The Effect of Transcutaneous Vagus Nerve Stimulation on Heart Rate Variability during Paced Breathing

Abstract

PurposeTranscutaneous vagus nerve stimulation (tVNS) is an effective, non‐invasive method of electrically stimulating the vagus nerve without surgical procedures and it is FDA‐approved to treat cluster headache and migraine. One approach of tVNS is to stimulate the auricle branch of the vagus nerve (tVNSab) by sending a small electrical current through the tragus of the ear. Previous evidence indicates that heart rate (HR) is lowered, indices of heart rate variability (HRV) are increased, and muscle sympathetic nerve activity is decreased following 10‐15 min of tVNSab. However, these previous investigations did not control for respiration, which can influence autonomic activity. Thus, we tested the hypotheses that tVNSab would lower heart rate and increase indices of HRV that reflect cardiac parasympathetic activity during paced breathing (PB).MethodsSeven healthy adults (age: 20 ± 3 y; BMI:19 ± 7 kg/m2, 3 women) completed two randomized visits; bilateral tVNSab (pulse width = 200 ms; pulse frequency = 30 Hz) or a time‐control visit (SHAM) in which electrodes were secured on the tragus, but no current was applied. A 3‐lead ECG was utilized to record cardiac rhythm and HR. After baseline (PRE), tVNSab/SHAM was initiated and continued throughout data collection. Data were collected at PRE and during each intervention (STIM) during 5 min of PB. During PB, participants breathed in concert to a metronome set at 15 breaths/min. The root mean square of successive differences (RMSSD) was chosen as a marker of HRV in the time‐domain, while the frequency domain was assessed via low‐frequency (LF) and high‐frequency (HF) power. Additionally, non‐linear HRV analysis was performed using Poincare plots to calculate standard deviation 1 (SD1) and 2 (SD2). Values are reported as mean ± SD.ResultsHR was not different at PRE (tVNSab: 73 ± 15; SHAM: 73 ± 10 bpm; P = 0.92) or during STIM (tVNSab: 74 ± 14; SHAM: 75 ± 11 bpm; P = 0.87). RMSSD was not different at PRE (tVNSab: 69 ± 67; SHAM: 62 ± 46 ms; P = 0.16) or during STIM (tVNSab: 69 ± 70; SHAM: 58 ± 48 ms; P = 0.06) and it did not change in either condition (tVNSab: P = 0.87; SHAM: P = 0.59). LF was different at PRE (tVNSab: 1160 ± 654; SHAM: 1916 ± 1917 ms2; P = 0.01) but not during STIM (tVNSab: 1382 ± 719; SHAM: 1802 ± 1730 ms2; P = 0.14) and it did not change in either condition (tVNSab: P = 0.56; SHAM: P = 0.89). HF was not different at PRE (tVNSab: 784 ± 505; SHAM: 1076 ± 692 ms2; P = 0.70) or during STIM (tVNSab: 1119 ± 804; SHAM: 1015 ± 711 ms2; P = 0.89) and it did not change in either condition (tVNSab: P = 0.46; SHAM: P = 0.99). SD1 was not different at PRE (tVNSab: 48 ± 46; SHAM: 46 ± 38 ms; P = 0.97) or during STIM (tVNSab: 52 ± 49; SHAM: 41 ± 25 ms; P = 0.13) and it did not change in either condition (tVNSab: P = 0.73; SHAM: P = 0.67). SD2 was not different at PRE (tVNSab: 108 ± 69; SHAM: 92 ± 48 ms; P = 0.55) or during STIM (tVNSab: 113 ± 60; SHAM: 105 ± 59 ms; P = 0.89) and it did not change in either condition (tVNSab: P = 0.97; SHAM: P = 0.70).ConclusionsThese preliminary data show that a single intervention of tVNSab did not reduce HR or alter HRV in healthy college‐aged adults during PB. Contrary to our hypotheses, these data indicate that tVNSab does not elicit changes to cardiac autonomic activity that reflect greater cardiac parasympathetic activity in young healthy adults.