, an index of cardiac-arterial baroreflex gain, decreased from rest to heavy exercise with and without beta(1)-blockade (P < 0.05). CONCLUSION: These findings suggest that the exercise intensity related reduction in cardiac-arterial baroreflex function at its operating point does not influence the dynamic control of MCA V(mean), even when the ability of exercise-induced increase in cardiac output is reduced by cardiac beta(1)-adrenergic blockade.

Standing up to the challenge of standing: a siphon does not support cerebral blood flow in humans.

Model studies have been advanced to suggest both that a siphon does and does not support cerebral blood flow in an upright position. If a siphon is established with the head raised, it would mean that internal jugular pressure reflects right atrium pressure minus the hydrostatic difference from the brain. This study measured spinal fluid pressure in the upright position, the pressure and the ultrasound-determined size of the internal jugular vein in the supine and sitting positions, and the internal jugular venous pressure during seated exercise. When the head was elevated approximately 25 cm above the level of the heart, internal jugular venous pressure decreased from 9.5 (SD 2.8) to 0.2 (SD 1.0) mmHg [n = 15; values are means (SD); P < 0.01]. Similarly, central venous pressure decreased from 6.2 (SD 1.8) to 0.6 (SD 2.6) mmHg (P < 0.05). No apparent lumen was detected in any of the 31 left or right internal veins imaged at 40 degrees head-up tilt, and submaximal (n = 7) and maximal exercise (n = 4) did not significantly affect internal jugular venous pressure. While seven subjects were sitting up, spinal fluid pressure at the lumbar level was 26 (SD 4) mmHg corresponding to 0.1 (SD 4.1) mmHg at the base of the brain. These results demonstrate that both for venous outflow from the brain and for spinal fluid, the prevailing pressure approaches zero at the base of the brain when humans are upright, which negates that a siphon supports cerebral blood flow.