Akiko Ushijima1, Nagaharu Fukuma, Yuko Kato, Noriko Aisu, Kyoichi Mizuno. 1. Division of Cardiology, Hepatology, Geriatrics, and Integrated Medicine, Department of Internal Medicine, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan. ushijima@nms.ac.jp
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 VO(2), lactic acid and BNP. HRR significantly correlated with the increment in heart rate (HR) from rest to peak exercise (DeltaHR) (r=0.30, p<0.05). When we divided DeltaHR into two phases at the anaerobic threshold (AT), HRR significantly correlated with DeltaHR (peak-AT) (r=0.409, p<0.01), but not with DeltaHR (AT-rest). There was a significant negative correlation between HRR and NE both at rest and at peak exercise (r=-0.286, p<0.05, r=-0.310, p<0.05). HRR was also correlated significantly with DeltaHR/logDeltaNE as an index of sensitivity to NE (r=0.421, p<0.01). Based on multiple regression analysis, DeltaHR and logDeltaNE 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.
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 VO(2), lactic acid and BNP. HRR significantly correlated with the increment in heart rate (HR) from rest to peak exercise (DeltaHR) (r=0.30, p<0.05). When we divided DeltaHR into two phases at the anaerobic threshold (AT), HRR significantly correlated with DeltaHR (peak-AT) (r=0.409, p<0.01), but not with DeltaHR (AT-rest). There was a significant negative correlation between HRR and NE both at rest and at peak exercise (r=-0.286, p<0.05, r=-0.310, p<0.05). HRR was also correlated significantly with DeltaHR/logDeltaNE as an index of sensitivity to NE (r=0.421, p<0.01). Based on multiple regression analysis, DeltaHR and logDeltaNE 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.
Authors: Felipe X Cepeda; Edgar Toschi-Dias; Cristiane Maki-Nunes; Maria Urbana P B Rondon; Maria Janieire N N Alves; Ana Maria F W Braga; Daniel G Martinez; Luciano F Drager; Geraldo Lorenzi-Filho; Carlos E Negrao; Ivani C Trombetta Journal: Sleep Date: 2015-07-01 Impact factor: 5.849