Sympathetic Excitation during Exercise as a Cause of Attenuated Heart Rate Recovery in Patients with Myocardial Infarction
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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) from rest to peak exercise (ΔHR) (r=0.30, p<0.05). When we divided ΔHR into two phases at the anaerobic threshold (AT), HRR significantly correlated with ΔHR (peak-AT) (r=0.409, p<0.01), but not with ΔHR (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 ΔHR/logΔNE as an index of sensitivity to NE (r=0.421, p<0.01). Based on multiple regression analysis, ΔHR and logΔNE predicted HRR (R2=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.
- 日本医科大学医学会の論文
日本医科大学医学会 | 論文
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