Reduction In Cerebral Blood Velocity Research Articles

High-intensity exercise does not protect against orthostatic intolerance following bedrest in 55- to 65-yr-old men and women.

Prolonged bedrest provokes orthostatic hypotension and intolerance of upright posture. Limited data are available on the cardiovascular responses of older adults to head-up tilt following bedrest, with no studies examining the potential benefits of exercise to mitigate intolerance in this age group. This randomized controlled trial of head-down bedrest (HDBR) in 55- to 65-yr-old men and women investigated if exercise could avert post-HDBR orthostatic intolerance. Twenty-two healthy older adults (11 female) underwent a strict 14-day HDBR and were assigned to either an exercise (EX) or control (CON) group. The exercise intervention included high-intensity, aerobic, and resistance exercises. Head-up tilt-testing to a maximum of 15 minutes was performed at baseline (Pre-Bedrest) and immediately after HDBR (R1), as well as 6 days (R6) and 4 weeks (R4wk) later. At Pre-Bedrest, three participants did not complete the full 15 minutes of tilt. At R1, 18 did not finish, with no difference in tilt end time between CON (422 ± 287 s) and EX (409 ± 346 s). No differences between CON and EX were observed at R6 or R4wk. At R1, just 1 participant self-terminated the test with symptoms, while 12 others reported symptoms only after physiological test termination criteria were reached. Finishers on R1 protected arterial pressure with higher total peripheral resistance relative to Pre-Bedrest. Cerebral blood velocity decreased linearly with reductions in arterial pressure, end-tidal CO2, and cardiac output. High-intensity interval exercise did not benefit post-HDBR orthostatic tolerance in older adults. Multiple factors were associated with the reduction in cerebral blood velocity leading to intolerance.

TILT TEST TOLERANCE AFTER TWO-WEEKS BED REST IN OLDER ADULTS IS NOT PROTECTED BY DAILY AEROBIC AND RESISTANCE EXERCISE

Abstract Bed rest is associated with increased risk of orthostatic intolerance on return to upright posture and, at least in young adults, regular exercise during bed rest is proposed as protective. 22 older adults (55-65 years, half women) participated in a randomized trial with 14-days of continuous 6-degree head-down bed rest. Half completed 60 min/day of aerobic and high-intensity interval cycling plus resistance exercises (Ex) while the other half were control (Con). A passive 80-degree head-up tilt (HUT) to a maximum of 15-min assessed orthostatic tolerance while cardio- and cerebrovascular responses were monitored to a pre-syncopal level of systolic blood pressure < 90 mmHg. In pre-bed rest baseline, all but 3 women (Ex) completed 15-min HUT. After 14-days bed rest, only 3 men (1 Ex) and 1 woman (Ex) completed 15-min with no differences in tolerance between men and women or Ex and Con. Vasovagal syncope presented in 5 participants (2 M-Con, 1 M-Ex, 1 F-Con, 1 F-Ex), most other non-finishers had progressive reduction in stroke volume without adequate vasoconstriction. Reductions in cerebral blood velocity measured during HUT by Doppler ultrasound revealed strong linear relationships to both end-tidal PCO2 and mean arterial pressure across all participants. These data indicate that neither older men nor older women were protected from orthostatic intolerance by 60-min per day exercise including high-intensity interval training. These data contrast with previous findings in younger adults in controlled trials of bed rest pointing to the need for greater understanding of mechanisms regulating blood pressure and brain blood flow.

Sodium bicarbonate ingestion mitigates the heat-induced hyperventilation and reduction in cerebral blood velocity during exercise in the heat.

