Key points: Anxiety disorders reduce both the heart rate variability (HRV) and the sensitivity of the cardiac baroreflex (BRS). This may lead to sudden cardiac death. To elucidate the mechanisms underlying these alterations, male rats were subjected to social defeat sessions that lead to an anxiety‐like state. In this model, HRV and BRS were reduced, reflex of a shift of the autonomic balance towards sympathetic predominance. Pharmacological blockade of the dorsomedial hypothalamus (DMH) reversed all cardiovascular alterations, whereas blockade of the nucleus tractus solitarii (NTS) 5‐HT₃receptor by the local or systemic administration of granisetron restored only baroreflex gains and the parasympathetic component of HRV. In conclusion, repeated social defeat in the rat leads to an anxiety‐like state, in which the DMH and the NTS are chronically activated and are responsible for dysautonomia. These regions may constitute new targets against sudden cardiac death. Abstract Anxiety disorders in humans reduce both the heart rate variability (HRV) and the sensitivity of the cardiac baroreflex (BRS). Both may contribute to sudden death. To elucidate the mechanisms underlying these alterations, male rats were subjected to social defeat sessions on four consecutive days. Five days later, the rats were found to be in an anxiety‐like state. At this time point, we analysed HRV and BRS in the defeated rats, with or without treatment with the anxiolytic chlordiazepoxide (CDZ). HRV was reduced after social defeat, due to changes in the autonomic balance favouring the sympathetic over the parasympathetic component. Spontaneous and pharmacological baroreflex gains were also reduced. CDZ abolished anxiety‐like symptoms as well as HRV and BRS alterations. Inhibition of the dorsomedial hypothalamus (DMH) with muscimol reversed all cardiovascular alterations, whereas blockade of the nucleus tractus solitarii (NTS) 5‐HT₃receptor by the local or systemic administration of granisetron restored only baroreflex gains and the parasympathetic component of HRV. In conclusion, repeated social defeat in the rat lead to an anxiety‐like state that was associated with lasting reduction in HRV and baroreflex gains. The DMH and the NTS were responsible for these chronic cardiovascular alterations. These regions may therefore constitute new therapeutic targets for reducing cardiac dysfunction and fibrillation in anxiety disorders.

Slow-paced breathing has been shown to enhance the self-regulation abilities of athletes via its influence on cardiac vagal activity. However, the role of certain respiratory parameters (i.e., inhalation/exhalation ratio and presence of a respiratory pause between respiratory phases) still needs to be clarified. The aim of this experiment was to investigate the influence of these respiratory parameters on the effects of slow-paced breathing on cardiac vagal activity. A total of 64 athletes (27 female; M_age = 22, age range = 18–30 years old) participated in a within-subject experimental design. Participants performed six breathing conditions within one session, with a 5 min washout period between each condition. Each condition lasted 5 min, with 30 respiratory cycles, and each respiratory cycle lasted 10 s (six cycles per minute), with inhalation/exhalation ratios of 0.8, 1.0, 1.2; and with or without respiratory pauses (0.4 s) between respiratory phases. Results indicated that the root mean square of successive differences (RMSSD), a marker of cardiac vagal activity, was higher when exhalation was longer than inhalation. The presence of a brief (0.4 s) post-inhalation and post-exhalation respiratory pause did not further influence RMSSD. Athletes practicing slow-paced breathing are recommended to use an inhalation/exhalation ratio in which the exhalation phase is longer than the inhalation phase.

Background and Purpose: Asthma is characterized by airway inflammation, mucus hypersecretion, and airway hyperresponsiveness. The use of nicotinic agents to mimic the cholinergic anti‐inflammatory pathway (CAP) controls experimental asthma. Yet, the effects of vagus nerve stimulation (VNS)‐induced CAP on allergic inflammation remain unknown.Experimental Approach: BALB/c mice were sensitized and challenged with house dust mite (HDM) extract and treated with active VNS (5 Hz, 0.5 ms, 0.05–1 mA). Bronchoalveolar lavage (BAL) fluid was assessed for total and differential cell counts and cytokine levels. Lungs were examined by histopathology and electron microscopy.Key Results: In the HDM mouse asthma model, VNS at intensities equal to or above 0.1 mA (VNS 0.1) but not sham VNS reduced BAL fluid differential cell counts and alveolar macrophages expressing α7 nicotinic receptors (α7nAChR), goblet cell hyperplasia, and collagen deposition. Besides, VNS 0.1 also abated HDM‐induced elevation of type 2 cytokines IL‐4 and IL‐5 and was found to block the phosphorylation of transcription factor STAT6 and expression level of IRF4 in total lung lysates. Finally, VNS 0.1 abrogated methacholine‐induced hyperresponsiveness in asthma mice. Prior administration of α‐bungarotoxin, a specific inhibitor of α7nAChR, but not propranolol, a specific inhibitor of β2‐adrenoceptors, abolished the therapeutic effects of VNS 0.1.Conclusion and Implications: Our data revealed the protective effects of VNS on various clinical features in allergic airway inflammation model. VNS, a clinically approved therapy for depression and epilepsy, appears to be a promising new strategy for controlling allergic asthma.