Exercise training enhances cardiac afferent inhibition of baroreflex function.

The influence of cardiac afferents on the arterial baroreflex regulation of renal sympathetic nerve activity (RSNA) was examined before and after an endurance training program. The 8-wk endurance exercise training program resulted in an exercise-induced bradycardia (decreased heart rates at rest and during a graded exercise test). At rest (210 +/- 6 vs. 242 +/- 10 beats/min) and during treadmill running at 15.0 m/min, 20% grade (287 +/- 5 vs. 390 +/- 5 beats/min) posttraining heart rates were lower than pretraining. In addition, when compared with a group of untrained rabbits, trained rabbits had a significantly higher heart weight-to-body weight ratio (1.9 +/- 0.02 vs. 2.8 +/- 0.017 g/kg). Rabbits were instrumented with a Doppler flow probe around the ascending aorta, Silastic catheter inserted into the pericardial sac, electrodes around the renal sympathetic nerves and catheters in the central ear artery and vein. Before training, cardiac afferent blockade (intrapericardial procainamide, 2%) did not significantly alter resting mean arterial pressure, cardiac index, systemic vascular resistance index or RSNA. After training, intrapericardial procainamide mean arterial pressure increased (P less than 0.05) resting (75 +/- 4 to 86 +/- 3 mmHg) and RSNA (100% to 175 +/- 15%). More importantly, cardiac afferent blockade did not alter the range (106 +/- 4 vs. 103 +/- 4%) or gain (4.1 +/- 0.3 vs. 3.4 +/- 0.3%/mmHg) of the baroreflex function curve in the untrained rabbit. However, after training, cardiac afferent blockade increased (P less than 0.05) the range (55 +/- 3 to 103 +/- 4%) and gain (1.5 +/- 0.07 to 3.9 +/- 0.2%/mmHg) of baroreflex regulation of RSNA.(ABSTRACT TRUNCATED AT 250 WORDS)