Hyperthermia during exercise in the heat causes minute ventilation ([Formula: see text]) to increase, which leads to reductions in arterial CO2 partial pressure ([Formula: see text]) and cerebral blood flow. On the other hand, sodium bicarbonate ingestion reportedly results in metabolic alkalosis, leading to decreased [Formula: see text] and increased [Formula: see text] during prolonged exercise in a thermoneutral environment. Here, we investigated whether sodium bicarbonate ingestion suppresses heat-induced hyperventilation and the resultant hypocapnia and cerebral hypoperfusion during prolonged exercise in the heat. Eleven healthy men ingested a solution of sodium bicarbonate (0.3 g/kg body wt) (NaHCO3 trial) or sodium chloride (0.208 g/kg) (NaCl trial). Ninety minutes after the ingestion, the subjects performed a cycle exercise for 60 min at 50% of peak oxygen uptake in the heat (35°C and 40% relative humidity). Esophageal temperature did not differ between the trials throughout (P = 0.56, main effect of trial). [Formula: see text] gradually increased with exercise duration in the NaCl trial, but the increases in [Formula: see text] were attenuated in the NaHCO3 trial (P = 0.01, main effect of trial). Correspondingly, estimated [Formula: see text] and middle cerebral artery blood velocity (an index of anterior cerebral blood flow) were higher in the NaHCO3 than the NaCl trial (P = 0.002 and 0.04, main effects of trial). Ratings of perceived exertion were lower in the NaHCO3 than the NaCl trial (P = 0.02, main effect of trial). These results indicate that sodium bicarbonate ingestion mitigates heat-induced hyperventilation and reductions in [Formula: see text] and cerebral blood velocity during prolonged exercise in the heat.NEW & NOTEWORTHY Hyperthermia causes hyperventilation and concomitant hypocapnia and cerebral hypoperfusion. The cerebral hypoperfusion may underlie central fatigue. We demonstrate that sodium bicarbonate ingestion reduces heat-induced hyperventilation and attenuates hypocapnia-related cerebral hypoperfusion during prolonged exercise in the heat. In addition, we show that sodium bicarbonate ingestion reduces ratings of perceived exertion during the exercise. This study provides new insight into the development of effective strategies for preventing central fatigue during exercise in the heat.

The effect of hypercapnia on regional cerebral blood flow regulation during progressive lower-body negative pressure.

Previous work indicates that dynamic cerebral blood flow (CBF) regulation is impaired during hypercapnia; however, less is known about the impact of resting hypercapnia on regional CBF regulation during hypovolemia. Furthermore, there is disparity within the literature on whether differences between anterior and posterior CBF regulation exist during physiological stressors. We hypothesized: (a) lower-body negative pressure (LBNP)-induced reductions in cerebral blood velocity (surrogate for CBF) would be more pronounced during hypercapnia, indicating impaired CBF regulation; and (b) the anterior and posterior cerebral circulations will exhibit similar responses to LBNP. In 12 healthy participants (6 females), heart rate (electrocardiogram), mean arterial pressure (MAP; finger photoplethosmography), partial pressure of end-tidal carbon dioxide (PETCO2), middle cerebral artery blood velocity (MCAv) and posterior cerebral artery blood velocity (PCAv; transcranial Doppler ultrasound) were measured. Cerebrovascular conductance (CVC) was calculated as MCAv or PCAv indexed to MAP. Two randomized incremental LBNP protocols were conducted (-20, -40, -60 and -80mmHg; three-minute stages), during coached normocapnia (i.e., room air), and inspired 5% hypercapnia (~ + 7mmHg PETCO2 in normoxia). The main findings were: (a) static CBF regulation in the MCA and PCA was similar during normocapnic and hypercapnic LBNP trials, (b) MCA and PCA CBV and CVC responded similarly to LBNP during normocapnia, but (c) PCAv and PCA CVC were reduced to a greater extent at -60mmHg LBNP (P = 0.029; P < 0.001) during hypercapnia. CBF regulation during hypovolemia was preserved in hypercapnia, and regional differences in cerebrovascular control may exist during superimposed hypovolemia and hypercapnia.

Acute reduction in cerebral blood velocity on supine-to-stand transition increases postural instability in young adults.

