Neuroendocrine activation in heart failure is modified by endurance exercise training.
OBJECTIVE
The purpose of this study was to determine whether endurance exercise training could buffer neuroendocrine activity in chronic heart failure patients.


BACKGROUND
Neuroendocrine activation is associated with poor long-term prognosis in heart failure. There is growing consensus that exercise may be beneficial by altering the clinical course of heart failure, but the mechanisms responsible for exercise-induced benefits are unclear.


METHODS
Nineteen heart failure patients (ischemic disease; New York Heart Association [NYHA] class II or III) were randomly assigned to either a training 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 and after 16 weeks.


RESULTS
The training group (n = 10; age = 61 +/- 6 years; EF = 30 +/- 6%) and control group (n = 9; age = 62 +/- 7 years; EF = 29 +/- 7%) did not differ in clinical findings at study entry. Resting levels of angiotensin II, aldosterone, 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; 146 +/- 23; 4.9 +/- 1.1; 35 +/- 10 control group). Peak exercise levels of angiotensin II, aldosterone, vasopressin and atrial natriuretic peptide in the exercise and control groups did not differ at study entry. After 16 weeks, rest and peak exercise hormone levels were unchanged in control patients. Peak exercise neurohormone levels were unchanged in the training group, but 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. Reduction in circulating neurohormones may have a beneficial impact on long-term prognosis.
Braith
R W
RW
Center for Exercise Science, College of Health and Human Performance, University of Florida, Gainesville 32611, USA. rbraith@hhp.ufl.edu
Welsch
M A
MA
Feigenbaum
M S
MS
Kluess
H A
HA
Pepine
C J
CJ
D000368:Aged; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D009320:Atrial Natriuretic Factor / Q000097:blood; D003327:Coronary Disease / Q000503:physiopathology / Q000534:rehabilitation; D015444:Exercise / Q000502:physiology*; D005260:Female; D006333:Heart Failure / Q000503:physiopathology / Q000534:rehabilitation*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009490:Neurosecretory Systems / Q000503:physiopathology*; D010807:Physical Endurance / Q000502:physiology*; D011379:Prognosis; D013318:Stroke Volume / Q000502:physiology; D016896:Treatment Outcome; D014667:Vasopressins / Q000097:blood
D014667:Vasopressins; D000804:Angiotensin II; D000450:Aldosterone; D009320:Atrial Natriuretic Factor