Background and Purpose-The relationship between middle cerebral artery (MCA) flow velocity (CFV) and cerebral blood flow (CBF) is uncertain because of unknown vessel diameter response to physiological stimuli. The purpose of this study was to directly examine the effect of a simulated orthostatic stress (lower body negative pressure [LBNP]) as well as increased or decreased end-tidal carbon dioxide partial pressure (P ET CO 2 ) on MCA diameter and CFV. Methods-Twelve subjects participated in a CO 2 manipulation protocol and/or an LBNP protocol. In the CO 2 manipulation protocol, subjects breathed room air (normocapnia) or 6% inspired CO 2 (hypercapnia), or they hyperventilated to Ϸ25 mm Hg P ET CO 2 (hypocapnia). In the LBNP protocol, subjects experienced 10 minutes each of Ϫ20 and Ϫ40 mm Hg lower body suction. CFV and diameter of the MCA were measured by transcranial Doppler and MRI, respectively, during the experimental protocols. Results-Compared with normocapnia, hypercapnia produced increases in both P ET CO 2 (from 36Ϯ3 to 40Ϯ4 mm Hg, PϽ0.05) and CFV (from 63Ϯ4 to 80Ϯ6 cm/s, PϽ0.001) but did not change MCA diameters (from 2.9Ϯ0.3 to 2.8Ϯ0.3 mm). Hypocapnia produced decreases in both P ET CO 2 (24Ϯ2 mm Hg, PϽ0.005) and CFV (43Ϯ7 cm/s, PϽ0.001) compared with normocapnia, with no change in MCA diameters (from 2.9Ϯ0.3 to 2.9Ϯ0.4 mm). During Ϫ40 mm Hg LBNP, P ET CO 2 was not changed, but CFV (55Ϯ4 cm/s) was reduced from baseline (58Ϯ4 cm/s, PϽ0.05), with no change in MCA diameter. Conclusions-Under the conditions of this study, changes in MCA diameter were not detected. Therefore, we conclude that relative changes in CFV were representative of changes in CBF during the physiological stimuli of moderate LBNP or changes in P ET CO 2 .

That insufficient sleep is associated with poor attention and performance deficits is becoming widely recognized. Fewer people are aware that chronic sleep complaints in epidemiological studies have also been associated with an increase in overall mortality and morbidity. This article summarizes findings of known effects of insufficient sleep on cardiovascular risk factors including blood pressure, glucose metabolism, hormonal regulation and inflammation with particular emphasis on experimental sleep loss, using models of total and partial sleep deprivation, in healthy individuals who normally sleep in the range of 7-8 hours and have no sleep disorders. These studies show that insufficient sleep alters established cardiovascular risk factors in a direction that is known to increase the risk of cardiac morbidity.

The dynamics of the cerebral vascular response to blood pressure changes in hypertensive humans is poorly understood. Because cerebral blood flow is dependent on adequate perfusion pressure, it is important to understand the effect of hypertension on the transfer of pressure to flow in the cerebrovascular system of elderly people. Therefore, we examined the effect of spontaneous and induced blood pressure changes on beat-to-beat and within-beat cerebral blood flow in three groups of elderly people: normotensive, controlled hypertensive, and uncontrolled hypertensive subjects. Cerebral blood flow velocity (transcranial Doppler), blood pressure (Finapres), heart rate, and end-tidal CO(2) were measured during the transition from a sit to stand position. Transfer function gains relating blood pressure to cerebral blood flow velocity were assessed during steady-state sitting and standing. Cerebral blood flow regulation was preserved in all three groups by using changes in cerebrovascular resistance, transfer function gains, and the autoregulatory index as indexes of cerebral autoregulation. Hypertensive subjects demonstrated better attenuation of cerebral blood flow fluctuations in response to blood pressure changes both within the beat (i.e., lower gain at the cardiac frequency) and in the low-frequency range (autoregulatory, 0.03-0.07 Hz). Despite a better pressure autoregulatory response, hypertensive subjects demonstrated reduced reactivity to CO(2). Thus otherwise healthy hypertensive elderly subjects, whether controlled or uncontrolled with antihypertensive medication, retain the ability to maintain cerebral blood flow in the face of acute changes in perfusion pressure. Pressure regulation of cerebral blood flow is unrelated to cerebrovascular reactivity to CO(2).

Objective-Neurovascular coupling may be involved in compensatory mechanisms responsible for preservation of gait speed in elderly people with cerebrovascular disease. Our study examines the association between neurovascular coupling in the middle cerebral artery and gait speed in elderly individuals with impaired cerebral vasoreactivity.Methods-Twenty-two fast and 20 slow walkers in the lowest quartile of cerebral vasoreactivity were recruited from the MOBILIZE Boston Study. Neurovascular coupling was assessed in bilateral middle cerebral arteries by measuring cerebral blood flow during the N-Back Task. Cerebral white matter hyperintensities were measured for each group using magnetic resonance imaging.Results-Neurovascular coupling was attenuated in slow compared to fast walkers (2.8% [CI 95%: −0.9-6.6] vs. 8.2% [CI 95%: 4.7-11.8]; p=0.02). The odds of being a slow walker were 6.4 (CI 95%: 1.7-24.9, p=0.007) if there was a high burden of white matter hyperintensity, however, this risk increased to 14.5 (CI 95%: 2.3-91.1, p=0.004) if neurovascular coupling was also attenuated.Interpretation-Our results suggest that intact neurovascular coupling may help preserve mobility in elderly people with cerebral microvascular disease.