Relative burst amplitude of muscle sympathetic nerve activity is an indicator of altered sympathetic outflow in chronic anxiety

Abstract

Relative burst amplitude of muscle sympathetic nerve activity (MSNA) is an indicator of augmented sympathetic outflow and contributes to greater vasoconstrictor responses. Evidence suggests anxiety-induced augmentation of relative MSNA burst amplitude in patients with panic disorder; thus we hypothesized that acute stress would result in augmented relative MSNA burst amplitude and vasoconstriction in individuals with chronic anxiety. Eighteen participants with chronic anxiety (ANX; 8 men, 10 women, 32 ± 2 yr) and 18 healthy control subjects with low or no anxiety (CON; 8 men, 10 women, 39 ± 3 yr) were studied. Baseline MSNA and 24-h blood pressure were similar between ANX and CON ( P > 0.05); however, nocturnal systolic blood pressure % dipping was blunted among ANX ( P = 0.02). Relative MSNA burst amplitude was significantly greater among ANX compared with CON immediately preceding (anticipation) and during physiological stress [2-min cold pressor test; ANX: 73 ± 5 vs. CON: 59 ± 3% arbitrary units (AU), P = 0.03] and mental stress (4-min mental arithmetic; ANX: 65 ± 3 vs. CON: 54 ± 3% AU, P = 0.02). Increases in MSNA burst frequency, incidence, and total activity in response to stress were not augmented among ANX compared with CON ( P > 0.05), and reduction in brachial artery conductance during cold stress was similar between ANX and CON ( P = 0.92). Relative MSNA burst amplitude during mental stress was strongly correlated with state ( P < 0.01) and trait ( P = 0.01) anxiety (State-Trait Anxiety Inventory), independent of age, sex, and body mass index. Thus in response to acute stress, both mental and physiological, individuals with chronic anxiety demonstrate selective augmentation in relative MSNA burst amplitude, indicating enhanced sympathetic drive in a population with higher risk for cardiovascular disease. NEW & NOTEWORTHY Relative burst amplitude of muscle sympathetic nerve activity in response to acute mental and physiological stress is selectively augmented in individuals with chronic anxiety, which is a prevalent condition that is associated with the development of cardiovascular disease. Augmented sympathetic burst amplitude occurs with chronic anxiety in the absence of common comorbidities. These findings provide important insight into the relation between anxiety, acute stress and sympathetic activation.

Keywords: MSNA; anxiety; blood pressure; mental stress.

Figures

Fig. 1.

Example baseline recordings (45 s) of muscle sympathetic nerve activity (MSNA) and electrocardiogram (ECG) in 5 individuals with moderate/high anxiety (A–E) and 5 control subjects with low/no anxiety (F–J). AU, arbitrary units; BMI, body mass index.

Fig. 2.

Mean summary data of relative muscle sympathetic nerve activity (MSNA) burst amplitude in control subjects with low/no anxiety and individuals with moderate/high anxiety during a 2-min baseline and during and after 2 min of cold stress (A; control: n = 18, anxiety: n = 18) and 4 min of mental stress (B; control: n = 15, anxiety: n = 13). Also shown is the anticipatory response in relative MSNA burst amplitude during the 2-min baseline periods before cold and mental stress compared with the resting 10-min baseline period at the beginning of the study (C). Data are expressed as means ± SE. AU, arbitrary units.

Fig. 3.

Mean summary data of muscle sympathetic nerve activity (MSNA) burst frequency (A and D), MSNA burst incidence (B and E), and MSNA total activity (C and F) in control subjects with low/no anxiety and individuals with moderate/high anxiety during a 2-min baseline and during and after 2 min of cold stress (control: n = 18, anxiety: n = 18) and 4 min of mental stress (mental arithmetic) (control: n = 15, anxiety: n = 13). Data are expressed as means ± SE. AU, arbitrary units; hb, heartbeats.

Fig. 4.

Mean summary data of % change in brachial artery conductance (A; control: n = 18, anxiety: n = 17) and mean arterial blood pressure (B; control: n = 18, anxiety: n = 18) during 2 min of cold stress in control subjects with low/no anxiety and individuals with moderate/high chronic anxiety. Brachial artery conductance could not be collected in 1 participant with high anxiety. Data are expressed as means ± SE. BL, baseline.

Fig. 5.

Correlational analyses between measures of anxiety (State-Trait Anxiety Inventory) and relative muscle sympathetic nerve activity (MSNA) burst amplitude (A) and MSNA burst incidence (B) during mental stress (I and II; mental arithmetic; control: n = 15, anxiety: n = 13) and cold stress (III and IV; control: n = 18, anxiety: n = 18). Data shown are MSNA responses during the latter half of mental stress (2 min avg.) and cold stress (1 min avg.), when peak responses tended to occur. BMI, body mass index.