This study was designed to examine the hypothesis that certain behavioral demands may tend to trigger sympathetic mechanisms which result in metabolically excessive cardiac output elevations. Oxygen consumption and cardiac output adjustments during a contrived reaction‐time shock‐avoidance task were compared to a cold pressor test in healthy young male adults. The linear cardiac output/oxygen consumption relationship generated by performance on a graded exercise task was used to assess the metabolic appropriateness of cardiac output adjustments to the reaction‐time task and cold pressor. The reaction‐time task was generally found to evoke metabolically excessive increases in cardiac output, while cardiac output adjustments to cold pressor were more consistent with changes in metabolic demands. However, the tasks were associated with similar heart rate responses, with a significant attenuation in stroke volume during cold pressor accounting for the differential alterations in cardiac output. This finding suggests a limited reliability for heart rate as an index of cardiac performance. The effects of propranolol, which was employed to evaluate the role of sympathetic influences, indicated that beta‐adrenergic mechanisms were responsible for mediating the cardiac output response to the reaction‐time task, but only partially contributed to the cold pressor response. Post‐hoc analyses of individual differences in cardiovascular reactivity to the reaction‐time task suggest that, for hyperreactive individuals, the coping responses evoked by this task may lead to tissue overperfusion with oxygen, thereby providing a stimulus for autoregulatory vascular reflexes which may be associated with the etiology of hypertensive disease.
In three experiments involving young adult males, beta‐adrenergic influences on heart rate and carotid dP/dt were evaluated as a function of the degree of individual control over stressful events. Beta‐adrenergic effects were more pronounced under conditions in which the subjects were either led to believe they had control or where some control was actually provided, i.e., a shock avoidance task. Beta‐adrenergic influences were either minimal or rapidly dissipated under conditions where no control was possible, i.e., the cold pressor, a pornographic film, inescapable shocks, or conditions which provided ready mastery of the task. Where beta‐adrenergic effects were maximal, systolic blood pressure was more appreciably elevated while diastolic blood pressure was less elevated than when beta‐adrenergic effects were minimal. A pharmacological blocking agent (propranolol) was used in one experiment to specify the extent the various cardiovascular changes were influenced by beta‐adrenergic activity. The results are discussed with respect to issues concerning stimulus parameters, blood pressure control mechanisms, individual differences in cardiovascular reactivity, and some methodological problems of the current study.
We studied the relationship between sympathetic neuronal function and left ventricular performance during stress in humans by analysis of endogenous catecholamine levels and systolic time intervals. The results showed that performance on a stressful cognitive task was accompanied by changes in plasma catecholamines, heart rate (HR), blood pressure (BP), and systolic time intervals. The cardiovascular responses were significantly correlated with plasma levels of epinephrine (E) and norepinephrine (NE). The relationship between plasma catecholamines and systolic time intervals is thought to reflect sympatho‐adrenomedullary impact on left ventricular performance during stress.
The main purpose of the present study was twofold: (a) to assess the relationship between defensive hostility (high hostility/high defensiveness) and additional heart rate reactivity during active coping and (b) to determine if the construct of anger-out might lend additional sensitivity to the predictive power of the defensive hostility model. Forty individuals were randomly assigned to complete a mental arithmetic task with or without the threat of shock. Participants also completed the Cook-Medley Hostility Inventory (Ho), the Marlowe-Crowne Social Desirability Scale (MC), and the Spielberger Anger Expression Scale. Defensive hostile subjects (high Ho/high MC) were significantly more reactive than any other subgroup. In addition, the combination of low Ho/high anger-out scores yielded a subgroup significantly less reactive than any other subgroup. These findings clarify the complex relationship of hostility and cardiovascular reactivity.
The purpose of this study was to compare the cardiopulmonary and hemodynamic adjustments to a physical (bicycle exercise) and behavioral (aversive reaction time) stressor. A related aim was to assess the role of beta‐adrenergic mechanisms in mediating these physiological responses. Thirty‐four subjects were exposed to both stressors while oxygen consumption, carbon dioxide production, pulmonary ventilation, end‐tidal oxygen and carbon dioxide, as well as heart rate were calculated breath‐by‐breath. Fourteen of these subjects were pretreated with 4 mg (iv) of propranolol hydrochloride. The remaining 20 subjects (intact) were subdivided post‐hoc into the 10 most and 10 least reactive on the basis of their heart rate response to the reaction time task. The results indicate that for the intact group both exercise and the reaction time task produced significant increases in heart rate although the magnitude of the heart rate change was reliably greater during exercise. Beta‐adrenergic blockade partially diminished the tachycardia to exercise but entirely abolished the tachycardia to behavioral stress. Interestingly, the most and least reactive subjects did not exhibit differential heart rate acceleration during exercise despite a reliable difference during the reaction time task. Oxygen consumption significantly increased to predictable levels during exercise but failed to change during the reaction time task for both the most and least reactive groups. These results suggest that the tachycardia elicited by the reaction time task in reactive subjects was not associated with an appropriate increase in oxygen consumption, relative to exercise, and may therefore be indicative of systemic overperfusion.
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