Sympathetic excitation during exercise as a cause of attenuated heart rate recovery in patients with myocardial infarction

Abstract

Background: Heart rate recovery (HRR) after exercise is known as a predictor of cardiac death in patients with heart disease. The mechanism is not fully understood, although a parasympathetic mechanism has been reported. To elucidate the factors that influence HRR, we evaluated the relationship of HRR with exercise performance and plasma norepinephrine (NE), lactic acid and B-type natriuretic peptide (BNP) responses to exercise testing. Methods: The study population consisted of 52 male patients (age 58 ± 9.6 years) who had experienced myocardial infarction without residual ischemia, uncompensated heart failure or atrial fibrillation. All subjects underwent a symptom-limited cardiopulmonary exercise test without a cool-down period and echocardiography. NE, lactic acid and BNP were measured at rest and at peak exercise. Results: HRR did not correlate with the left ventricular ejection fraction, peak VO2,lactic acid and BNP. HRR significantly correlated with the increment in heart rate(HR)fromrestto peak exercise (AHR) (r=0.30, p<0.05). When we divided AHR into two phases at the anaerobic threshold (AT), HRR significantly correlated with AHR (peak-AT) (r=0.409, p<0.01), but not with AHR (AT-rest). There was a significant negative correlation between HRR andNEboth at rest and at peak exercise (r=-0.286, p<0.05, r=-0.310, p<0.05). HRR was also correlated significantly with AHR/logANE as an index of sensitivity to NE (r=0.421, p<0.01). Based on multiple regression analysis, AHR and logANE predicted HRR (R 2=0.467, p=0.0027). Conclusions: Present findings suggest that enhanced sympathetic excitation at maximum exercise suppresses parasympathetic reactivation and results in attenuation of HRR.