We tested the hypothesis that transient deficits in cerebral blood flow are associated with postural sway. In 19 young, healthy adults, we examined the association between the drop in cerebral blood flow during supine-to-stand transitions, indexed by transcranial Doppler ultrasound [middle cerebral artery blood velocity at diastole (MCAdv)] and near-infrared spectroscopy [tissue saturation index (TSI)] and the center of pressure displacement while standing. Participants performed transitions under three conditions aimed at progressively increasing the drop in MCAdv, in a randomized order: 1) a control transition (Con); 2) a transition that coincided with deflation of bilateral thigh cuffs; and 3) a transition that coincided with both thigh-cuff deflation and 90 s of prior hyperventilation (HTC). The deficit in diastolic blood velocity (MCAdv deficit) was quantified as the difference between MCAdv and its preceding baseline value, summed over 10 s, beginning at the MCAdv nadir. Compared with Con, HTC led to greater drops in MCAdv (P = 0.003) and TSI (P < 0.001) at nadir. The MCAdv deficit was positively associated with the center of pressure displacement vector-average using repeated-measures correlation (repeated-measures correlation coefficient = 0.56, P < 0.001). An a posteriori analysis identified a sub-group of participants that showed an exaggerated increase in MCAdv deficit and greater postural instability in both the anterior-posterior (P = 0.002) and medial-lateral (P = 0.021) directions in response to the interventions. These findings support the theory that individuals who experience greater initial cerebral hypoperfusion on standing may be at a greater risk for falls.NEW & NOTEWORTHY Dizziness and risk for falls after standing might link directly to reduced delivery of oxygen to the brain. By introducing challenges that increased the drop in brain blood flow in healthy young adults, we have shown for the first time a direct link to greater postural instability. These results point to a need to measure cerebral blood flow and/or oxygenation after postural transitions in populations, such as older adults, to assist in fall risk assessment.

Responses of cerebral blood velocity and tissue oxygenation to low-frequency oscillations during simulated haemorrhagic stress in humans.

What is the central question of this study? Do low-frequency oscillations in arterial pressure and cerebral blood velocity protect cerebral blood velocity and oxygenation during central hypovolaemia? What is the main finding and its importance? Low-frequency oscillations in arterial pressure and cerebral blood velocity attenuate reductions in cerebral oxygen saturation but do not protect absolute cerebral blood velocity during central hypovolaemia. This finding indicates the potential importance of haemodynamic oscillations in maintaining cerebral oxygenation and therefore viability of tissues during challenges to cerebral blood flow and oxygen delivery. Tolerance to both real and simulated haemorrhage varies between individuals. Exaggerated low-frequency (∼0.1Hz) oscillations in mean arterial pressure and brain blood flow [indexed via middle cerebral artery velocity (MCAv)] have been associated with improved tolerance to reduced central blood volume. The mechanism for this association has not been explored. We hypothesized that inducing low-frequency oscillations in arterial pressure and cerebral blood velocity would attenuate reductions in cerebral blood velocity and oxygenation during simulated haemorrhage. Fourteen subjects (11men and three women) were exposed to oscillatory (0.1 and 0.05Hz) and non-oscillatory (0Hz) lower-body negative pressure profiles with an average chamber pressure of -60mmHg (randomized and counterbalanced order). Measurements included arterial pressure and stroke volume via finger photoplethysmography, MCAv via transcranial Doppler ultrasound, and cerebral oxygenation of the frontal lobe via near-infrared spectroscopy. Tolerance was higher during the two oscillatory profiles compared with the 0Hz profile (0.05Hz, P=0.04; 0.1Hz, P=0.09), accompanied by attenuated reductions in stroke volume (P<0.001) and cerebral oxygenation of the frontal lobe (P≤0.02). No differences were observed between profiles for reductions in mean arterial pressure (P=0.17) and MCAv (P=0.30). In partial support of our hypothesis, cerebral oxygenation, but not cerebral blood velocity, was protected during the oscillatory profiles. Interestingly, more subjects tolerated the oscillatory profiles compared with the static 0Hz profile, despite similar arterial pressure responses. These findings emphasize the potential importance of haemodynamic oscillations in maintaining perfusion and oxygenation of cerebral tissues during haemorrhagic stress.

Post-exercise syncope: Wingate syncope test and visual-cognitive function.

