Breath-hold diving as a tool to harness a beneficial increase in cardiac vagal tone
Author: Pierrick Martinez1, Mathias Dutschmann2, Vincent Épercieux3, Géraud Gourjon4, Fabrice Joulia5
Affiliation:
1 Laboratory « Jeunesse - Activité Physique et Sportive- Santé » (J-AP2S), University of Toulon, Toulon, France. Electronic address: pierrick.martinez@ifoga.fr.
2 Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, University Hospitals Cleveland Medical Center and Case Western Reserve University, Cleveland, OH 44106, USA; Center for Sleep Disorders Research, Louis Stokes Cleveland VA Medical Center and Case Western Reserve University, Cleveland, OH 44106, USA.
3 Aix Marseille Univ., CNRS, IBDM, Institut de Biologie du Développement de Marseille, Marseille, France.
4 Scientific and Osteopathic Research Department, Institut de Formation en Ostéopathie du Grand Avignon, 403 Rue Marcel Demonque, Avignon, France.
5 Laboratory « Jeunesse - Activité Physique et Sportive- Santé » (J-AP2S), University of Toulon, Toulon, France; Center for Cardiovascular and Nutrition Research C2VN, INSERM 1263 INRAE 1260 Aix Marseille Université, Marseille, France.
Conference/Journal: Respir Physiol Neurobiol
Date published: 2025 Mar 15
Other:
Pages: 104416 , Special Notes: doi: 10.1016/j.resp.2025.104416. , Word Count: 275
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.
Keywords: Bradycardia; Cardiac Vagal Tone; Diving; Kölliker-Fuse Nucleus; postinspiration, glottal adduction; pre-Bötzinger complex.
PMID: 40096873 DOI: 10.1016/j.resp.2025.104416
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