Acute cholesterol responses to mental stress and change in posture.

BACKGROUND: Serum lipid levels vary widely within individuals, but the causes of these fluctuations are poorly understood. One area of research concerns elevations in cholesterol concentration in response to emotional stress. In a laboratory-based experiment, we compared the effects of acute mental stress and postural change (standing) on serum cholesterol concentration. In addition, plasma volume was indirectly monitored to determine whether cholesterol changes with mental stress, if present, were a function of hemoconcentration. METHODS: Twenty-six men attended two laboratory sessions, each consisting of baseline (30 minutes), task (20 minutes), and recovery (30 minutes) periods. Subjects rested in the supine position during the baseline and recovery periods. During the task period of one session, subjects performed a mental task (Stroop test and mental arithmetic); during the other session, the subjects stood for the task period. RESULTS: Both mental stress and standing elicited significant elevations in heart rate, blood pressure, and plasma catecholamine concentrations, relative to the baseline and recovery periods. Both the mental and orthostatic tasks also significantly increased serum cholesterol concentration (by 0.10 and 0.57 mmol/L [3.7 and 21.9 mg/dL], respectively), as well as hemoglobin level and hematocrit. Cholesterol elevations with standing were reversible, while those resulting from mental stress persisted through the recovery period. When values were corrected for concomitant hemoconcentration, no net change in serum cholesterol level occurred during either task. CONCLUSIONS: Acute mental stress can produce rapid elevations in serum cholesterol concentration. It can also increase hemoglobin concentration and hematocrit (ie, reduce plasma volume). Therefore, increases in serum cholesterol level after acute mental stress are analogous to those with standing and may reflect hemoconcentration rather than altered lipoprotein metabolism.

Lymphocyte subset redistribution during acute laboratory stress in young adults: mediating effects of hemoconcentration.

Acute psychological stress is known to alter the distribution of circulating lymphocyte subsets and also to cause a reduction of plasma volume. Data were reanalyzed from 4 previously reported studies (E. A. Bachen et al., 1995; T. B. Herbert et al., 1994; A. L. Marsland, S. B. Manuck, T. V. Fazzari, C. J. Stewart, & B. S. Rabin, 1995; A. L. Marsland, S. B. Manuck, P. Wood, et al., 1995) to determine the extent to which changes in the concentration of lymphocyte subsets are attributable to such hemoconcentration. Meta-analytic procedures showed circulating concentrations of T-suppressor/cytotoxic (CD8) and natural killer (NK) cells to increase following acute laboratory challenge, whereas T-helper (CD4) and B- (CD19) cell populations did not change. Adjustments for concomitant hemoconcentration reduced the magnitude of stress-related increases in CD8 and NK cells significantly and revealed a decrease in CD4 and CD19 cell concentrations from baseline to stress measurements. These data provide evidence (a) that increases in circulating numbers of CD8 and NK cells following acute stress are partially attributable to hemoconcentration and (b) that CD4 and CD19 cell concentrations decrease during acute stress when hemoconcentration is taken into account.

Behaviorally-evoked plasma catecholamine response and 24-hour excretion of urinary catecholamines among cardiac and vascular reactors.

Individuals differ in the cardiac and vascular processes that underlie blood pressure elevations evoked by environmental stimuli; such differences may reflect variability in sympathoadrenal response. We separated 108 healthy, young-adult males into those with predominant elevations in either cardiac output or peripheral resistance when exposed to psychological challenges. We then asked if they differed on other measures of cardiovascular response, concomitant plasma catecholamine reactions or 24-h urinary excretion of catecholamines. Cardiac reactors, relative to vascular reactors, showed reduced cardiac pre-ejection period, a smaller reduction in stroke volume, and elevated plasma epinephrine response and 24-h urinary epinephrine excretion. Vascular reactors, relative to cardiac reactors, responded to mental stress with more elevated diastolic blood pressure, a rise in peripheral resistance and pulse wave velocity, and a greater reduction in stroke volume. Vascular reactors, however, did not show plasma norepinephrine response or 24-h urinary norepinephrine excretion that was greater than cardiac reactors. The results provide partial support for the hypothesis that variability in sympathoadrenal activity contributes to individual differences in cardiac and vascular reactivity, and extend prior observations by demonstrating covariation of behaviorally-elicited cardiac reactivity with the 24-h excretion of epinephrine.

Relationship of cardiovascular reactivity and anger expression to serum lipid concentrations in healthy young men.

