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Abstract: We examined how cerebral blood flow velocity (CBV) and neurovascular coupling is influenced by exercise. Blood velocities in the posterior and middle cerebral arteries (PCAv and MCAv) during rest and cycling exercise at 60% estimated maximal oxygen consumption were measured. Neurovascular coupling was quantified as the ΔPCAv with visual stimulation. During exercise, despite a 15.2±13.6% and 26.1±22.5% increase from rest in the MCAv and PCAv, respectively, neurovascular coupling was unaltered. Thus, despite regionally heterogeneous elevations in CBV during exercise, neurometabolic coupling is maintained. [Copyright &y& Elsevier]

Abstract: We investigated regional changes in cerebral artery velocity during incremental exercise while breathing normoxia (21% O2), hyperoxia (100% O2) or hypoxia (16% O2) [n =10; randomized cross over design]. Middle cerebral and posterior cerebral arterial velocities (MCAv and PCAv) were measured continuously using transcranial Doppler ultrasound. At rest, only PCAv was reduced (−7%; P =0.016) with hyperoxia. During low-intensity exercise (40% workload maximum [Wmax]) MCAv (+17cms−1; +14cms−1) and PCAv (+9cms−1; +14cms−1) were increased above baseline with normoxia and hypoxia, respectively (P <0.05). The absolute increase from rest in MCAv was greater than the increase in PCAv between 40 and 80% Wmax with normoxia; this greater increase in MCAv was also evident at 60% Wmax with hypoxia and hyperoxia. Hyperoxic exercise resulted in larger absolute (+19cms−1) and relative (+40%) increases in PCAv compared with normoxia. Our findings highlight the selective changes in PCAv during hyperoxic incremental exercise. [Copyright &y& Elsevier]

Abstract: Nitric oxide (NO) is a potent vasodilator that regulates pulmonary vascular tone. During ascent to high altitude, pulmonary vascular tone increases leading to pulmonary hypertension. To explore the mechanisms underpinning this effect, we investigated the relationship between exhaled NO (; nmHg) and pulmonary artery systolic pressure (PASP; mmHg) in 11 healthy adults during hypoxic challenge at sea level [with oxygen saturations () of 80% and 90%] and at intervals during graded ascent to 5050m. During normobaric hypoxia, PASP progressively increased from 22.7mmHg to 33.5mmHg (p =0.006), whilst remained unchanged. In contrast, during ascent to high altitude, PASP increased progressively from 22.7mmHg to 39.1mmHg (p <0.001), but decreased from 18.8nmHg to 9.0nmHg (p <0.001). However, after appropriate adjustments, had no significant effect on PASP at altitude (p =0.309). These findings indicate that although exhaled NO decreases with altitude, it does not appear to be a major contributor to hypoxic pulmonary vasoconstriction. [Copyright &y& Elsevier]

Abstract: There is considerable utility in the use of transcranial Doppler ultrasound (TCD) to assess cerebrovascular function. The brain is unique in its high energy and oxygen demand but limited capacity for energy storage that necessitates an effective means of regional blood delivery. The relative low cost, ease-of-use, non-invasiveness, and excellent temporal resolution of TCD make it an ideal tool for the examination of cerebrovascular function in both research and clinical settings. TCD is an efficient tool to access blood velocities within the cerebral vessels, cerebral autoregulation, cerebrovascular reactivity to CO2, and neurovascular coupling, in both physiological states and in pathological conditions such as stroke and head trauma. In this review, we provide: (1) an overview of TCD methodology with respect to other techniques; (2) a methodological synopsis of the cerebrovascular exam using TCD; (3) an overview of the physiological mechanisms involved in regulation of the cerebral blood flow; (4) the utility of TCD for assessment of cerebrovascular pathology; and (5) recommendations for the assessment of four critical and complimentary aspects of cerebrovascular function: intra-cranial blood flow velocity, cerebral autoregulation, cerebral reactivity, and neurovascular coupling. The integration of these regulatory mechanisms from an integrated systems perspective is discussed, and future research directions are explored. [Copyright &y& Elsevier]

Moving rapidly from a supine to a standing posture is a common daily activity, yet a significant physiological challenge. Syncope can result from the development of initial orthostatic hypotension (IOH) involving a transient fall in systolic/diastolic blood pressure (BP) of >40/20 mm Hg within the first 15 s, and/or a delayed orthostatic hypotension (DOH) involving a fall in systolic/diastolic BP of >20/10 mm Hg within 15 min of posture change. Although epidemiological data indicate a heightened syncope risk in the morning, little is known about the diurnal variation in the IOH and DOH mechanisms associated with postural change. The authors hypothesized that the onset of IOH and DOH occurs sooner, and the associated cardiorespiratory and cerebrovascular changes are more pronounced, in the early morning. At 06:00 and 16:00 h, 17 normotensive volunteers, aged 26 ± 1 yrs (mean ± SE), completed a protocol involving supine rest, an upright stand, and a 60° head-up tilt (HUT) during which continuous beat-to-beat measurements of middle cerebral artery velocity (MCAv), mean arterial BP (MAP), heart rate, and end-tidal P co2 (PET co2) were obtained. Mean MCAv was ∼12% lower at baseline in the morning ( p ≤ .01) and during the HUT ( p < .01), despite a morning elevation in PET co2 by ∼2.2 mm Hg ( p = .01). The decline in MAP during initial standing (morning vs. afternoon: 50% ± 4% vs. 49% ± 3%) and HUT (39% ± 3% vs. 38% ± 3%) did not vary with time-of-day ( p > .30). In conclusion, although there is a marked reduction in MCAv in the morning, there is an absence of diurnal variation in the onset of and associated physiological responses associated with IOH and DOH. These responses, at least in this population, are unlikely contributors to the diurnal variation in orthostatic tolerance. (Author correspondence: ) [ABSTRACT FROM AUTHOR]