This study tested various sources of changes in respiratory
sinus arrhythmia (RSA). Twenty-two healthy participants
participated in three experimental conditions (mental stress,
relaxation, and mild physical exercise) that each consisted
of three breathing parts (normal breathing, breathing compressed
room air, and breathing compressed 5% CO2-enriched
air). Independent contributions to changes in RSA were found
for changes in tonic vagal modulation of heart rate, central
respiratory drive (i.e., PaCO2), respiratory depth,
and respiratory frequency. The relative contributions to changes
in RSA differed for mental stress and physical exercise. It
is concluded that uncorrected RSA will suffice to index
within-subject changes in tonic vagal modulation of heart rate
in most situations. However, if the central respiratory drive
is expected to change, RSA should ideally be corrected for changes
in PaCO2, respiratory depth, and respiratory frequency.

The extent to which variation in posture and respiration can confound pre-ejection period and respiratory sinus arrhythmia (RSA) as indices of cardiac sympatho-vagal activity was examined. Within-subjects changes in these measures were assessed in 36 subjects during different postures and (paced) respiratory frequencies. Changes from supine to sitting to standing led to reduced RSA values and longer pre-ejection periods, reflecting the known decrease in vagal but not the increase of sympathetic activity. Multilevel path analysis showed that within-subjects changes in sympatho-vagal balance were faithfully reflected by changes in interbeat interval, but imperfectly by changes in RSA and pre-ejection period. It was concluded that pre-ejection period should be stratified for posture and RSA for respiratory frequency to reliably index changes in sympatho-vagal balance when these factors are prone to change (e.g., during 24-h ambulatory recording)

The hypothesis that biased symptom perception toward excessive symptoms is common when relatively normal chronic patients enter symptom-relating situations, irrespective of emotional variables, was tested in 19 women with severe asthma, 18 with somatization-like characteristics, and 18 controls. Each underwent three experimental conditions: mental stress, resting, and physical exercise. Each condition included three breathing conditions: breathing normally, normal compressed air, and 5.5% CO2-enriched compressed air. Results yielded no group differences in physiological measures, e.g. elevated CO2 in exhaled air (end-tidal partial pressure of CO2, PetCO2), or lung function. Asthma patients experienced more breathlessness, and somatization-like participants more breathlessness, miscellaneous symptoms, and subjective stress than controls. Although these differences suggested acquired biased symptom perception, as it turned out, breathlessness in asthmatics was more influenced by PetCO2 and less by subjective stress compared to controls. Likewise, breathlessness in somatization-like participants was similarly influenced by PetCO2 and subjective stress compared to controls, and miscellaneous symptoms were even more influenced by PetCO2 and less by subjective stress compared to controls. It was concluded that acquired sensitivity to physiological activity associated with habitual symptoms may account for excessive symptoms in patients with chronic health problems.

People with medically unexplained symptoms (MUS) often have a comorbid history of stress and negative affect. Although the verbal-cognitive and (peripheral) physiological stress systems have shown a great degree of independence, at the same time it is claimed that chronic stress and negative affect can result in a disregulated physiological stress system, which may lead to MUS. Previous studies could not demonstrate a straightforward between subject relationship between MUS and stress physiology, supporting the view of independence. The aim of the current study was to further explore this relationship using an improved methodology based on ecologically valid 24-h real-life ambulatory recordings. Seventy-four participants (19 male; 55 female) with heterogeneous MUS were compared with 71 healthy controls (26 male; 45 females). Momentary experienced somatic complaints and mood, heart rate, cardiac autonomic activity, respiration and saliva cortisol were monitored using electronic diary and ambulatory registration devices. Participants with MUS reported much more momentary complaints and negative affect as compared to controls. Although MUS seemed to be associated with elevated heart rate and reduced low and very-low frequency heart period variability, these effects disappeared after controlling for differences in sports behaviour. No group differences were found for cardiac autonomic activity, respiration, end-tidal CO2 and saliva cortisol. Our 24-h real-life ambulatory study did not support the existence of a connection between MUS and disregulated peripheral stress physiology. Future studies may instead focus on central measures to reveal potential abnormalities such as deviant central processing of visceral signals in MUS patients.

The extent to which various measures of ambulatory respiratory sinus arrhythmia (RSA) capture the same information across conditions in different subjects remains unclear. In this study the root mean square of successive differences (RMSSD), peak valley RSA (pvRSA), and high frequency power (HF power) were assessed during ambulatory recording in 84 subjects, of which 64 were retested after about 3 years. We used covariance structure modeling to test the equality of the correlations among three RSA measures over two test days and three conditions (daytime sitting or walking and nighttime sleep) and in groups with low, medium, and high mean heart rate (HR), or low, medium, and high mean respiration rate (RR). Results showed that ambulatory RMSSD, pvRSA, and HF power are highly correlated and that their correlation is stable across time, ambulatory conditions, and a wide range of resting HR and RR values. RMSSD appears to be the most cost-efficient measure of RSA.

The purpose of the current study was to validate the change in thoracic impedance (dZ) derived respiratory signal obtained from four spot electrodes against incidental spirometry. Additionally, a similar validation was performed for a dual respiratory belts signal to compare the relative merit of both methods. Participants were 38 healthy adult subjects (half male, half female). Cross-method comparisons were performed at three (paced) respiration frequencies in sitting, supine and standing postures. Multilevel regression was used to examine the within- and between-subjects structure of the relationship between spirometric volume and the respiratory amplitude signals obtained from either dZ or respiratory belts. Both dZ derived respiratory rate and dual belts derived respiratory rate accurately reflected the pacing frequencies. For both methods, fixed factors indicated acceptable but posture-specific regression on spirometric volume. However, random factors indicated large individual differences, which was supported by variability of gain analyses. It was concluded that both the dZ and dual belts methods can be used for measurement of respiratory rate and within-subjects, posture-specific, changes in respiratory volume. The need for frequent subject-specific and posture-specific calibration combined with relatively large measurement errors may strongly limit the usefulness of both methods to assess absolute tidal volume and minute ventilation in ambulatory designs.

