This study examined chronic and short-term stress effects on heart rate variability (HRV), comparing time, frequency and phase domain (complexity) measures in 50 healthy adults. The hassles frequency subscale of the combined hassles and uplifts scale (CHUS) was used to measure chronic stress. Shortterm stressor reactivity was assessed with a speech task. HRV measures were determined via surface electrocardiogram (ECG). Because respiration rate decreased during the speech task (p < .001), this study assessed the influence of respiration rate changes on the effects of interest. A series of repeatedmeasures analyses of covariance (ANCOVA) with Bonferroni adjustment revealed that short-term stress decreased HR D2 (calculated via the pointwise correlation dimension PD2) (p < .001), but increased HR mean (p < .001), standard deviation of R-R (SD RR ) intervals (p < .001), low (LF) (p < .001) and high frequency band power (HF) (p = .009). Respiratory sinus arrhythmia (RSA) and LF/HF ratio did not change under short-term stress. Partial correlation adjusting for respiration rate showed that HR D2 was associated with chronic stress (r = −.35, p = .019). Differential effects of chronic and short-term stress were observed on several HRV measures. HR D2 decreased under both stress conditions reflecting lowered functionality of the cardiac pacemaker. The results confirm the importance of complexity metrics in modern stress research on HRV.
Selected examples from man and canine experiments with time series of reticular neurons, respiration, arterial blood pressure, and cutaneous forehead blood content fluctuations were analyzed using multiscaled Time-Frequency-Distribution (TFD), Post-Event-Scan (PES), and Pointwise Transinformation (PTI), resp.. We found in both experiments a "0.15 Hz rhythm" which exhibited periods of spindle wave epochs (increasing and decreasing amplitudes) to be phase synchronized with respiration at 1:2, 1:1 and 2:1 integer number ratios. At times of these wave-epochs and n:m phase-synchronization, the "0.15 Hz rhythm" appeared also in heart rate and arterial blood pressure fluctuations. If phase synchronization of the "0.15 Hz rhythm" with respiration was established at a 1:1 integer number ratio, it was maintained throughout and resulted in consensualization of all cardio-vascular-respiratory oscillations at 0.15 Hz. Analysis of a canine experiment supplied evidence that the emergence of the "0.15Hz rhythm" and n:m phase synchronization appears to result from a decline in the level of the general activity of the organism which was associated with a decline in the level of activity of reticular neurons in the lower brainstem network. These findings corroborate the notion of the "0.15 Hz rhythm" to be a state marker of the `trophotropic mode of operation` which was introduced by W.R. Hess.
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