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INTEGRATIVE |
1 Department of Anaesthesia, The Copenhagen Muscle Research Centre, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark
Intense exercise decreases the cerebral metabolic ratio of oxygen to carbohydrates [O2/(glucose +
lactate)], but whether this ratio is influenced by adrenergic stimulation is not known. In eight males, incremental cycle ergometry increased arterial lactate to 15.3 ± 4.2 mM (mean ± S.D.) and the arterial–jugular venous (a–v) difference from –0.02 ± 0.03 mM at rest to 1.0 ± 0.5 mM (P < 0.05). The a–v difference for glucose increased from 0.7 ± 0.3 to 0.9 ± 0.1 mM (P < 0.05) at exhaustion and the cerebral metabolic ratio decreased from 5.5 ± 1.4 to 3.0 ± 0.3 (P < 0.01). Administration of a non-selective β-adrenergic (β1 + β2) receptor antagonist (propranolol) reduced heart rate (69 ± 8 to 58 ± 6 beats min–1) and exercise capacity (239 ± 42 to 209 ± 31 W; P < 0.05) with arterial lactate reaching 9.4 ± 3.6 mM. During exercise with propranolol, the increase in a–v lactate difference (to 0.5 ± 0.5 mM; P < 0.05) was attenuated and the a–v glucose difference and the cerebral metabolic ratio remained at levels similar to those at rest. Together with the previous finding that the cerebral metabolic ratio is unaffected during exercise with administration of the β1-receptor antagonist metropolol, the present results suggest that the cerebral metabolic ratio decreases in response to a β2-receptor mechanism.
(Received 22 January 2008;
accepted after revision 7 April 2008;
first published online 10 April 2008)
Corresponding author T. S. Larsen: Department of Anaesthesia, Rigshospitalet 2041, Blegdamsvej 9, DK 2100, Copenhagen Ø, Denmark. Email: tseifert78{at}gmail.com
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