Voluntary breath-holds can be sustained for a long time following training, but ultimately, regardless of duration, the asphyxic break-point is reached and the apnoea terminated. The physiological changes occurring during the apnoea include a marked increase in sympathetically-mediated vasoconstriction in non-essential organs, such as skeletal muscle, spleen and kidney, while the brain is protected by a marked increase in perfusion. What is not understood is what happens to cardiac vagal activity. Here, we performed microelectrode recordings from the right cervical vagus nerve in healthy participants [both trained breath-hold divers (n = 10) and untrained controls (n = 10)] during tidal breathing, slow-deep breathing, an inspiratory-capacity apnoea and an end-expiratory apnoea. Using cross-correlation analysis of multi-unit neural activity, we tested the hypothesis that breath-hold divers would have greater cardiac modulation of vagal activity, which primarily reflects the discharge of cardiac afferents, particularly during a maximal apnoea. We showed that there were no differences in cardiac modulation of vagus nerve activity either during tidal breathing or during any of the respiratory manoeuvres, nor was there a difference in cardiac modulation during the static phase of a maximal apnoea or when involuntary breathing movements occurred before reaching the asphyxic break-point. We conclude that changes in vagal sensory inputs from the heart are not responsible for the marked tolerance to asphyxia shown by breath-hold divers.