Physical exercise increases middle cerebral artery blood flow velocity

Hellström, G; Wahlgren, Nils

doi:10.1007/bf00258249

Cited by 42 publications

(43 citation statements)

References 13 publications

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“…As expected (17,25,30), we observed an exerciseinduced increase in BP as well as an increase in CBFV. Exercise also significantly increased the power of LF oscillations of BP, most likely related to increased sympathetic drive (42, 50a).…”

Section: Discussionsupporting

confidence: 89%

“…During increasing levels of physical effort, cerebral perfusion is not only driven by increasing BP and heart rate (HR) but also has to adjust to high levels of sympathetic activity and to altered metabolism with changes in PO 2 and PCO 2 . With increasing muscle metabolism, PO 2 in the blood decreases, whereas PCO 2 increases, unless augmented respiration compensates for the higher O 2 demand and production of CO 2 (17,35,54). Cerebral autoregulation has to counterbalance all the cardiovascular and metabolic responses to physical effort.…”

mentioning

confidence: 99%

“…With increasing muscle metabolism, PO 2 in the blood decreases, whereas PCO 2 increases, unless augmented respiration compensates for the higher O 2 demand and production of CO 2 (17,35,54). Cerebral autoregulation has to counterbalance all the cardiovascular and metabolic responses to physical effort.…”

mentioning

confidence: 99%

“…Cerebral autoregulation has to counterbalance all the cardiovascular and metabolic responses to physical effort. Although some studies suggest that CBF velocity (CBFV) and CBF remain stable despite physical effort (15), several others found an increase in CBFV (14,17,30) as well as regional CBF (10,55) and global CBF during exercise (24,51).…”

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confidence: 99%

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Dynamic cerebral autoregulation remains stable during physical challenge in healthy persons

Bryś

Brown²,

Marthol³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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. Dynamic cerebral autoregulation remains stable during physical challenge in healthy persons. Am J Physiol Heart Circ Physiol 285: H1048-H1054, 2003; 10.1152/ajpheart.00062.2003.-The effects of physical activity on cerebral blood flow (CBF) and cerebral autoregulation (CA) have not yet been fully evaluated. There is controversy as to whether increasing heart rate (HR), blood pressure (BP), and sympathetic and metabolic activity with altered levels of CO2 might compromise CBF and CA. To evaluate these effects, we studied middle cerebral artery blood flow velocity (CBFV) and CA in 40 healthy young adults at rest and during increasing levels of physical exercise. We continuously monitored HR, BP, endexpiratory CO 2, and CBFV with transcranial Doppler sonography at rest and during stepwise ergometric challenge at 50, 100, and 150 W. The modulation of BP and CBFV in the low-frequency (LF) range (0.04-0.14 Hz) was calculated with an autoregression algorithm. CA was evaluated by calculating the phase shift angle and gain between BP and CBFV oscillations in the LF range. The LF BP-CBFV gain was then normalized by conductance. Cerebrovascular resistance (CVR) was calculated as mean BP adjusted to brain level divided by mean CBFV. HR, BP, CO 2, and CBFV increased significantly with exercise. Phase shift angle, absolute and normalized LF BP-CBFV gain, and CVR, however, remained stable. Stable phase shift, LF BP-CBFV gain, and CVR demonstrate that progressive physical exercise does not alter CA despite increasing HR, BP, and CO 2. CA seems to compensate for the hemodynamic effects and increasing CO2 levels during exercise.cross-spectral analysis; low-frequency blood pressure-cerebral blood flow velocity gain; phase shift angle; cerebrovascular resistance CEREBRAL AUTOREGULATION normally ensures that cerebral blood flow (CBF) remains relatively constant despite fluctuations in blood pressure (BP), provided that mean BP remains within the range of autoregulation, usually from 50 to 170 mmHg (6,21,37). If BP exceeds these limits, CBF increases, initially in a curvilinear relation, and then follows BP passively in a linear relation (21, 31). During increasing levels of physical effort, cerebral perfusion is not only driven by increasing BP and heart rate (HR) but also has to adjust to high levels of sympathetic activity and to altered metabolism with changes in PO 2 and PCO 2 . With increasing muscle metabolism, PO 2 in the blood decreases, whereas PCO 2 increases, unless augmented respiration compensates for the higher O 2 demand and production of CO 2 (17,35,54). Cerebral autoregulation has to counterbalance all the cardiovascular and metabolic responses to physical effort. Although some studies suggest that CBF velocity (CBFV) and CBF remain stable despite physical effort (15), several others found an increase in CBFV (14, 17, 30) as well as regional CBF (10, 55) and global CBF during exercise (24, 51).During cardiovascular changes as they occur with increasing physical challenge, cerebral autoregulation can be evaluated b...

