Slow breathing and hypoxic challenge activated discrete brainstem nuclei and corticostriatal circuitry, highlighting the neural substrates of cardiorespiratory control.
What are the central neural substrates and cardiorespiratory consequences of slow breathing and hypoxic challenge in healthy volunteers?
Slow breathing and hypoxic challenge engage discrete brainstem nuclei and corticostriatal circuitry to regulate physiological cardiorespiratory responses.
p-value: p=<0.05
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.
Critchley et al. (Thu,) conducted a other in Healthy volunteers (n=20). Slow breathing and hypoxic challenge vs. Normal rate breathing (9.9 breaths/min); normoxic air was evaluated on Regional brain activity (BOLD fMRI signal) during slow breathing and hypoxia (p=<0.05). Slow breathing and hypoxic challenge activated discrete brainstem nuclei and corticostriatal circuitry, highlighting the neural substrates of cardiorespiratory control.