Slow breathing and hypoxic challenge: cardiorespiratory consequences and their central neural substrates.

Author: Critchley HD1, Nicotra A2, Chiesa PA3, Nagai Y4, Gray MA5, Minati L6, Bernardi L7.
Affiliation:
1Brighton and Sussex Medical School, University of Sussex, Brighton, United Kingdom; Sackler Centre for Consciousness Science, University of Sussex, Brighton, United Kingdom. 2Imperial College Healthcare NHS Trust, London, United Kingdom. 3Department of Psychology, Sapienza University of Rome, Rome, Italy; Ghermann Laboratory, University of Queensland, Queensland, Australia. 4Brighton and Sussex Medical School, University of Sussex, Brighton, United Kingdom. 5IRCCS, Fondazione Santa Lucia, Rome, Italy. 6IRCCS, Fondazione Neurologico Carlo Besta, Milano, Italy. 7Department of Internal Medicine, University of Pavia and Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.
Conference/Journal: PLoS One.
Date published: 2015 May 14
Other: Volume ID: 10 , Issue ID: 5 , Pages: e0127082 , Special Notes: doi: 10.1371/journal.pone.0127082 , Word Count: 247



Controlled slow breathing (at 6/min, a rate frequently adopted during yoga practice) can benefit cardiovascular function, including responses to hypoxia. We tested the neural substrates of cardiorespiratory control in humans during volitional controlled breathing and hypoxic challenge using functional magnetic resonance imaging (fMRI). Twenty healthy volunteers were scanned during paced (slow and normal rate) breathing and during spontaneous breathing of normoxic and hypoxic (13% inspired O2) air. Cardiovascular and respiratory measures were acquired concurrently, including beat-to-beat blood pressure from a subset of participants (N = 7). Slow breathing was associated with increased tidal ventilatory volume. Induced hypoxia raised heart rate and suppressed heart rate variability. Within the brain, slow breathing activated dorsal pons, periaqueductal grey matter, cerebellum, hypothalamus, thalamus and lateral and anterior insular cortices. Blocks of hypoxia activated mid pons, bilateral amygdalae, anterior insular and occipitotemporal cortices. Interaction between slow breathing and hypoxia was expressed in ventral striatal and frontal polar activity. Across conditions, within brainstem, dorsal medullary and pontine activity correlated with tidal volume and inversely with heart rate. Activity in rostroventral medulla correlated with beat-to-beat blood pressure and heart rate variability. Widespread insula and striatal activity tracked decreases in heart rate, while subregions of insular cortex correlated with momentary increases in tidal volume. Our findings define slow breathing effects on central and cardiovascular responses to hypoxic challenge. They highlight the recruitment of discrete brainstem nuclei to cardiorespiratory control, and the engagement of corticostriatal circuitry in support of physiological responses that accompany breathing regulation during hypoxic challenge.
PMID: 25973923

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