Parasympathetic contribution to bradycardia induced by endurance training in man

Seven normal subjects of sedentary habits were submitted to a 10 week period of endurance physical training on a cycloergometer. The training programme produced a mean 15.6 ± 1.4% (± SE) increase in O2max (from 39.7 ± 2.0 ml·kg−1·min−1 to 45.9 ± 2.4 ml·kg−1·min−1) and a reduction in resting heart rate (HR) from 69 ± 1.9 to 58 ± 1.7 beats·min−1 in the supine position. After pharmacological blockade of the parasympathetic system with atropine sulphate, HR rose on average by 53 ± 3.9 beats·min−1 before training and 47 ± 3.6 beats·min−1 after training, the difference being statistically nonsignificant. The magnitude of respiratory sinus arrhythmia (RSA) was similar before and after the period of physical conditioning. The respiratory variation in HR(ΔHR) at the 1 litre tidal volume was 20 ± 2.4 beats·min−1 and 20 ± 2.6 beats·min−1 before and after training, respectively. At the 2 litre tidal volume, these values were 25 ± 3.2 and 27 ± 4.5 beats·min−1. Similar results were obtained with the RSA test when a group of 13 sedentary individuals (O2max = 39.4 ± 1.3 ml·kg−1·min−1) was compared with a group of 7 athletes who are medium distance runners (O2max = 53.8 ± 1.3 ml·kg−1·min−1). Although it is possible that the RSA value does not necessarily reflect changes in parasympathetic tonus, the present results clearly show that increased endurance capacity is not accompanied by increased RSA values. In addition, the HR response to pharmacological blockade did not suggest any parasympathetic participation in bradycardia induced by physical training.