Breath-hold diving as a tool to harness a beneficial increase in cardiac vagal tone.

Here we review central mechanisms that mediate the diving bradycardia and propose that breath-hold diving (BH-D) is a powerful therapeutic tool to improve cardiac vagal tone (CVT). Physiological fluctuations in CVT are known as the respiratory heart rate variability (respirHRV) and involve two respiratory-related brainstem mechanisms. During inspiration pre-Bötzinger complex (pre-BötC) neurons inhibit cardiac vagal motor neurons to increase heart rate and subsequently cardiac vagal disinhibition and a decrease in heart rate is associated with a Kölliker-Fuse (KF) nucleus-mediated partial glottal constriction during early expiration. Both KF and pre-BötC receive direct descending cortical inputs that could mediate volitional glottal closure as critical anatomical framework to volitionally target brainstem circuits that generate CVT during BH-D. Accordingly we show that volitional and reflex glottal closure during BH-D appropriates the respirHRV core network to mediate the diving bradycardia via converging trigeminal afferents inputs from the nose and forehead. Additional sensory inputs linked to prolonged BH-D after regular training further increase CVT during the acute dive and can yield a long-term increase in CVT. Centrally, evidence of Hebbian plasticity within respirHRV/BH-D core circuit further support the notion that regular BH-D exercise can yield a permanent increase in CVT specifically via a sensitization of synapse involved in the generation of the respirHRV. Contrary to other regular physical activity, BH-D reportedly does not cause structural remodeling of the heart and therefore we suggest that regular BH-D exercise could be employed as a save and non-invasive approach to treat sympathetic hyperactivity, particularly in elderly patients with cardio-vascular predispositions.