Cerebral blood flow and metabolism during exercise. Prog Neurobiol

The Copenhagen Muscle Research Centre, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, Blegdamsvej 9, DK-2100 Copenhagen, Denmark
Progress in Neurobiology (Impact Factor: 9.99). 08/2000; 61(4):397-414. DOI: 10.1016/S0301-0082(99)00057-X


During exercise regional cerebral blood flow (rCBF), as blood velocity in major cerebral arteries and also blood flow in the internal carotid artery increase, suggesting an increase in blood flow to a large part of the brain. Such an increase in CBF is independent of the concomitant increase in blood pressure but is modified by the alteration in arterial carbon dioxide tension (PaCO2). Also, the increase in middle cerebral artery mean blood velocity (MCA Vmean) reported with exercise appears to depend on the ability to increase cardiac output (CO), as demonstrated in response to beta-1 blockade and in patients with cardiac insufficiency or atrial fibrillation.Near-infrared spectroscopy (NIRS) determined cerebral oxygenation supports the alterations in MCA Vmean during exercise. Equally, the observation that the cerebrovascular CO2-reactivity appears to be smaller in the standing than in the sitting and especially in the supine position could relate to the progressively smaller CO.In contrast, during exercise “global” cerebral blood flow (gCBF), as determined by the Kety–Schmidt technique is regarded as being constant. One limitation of the Kety–Schmidt method for measuring CBF is that blood flow in the two internal jugular veins depends on the origin of drainage and it has not been defined which internal jugular venous flow is evaluated. Such a consideration is equally relevant for an evaluation of cerebral metabolism during exercise.While the regional cerebral uptake of oxygen (O2) increases during exercise, the global value is regarded as being constant. Yet, during high intensity exercise lactate is taken up by the brain and its O2 uptake also increases. Furthermore, in the initial minutes of recovery immediately following exercise, brain glucose and O2 uptake are elevated and lactate uptake remains high.A maintained substrate uptake by the brain after exercise suggests a role for brain glycogen in cerebral activation, but the fate of brain substrate uptake has not yet been determined.

