Effects of hypoxia and hypercapnia on human HRV and respiratory sinus arrhythmia

Abstract

Purpose: Hypercapnia increases minute ventilation (V'E) with little effect on heart rate (HR), whereas hypoxia may increase HR without affecting V'E. However, the effects of hypercapnia and hypoxia on both heart rate variability (HRV) and the clustering of heart beats during spontaneous breathing (respiratory sinus arrhythmia -RSA), are not clear. Methods: In this study, 10 human volunteers breathed room air (RA), hypercapnic (5% CO 2 ) or hypoxic (10% O 2 ) gas mixtures, each for 6 min, while resting supine. ECG, mean arterial pressure (MAP), ventilatory flow, inhaled and exhaled fractions of CO 2 and O 2 , were recorded throughout. Results: Both V'E and MAP increased with 5% CO 2 , with no change in HR. Hypoxia did not change ventilation but increased HR. High frequency components of HRV, and the relative proportion of heart beats occurring during inhalation increased with 5% CO 2 , but neither changed with 10% O 2 . Conclusion: Increased RSA concomitant with increased MAP suggests RSA -vagal dissociation with hypercapnia. Elevated heart rate with acute hypoxia with no change in either frequency components of HRV or the distribution of heart beats during ventilation, suggested that clustering of heart beats may not be a mechanism to improve ventilation-perfusion matching during hypoxia.Keywords: autonomic nervous system, spectral analysis, cardiovascular control, heart rate variability, hypoxia, hypercapniaOscillations in the human heart rate at rest contribute to heart rate variability (HRV) (1, 18, 21, 23), and may indicate cardiac sympatho-vagal balance (7). Low (LF: 0-0.04 Hz), middle (MF: 0.04-0.15 Hz) and high (HF: 0.15-0.4 Hz) frequency bands form part of this variability and are often determined by spectral analysis of an R-R interval tachogram using fast Fourier transform (FFT). The influence of both hypoxia and hypercapnia on resting HRV has been studied at rest, but with equivocal results regarding changes in the frequency domain (37). Hypoxia may decrease HRV total power (TP) (6, 14, 29) and decrease both MF and HF power (3,6,21,23,24,29). However, hypoxia may decrease HF and increase MF power (14), or have no effect on HF power while increasing MF power (15). Hypercapnia stimulates ventilation and therefore increases HF power (usually with a concomitant decrease in MF power), but has little or no effect on resting heart rate. These equivocal findings emphasize the complex interaction between ambient PO 2 , PCO 2 , and autonomic nervous system function (10, 30). Hypoxia and hypercapnia may also influence respiratory sinus arrhythmia (RSA) -a measure synonymous with the HF component of HRV (31). RSA is due to the modulatory effects of pulmonary ventilation on vagal activity (2, 7) and reflects the preferential

Effects of Hypoxia on Heart Rate Variability in Healthy Individuals: A Systematic Review

“…Although the effects of hypoxia on cardiac autonomic modulation are well studied, 10,21,22 even after a rigorous selection criterion of the articles, experimental protocols are considerably different. The results found are shown in Table 1.…”

“…The difference between RG and SG (Table 1) indicates that SG has an increased sympathetic modulation associated with decreased vagal modulation during exposure to NH. In the study by Brown et al 22 although the level of oxygen used was 10% FiO 2 ~5500 m and increases in HR were found, in LFnu and HFnu components no differences were found in the normoxic condition. This study conducted a six-minute analysis during normoxia (21% O 2 ), hypercapnia (5% CO 2 ) and hypoxia (10% O 2 ) at 5-minute intervals of normoxia between conditions and in a randomized manner.…”

“…Among the selected studies, some had short exposure to hypoxia -of around 6-15 minutes, 8,11,[21][22][23][24][25] while others had longer exposure periods of one to twelve hours. 4,12 Furthermore, the studies used gradual rise protocols 10,12,26 or sudden exposure to hypoxia.…”

“…4,12 Furthermore, the studies used gradual rise protocols 10,12,26 or sudden exposure to hypoxia. 8,11,20,[22][23][24][25][26] The length of stay and type of rise to a simulated altitude could generate different cardiac autonomic modulation responses, as shown in the table 1. 12,27,28 Likewise, the different levels of oxygen used in the studies, ranging from 19% to 9.6% of FiO 2 10,21,23 also appear to induce different HRV responses.…”

“…9, [21][22][23][24] Although those studies differ in the type of hypoxia, one of them being in hypobaric environment 9 and the others in normobaric environment. 21,24 Furthermore, other studies using a similar level of hypoxia also had varied responses in cardiac autonomic modulation both in HH 26 and NH.…”