Effects of long-term exercise training on autonomic control in myocardial infarction patients

DG Martinez, JC Nicolau, RL Lage, E Toschi-Dias… - …, 2011 - Am Heart Assoc
DG Martinez, JC Nicolau, RL Lage, E Toschi-Dias, LDNJ de Matos, MJNN Alves
Hypertension, 2011Am Heart Assoc
Autonomic dysfunction, including baroreceptor attenuation and sympathetic activation, has
been reported in patients with myocardial infarction (MI) and has been associated with
increased mortality. We tested the hypotheses that exercise training (ET) in post-MI patients
would normalize arterial baroreflex sensitivity (BRS) and muscle sympathetic nerve activity
(MSNA), and long-term ET would maintain the benefits in BRS and MSNA. Twenty-eight
patients after 1 month of uncomplicated MI were randomly assigned to 2 groups, ET (MI-ET) …
Autonomic dysfunction, including baroreceptor attenuation and sympathetic activation, has been reported in patients with myocardial infarction (MI) and has been associated with increased mortality. We tested the hypotheses that exercise training (ET) in post-MI patients would normalize arterial baroreflex sensitivity (BRS) and muscle sympathetic nerve activity (MSNA), and long-term ET would maintain the benefits in BRS and MSNA. Twenty-eight patients after 1 month of uncomplicated MI were randomly assigned to 2 groups, ET (MI-ET) and untrained. A normal control group was also studied. ET consisted of three 60-minute exercise sessions per week for 6 months. We evaluated MSNA (microneurography), blood pressure (automatic oscillometric method), heart rate (ECG), and spectral analysis of RR interval, systolic arterial pressure (SAP), and MSNA. Baroreflex gain of SAP-RR interval and SAP-MSNA were calculated using the α-index. At 3 to 5 days and 1 month after MI, MSNA and low-frequency SAP were significantly higher and BRS significantly lower in MI patients when compared with the normal control group. ET significantly decreased MSNA (bursts per 100 heartbeats) and the low-frequency component of SAP and significantly increased the low-frequency component of MSNA and BRS of the RR interval and MSNA. These changes were so marked that the differences between patients with MI and the normal control group were no longer observed after ET. MSNA and BRS in the MI-untrained group did not change from baseline over the same time period. ET normalizes BRS, low-frequency SAP, and MSNA in patients with MI. These improvements in autonomic control are maintained by long-term ET. These findings highlight the clinical importance of this nonpharmacological therapy based on ET in the long-term treatment of patients with MI.
Am Heart Assoc