Beat‐to‐beat modulation of atrioventricular conduction during dynamic exercise in the elite athletes

Abstract

PR interval shortens due to an extrinsic neural mechanism during exercise as well as PP interval. On the contrary, PR interval lengthens due to an intrinsic mechanism of the atrioventricular (AV) node, when PP interval is decreased by atrial pacing. Long-term endurance training lowers baseline heart rate (HR) and augments its variability. However, it remains unknown how endurance training modifies the extrinsic and intrinsic mechanisms controlling AV conduction. To answer this question, we compared the responses in PP, RR, and PR intervals during dynamic exercise between sedentary subjects and elite athletes, who performed ergometer exercise to increase HR to 160 beats/min from baseline. Although the mean PP and RR intervals similarly decreased during exercise, the variation of RR interval became much smaller than that of PP interval. In contrast, the PR interval variation tended to increase during exercise, despite shortened mean PR interval. A strong inverse relationship between PP interval and the subsequent change in PR interval was recognized during exercise, indicating that PR interval changed due to the intrinsic AV nodal mechanism as opposed to fluctuation in PP interval. Although the fundamental characteristics of the exercise-induced response in PR interval were the same between both groups, the intrinsic AV nodal mechanism in the athletes started to operate at a longer PP interval. The intrinsic mechanism of AV node is likely to cancel fluctuation in atrial excitation rhythm during exercise so as to stabilize ventricular excitation rhythm. We suggest that long-term endurance training allows the intrinsic AV nodal function to operate at a lower HR.