PURPOSE: One hypothesis by which exercise-based cardiac rehabilitation (CR) reduces mortality and cardiac events in patients with coronary artery disease invokes a beneficial effect of exercise on autonomic modulation. This study aimed to evaluate the autonomic effects of CR in patients with coronary artery disease. METHODS: Participants referred to phase 2 CR underwent 4 bicycle stress tests, 2 before starting CR and 2 after. On visits 1 and 3, a symptom-limited bicycle stress test was performed. On visits 2 and 4, the subject exercised to the same workload, but atropine was administered during maximal exercise to achieve parasympathetic blockade. Parasympathetic effect in exercise recovery was computed before and after CR. Heart rate variability for each segment was also quantified. Plasma catecholamine levels were obtained at baseline, peak exercise, and during recovery. RESULTS: Seventeen subjects (age 56 ± 10 years; 4 women) were enrolled. Six completed the post-CR testing. There was a significant increase in parasympathetic effect during exercise recovery post-CR (P < .001). There was also a significant increase in heart rate variability during exercise recovery post-CR (P < .001). Resting catecholamine levels were not different pre- and post-CR (NS). Post-CR, there was a blunted increase in peak exercise plasma catecholamine levels compared with those seen pre-CR, but this was not statistically significant. CONCLUSIONS: We demonstrated a shift toward increased parasympathetic and possibly, blunted sympathetic effect in this cohort after completion of an exercise-based CR program. Our findings provide insight into the mechanism for the observed changes in exercise parameters following exercise training, and the improved outcomes seen after CR.
PURPOSE: One hypothesis by which exercise-based cardiac rehabilitation (CR) reduces mortality and cardiac events in patients with coronary artery disease invokes a beneficial effect of exercise on autonomic modulation. This study aimed to evaluate the autonomic effects of CR in patients with coronary artery disease. METHODS:Participants referred to phase 2 CR underwent 4 bicycle stress tests, 2 before starting CR and 2 after. On visits 1 and 3, a symptom-limited bicycle stress test was performed. On visits 2 and 4, the subject exercised to the same workload, but atropine was administered during maximal exercise to achieve parasympathetic blockade. Parasympathetic effect in exercise recovery was computed before and after CR. Heart rate variability for each segment was also quantified. Plasma catecholamine levels were obtained at baseline, peak exercise, and during recovery. RESULTS: Seventeen subjects (age 56 ± 10 years; 4 women) were enrolled. Six completed the post-CR testing. There was a significant increase in parasympathetic effect during exercise recovery post-CR (P < .001). There was also a significant increase in heart rate variability during exercise recovery post-CR (P < .001). Resting catecholamine levels were not different pre- and post-CR (NS). Post-CR, there was a blunted increase in peak exercise plasma catecholamine levels compared with those seen pre-CR, but this was not statistically significant. CONCLUSIONS: We demonstrated a shift toward increased parasympathetic and possibly, blunted sympathetic effect in this cohort after completion of an exercise-based CR program. Our findings provide insight into the mechanism for the observed changes in exercise parameters following exercise training, and the improved outcomes seen after CR.
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