Table 1.
Respiratory | Generally coincides with increased tidal volume and may enhance diaphragmatic excursion [16, 18] Enhances ventilation efficiency and arterial oxygenation via alveolar recruitment, and distension and reduction of alveolar dead space [23, 24] Moderates chemoreflex sensitivity [21] |
Cardiovascular | Increases venous return → increases filling of the right heart → increases stroke volume → increases cardiac output [29, 30, 32, 35] Causes blood pressure pulse fluctuations to synchronise with heart beat rhythm [29] Synchronisation of vasomotion [34] May entrain and enhance vasomotion (and microflow), i.e. to improve blood oxygenation [34] Increases HRV and blood pressure fluctuations [21, 41, 42, 62] May decrease mean blood pressure [30, 41, 43, 44] |
Cardiorespiratory | Augments LF HRV and baroreflex sensitivity [41, 60, 65, 66, 77] Increases RSA (maximises around 6 breaths per min (resonant frequency)) [41, 61, 62, 72–75] Improves pulmonary gas exchange efficiency [45, 47, 48, 78–80], minimises cardiac work [74, 80, 81], buffers blood pressure fluctuations [29, 35] Clustering of heartbeats within inspiratory phase (cardiorespiratory coupling) [46, 47] Synchronisation of pulse harmonics of blood flow and heart rhythm [29] |
Autonomic nervous system | Increases vagal activity (vagal tone) [42, 103] Shift towards parasympathetic dominance [42, 105] Augments vagal power (entrainment of cardiac resetting by vagus to respiration phases) [97, 103] Optimises acetylcholine release and hydrolysis at SA node [67, 76] Enhances phasic modulation of sympathetic activity [104, 106] Improves autonomic responsiveness to physical perturbations (i.e. standing) [107] Optimises sympathovagal balance [107] |
Hypotheses and plausible speculations are italicised.