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Updated: Aug 18, 2026

A Pacing-Controlled Procedure for the Assessment of Heart Rate-Dependent Diastolic Functions in Murine Heart Failure Models
Published on: July 21, 2023
Beat-to-beat modulation of atrioventricular conduction during dynamic exercise in humans
Tomoko Nakamoto1, Kanji Matsukawa, Jun Murata
1Department of Physiology, Graduate School of Health Sciences, Hiroshima University, Minami-ku, Hiroshima, 734-8551 Japan.
Abstract:
A complex balance between extrinsic neural and intrinsic mechanisms is responsible for regulating atrioventricular (AV) conduction. We hypothesized that atrial excitation interval is shortened during dynamic exercise by extrinsic cardiac autonomic activity and that if AV conduction time responds inversely to fluctuation in atrial rhythm, ventricular excitation interval will be maintained at the predetermined cardiac cycle length. To examine such inverse relationship between PP interval and the subsequent change in PR interval (DeltaPR), we analyzed the beat-to-beat changes in PP, PR, and RR intervals during stair-stepping exercise for 10 min in 11 sedentary and 9 trained subjects. In the sedentary group, the average PR interval significantly shortened during exercise, in parallel with the reduction in the average PP and RR intervals. The variance of PP and RR intervals was also significantly decreased during exercise. The reduction in the variance of RR interval was, however, much greater than that of PP interval, implying that AV conduction time changes inversely to fluctuation in atrial excitation rhythm. Indeed, the variance of PR interval was augmented during exercise and there was a clear inverse relationship between PP and DeltaPR intervals. Although trained subjects were characterized by their lower heart rate response during dynamic exercise, the responses in the variability of PP, PR, and RR intervals were fundamentally identical with those in sedentary subjects. We conclude that the AV nodal mechanism that operates at a higher level of heart rate during dynamic exercise may cancel fluctuation in atrial excitation interval and keep ventricular excitation rhythm at the predetermined cardiac cycle length.
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