Snyder, Eric M.

Abstract Workplace stress is one of the main sources of stress for adults, although physiological and cognitive factors may impact each person's stress response. Numerous studies have shown heart rate, heart rate variability, neural activity, and cognitive performance are affected by stress. Additionally, visual and auditory stimuli in one's environment have been shown to affect individuals' reaction to stressful events. To our knowledge, few studies have examined how each of these physiological and cognitive measures relate to one's perception of stress, the ability to recover from stress, and what environmental factors may help with stress recovery. Here, 80 healthy adults performed a laboratory-controlled stress induction task where they experienced and recovered from an acute psychological stressor (Trier Social Stress Test, TSST, using verbal math skills and a public presentation that was videotaped). Throughout the assessment, heart rate, heart rate variability, and neural activity were measured using wearable devices to assess changes before, during, and after the stressor. Additionally, participants were assessed their perceived stress levels at specific times throughout the assessment. After the psychological stressor, participants were randomly assigned to one of four recovery conditions within a multisensory relaxation room: Control (C), Auditory Only (A), Visual Only (V), or Combined Auditory and Visual (AV). During the stressor, anxiety, heart rate, and beta EEG power increased and high-frequency power and heart rate variability decreased, confirming participants reactivity to the stressor ( P < 0.01 for all vs. baseline). Only the V and AV conditions led to notable reductions in anxiety (15 and 17%, respectively) vs. the C condition, but these did not reach statistical significance. There was no difference between V and AV, suggesting a stronger impact of V. We observed no differences between conditions during recovery for HR and HRV. Overall, these findings suggest the visual features of the relaxation room impacted self-reported anxiety, however physiological and neurological effects did not demonstrate a statistically meaningful response.

Cardiogenic pulmonary edema is a life-threatening complication in patients with heart failure (HF) resulting from increased alveolar Cl- secretion and inhibition of alveolar epithelial Na+ channels (ENaC). Not all HF patients develop pulmonary edema, despite similar clinical characteristics, suggesting a genetic component to edema formation in response to cardiac failure. The ENaC are crucial for alveolar fluid clearance, with the alpha subunit demonstrating particular importance. We have previously found that genetic variation of the alpha subunit (SCNN1A) of ENaC, an alanine (A) to threonine (T) substitution, influences ion regulation during exercise and in response to albuterol. In the present study, we sought to determine the influence of the threonine variant (T663; AT/TT group) on lung fluid regulation in response to normobaric hypoxia, an environmental condition known to increase pulmonary capillary hydrostatic stress in healthy humans. Lung ion and fluid changes were assessed using exhaled Na+ (ENa+) and the lung diffusing capacity for carbon monoxide and nitric oxide (DLCO and DLNO, respectively) to determine alveolar-capillary membrane conductance (DM). 19 healthy subjects (n=8 vs. 11, %female=50 vs. 62%, age=27±1 vs. 28±2yrs., ht=171±3 vs. 173±2cm, wt=69±6 vs.72±3kg , BMI=23±1 vs.24±1kg/m2 , for AA and AT/TT, respectively) completed two overnight visits in a hypoxic tent simulating just over 5,400m. The visits were randomized to inhaled placebo (P) or inhaled amiloride (Aml, 1.5mg in 5ml normal saline, used to inhibit ENaC activity) with ENa+, DLCO, and DM assessed at baseline and following 12 hours of hypoxic exposure. There was an effect of genotype on the ENa+ response to hypoxia with placebo that was abolished with amiloride, but no effect of genotype on the diffusing capacity of the lung (Table). These results suggest that genetic variation of SCNN1A may influence ion regulation in the lung under conditions of elevated hydrostatic stress.