The relationship between behaviorally evoked cardiovascular reactivity, preferred mode of anger expression, and serum lipid concentrations was examined in 63 healthy, young adult males. Subjects derived from three studies, each evaluating cardiovascular response to laboratory stressors. All participants completed the Spielberger Anger Expression Scale and provided fasting blood samples for lipid determinations. A significant negative correlation, calculated by meta-analytic procedures, was noted between a baseline-free measure of heart rate reactivity and high density lipoprotein-cholesterol (HDL-C) concentrations (r = -0.26, p = 0.05). However, the previously reported relationship between cardiovascular reactivity and elevated total serum cholesterol (TSC) was not found. Additionally, men scoring high on a self-report measure of the tendency to express anger outwardly had significantly higher HDL-C concentrations than men scoring low on this measure (r = 0.30, p = 0.02); when subjects were stratified by level of cardiovascular reactivity, this relationship was apparent only among those showing the greatest magnitude of heart rate and blood pressure responses to acute mental stress.

Active coping and cardiovascular reactivity: a multiplicity of influences.

OBJECTIVE: Active coping enhances cardiovascular response presumably by beta-adrenergically mediated myocardial activation. This study examined impedance-derived hemodynamic parameters underlying blood pressure response to two laboratory tasks requiring active coping, performed either with or without an appetitive (i.e., monetary) incentive. METHOD: Forty-eight healthy, young men completed the Stroop Color-Word Test and Mirror Tracing. Half received no incentive, whereas half were provided with a monetary incentive as an active coping manipulation. Task-related changes in blood pressure, heart rate, systolic time intervals, and hemodynamic parameters were monitored. Psychological responses to the tasks were also obtained. RESULTS: On average, incentive virtually doubled blood pressure response to both Stroop and Mirror Tracing. The change in blood pressure was explained predominantly by a concomitant increase in total peripheral resistance. Heart rate response was also enhanced substantially with incentive. Individuals in the incentive condition reported greater interest in the task, but less perceived control, than persons in the no-incentive condition. CONCLUSIONS: The incentive-related increase in total peripheral resistance, combined with an absence of enhanced stroke volume, cardiac output, or preejection period response, indicates that active coping may, under certain conditions, elevate blood pressure via increased systemic resistance, presumably reflecting alpha-adrenergic activation. Furthermore, the enhanced heart rate associated with incentive may reflect a withdrawal of parasympathetic influence.

Cardiovascular reactivity and the course of immune response to an acute psychological stressor.

This study evaluated the temporal nature of cellular immune responses, as well as the effects of cardiovascular reactivity on immune responses after exposure to an acute psychological stressor. Lymphocyte subsets and lymphocyte proliferative response to phytohemagglutinin were assessed at baseline and at 5 and 21 minutes after stressor onset in the experimental group and at the same time points in a nonstressor control group. By 5 minutes after stressor onset, the number of CD8 suppressor/cytotoxic T and CD16/56 natural killer cells increased and proliferative response to phytohemagglutinin decreased. These changes were maintained at 21 minutes. Those subjects showing the greatest cardiovascular reactivity had the largest immune alterations. These data did not indicate that gender significantly moderated immune responses. Results are consistent with the hypothesis that sympathetic activation mediates stressor-induced quantitative alterations of peripheral blood lymphocyte subpopulations and nonspecific mitogen stimulated proliferation.

Lymphocyte subset and cellular immune responses to a brief experimental stressor.

To evaluate effects of acute mental stress on aspects of cellular immunity, lymphocyte populations and phytohemagglutinin (PHA)-stimulated T-cell mitogenesis were measured in 33 healthy young men, both before and immediately following subjects' performance of a frustrating, 21-minute laboratory task (Stroop test). Relative to baseline evaluations, post-task measurements showed a significant reduction in mitogenesis and alterations in various circulating lymphocyte populations; the latter included a diminished T-helper/T-suppressor cell ratio and an elevation in the number of natural killer cells. Eleven subjects assigned to a control (unstressed) condition exhibited no changes in lymphocyte populations, but did show an increase in T-cell proliferation, compared with pretask measurements.

Adrenergic blockade ameliorates cellular immune responses to mental stress in humans.

This study evaluated the sympathoadrenal modulation of behaviorally evoked immune responses by administration of a nonselective adrenoceptor antagonist (labetalol) to subjects exposed to mental stress. In a 2 x 2 factorial design, subjects were assigned to a labetalol or saline condition and, within each condition, were exposed either to acute laboratory stress or no stress (control). Lymphocyte subsets, natural killer (NK) cell cytotoxicity, and T cell proliferation to phytohemagglutinin and concanavalin A were assessed pre-experimentally, at baseline after infusion and after 18 minutes of mental stress (or rest). By comparison with the other three conditions, the saline-stress group showed a greater peripheral NK cell number and cytotoxicity, lower mitogenic response to phytohemagglutinin and concanavalin A, and diminished ratio of CD4:CD8 cells after the stressor. As predicted, immune responses did not differ among the remaining groups (labetalol-stress, saline-rest, labetalol-rest). Group differences in NK cell cytotoxicity were not significant after controlling for differences in NK cell numbers. These findings demonstrate that the occurrence of certain immunologic responses to acute psychological stress are dependent on concomitant activation of the sympathetic nervous system.