BROWNLEY, K. A., A. L. HINDERLITER, S. G. WEST, S. S. GIRDLER, A. SHERWOOD, and K. C. LIGHT. Sympathoadrenergic Mechanisms in Reduced Hemodynamic Stress Responses after Exercise. Med. Sci. Sports Exerc., Vol. 35, No. 6, pp. 978–986, 2003.
Purpose: This study examines the acute effects of moderate aerobic exercise on 1) hemodynamic and sympathetic activity during behavioral stress and 2) β-adrenergic receptor responsivity in a biracial sample of 24 sedentary adults.
Methods: Before and after exercise, blood pressure (BP), impedance-derived cardiovascular measures, and plasma norepinephrine (NE) and epinephrine (EPI) were assessed during mental arithmetic and active speech tasks, and β-adrenergic receptor responsivity was assessed using a standard isoproterenol challenge procedure.
Results: After exercise, BP, NE, and EPI responses to stress were reduced (0.0001 <P < 0.08), preejection period (PEP) was elongated (P < 0.0001), and β1- and β2-receptor responsivity (P < 0.02) was enhanced. Approximately 65% of the prepost exercise mean arterial pressure response difference could be accounted for by changes in sympathetic factors, with change in NE and PEP being the single best predictors.
Conclusions: Reduced BP responses to stress after acute exercise are strongly linked to a decrease in sympathetic drive, as evidenced by reduced NE responses and elongation of the PEP. Coincident with this overall dampening of the hemodynamic response to stress, increases in cardiac and vascular β-adrenergic receptor responsivity occur. These findings may have important implications for future translational studies that seek to articulate the mechanisms through which regular aerobic exercise reduces the risks of hypertensive and coronary heart disease.
It has been suggested that heightened sympathetic responses to behavioral stress may be a marker for increased cardiovascular disease risk due to other pathological processes, or perhaps even play a causal role in the etiology of hypertension (15,20). Although the precise mechanisms underlying these associations are not completely understood, it is thought that recurrent exposure to increased hemodynamic load may promote deleterious structural and/or functional adaptations in the myocardium or systemic vasculature that, in turn, depress cardiac output (CO) and elevate total peripheral resistance (TPR) in a manner predisposing to the development of established hypertension. Conversely, aerobic exercise training is strongly associated with reduced risk of hypertension and cardiovascular morbidity and mortality (13,19), and cross-sectional studies indicate a link between aerobic fitness and reduced sympathetic responses to stress (30). This collection of observations has led to the speculation that regular participation in an aerobic exercise program may lower cardiovascular risk by attenuating sympathetic responses to stress in a cumulative manner, thereby limiting exposure to the presumed pathophysiological sequelae of repeated hypersympathetic arousal. Although this proposition has yet to be confirmed through longitudinal investigation, a growing body of literature linking acute moderate-intensity exercise with reduced cardiovascular responses to stress is emerging.
Exercise may directly reduce autonomic and neuroendocrine responses to behavioral challenge. Several studies, including our own (3,32), have shown reduced blood pressure (BP) responsiveness to behavioral challenge after a single episode of moderate to high-intensity aerobic exercise (1,6,27). Postexercise inhibition of BP responsiveness to stress has been observed both in controlled laboratory as well as ambulatory settings—the latter findings, in particular, suggesting that acute exercise may modulate the physiological impact of everyday stress on resting BP. Despite the consistency of these findings, however, relatively less is understood about the physiological mechanisms underlying this phenomenon.
Peronnet et al. (26) reported a nearly 50% reduction in plasma epinephrine response to the Stroop test in young, healthy male subjects after 2 h of low-intensity cycling. This study, however, did not find a significant postexercise reduction in BP response to the Stroop. Therefore, it is unclear from this study to what extent, if at all, the observed postexercise alteration in adrenomedullary activity influenced cardiovascular responsiveness during stress exposure. Previously, our research group (32) and others (6) observed marked reductions in peripheral vasoconstriction during behavioral stress tasks administered after acute exercise. However, these studies did not assess peripheral or myocardial mechanisms responsible for these effects. Therefore, the present study was designed to systematically examine alterations in cardiovascular, neuroendocrine, and β-adrenergic receptor-mediated functioning at rest and in response to behavioral challenge after a single 20-min bout of moderate-intensity aerobic bicycle exercise.
The two primary objectives of the present study were to 1) replicate earlier findings of reduced cardiovascular stress responses in sedentary individuals after acute moderate-intensity exercise, and 2) examine whether such reductions may be due to diminished sympathoadrenergic activity.