Copyright © 1999 by the European Society of Cardiology.
Resting muscle sympathetic nerve activity and peak oxygen uptake in heart failure and normal subjects
Division of Cardiology and Harrowston Heart Failure Clinic, Mount Sinai Hospital
Division of Cardiology, The Toronto Hospital
The Centre for Cardiovascular Research, University of Toronto, Toronto, Ontario, Canada
revised November 24, 1998; accepted November 26, 1998
Abstract
Aims Exercise intolerance and increased efferent vasoconstrictor traffic to muscle are two characteristics of heart failure that have not been explicitly linked. We tested the hypothesis that peak oxygen consumption is inversely related to resting muscle sympathetic nerve activity in heart failure.
Methods and Results We recorded peroneal muscle sympathetic nerve activity in 17 treated heart failure patients (16 men,1 woman; mean ejection fraction of 26·0±3·2% (SE)) and 17 age-matched healthy subjects (16 men, 1 woman). Oxygen consumption was measured during cycle ergometry to maximal effort. In heart failure and normal subjects, mean peak oxygen consumption was 20·6±1·7 vs 32·2±2·6ml.kg1.min1(P<0·0001) and mean muscle sympathetic activity was 49·3±2·8 vs 33·0±3·3 bursts.min1(P<·0007) respectively. When age was accounted for by multiple regression analysis, there was a significant relationship between peak oxygen consumption and burst frequency in heart failure (P<0·02) but not in healthy subjects. The percent of predicted peak oxygen consumption achieved (based on age, sex and body size) was inversely related to muscle sympathetic nerve burst frequency in heart failure (r=0·71, P<0·0014) but not in normal subjects (r=0·44, P<0·08;P<0·0001 for this comparison).
Conclusion Reduced exercise capacity in heart failure is related to increased efferent sympathetic traffic to calf muscle. These observations are consistent with the concept of a peripheral neurogenic limit to exercise in heart failure.
Key Words: Heart failure oxygen consumption sympathetic nerve activity exercise capacity ejection fraction
f1 Correspondence : John S. Floras, Division of Cardiology, Mount Sinai Hospital, Suite 1614, 600 University Avenue, Toronto, Ontario, M5G 1X5, Canada.
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