EVALUATION OF BETA-ADRENERGIC INFLUENCES ON CARDIOVASCULAR AND METABOLIC ADJUSTMENTS TO PHYSICAL AND PSYCHOLOGICAL STRESS
EVALUATION OF BETA-ADRENERGIC INFLUENCES ON CARDIOVASCULAR AND METABOLIC ADJUSTMENTS TO PHYSICAL AND PSYCHOLOGICAL STRESS
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DOI：
10.1111/j.1469-8986.1986.tb00602.x
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发表时间：
1986-01-01
期刊：
影响因子：
3.7
通讯作者：
LANGER, AW
中科院分区：
文献类型：
--
作者：
SHERWOOD, A;ALLEN, MT;LANGER, AW
本研究旨在检验以下假设：某些行为需求可能会触发交感神经机制，从而导致代谢性心输出量过度升高。在健康年轻男性中，将人为的反应时间避免电击任务期间的耗氧量和心输出量调整与冷加压测试进行比较。通过分级运动任务的表现产生的线性心输出量/耗氧量关系用于评估心输出量调整对反应时间任务和冷加压剂的代谢适当性。通常发现反应时间任务会引起心输出量的代谢过度增加，而冷加压的心输出量调整更符合代谢需求的变化。然而，这些任务与相似的心率反应相关，冷加压期间每搏输出量显着减弱，导致心输出量的差异变化。这一发现表明心率作为心脏功能指标的可靠性有限。用于评估交感神经影响作用的普萘洛尔的作用表明，β-肾上腺素能机制负责介导对反应时间任务的心输出量反应，但仅部分促进冷加压反应。对反应时间任务心血管反应性个体差异的事后分析表明，对于反应过度的个体，该任务引起的应对反应可能导致组织过度灌注氧气，从而刺激血管自动调节反射，这可能与高血压病的病因有关。
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.