Adequate cerebral perfusion is necessary to maintain consciousness in upright humans. Following maximal anaerobic exercise, cerebral perfusion can become compromised and result in syncope. It is unknown whether post‐exercise reductions in cerebral perfusion can lead to visual‐cognitive deficits prior to the onset of syncope, which would be of concern for emergency workers and warfighters, where critical decision making and intense physical activity are combined. Therefore, the purpose of this experiment was to determine if reductions in cerebral blood velocity, induced by maximal anaerobic exercise and head‐up tilt, result in visual‐cognitive deficits prior to the onset of syncope. Nineteen sedentary to recreationally active volunteers completed a symptom‐limited 60° head‐up tilt for 16 min before and up to 16 min after a 60 sec Wingate test. Blood velocity of the middle cerebral artery was measured using transcranial Doppler ultrasound and a visual decision‐reaction time test was assessed, with independent analysis of peripheral and central visual field responses. Cerebral blood velocity was 12.7 ± 4.0% lower (mean ± SE; P < 0.05) after exercise compared to pre‐exercise. This was associated with a 63 ± 29% increase (P < 0.05) in error rate for responses to cues provided to the peripheral visual field, without affecting central visual field error rates (P = 0.46) or decision‐reaction times for either visual field. These data suggest that the reduction in cerebral blood velocity following maximal anaerobic exercise contributes to visual‐cognitive deficits in the peripheral visual field without an apparent affect to the central visual field.

Elevated local skin temperature impairs cutaneous vasoconstrictor responses to a simulated haemorrhagic challenge while heat stressed

During a simulated haemorrhagic challenge, syncopal symptoms develop sooner when individuals are hyperthermic relative to normothermic. This is due, in part, to a large displacement of blood to the cutaneous circulation during hyperthermia, coupled with inadequate cutaneous vasoconstriction during the hypotensive challenge. The influence of local skin temperature on these cutaneous vasoconstrictor responses is unclear. This project tested the hypothesis that local skin temperature modulates cutaneous vasoconstriction during simulated haemorrhage in hyperthermic humans. Eight healthy participants (four men and four women; 32 ± 7 years old; 75.2 ± 10.8 kg) underwent lower-body negative pressure to presyncope while heat stressed via a water-perfused suit sufficiently to increase core temperature by 1.2 ± 0.2 °C. At forearm skin sites distal to the water-perfused suit, local skin temperature was either 35.2 ± 0.6 (mild heating) or 38.2 ± 0.2 °C (moderate heating) throughout heat stress and lower-body negative pressure, and remained at these temperatures until presyncope. The reduction in cutaneous vascular conductance during the final 90 s of lower-body negative pressure, relative to heat-stress baseline, was greatest at the mildly heated site (-10 ± 15% reduction) relative to the moderately heated site (-2 ± 12%; P = 0.05 for the magnitude of the reduction in cutaneous vascular conductance between sites), because vasoconstriction at the moderately heated site was either absent or negligible. In hyperthermic individuals, the extent of cutaneous vasoconstriction during a simulated haemorrhage can be modulated by local skin temperature. In situations where skin temperature is at least 38 °C, as is the case in soldiers operating in warm climatic conditions, a haemorrhagic insult is unlikely to be accompanied by cutaneous vasoconstriction.

Effects of aging on the cerebrovascular orthostatic response

When healthy subjects stand up, it is associated with a reduction in cerebral blood velocity and oxygenation although cerebral autoregulation would be considered to prevent a decrease in cerebral perfusion. Aging is associated with a higher incidence of falls, and in the elderly falls may occur particularly during the adaptation to postural change. This study evaluated the cerebrovascular adaptation to postural change in 15 healthy younger (YNG) vs. 15 older (OLD) subjects by recordings of the near-infrared spectroscopy-determined cerebral oxygenation (cO₂Hb) and the transcranial Doppler-determined mean middle cerebral artery blood velocity (MCA V(mean)). In OLD (59 (52-65) years) vs. YNG (29 (27-33) years), the initial postural decline in mean arterial pressure (-52 ± 3% vs. -67 ± 3%), cO₂Hb (-3.4 ± 2.5 μmoll(-1) vs. -5.3 ± 1.7 μmoll(-1)) and MCA V(mean) (-16 ± 4% vs. -29 ± 3%) was smaller. The decline in MCA V(mean) was related to the reduction in MAP. During prolonged orthostatic stress, the decline in MCA V(mean)and cO(2)Hb in OLD remained smaller. We conclude that with healthy aging the postural reduction in cerebral perfusion becomes less prominent.

