BACKGROUND: Exercise and its recovery period are associated with increased risk of death relative to sedentary periods. They are also accompanied by dynamic changes in autonomic tone. Little information is available regarding parasympathetic effects during high-intensity exercise and recovery. METHODS: Ten normal subjects (five women; age 33 +/- 2 years) underwent exercise testing on a bicycle ergometer. On day 1, subjects exercised to maximum tolerated workload using a graded protocol with 5 minutes at maximal workload (peak heart rate achieved 174.7 +/- 5.4 bpm). On day 2, subjects performed the identical exercise protocol as on day 1; 1 minute into the maximum exercise stage, atropine (0.04 mg/kg) was administered. Heart rate was recorded every minute during exercise, and an electrocardiogram was recorded every minute in recovery for 10 minutes. The parasympathetic effect on heart rate was defined by the difference in heart rate with and without atropine. RESULTS: The parasympathetic effect during maximal exercise was 3.4 to 6 bpm (p < .05). During recovery, a large parasympathetic effect on heart rate was noted by 1 minute (22.8 bpm; p < .0002), increased until 4 minutes, and then remained stable until 10 minutes. Despite faster heart rates with parasympathetic blockade, the P-R interval was shorter (p < .002), consistent with a significant parasympathetic effect on the atrioventricular node in recovery. Evaluation of the Q-T-R-R relationship on the 2 days demonstrated significant changes in both the slope (p < .0001) and the intercept (p < .0001), consistent with a modification of ventricular repolarization by parasympathetic tone in recovery. CONCLUSION: These data indicate that in normal subjects, parasympathetic effects persist during high-intensity exercise and are prominent in the early phases of recovery. These parasympathetic effects may play an important role in prevention of sudden cardiac death during these periods of increased risk.
BACKGROUND: Exercise and its recovery period are associated with increased risk of death relative to sedentary periods. They are also accompanied by dynamic changes in autonomic tone. Little information is available regarding parasympathetic effects during high-intensity exercise and recovery. METHODS: Ten normal subjects (five women; age 33 +/- 2 years) underwent exercise testing on a bicycle ergometer. On day 1, subjects exercised to maximum tolerated workload using a graded protocol with 5 minutes at maximal workload (peak heart rate achieved 174.7 +/- 5.4 bpm). On day 2, subjects performed the identical exercise protocol as on day 1; 1 minute into the maximum exercise stage, atropine (0.04 mg/kg) was administered. Heart rate was recorded every minute during exercise, and an electrocardiogram was recorded every minute in recovery for 10 minutes. The parasympathetic effect on heart rate was defined by the difference in heart rate with and without atropine. RESULTS: The parasympathetic effect during maximal exercise was 3.4 to 6 bpm (p < .05). During recovery, a large parasympathetic effect on heart rate was noted by 1 minute (22.8 bpm; p < .0002), increased until 4 minutes, and then remained stable until 10 minutes. Despite faster heart rates with parasympathetic blockade, the P-R interval was shorter (p < .002), consistent with a significant parasympathetic effect on the atrioventricular node in recovery. Evaluation of the Q-T-R-R relationship on the 2 days demonstrated significant changes in both the slope (p < .0001) and the intercept (p < .0001), consistent with a modification of ventricular repolarization by parasympathetic tone in recovery. CONCLUSION: These data indicate that in normal subjects, parasympathetic effects persist during high-intensity exercise and are prominent in the early phases of recovery. These parasympathetic effects may play an important role in prevention of sudden cardiac death during these periods of increased risk.
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