Abstract
1352 Following an acute bout of exercise there is a persistent and unexplained rise in systemic vascular conductance that is not completely offset by an increase in cardiac output. These hemodynamic changes manifest in a postexercise hypotension, often sustained for ∼2 hours in healthy normotensive individuals. PURPOSE: Determine the potential role of the cutaneous circulation in postexercise hypotension. METHODS: Studies were performed in a temperature controlled laboratory maintained between 22 and 24°C. Arterial blood pressure was measured via an automated sphygmomanometer (Dinamap), and core body temperature was measured with an ingestible temperature pill (HQI). Red blood cell flux (laser Doppler flowmetry; Moore DRT4) was monitored at four skin sites (chest, forearm, thigh, and shin) and cutaneous vascular conductance (CVC) was calculated (red blood cell flux/mean arterial pressure) and scaled as % maximal CVC (local heating to 43°C). Five subjects (3 men and 2 women; age 23 ± 2; VO2 peak 44.3 ± 1.9) volunteered for this study. Following 30 minutes of supine rest, subjects exercised on a bicycle ergometer for one hour at 60% of their peak VO2. Subjects were then positioned supine for 90 minutes. RESULTS: Exercise elicited Friday, June 4, 2004 day, day postexercise hypotension reaching a nadir at 50 minutes postexercise (73 ± 2 vs. 79 ± 2 mmHg pre-exercise; p<0.05). Core body temperature increased with exercise (38.1 ± 0.1 vs. 36.9 ± 0.2°C pre-exercise; p<0.05), returning to pre-exercise values at 50 minutes postexercise (37.0 ± 0.1°C vs. pre-exercise; p = 0.6). CVC at all four skin sites was elevated immediately after the exercise bout (14.8 ± 2.1 vs. 8.2 ± 1.5%CVCmax pre-exercise; p<0.05). Importantly, CVC at all four skin sites returned to pre-exercise values 60 minutes postexercise (7.7 ± 1.5%CVCmax vs. pre-exercise; p = 0.7), however mean arterial pressure remained significantly reduced (74 ± 2 mmHg vs. pre-exercise; p<0.05). CONCLUSION: Although transient changes in CVC occur postexercise, they do not appear to play an obligatory role in mediating postexercise hypotension under thermoneutral conditions. Supported by AHA grant: 30403Z
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