Heat stress reduces cerebral blood velocity and markedly impairs orthostatic tolerance in humans

Orthostatic tolerance is reduced in the heat-stressed human. This study tested the following hypotheses: 1) whole body heat stress reduces cerebral blood velocity (CBV) and increases cerebral vascular resistance (CVR); and 2) reductions in CBV and increases in CVR in response to an orthostatic challenge will be greater while subjects are heat stressed. Fifteen subjects were instrumented for measurements of CBV (transcranial ultrasonography), mean arterial blood pressure (MAP), heart rate, and internal temperature. Whole body heating increased both internal temperature (36.4+/-0.1 to 37.3+/-0.1 degrees C) and heart rate (59+/-3 to 90+/-3 beats/min); P<0.001. Whole body heating also reduced CBV (62+/-3 to 53+/-2 cm/s) primarily via an elevation in CVR (1.35+/-0.06 to 1.63+/-0.07 mmHg.cm-1.s; P<0.001. A subset of subjects (n=8) were exposed to lower-body negative pressure (LBNP 10, 20, 30, 40 mmHg) in both normothermic and heat-stressed conditions. During normothermia, LBNP of 30 mmHg (highest level of LBNP achieved by the majority of subjects in both thermal conditions) did not significantly alter CBV, CVR, or MAP. During whole body heating, this LBNP decreased MAP (81+/-2 to 75+/-3 mmHg), decreased CBV (50+/-4 to 39+/-1 cm/s), and increased CVR (1.67+/-0.17 to 1.92+/-0.12 mmHg.cm-1.s); P<0.05. These data indicate that heat stress decreases CBV, and the reduction in CBV for a given orthostatic challenge is greater during heat stress. These outcomes reduce the reserve to buffer further decreases in cerebral perfusion before presyncope. Increases in CVR during whole body heating, coupled with even greater increases in CVR during orthostasis and heat stress, likely contribute to orthostatic intolerance.

Orthostatic tolerance, cerebral oxygenation, and blood velocity in humans with sympathetic failure.

Patients with orthostatic hypotension due to sympathetic failure become symptomatic when standing, although their capability to maintain cerebral blood flow is reported to be preserved. We tested the hypothesis that in patients with sympathetic failure, orthostatic symptoms reflect reduced cerebral perfusion with insufficient oxygen supply. This study addressed the relationship between orthostatic tolerance, mean cerebral artery blood velocity (V(mean), determined by transcranial Doppler ultrasonography), oxygenation (oxyhemoglobin [O(2)Hb], determined by near-infrared spectroscopy), and mean arterial pressure at brain level (MAP(MCA), determined by finger arterial pressure monitoring [Finapres]) in 9 patients (aged 37 to 70 years; 4 women) and their age- and sex-matched controls during 5 minutes of standing. Supine MAP(MCA) (108+/-14 versus 86+/-14 mm Hg) and V(mean) (84+/-21 versus 62+/-13 cm. s(-1)) were higher in the patients. After 5 minutes of standing, MAP(MCA) was lower in the patients (31+/-14 versus 72+/-14 mm Hg), as was V(mean) (51+/-8 versus 59+/-9 cm. s(-1)), with a larger reduction in O(2)Hb (-11. 6+/-4 versus -6.7+/-4.5 micromol. L(-1)). Four patients terminated standing after 1 to 3.5 minutes. In these symptomatic patients, the orthostatic fall in V(mean) was greater (45+/-6 versus 64+/-10 cm. s(-1)), and the orthostatic decrease in O(2)Hb (-12.0+/-3.3 versus -7.6+/-3.9 micromol. L(-1)) tended to be larger. The reduction in MAP(MCA) was larger after 10 seconds of standing, and MAP(MCA) was lower after 1 minute (25+/-8 versus 40+/-6 mm Hg). In patients with sympathetic failure, the orthostatic reduction in cerebral blood velocity and oxygenation is larger. Patients who become symptomatic within 5 minutes of standing are characterized by a pronounced orthostatic fall in blood pressure, cerebral blood velocity, and oxygenation manifest within the first 10 seconds of standing.