Moderate exercise induces different autonomic modulations of sinus and AV node.

BACKGROUND

The routine determination of heart rate variability (HRV) from surface ECGs is based on RR intervals because of the difficulty to precisely locate the P-wave fiducial point on surface ECG recordings. The aim of the study was to assess the changes of RR, PP, and PR intervals at rest and during moderate exercise. The time intervals were determined from atrial and ventricular pacemaker-mediated intracardiac electrograms.

METHODS

Ten patients in sinus rhythm with intrinsic AV node conduction who had received the dual-chamber pacemaker Logos (Biotronik) were included. High-resolution atrial and ventricular intracardiac electrograms were transmitted at rest in supine position and during walking to a portable external recorder. Recording sequences of 150 successive heart cycles were used for HRV analyses after computer-assisted triggering of P and R events. The HRV-index SDNN and power spectral densities for the low (LF; 0.04-0.15 Hz) as well as high (HF; 0.15-0.40 Hz) frequency bands were determined.

RESULTS

SDNN decreased from 26.0 +/- 8.1 ms at rest to 18.3 +/- 4.2 ms during exercise for the PP intervals (P < 0.05) and from 26.8 +/- 8.1 to 18.4 +/- 4.1 ms for the RR intervals (P < 0.05). The LF/HF ratio increased from 2.02 +/- 1.3 to 4.5 +/- 1.5 in the atrium (P < 0.05) and from 2.0 +/- 1.2 to 5.2 +/- 1.9 in the ventricle P < 0.05). Comparing atrial and ventricular HRV at both activity levels, no significant differences were observed for the power of LF and HF spectral components. Regarding the PR intervals SDNN, the total power and the LF/HF ratio did not significantly change during exercise.

CONCLUSIONS

The described technique enabled to record intracardiac electrograms not only at rest, but also during moderate exercise and to use them for HRV evaluation. The changes of PP and RR, but not of the PR intervals, during exercise indicate that autonomic inputs to the sinus node and AV node are independent from each other. The ventricular HRV seems to derive mainly from variations of the sinus node pulse formation.