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Maintained cerebral metabolic ratio during exercise in patients with β‐adrenergic blockade
Author(s) -
Gam Christiane M. B.,
Rasmussen Peter,
Secher Niels H.,
Seifert Thomas,
Larsen Fin S.,
Nielsen Henning B.
Publication year - 2009
Publication title -
clinical physiology and functional imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.608
H-Index - 67
eISSN - 1475-097X
pISSN - 1475-0961
DOI - 10.1111/j.1475-097x.2009.00889.x
Subject(s) - medicine , propranolol , brachial artery , endocrinology , jugular vein , adrenergic , carbohydrate metabolism , blockade , anesthesia , cardiology , receptor , blood pressure
Summary Background: Decreased cerebral metabolic ratio (CMR) [molar uptake of O 2 versus molar uptake of (glucose + ½ lactate)] during exercise is attenuated by intravenous administration of the non‐selective β‐adrenergic receptor antagonist propranolol. We evaluated to what extent cirrhotic patients in oral treatment with propranolol are able to mobilize brain non‐oxidative carbohydrate metabolism. Methods: Incremental cycle ergometry to exhaustion (86 ± 4·2 W; mean ± SD) was performed in eight cirrhotic patients instrumented with a catheter in the brachial artery and one retrograde in the right internal jugular vein. Healthy subjects form the control group. Results: In β‐blocked cirrhotic patients arterial lactate increased from 1·5 ± 0·3 to 5·1 ± 0·8 mM ( P <0·05) and the arterial–jugular venous difference (a–v diff) from −0·01 ± 0·03 to 0·30 ± 0·05 mM ( P <0·05) at rest and during exercise, respectively. During exercise the glucose a–v diff of 0·46 ± 0·06 mM remained at a level similar to rest (0·54 ± 0·03 mM) and at exhaustion the CMR was not significantly changed (5·8 ± 1·1 versus 6·0 ± 0·6). In controls, CMR decreased from 5·6 ± 0·9 at rest to 3·4 ± 0·7 ( P <0·05) during maximal exercise and at a lactate level comparable to that achieved by the patients it was 3·8 ± 0·4. Conclusion: During exhaustive exercise in cirrhotic patients the CMR is maintained and a significant cerebral uptake of lactate is demonstrated. The data suggest that oral treatment with a non‐selective β‐adrenergic receptor antagonist attenuates cerebral non‐oxidative metabolism.