Cardiac vagal control and respiratory sinus arrhythmia during hypercapnia in humans

Abstract

Normoxic hypercapnia may increase high-frequency (HF) power in heart rate variability (HRV) and also increase respiratory sinus arrhythmia (RSA). Low-frequency (LF) power may remain unchanged. In this study, 5-min ECG recordings (N = 10) were analyzed in time and frequency domains while human subjects breathed normoxic 5% CO2 (5%CO2) or room air (RA). Tidal volume (VT), inhalatory (TI), and exhalatory (TE) times of breaths in the final minute were measured. ECG time domain measures were unaffected by CO2 inhalation (P > 0.05). Following natural logarithmic transformation (LN), LFLN was unaltered (RA: 7.14 ± 0.95 vs. 5%CO2: 7.35 ± 1.12, P > 0.05), and HFLN increased (RA: 7.65 ± 1.37 vs. 5%CO2: 8.58 ± 1.11, P < 0.05) with CO2 inhalation. When changes in total power (NU) were corrected, LFNU decreased (RA: 34.4 ± 22.9 vs. 5%CO2: 23.8 ± 23.1, P < 0.01), and HFNU increased (RA: 56.5 ± 22.3 vs. 5%CO2: 66.8 ± 22.9, P < 0.01) with CO2 inhalation. TI (RA: 2.0 ± 1.0 vs. 5%CO2: 1.9 ± 0.8 s) and TE (RA: 2.5 ± 1.1 vs. 5%CO2: 2.4 7plusmn; 0.9 s) remained unchanged, but V T increased with CO2 inhalation (RA: 1.1 ± 0.3 vs. 5%CO2: 2.0 ± 0.8 L, P < 0.001). Heart rates during inhalation (RA: 35.2 ± 4.4, 5%CO2: 34.5 ± 4.8 beats min-1) were different from heart rates during exhalation (RA: 28.8 ± 4.4, 5%CO2: 29.1 ± 3.1 beats min-1). Hypercapnia did not increase the clustering of heart beats during inhalation, and we suggest that the HF component may not adequately reflect RSA.