CONTEXT: It has been hypothesized that depression is associated with lower heart rate variability and decreased cardiac vagal control. This may play an important role in the risk of cardiovascular disease among depressed individuals.
OBJECTIVE: To determine whether heart rate variability was lower in depressed individuals than in healthy controls in a large adult sample.
DESIGN: Cross-sectional analyses from a large depression cohort study.
SETTING: The Netherlands Study of Depression and Anxiety.
PARTICIPANTS: Two thousand three hundred seventy-three individuals (mean age, 41.8 years; 66.8% female) who participated in the Netherlands Study of Depression and Anxiety. Included were 524 controls, 774 individuals with a diagnosis of major depressive disorder (MDD) earlier in life (remitted MDD), and 1075 individuals with current MDD based on the Composite International Diagnostic Interview. This sample was sufficiently powered to examine the confounding effects of lifestyle, comorbid anxiety, and antidepressants.
MAIN OUTCOME MEASURES: The standard deviation of normal-to-normal beats (SDNN) and cardiac vagal control, as indexed by respiratory sinus arrhythmia (RSA), were measured during 1(1/2) hours of ambulatory recording of electrocardiograms and thorax impedance. Multivariate analyses were conducted to compare SDNN and RSA across depression groups after adjustment for demographics, health, lifestyle, comorbid anxiety, and psychoactive medication.
RESULTS: Individuals with remitted and current MDD had a lower mean SDNN and RSA compared with controls (SDNN, 3.1-5.7 milliseconds shorter, P < or = .02; RSA, 5.1-7.1 milliseconds shorter, P < .001; effect size, 0.125-0.269). Comorbid anxiety and lifestyle did not reduce these associations. However, accounting for psychoactive medication removed the association with SDNN and strongly attenuated the association with RSA. Depressed individuals who were using selective serotonin reuptake inhibitors, tricyclic antidepressants, or other antidepressants had significantly shorter SDNNs and RSAs (effect size, 0.207-0.862) compared with controls and depressed individuals not taking medication. CONCLUSIONS: This study shows that depression is associated with significantly lowered heart rate variability. However, this association appears to be mainly driven by the effect of antidepressants.

A non-clinical group high on heterogeneous medically unexplained symptoms (MUS; n=97) was compared with healthy controls (n=66) on the within-subject relationships between physiological measures using multilevel path analysis. Momentary experienced somatic complaints, mood (tension and depression), cardiac autonomic activity (inter-beat intervals, pre-ejection period (PEP), and respiratory sinus arrhythmia (RSA)) and respiration (rate and partial pressure of CO2 at the end of a normal expiration) were monitored for 24 h using electronic diary and ambulatory devices. Relationships between measures were controlled for diurnal variation and individual means. Only subtle group differences were found in the diurnal rhythm and in the within-subject relationships between physiological measures. For participants high on MUS, within-subject changes in bodily symptoms were related to changes in mood, but only marginally to the physiological measures. Results of the current path analysis confirm the subordinate role of cardiac autonomic and respiratory parameters in MUS.

Although many musicians perceive music performance anxiety (MPA) as a significant problem, studies about the psychobiological and performance-related concomitants of MPA are limited. Using the biopsychosocial model of challenge and threat as theoretical framework, we aim to investigate whether musicians’ changes in their psychobiological responses and performance quality from a private to a public performance are moderated by their general MPA level. According to the challenge and threat framework, individuals are in a threat state when the perceived demands of a performance situation outweigh the perceived resources, whereas they are in a challenge state when the perceived resources outweigh the perceived demands. The resources-demands differential (resources minus demands) and the cardiovascular challenge-threat index (sum of cardiac output and reverse scored total peripheral resistance) are the main indices of these states. We postulate that the relationship between general MPA level and performance quality is mediated by these challenge and threat measures.

Speech production interferes with the measurement of changes in cardiac vagal activity during acute stress by attenuating the expected drop in heart rate variability. Speech also induces cardiac sympathetic changes similar to those induced by psychological stress. In the laboratory, confounding of physiological stress reactivity by speech may be controlled experimentally. In ambulatory assessments, however, detection of speech episodes would be necessary to separate the physiological effects of psychosocial stress from those of speech. Using machine learning (https://osf.io/bk9nf), we trained and tested speech classification models on data from 56 participants (ages 18–39) under controlled laboratory conditions. They were equipped with privacy-secure wearables measuring thoracoabdominal respiratory inductance plethysmography (RIP from a single and a dual-band set-up), thoracic impedance pneumography, and an upper sternum positioned unit with triaxial accelerometers and gyroscopes. Following an 80/20 train-test split, nested cross-validations were run with the machine learning algorithms XGBoost, gradient boosting, random forest, and logistic regression on the training set to get generalized performance estimates. Speech classification by the best model per method was then validated in the test set. Speech versus no-speech classification performance (AUC) for both nested cross-validation and test set predictions was excellent for thorax–abdomen RIP (nested cross-validation: 96.6%, test set prediction: 98.5%), thorax-only RIP (97.5%, 99.1%), impedance (97.0%, 97.8%), and accelerometry (99.3%, 99.6%). The sternal accelerometer method outperformed others. These open-access models leveraging biosignals have the potential to also work in daily life settings. This could enhance the trustworthiness of ambulatory psychophysiology, by enabling detection of speech and controlling for its confounding effects on physiology.