Neuroendocrine activation in heart failure is modified by endurance exercise training

Citation
Rw. Braith et al., Neuroendocrine activation in heart failure is modified by endurance exercise training, J AM COL C, 34(4), 1999, pp. 1170-1175
Citations number
42
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
07351097 → ACNP
Volume
34
Issue
4
Year of publication
1999
Pages
1170 - 1175
Database
ISI
SICI code
0735-1097(199910)34:4<1170:NAIHFI>2.0.ZU;2-D
Abstract
OBJECTIVES The purpose of this study was to determine whether endurance exe rcise training could buffer neuroendocrine activity In chronic heart failur e patients. BACKGROUND Neuroendocrine activation is associated with poor long-term prog nosis in heart failure. There is growing consensus that exercise may be ben eficial by altering the clinical course of heart failure, but the mechanism s responsible for exercise-induced benefits are unclear. METHODS Nineteen heart failure patients (ischemic disease; New York Heart A ssociation [NYHA] class II or III) were randomly assigned to either a train ing group or to a control group. Exercise training consisted of supervised walking three times a week for 16 weeks at 40% to 70% of peak oxygen uptake . Medications were unchanged. Neurohormones were measured at study entry an d after 16 weeks. RESULTS The training group (n = 10; age = 61 +/- 6 years; EF = 30 +/- 6%) a nd control group (n = 9; age = 62 +/- 7 years; EF = 29 +/- 7%) did not diff er in clinical findings at study entry. Resting levels of angiotensin II, a ldosterone, vasopressin and atrial natriuretic peptide in the training and control groups did not differ at study entry (5.6 +/- 1.3 pg/ml; 158 +/- 38 pg/ml; 6.1 +/- 2.0 pg/ml; 37 +/- 8 pg/ml training group vs. 4.8 +/- 1.2; 1 46 +/- 23; 4.9 +/- 1.1; 35 +/- 10 control group). Peak exercise levels of a ngiotensin II, aldosterone, vasopressin and atrial natriuretic peptide in t he exercise and control groups did not differ at study entry. After 16 week s, rest and peak exercise hormone levels were unchanged in control patients . Peak exercise neurohormone levels were unchanged in the training group, b ut resting levels were significantly (p < 0.001) reduced (angiotensin -26%; aldosterone -32%; vasopressin -30%; atrial natriuretic peptide -27%). CONCLUSIONS Our data indicate that 16 weeks of endurance exercise training modified resting neuroendocrine hyperactivity in heart failure patients. Re duction in circulating neurohormones may have a beneficial impact on long-t erm prognosis. (J Am Coll Cardiol 1999;34:1170-5) (C) 1999 by the American College of Cardiology.