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Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Dynamic cerebral autoregulation remains stable during physical challenge in healthy persons

Bryś

Brown²,

Marthol³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…The increase in the MFV of the MCA reflects a CBF increase. This may be the result of the vasoneuronal coupling, which means that the activation of certain cerebral regions needs more perfusion [22, 23, 24]. These conclusions are, however, indirect because we used non-invasive, rather than invasive measurement methods.…”

Section: Discussionmentioning

confidence: 96%

Delayed Cerebrovascular Autoregulatory Response to Ergometer Exercise in Normotensive Elderly Humans

Heckmann

Brown²,

Cheregi³

et al. 2003

Cerebrovasc Dis

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Background: Relatively little is known about physiological cerebrovascular haemodynamics during physical stress in elderly healthy individuals. The aim of this study was to determine the effect of ergometer stress on cerebrovascular haemodynamics in elderly healthy individuals in comparison with young healthy individuals, using non-invasive methods. Methods: Continuous middle cerebral artery blood flow velocity (CBFV; transcranial Doppler ultrasound), beat-to-beat blood pressure, heart rate and transcutaneous pCO₂ were measured in response to 3 min ergometer exercise stress in 18 elderly healthy subjects (mean age ± SD 66.5 ± 5.8 years) and 18 healthy young subjects (mean age ± SD 29.4 ± 4.7 years). Pulsatility index (PI) was used as a parameter for cerebrovascular resistance. The subjects were in a supine position with an elevated trunk and performed exercise by pedalling on an ergometer, generating 75–100 W. Statistical analysis was carried out using MANOVA, a general linear model with repeated measures. Results: In both groups, blood pressure increased significantly (p < 0.001) with time during exercise, with no significant differences between the groups or regarding interaction (time sequence/group factor). Heart rate increased significantly with time during exercise (p < 0.001) and was significantly more prominent (p = 0.002) and prolonged (p < 0.001) in the young group. pCO₂ did not differ with time or between the groups and with regard to interaction. Mean CBFV (MFV) increased significantly during time (p < 0.001). Between the groups, there was no significant difference (p = 0.836), but with regard to interaction (time sequence/group factor), there was a significant delay in MFV increase in the group of young subjects (p = 0.002). The PI, a measure of cerebrovascular resistance, increased significantly with time without significant differences between the groups (p = 0.061), but was significantly delayed in the elderly regarding the interaction time sequence/group factor (p < 0.001). Conclusion: The cerebrovascular changes during ergometer exercise may reflect the combined activation of the cerebrovascular autoregulative mechanisms (predominantly neurogenic and myogenic). In healthy normotensive elderly subjects, cerebral autoregulatory capacity is retained but delayed in response to ergometer stress compared with young healthy subjects. We speculate that these findings may contribute to a higher risk of cerebral hypoperfusion in the elderly.

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Cocaine-Induced Cerebral Vasoconstriction Detected in Humans With Magnetic Resonance Angiography

Kaufman

Levin

Ross

et al. 1998

JAMA

189

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Context.-Clinical observations and case reports suggest that there are important cerebrovascular complications of cocaine use, but no studies have documented a direct link. Objective.-To determine whether low-dose cocaine administration induces cerebral vasoconstriction in healthy cocaine users. Design.-Randomized controlled trial. Subjects.-Twenty-four healthy and neurologically normal men (mean age, 29 years) reporting median cocaine use of 8 lifetime exposures (range, 3 to Ͼ40). Intervention.-Double-blind intravenous administration of cocaine (0.4 or 0.2 mg/kg) or placebo, with cerebral magnetic resonance angiography performed at baseline and 20 minutes following infusion. Main Outcome Measure.-Cocaine-induced angiographic change indicative of vasoconstriction, as independently and concordantly rated by 2 reviewers blind to treatment condition. Results.-Cocaine-induced cerebral vasoconstriction in a dose-related fashion (P=.03), with angiograms indicative of vasoconstriction found in 5 of 8 and 3 of 9 subjects receiving 0.4-and 0.2-mg/kg cocaine, respectively, compared with 1 of 7 subjects administered placebo. Outcome stratification by frequency of self-reported lifetime cocaine use (3-10 times, 11-40 times, or Ͼ40 times) revealed a statistically stronger dose-related effect (PϽ.001), suggesting that greater lifetime cocaine use was associated with a greater likelihood of vasoconstriction. Conclusions.-Cocaine administration induced dose-related cerebral vasoconstriction on magnetic resonance angiograms. These changes occurred at low cocaine doses and in the absence of other risk factors, including polydrug abuse, hypertension, or cerebrovascular disease. Outcome stratification by prior cocaine use statistically strengthened the relationship between cocaine administration and vasoconstriction, suggesting that cocaine may have a cumulative residual effect in promoting cerebrovascular dysfunction.

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Physical exercise increases middle cerebral artery blood flow velocity

Cited by 42 publications

References 13 publications

Dynamic cerebral autoregulation remains stable during physical challenge in healthy persons

Dynamic cerebral autoregulation remains stable during physical challenge in healthy persons

Delayed Cerebrovascular Autoregulatory Response to Ergometer Exercise in Normotensive Elderly Humans

Cocaine-Induced Cerebral Vasoconstriction Detected in Humans With Magnetic Resonance Angiography

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