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To determine the adaptations of the autonomic nervous system in the control of heart rate and blood pressure induced by endurance training, 10 competitive cyclists aged 27 +/- 7 years and 10 age-, weight- and height-matched sedentary controls were subjected to Power Spectral Analysis of the RR interval and of blood pressure at supine rest and during submaximal cycloergometric exercise test in the supine position at 20% and 40% of maximal workload. At rest, the high-frequency (HF) power of the RR interval was higher in cyclists (p < 0.05) compared to controls, whereas the power spectrum of both systolic and diastolic blood pressure did not differ between cyclists and controls. During exercise the variance, the low-frequency (LF) and the HF power of the RR interval decreased significantly (p < 0.005) and similarly in cyclists and controls. The LF/HF ratio of the RR interval increased (p < 0.001) and the alfa index of baroreflex sensitivity decreased (p < 0.05) without differences between cyclists and controls. The variance of both systolic and diastolic blood pressure increased (p < 0.001 and p < 0.005, respectively) as well as the HF power of systolic blood pressure (p < 0.001) similarly in cyclists and in controls. In conclusion, the data of the present study suggest that competitive cycling causes an enhanced vagal drive to the sinus node, whereas the neural control of blood pressure is not affected. During exercise a vagal withdrawal and a sympathetic activation in the neural control of heart rate, together with a reduction of baroreflex sensitivity are operative. These changes are similar in cyclists and controls.

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To examine the effect of long term strength training on heart rate and blood pressure, measured in different conditions, and on their variability, thirty healthy, previously sedentary men were randomized into a training and a control group. The strength training program consisted of 48 training sessions on a multigym apparatus at a frequency of 3 sessions each week, involving leg press, bench press, leg curl, shoulder press, leg extension and sit ups. The control group was asked not to change their sedentary lifestyle. In the subjects of the training group the load could be increased significantly for all exercises (p < 0.01). Heart rate and blood pressure were measured at rest in the supine and sitting position, during 24 hours with a non-invasive ambulatory device and during an exercise test on a cycloergometer. Repeated measures analysis of variance did not show an effect of strength training on heart rate or on blood pressure. In addition, power spectral analysis of the RR interval (ECG) and of the beat-to-beat blood pressure in the supine subject revealed similar total, low frequency and high frequency power before and after training, indicating that the neural control of both heart rate and blood pressure was not affected by a 16-week program of strength training.

The effect of semi-supine long lasting exercise to exhaustion [61 (SD 10) min] on left ventricular systolic performance was studied by echocardiography in 16 young healthy volunteers. During the incremental phase of exercise, the ejection fraction increased from 65.2 (SD 4.1)% to 80.1 (SD 4.8)% (P < 0.0001), then it levelled off up to the end of exercise [81.7 (SD 4.4)%, P < 0.0001 vs rest]. During recovery, the ejection fraction rapidly and steadily decreased to a value similar to that at rest [66.1 (SD 5.0)%, n.s.). A similar pattern was shown by the systolic blood pressure/end-systolic volume coefficient, which rose from 3.2 (SD 0.8) mmHg.ml-1 to 7.5 (SD 2.7) mmHg.ml-1 (P < 0.0001) in the initial phase and subsequently did not change until the end of exercise [7.0 (SD 2.2) mmHg.ml-1, P < 0.0001 vs rest], to fall sharply after the cessation of exercise [2.9 (SD 1.1) mmHg.ml-1 at the 10th min, n.s. vs rest]. Exercise and recovery indices of left ventricular performance were not correlated with exercise duration, maximal heart rate and increase in free fatty acids. The present results indicated that, after the initial increase, left ventricular performance remained elevated during prolonged high intensity exercise and that conclusions on exercise cardiac performance drawn from postexercise data can be misleading.