OBJECTIVES: Vagally mediated heart rate recovery after exercise was assessed in patients with chronic heart failure and in well trained athletes by analyzing the postexercise heart rate decay. BACKGROUND: Vagal reactivation is an important cardiac deceleration mechanism after exercise. However, alterations of this mechanism under pathologic conditions have not been characterized because of the lack of a specific index. METHODS: To find a vagally mediated component of heart rate recovery, the time constants of the beat-by-beat heart rate decay for the first 30 s (T30) and the first 120 s (T120) after exercise were obtained at six levels of exercise in eight normal volunteers: 1) at maximal exercise, 2) at anaerobic threshold, 3) at anaerobic threshold with propranolol administration, 4) at anaerobic threshold with atropine administration, 5) at anaerobic threshold with concomitant administration of both drugs, and 6) at 50% of anaerobic threshold. To investigate the effects of heart failure and endurance training on vagally mediated heart rate recovery, T30 and T120 at anaerobic threshold were obtained in 20 patients with chronic heart failure and in 9 cross-country skiers. RESULTS: In normal volunteers, T30 and T120 were markedly prolonged by atropine administration, indicating that both time constants are mediated by vagal reactivation. Moreover, T30 was almost independent of the exercise intensity and sympathetic blockade, whereas T120 was affected by sympathetic nerve activity and exercise work load. These results indicate that T30 is mediated primarily by vagal reactivation, independent of sympathetic withdrawal, and is significantly smaller in athletes (p < 0.01) and significantly larger in patients with chronic heart failure (p < 0.01) than that in respective age-matched normal control subjects. CONCLUSIONS: The T30 value could be a specific index for vagally mediated heart rate recovery. Vagally mediated heart rate recovery after exercise is accelerated in well trained athletes but blunted in patients with chronic heart failure.
OBJECTIVES: Vagally mediated heart rate recovery after exercise was assessed in patients with chronic heart failure and in well trained athletes by analyzing the postexercise heart rate decay. BACKGROUND: Vagal reactivation is an important cardiac deceleration mechanism after exercise. However, alterations of this mechanism under pathologic conditions have not been characterized because of the lack of a specific index. METHODS: To find a vagally mediated component of heart rate recovery, the time constants of the beat-by-beat heart rate decay for the first 30 s (T30) and the first 120 s (T120) after exercise were obtained at six levels of exercise in eight normal volunteers: 1) at maximal exercise, 2) at anaerobic threshold, 3) at anaerobic threshold with propranolol administration, 4) at anaerobic threshold with atropine administration, 5) at anaerobic threshold with concomitant administration of both drugs, and 6) at 50% of anaerobic threshold. To investigate the effects of heart failure and endurance training on vagally mediated heart rate recovery, T30 and T120 at anaerobic threshold were obtained in 20 patients with chronic heart failure and in 9 cross-country skiers. RESULTS: In normal volunteers, T30 and T120 were markedly prolonged by atropine administration, indicating that both time constants are mediated by vagal reactivation. Moreover, T30 was almost independent of the exercise intensity and sympathetic blockade, whereas T120 was affected by sympathetic nerve activity and exercise work load. These results indicate that T30 is mediated primarily by vagal reactivation, independent of sympathetic withdrawal, and is significantly smaller in athletes (p < 0.01) and significantly larger in patients with chronic heart failure (p < 0.01) than that in respective age-matched normal control subjects. CONCLUSIONS: The T30 value could be a specific index for vagally mediated heart rate recovery. Vagally mediated heart rate recovery after exercise is accelerated in well trained athletes but blunted in patients with chronic heart failure.
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