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

¹Department of Ergonomics, University of Toulon-Var, La Garde; and ²Laboratory I3S, University of Nice-Sophia Antipolis, Sophia Antipolis, France

Submitted 29 July 2004 ; accepted in final form 17 September 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 (F_RSA, in Hz) and amplitude (A_RSA, in ms) were then extracted from all recordings. A_RSA was calculated with short-time Fourier transform. First, measurements of F_RSA and A_RSA were performed from data obtained during a graded and maximal exercise test. Influences of different ventilation regimens [changes in tidal volume (V_T) and respiratory frequency (F_R)] on A_RSA were then tested during submaximal [70% peak O₂ consumption (O_2peak)] rectangular exercise bouts. Under graded and maximal exercise conditions, A_RSA decreased from the beginning of exercise to 61.9 ± 3.8% O_2peak and then increased up to peak exercise. During the paced breathing protocol, normoventilation (69.4 ± 8.8 l/min), hyperventilation (81.8 ± 8.3 l/min), and hypoventilation (56.4 ± 6.2 l/min) led to significantly (P < 0.01) different A_RSA values (3.8 ± 0.5, 4.6 ± 0.8, and 2.9 ± 0.5 ms, respectively). In addition, no statistical difference was found in A_RSA when ventilation was kept constant, whatever the F_R-V_T 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

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