Cerebral metabolic response to submaximal exercise

Cerebral metabolic response to submaximal exercise Abstract We studied cerebral oxygenation and metabolism during submaximal cycling in 12 subjects. At two work rates, middle cerebral artery blood velocity increased from 62 ± 3 to 63 ± 3 and 70 ± 5 cm/s as did cerebral oxygenation determined by near-infrared spectroscopy. Oxyhemoglobin increased by 10 ± 3 and 25 ± 3 μmol/l ( P < 0.01), and there was no significant change in brain norepinephrine spillover. The arterial-to-internal-jugular-venous (a-v) difference for O 2 decreased at low-intensity exercise (from 3.1 ± 0.1 to 2.9 ± 0.1 mmol/l; P < 0.05) and recovered at moderate exercise (to 3.3 ± 0.1 mmol/l). The profile for glucose was similar: its a-v difference tended to decrease at low-intensity exercise (from 0.55 ± 0.05 to 0.50 ± 0.02 mmol/l) and increased during moderate exercise (to 0.64 ± 0.04 mmol/l; P < 0.05). Thus the molar ratio (a-v difference, O 2 to glucose) did not change significantly. However, when the a-v difference for lactate (0.02 ± 0.03 to 0.18 ± 0.04 mmol/l) was taken into account, the O 2 -to-carbohydrate ratio decreased (from 6.1 ± 0.4 to 4.7 ± 0.3; P < 0.05). The enhanced cerebral oxygenation suggests that, during exercise, cerebral blood flow increases in excess of the O 2 demand. Yet it seems that during exercise not all carbohydrate taken up by the brain is oxidized, as brain lactate metabolism appears to lower the balance of O 2 -to-carbohydrate uptake. blood pressure epinephrine glucose heart rate lactate near-infrared spectroscopy norepinephrine norepinephrine spillover Footnotes Address for reprint requests and other correspondence: K. Ide, Dept. of Anesthesia, Rigshospitalet 2041, Blegdamsvej 9, DK-2100 Copenhagen, Denmark (E-mail: Ide@rh.dk ). This study was supported by Danish National Research Foundation Grant 504–4 and Danish Medical Research Council Grant 9502885. The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. §1734 solely to indicate this fact. Copyright © 1999 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Physiology The American Physiological Society

Cerebral metabolic response to submaximal exercise

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
8750-7587
eISSN
1522-1601
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Abstract

Abstract We studied cerebral oxygenation and metabolism during submaximal cycling in 12 subjects. At two work rates, middle cerebral artery blood velocity increased from 62 ± 3 to 63 ± 3 and 70 ± 5 cm/s as did cerebral oxygenation determined by near-infrared spectroscopy. Oxyhemoglobin increased by 10 ± 3 and 25 ± 3 μmol/l ( P < 0.01), and there was no significant change in brain norepinephrine spillover. The arterial-to-internal-jugular-venous (a-v) difference for O 2 decreased at low-intensity exercise (from 3.1 ± 0.1 to 2.9 ± 0.1 mmol/l; P < 0.05) and recovered at moderate exercise (to 3.3 ± 0.1 mmol/l). The profile for glucose was similar: its a-v difference tended to decrease at low-intensity exercise (from 0.55 ± 0.05 to 0.50 ± 0.02 mmol/l) and increased during moderate exercise (to 0.64 ± 0.04 mmol/l; P < 0.05). Thus the molar ratio (a-v difference, O 2 to glucose) did not change significantly. However, when the a-v difference for lactate (0.02 ± 0.03 to 0.18 ± 0.04 mmol/l) was taken into account, the O 2 -to-carbohydrate ratio decreased (from 6.1 ± 0.4 to 4.7 ± 0.3; P < 0.05). The enhanced cerebral oxygenation suggests that, during exercise, cerebral blood flow increases in excess of the O 2 demand. Yet it seems that during exercise not all carbohydrate taken up by the brain is oxidized, as brain lactate metabolism appears to lower the balance of O 2 -to-carbohydrate uptake. blood pressure epinephrine glucose heart rate lactate near-infrared spectroscopy norepinephrine norepinephrine spillover Footnotes Address for reprint requests and other correspondence: K. Ide, Dept. of Anesthesia, Rigshospitalet 2041, Blegdamsvej 9, DK-2100 Copenhagen, Denmark (E-mail: Ide@rh.dk ). This study was supported by Danish National Research Foundation Grant 504–4 and Danish Medical Research Council Grant 9502885. The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. §1734 solely to indicate this fact. Copyright © 1999 the American Physiological Society

Journal

Journal of Applied PhysiologyThe American Physiological Society

Published: Nov 1, 1999

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