Regional cerebral artery mean flow velocity and blood flow during dynamic exercise in humans

Jørgensen, Lise Bolt; Perko, G.; Secher, Niels H.

doi:10.1152/jappl.1992.73.5.1825

Cited by 189 publications

(159 citation statements)

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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%

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%

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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“…Consistent increases in middle cerebral artery blood velocity (MCAV) have been observed from rest to submaximal whole body normoxic exercise (50,52,62), whereas other cerebral arteries did not show a similar increase (55). Changes in CBF during exercise depend on cerebral areas being activated and are distributed heterogeneously within the brain (58), global CBF as measured with the Kety-Schmidt method remaining relatively constant from rest to maximal exercise (62).…”

Section: Cerebral Blood Flowmentioning

confidence: 86%

Cerebral perturbations during exercise in hypoxia

Vergès

Rupp

Jubeau

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Reduction of aerobic exercise performance observed under hypoxic conditions is mainly attributed to altered muscle metabolism due to impaired O 2 delivery. It has been recently proposed that hypoxia-induced cerebral perturbations may also contribute to exercise performance limitation. A significant reduction in cerebral oxygenation during whole body exercise has been reported in hypoxia compared with normoxia, while changes in cerebral perfusion may depend on the brain region, the level of arterial oxygenation and hyperventilation induced alterations in arterial CO 2. With the use of transcranial magnetic stimulation, inconsistent changes in cortical excitability have been reported in hypoxia, whereas a greater impairment in maximal voluntary activation following a fatiguing exercise has been suggested when arterial O 2 content is reduced. Electromyographic recordings during exercise showed an accelerated rise in central motor drive in hypoxia, probably to compensate for greater muscle contractile fatigue. This accelerated development of muscle fatigue in moderate hypoxia may be responsible for increased inhibitory afferent signals to the central nervous system leading to impaired central drive. In severe hypoxia (arterial O 2 saturation Ͻ70 -75%), cerebral hypoxia per se may become an important contributor to impaired performance and reduced motor drive during prolonged exercise. This review examines the effects of acute and chronic reduction in arterial O 2 (and CO2) on cerebral blood flow and cerebral oxygenation, neuronal function, and central drive to the muscles. Direct and indirect influences of arterial deoxygenation on central command are separated. Methodological concerns as well as future research avenues are also considered. cerebral perfusion; cerebral oxygenation; cortex excitability; central motor command; endurance WITH THE EXCEPTION of very short or static exercises performed at a high percentage of maximal power (15,19,83), hypoxia deteriorates exercise performance (7, 82). In particular, the maximal aerobic workload (Ẇ max ) that can be sustained during exercise involving large muscle groups (e.g., cycling) is considerably lower in hypoxia compared with normoxia. The difference between these two environmental conditions increases progressively with the reduction in oxygen inspiratory pressure (PI O 2 ) (36) and is affected by subjects' fitness so that subjects with elevated maximal aerobic capacity are more affected by hypoxia (41).The origin of exercise performance limitation in hypoxia is still under debate, since the consequences of reduced blood O 2 affect the whole organism. This limitation has been attributed to a lowered O 2 partial pressure in arterial blood (Pa O 2 ) reducing arterial O 2 content and O 2 delivery to tissues with critical consequences on muscle metabolism and contraction (1, 46). Magnetic nerve stimulation has confirmed the effects of reduced arterial oxygenation on dynamic (12, 111) and static (54) exercise-induced alterations in muscle contractility. Reduced muscle O...

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“…Surprisingly, in both studies the relative increases in V mean were generally smaller than for CBF, and this finding cannot be explained by activation of brain regions supplied by the anterior cerebral artery. 7 In a later study from the same group, a more robust method (SPECT scanning) for determination of global CBF was applied, and it was then found that global CBF remained constant, whereas V mean still increased. 15 This inconsistency is not readily explained, and we believe that changes in the diameter of the MCA may take place in dynamic exercise, eg, the activation of the sympathetic nervous system may constrict the larger cerebral resistance vessels concomitant to an autoregulatory dilation of the smaller resistance vessels.…”

Section: Discussionmentioning

confidence: 99%

Transcranial Doppler is valid for determination of the lower limit of cerebral blood flow autoregulation.

Larsen

Olsen

Hansen

et al. 1994

Stroke

261

152

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Background and Purpose This study validates transcranial Doppler sonography (TCD) for determination of the lower limit of cerebral blood flow (CBF) autoregulation and establishes a relation between global CBF and mean flow velocity (V mean ) in the middle cerebral artery.Methods Relative changes in CBF and in V mean were compared in 12 normal volunteers (2 women and 10 men; median age, 30 years [range, 21 to 61 years]). Catheters was placed in the left radial artery and in the bulb of the right internal jugular vein, respectively. Baseline CBF was measured by single-photon emission computed tomography scanning; concomitantly, blood samples were drawn for calculation of the cerebral arteriovenous oxygen difference. Then changes in mean arterial pressure (MAP) were induced, and relative changes in global CBF were calculated according to Fick's principle assuming a constant cerebral oxygen metabolism. MAP was increased 30 mm Hg by norepinephrine infusion and was decreased by lower body negative pressure. V raean was

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Regional cerebral artery mean flow velocity and blood flow during dynamic exercise in humans

Cited by 189 publications

References 0 publications

Dynamic cerebral autoregulation remains stable during physical challenge in healthy persons

Dynamic cerebral autoregulation remains stable during physical challenge in healthy persons

Cerebral perturbations during exercise in hypoxia

Transcranial Doppler is valid for determination of the lower limit of cerebral blood flow autoregulation.

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