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Available from: Kojiro Ide, Apr 29, 2014
    • "At higher intensities of exercise, CBF and cerebral oxygenation tend to plateau and even return to resting levels, in line with the hyperventilation-induced fall in arterial carbon dioxide tension (P aCO 2 ) (Ide & Secher, 2000; Ogoh et al. 2005). Age-related impairments in regulation of the skeletal muscle vasculature have been reported both at rest and especially during exercise, partly due to exaggerated sympathetic vasoconstriction, endothelial dysfunction and attenuated metabolic vasodilatation (Dinenno & Joyner, 2006; Proctor & Parker, 2006; Schrage et al. 2007; Kirby et al. 2012; Phillips et al. 2012). "
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    ABSTRACT: Age is one of the most important risk factors for dementia and stroke. Examination of the cerebral circulatory responses to acute exercise in the elderly may help to pinpoint the mechanisms by which exercise training can reduce the risk of brain diseases, inform the optimisation of exercise training programmes and assist with the identification of age-related alterations in cerebral vascular function. During low-to-moderate intensity dynamic exercise, enhanced neuronal activity is accompanied by cerebral perfusion increases of ∼10-30%. Beyond ∼60-70% maximal oxygen uptake, cerebral metabolism remains elevated but perfusion in the anterior portion of the circulation returns towards baseline, substantively because of a hyperventilation-mediated reduction in the partial pressure of arterial carbon dioxide (PaCO2 ) and cerebral vasoconstriction. Cerebral perfusion is lower in older individuals, both at rest and during incremental dynamic exercise. Nevertheless, the increase in the estimated cerebral metabolic rate for oxygen and the arterial-internal jugular venous differences for glucose and lactate are similar in young and older individuals exercising at the same relative exercise intensities. Correction for the age-related reduction in PaCO2 during exercise by the provision of supplementary CO2 is suggested to remove ∼50% of the difference in cerebral perfusion between young and older individuals. A multitude of candidates could account for the remaining difference, including cerebral atrophy, enhanced vasoconstrictor and blunted vasodilatory pathways. In summary, age-related reductions in cerebral perfusion during exercise are partly associated with a lower PaCO2 in exercising older individuals, nevertheless the cerebral extraction of glucose, lactate and oxygen appear to be preserved. This article is protected by copyright. All rights reserved.
    The Journal of Physiology 10/2015; DOI:10.1113/JP271081 · 5.04 Impact Factor
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    • "The major explanation of this phenomenon is cerebral vasoconstriction (less exercise vasodilatation) induced by hypocapnia during heavy exercise intensities (Bhambhani et al., 2007). Indeed CO 2 is an important vasodilatator of the cerebral vasculature during exercise (Ide and Secher, 2000; Seifert and Secher, 2011). Bhambhani et al. (2007) reported closed relationships between RCP and Th COx in healthy subjects. "
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    ABSTRACT: The study examined whether the aerobic fitness level modifies the cerebral oxygenation response to incremental ramp exercise, and more specifically the decline in cerebral oxygenation from heavy exercise up to maximal intensities.11 untrained (V˙O2max 47.3 ± 4.0 ml.min−1.kg−1) and 13 endurance-trained (V˙O2max 61.2 ± 8.0 ml.min−1.kg−1) healthy men performed a maximal ramp cycle exercise. Left prefrontal cortex oxygenation (ΔHbO2) was monitored by near-infrared spectroscopy. A cerebral oxygenation threshold decline (ThCOx) during exercise was determined. ThCox occurred in all subjects but for higher V˙O2 (mL.min−1.kg−1) in endurance-trained than in untrained subjects (P < 0.01). At submaximal exercise intensity corresponding to ThCOx, ΔHbO2 was higher in endurance-trained than in untrained subjects (P < 0.05). V˙O2 at ThCox was related to V˙O2 at respiratory compensation point (n = 24, r = 0.93, P < 0.001) and to V˙O2max (n = 24, r = 0.92, P < 0.001). These findings indicate that above the respiratory compensation point the prefrontal O2 demand exceeds the supply in untrained and in endurance-trained subjects. In addition, the occurrence of ThCOx was delayed to higher absolute exercise intensities in endurance-trained in relation with their higher V˙O2max than untrained men. These results demonstrated that aerobic fitness influences cerebral oxygenation during exercise.
    Respiratory Physiology & Neurobiology 10/2014; 205. DOI:10.1016/j.resp.2014.10.009 · 1.97 Impact Factor
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    • "Here, we investigated the vascular mechanisms underlying the hemodynamic response function in the superficial layers of the cortex in response to exercise. Previous work on the existence, localization and even direction of cerebral blood flow and volume changes during exercise are contentious (reviewed in (Ide and Secher, 2000)), with some studies showing no changes (Globus et al., 1983), some showing global, non-specific increases (Herholz et al., 1987), and other showing localized increases (Jørgensen et al., 1992; Linkis et al., 1995). One explanation for the discrepancies among these studies, which use different methodologies and durations of exercise, is that different techniques have different sensitivity to arterial versus venous changes. "
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    ABSTRACT: Voluntary locomotion is accompanied by large increases in cortical activity and localized increases in cerebral blood volume (CBV). We sought to quantitatively determine the spatial and temporal dynamics of voluntary locomotion-evoked cerebral hemodynamic changes. We measured single vessel dilations using two-photon microscopy and cortex-wide changes in CBV-related signal using intrinsic optical signal (IOS) imaging in head-fixed mice freely locomoting on a spherical treadmill. During bouts of locomotion, arteries dilated rapidly, while veins distended slightly and recovered slowly. The dynamics of diameter changes of both vessel types could be captured using a simple linear convolution model. Using these single vessel measurements, we developed a novel analysis approach to separate out spatially and temporally distinct arterial and venous components of the location-specific hemodynamic response functions (HRF) for IOS. The HRF of each pixel of was well fit by a sum of a fast arterial and a slow venous component. The HRFs of pixels in the limb representations of somatosensory cortex had a large arterial contribution, while in the frontal cortex the arterial contribution to the HRF was negligible. The venous contribution was much less localized, and was substantial in the frontal cortex. The spatial pattern and amplitude of these HRFs in response to locomotion in the cortex were robust across imaging sessions. Separating the more localized, the arterial component from the diffuse venous signals will be useful for dealing with the dynamic signals generated by naturalistic stimuli. Copyright © 2014. Published by Elsevier Inc.
    NeuroImage 10/2014; 105. DOI:10.1016/j.neuroimage.2014.10.030 · 6.36 Impact Factor
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