Hemodynamic and Autonomic Adjustments to Real Life Stress Conditions in Humans

Abstract

Abstract-Psychological stress represents a risk factor for hypertension, but mechanisms are not known in detail. In this investigation we tested the hypothesis that real-life stress conditions produce changes in autonomic cardiac and vascular regulation that might differ in magnitude. University students, a well-established model of mild real-life stress, were examined shortly before a university examination, and a second time 3 months afterward, during holiday. Autonomic cardiovascular regulation was assessed by a noninvasive approach, based on autoregressive analysis of RR interval variability (V) and of systolic arterial pressure (SAP) V. The overall level of stress in the two sessions was gauged from the elevated salivary cortisol (5.6Ϯ0.5 versus 2.4Ϯ0.2 ng/mL, PϽ0.05) and altered cytokine profile (PϽ0.05). During the stress day, the RR interval was reduced and arterial pressure increased significantly; simultaneously, the normalized low frequency component of RRV (a marker of sympathetic modulation of the sinoatrial node) was increased and the index ␣ (a measure of baroreflex gain) reduced. Concomitantly, the autonomic response to the sympathetic excitation produced by standing was altered: cardiac response was impaired and vascular responsiveness increased. Markers of autonomic regulation of the sinoatrial node correlated significantly with cortisol levels, both at rest and also considering standing induced changes, suggesting a gradual range of effects. The data support the concept that mild real-life stress increases arterial pressure and impairs cardiovascular homeostasis. These changes, assessable with spectral analysis of cardiovascular variability, might contribute, in susceptible individuals, to the link between psychological stress and increased cardiovascular risk of hypertension. Key Words: autonomic nervous system Ⅲ baroreceptors Ⅲ stress hormones Ⅲ risk factors T he importance and nature of the complex, multifarious mechanisms linking psychological stress to arterial hypertension 1,2 have been extensively explored in simulated conditions. In laboratory models, mental stress leads to a rise in arterial pressure and heart rate, by way of altered neural cardiovascular regulation, typically consisting of increased sympathetic activity 3-5 and reduced baroreflex gain, 6,7 coupled to a prolonged endothelial dysfunction. 8,9 Sympathetic activation is noninvasively recognized by spectral analysis of RR variability, 10,11 indicating a predominant low frequency (LF) component of RR variability, in conditions of acute laboratory stress. 7 Data from laboratory experiments, however, are limited by their intrinsic artificiality and by the fact that some of the more efficacious models, such as public speaking and mental arithmetic, might involve changes in respiration that could obscure the interpretation of results, particularly when autonomic regulation is inferred solely by spectral analysis of RR variability. 12 Conversely, the effects of real-life psychological stressors on cardiovascular regulations, al...

Risk Indices Associated with the Insulin Resistance Syndrome, Cardiovascular Disease, and Possible Protection with Yoga: A Systematic Review

“…8,15,16,18 -20 Increased sympathetic activity, enhanced cardiovascular reactivity, and reduced parasympathetic tone have also been strongly implicated in the pathogenesis of IRS 10,[21][22][23][24][25][26][27][28][29] and in the development and progression of atherosclerosis 27,28,30,31 and cardiovascular disease. 21,25,28 -36 In addition, recent research offers compelling evidence that chronic psychological stress and negative affective states contribute significantly to the pathogenesis and progression of insulin resistance, [37][38][39][40][41] glucose intolerance, 38 hypertension, [42][43][44][45][46] dyslipidemia, 38,41,47 and other IRS-related conditions 28,37,48 -55 and ultimately, increase risk for CVD morbidity and mortality. 28,32,43,44,46,52,56 -60 Not only can IRS-related conditions be exacerbated by lifestyle variables, such as smoking, lack of exercise, and poor diet, but these conditions can interact with one another in a destructive manner, 61 likely accounting for their synergistic effect on CVD risk.…”

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“…30 As in a previous study on the autonomic effects of acute and chronic stress, 18,27 all of the subjects filled out a self-administered questionnaire providing nominal self-rated scales that focus on overall stress, tiredness perception, and stress-related symptoms. The overall stress and tiredness perception scale 18,27 uses Likert linear analogue scales from 0 ("no perception") to 10 ("strong perception") to approximate the perceived overall stress and tiredness levels. The Subjective Stress-Related Somatic Symptoms Questionnaire (4S-Q) 18,27 inquires about 18 somatic symptoms accounting for the majority of somatic complaints.…”

“…According to the sympatho-vagal model, as applied in our laboratory, and on the basis of a strong coherence between similar oscillations in the variability of the RR interval and of muscle sympathetic efferent activity, 31 the low-frequency component ([LF] in normalized units) represents a marker of oscillatory sympathetic modulation of the senoatrial node, whereas the high-frequency component ([HF] nu) is a marker of vagal oscillatory modulation. [21][22][23][24][25][26][27][28] …”

“…To partly overcome these problems, we developed and tested a noninvasive, nonintrusive methodology to simultaneously study multiple dimensions of stress in the clinical laboratory, addressing both autonomic changes and symptoms profiles. 18,27 …”

“…Obviously, this design imposes technical constraints, suggesting the use of simple, noninvasive methodologies, such as spectral analysis of RR variability. This technique provides quantitative markers of autonomic regulation [21][22][23][24] capable of distinguishing between different autonomic profiles as related to posture, 25 psychological stress, 18,26,27 or various grades of hypertension. 24 Notably, RR variability may be assessed onsite with very simple telemedicine techniques, providing results highly consistent with those obtained in the clinical laboratory.…”