Alan W. Langer

Some Working Hypotheses on the Significance of Behaviorally Evoked Cardiovascular Reactivity to Pathophysiology

A guiding hypothesis inherent in research on the role of behavioral influences in the etiology of cardiovascular pathophysiology is that repeated occurrences of environmentally induced myocardial, vascular, and blood pressure (BP) reactivity is the means by which life’s events are translated into the disease process (Folkow 1982). While this assumption appears to have a certain face validity, there is evidence to indicate that reactivity per se does not have invariable pathophysiological consequences, since there are circumstances where reactivity serves a necessary adaptive function. For example, pressor responses facilitate tissue perfusion when one exercises (Obrist 1981) or changes state from sleep to awake (Floras et al. 1978). On other occasions, reactivity may reflect nothing more than a momentary disruption in the efficiency with which the individual adjusts cardiovascularly to the ever-changing events in the interaction of the organism and its environment (Obrist et al. 1970; Obrist 1984). The most definitive evidence implicating this interaction, and hence reactivity, in the development of cardiovascular disease, is from animal models (Lawler et al. 1981; Anderson et al. 1983; Kaplan et al. 1983; Manuck et al. 1983). But caution must be exerted in generalizing from such data, since we are not certain how much one can liken these models to the human condition. This paper is intended first to briefly overview some of the evidence which places some reservations on this hypothesis, and secondly to propose some specific hypotheses that attempt to provide a perspective of how we might better decipher when reactivity has the pathophysiological consequences we seek to ascertain. This discussion is most relevant to the hypertensive process but is also applicable to coronary heart disease, to the extent that hypertension is instrumental in the development of atherosclerosis.

The Integration and Differentiation of Cardiovascular and Metabolic Responses to Stress

The problem of clarifying how cardiac and metabolic (somatic) processes interact over a wide range of behavioral conditions which have been variously characterized as stressful has been of long standing interest to both physiologists and psychophysiologists alike. Not only are the relationships among these events rather complex from a physiological point of view, but also from a behavioral standpoint. For example, the term stress refers to a rather heterogeneous set of events such as heat stress, cold stress, exhaustion, infection, trauma, anxiety, nervous tension, strain, and even physical exertion and exercise. Furthermore, even when the analysis is limited to only one type of stress, such as psychological stress, the welter of results that emerge are somewhat difficult to summarize. This difficulty can, in part, be ascribed to the facts that many of the studies reported frequently operationalize stress using different experimental paradigms and involve experiments conducted on various species. Moreover, even where the focus is limited to outcomes with human volunteers, the populations from which samples have been selected often vary along many important dimensions. Notwithstanding these difficulties, the scope of the present chapter will be delimited to one which focuses on the cardiac-metabolic (somatic) interactions which take place during physical (exercise) and psychological stress.

Biofeedback-Assisted Heart Rate Deceleration: Specificity of Cardiovascular and Metabolic Effects in Normal and High Risk Subjects

An important theoretical issue in cardiovascular psychophysiology is whether biofeedback-assisted alterations in heart rate (HR) reflect only changes in cardiac function, are mediated indirectly by changes in somatic or respiratory responses, or reflect a common central nervous system integration of cardiac-somatic activity. In this connection, the first position was advanced by Miller and collaborators (Miller and DiCara, 1967; Miller and Banuazizi, 1968; DiCara and Miller, 1968), who argued that operant control of HR could be obtained in the absence of somatic mediation. This series of studies, employing the curarized preparation, putatively demonstrated that appreciable bidirectional HR changes could be conditioned independent of somatomotor activity. On the other hand, Obrist (1981) and others have been concerned with the common central coupling of cardiac and somatic processes during both classical (Obrist, 1968) and operant HR conditioning procedures. In an early classical aversive conditioning study with humans, a strong relationship between the magnitude and direction of phasic HR and somatomotor activity was noted (Obrist, 1968). Similarly, concomitant changes in HR and somatic activity were found during an operant conditioning paradigm that employed visual binary HR feedback for both HR acceleration and deceleration and a shock avoidance contingency (Obrist, Galosy, Lawler, Gaebelein, Howard and Shanks, 1975).