Influences of breathing patterns on respiratory sinus arrhythmia in humans during exercise

Abstract

Blain, Grégory, Olivier Meste, and Stéphane Bermon. Influences of breathing patterns on respiratory sinus arrhythmia in humans during exercise. Am J Physiol Heart Circ Physiol 288: H887-H895, 2005. First published September 23, 2004 doi:10.1152/ajpheart. 00767.2004.-Persistence of respiratory sinus arrhythmia (RSA) has been described in humans during intense exercise and attributed to an increase in ventilation. However, the direct influence of ventilation on RSA has never been assessed. The dynamic evolution of RSA and its links to ventilation were investigated during exercise in 14 healthy men using an original modeling approach. An evolutive model was estimated from the detrended and high-pass-filtered heart period series. The instantaneous RSA frequency (FRSA, in Hz) and amplitude (ARSA, in ms) were then extracted from all recordings. ARSA was calculated with short-time Fourier transform. First, measurements of FRSA and ARSA were performed from data obtained during a graded and maximal exercise test. Influences of different ventilation regimens [changes in tidal volume (VT) and respiratory frequency (FR)] on ARSA were then tested during submaximal [70% peak O2 consumption (V O2 peak)] rectangular exercise bouts. Under graded and maximal exercise conditions, ARSA decreased from the beginning of exercise to 61.9 Ϯ 3.8% V O2 peak and then increased up to peak exercise. During the paced breathing protocol, normoventilation (69.4 Ϯ 8.8 l/min), hyperventilation (81.8 Ϯ 8.3 l/min), and hypoventilation (56.4 Ϯ 6.2 l/min) led to significantly (P Ͻ 0.01) different ARSA values (3.8 Ϯ 0.5, 4.6 Ϯ 0.8, and 2.9 Ϯ 0.5 ms, respectively). In addition, no statistical difference was found in ARSA when ventilation was kept constant, whatever the FR-VT combinations. Those results indicate that RSA persists for all exercise intensities and increases during the highest intensities. Its persistence and increase are strongly linked to both the frequency and degree of lung inflation, suggesting a mechanical influence of breathing on RSA. cardiorespiratory coupling; heart period variability; paced breathing; time-varying model

Cardiac Vagal Control and Respiratory Sinus Arrhythmia during Hypercapnia in Humans

“…It is interesting, however, that the greater variability of V T did not translate into greater variability in arterial pressure [19]. The amplitude of RSA, as indicated by the HF component of HRV, was proportionally increased or reduced by increases or decreases in V T , respectively, when B f was kept constant [29], thus suggesting a direct influence of lung inhalation on HF amplitude. Others [30] have reported that phasic inputs from pulmonary and thoracic stretch receptors make only a small contribution to R-R variability at respiratory frequency, though it has been suggested that changes in both B f and V T be taken into account when using HRV to explore cardiac autonomic regulation [31].…”

Effect of exercise mode on heart rate variability during steady state exercise

“…Contrary to previous studies (Cottin et al 2004;Tulppo et al 1999), the current study examined steady-state submaximal exercise of various modes with greater HRV maintained during UB exercise compared to WB and LB exercise, despite the same HR (Tables 2, 3). The greater HRV during UB may reflect greater respiratory-induced sinus arrhythmia as changes in respiration, particularly respiratory rate, have been reported to alter HRV (Blain et al 2005;Brown et al 1993). However, this was unlikely in the current study given that Resp was significantly lower for LB compared to WB with similar HRV, while Resp was similar between WB and UB with significantly greater HRV for UB compared to WB.…”

Influence of cold water face immersion on post-exercise parasympathetic reactivation

“…The Wingate test was aimed at markedly increasing sympathetic and reducing vagal activities (Goulopoulou et al 2006) prior to the start of the submaximal exercise bout, so that the confounding effect of sympathetic overactivity (i.e., interaction; Levy 1971) on the post-exercise parasympathetic reactivation response to both recovery conditions could be investigated. As well, analyzing autonomic responses to submaximal, but not maximal exercise, was designed to observe the influence of the presumed sympathetic overactivity on post-exercise HRV indices, whilst eliminating the potential confounding mechanical effects of high minute ventilation on the HF power density (Blain et al 2005). …”