POSTEXERCISE HYPOTENSION - KEY FEATURES, MECHANISMS, AND CLINICAL-SIGNIFICANCE

Citation
Mj. Kenney et Dr. Seals, POSTEXERCISE HYPOTENSION - KEY FEATURES, MECHANISMS, AND CLINICAL-SIGNIFICANCE, Hypertension, 22(5), 1993, pp. 653-664
Citations number
99
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0194911X
Volume
22
Issue
5
Year of publication
1993
Pages
653 - 664
Database
ISI
SICI code
0194-911X(1993)22:5<653:PH-KFM>2.0.ZU;2-B
Abstract
Recent investigations have demonstrated that there is a sustained redu ction in arterial blood pressure after a single bout of exercise, ie, postexercise hypotension (PEH). The purpose of this discussion is to i ntegrate the available information on this topic and to review studies using sustained stimulation of somatic afferents in experimental rats as a model to study the role of somatic afferents in PEH. PEH occurs in response to several types of large-muscle dynamic exercise (ie, wal king, running, leg cycling, and swimming) at submaximal intensities gr eater than 40% of peak aerobic capacity and exercise durations general ly between 20 and 60 minutes. PEH is observed in both normotensive and hypertensive humans and in spontaneously hypertensive rats but is gen erally greater in magnitude in hypertensive subjects. The maximal exer cise-induced reductions in systolic and diastolic arterial blood press ures have been on average 18 to 20 and 7 to 9 mm Hg, respectively, in hypertensive humans and 8 to 10 and 3 to 5 mm Hg, respectively, in nor motensive humans. PEH has been reported to persist for 2 to 4 hours un der laboratory conditions. Whether PEH is sustained for a prolonged pe riod of time under free-living conditions remains controversial, altho ugh the results of one study indicate that PEH can persist for up to 1 3 hours. Possible mechanisms involved in mediating postexercise and po ststimulation reductions in arterial blood pressure include decreased stroke volume and cardiac output; reductions in limb vascular resistan ce, total peripheral resistance, and muscle sympathetic nerve discharg e; group III somatic afferent activation; altered baroreceptor reflex circulatory control; reduced vascular responsiveness to alpha-adrenerg ic receptor-mediated stimulation; and activation of endogenous opioid and serotonergic systems. It appears that the magnitude of PEH in hype rtensive subjects is clinically significant; however, more investigati on is required to determine if the duration is sufficient under real-l ife conditions to contribute to the reduction in blood pressure observ ed with chronic exercise conditioning.