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1 Human Physiology, University of Oregon, Eugene, OR, USA
* To whom correspondence should be addressed. E-mail: halliwil{at}uoregon.edu.
Following an acute bout of exercise there is an unexplained elevation in systemic vascular conductance that is not completely offset by an increase in cardiac output, resulting in a postexercise hypotension. The contribution of the splanchnic and renal circulations were examined in a companion paper (Pricher et al.). The purpose of this study was to determine the contribution of the cutaneous circulation in postexercise hypotension under thermoneutral conditions (~23°C). Arterial blood pressure was measured via an automated sphygmomanometer, internal temperature was measured via an ingestible pill, and skin temperature was measured with 8 thermocouples. Red blood cell flux (laser Doppler flowmetry) was monitored at four skin sites (chest, forearm, thigh, and leg) and cutaneous vascular conductance (CVC) was calculated (red blood cell flux/mean arterial pressure) and scaled as % maximal CVC (local heating to 43°C). Ten subjects (6 men and 4 women; age 23 ± 1 yrs; VO2peak 45.8 ± 2.0 ml kg-1 min-1) volunteered for this study. Following supine rest (30 min), subjects exercised on a bicycle ergometer for 1 hour at 60% of their VO2peak and were then positioned supine for 90 minutes. Exercise elicited a postexercise hypotension reaching a nadir at 46.0 ± 4.5 minutes postexercise (77 ± 1 vs. 82 ± 2 mmHg preexercise; P < 0.05). Internal temperature increased (38.0 ± 0.1 vs. 36.7 ± 0.1°C preexercise; P < 0.05), remaining elevated at 90 minutes postexercise (36.9 ± 0.1°C vs. preexercise; P < 0.5). CVC at all four skin sites was elevated by the exercise bout (P < 0.05), returning to preexercise values within 50 minutes postexercise (P > 0.05). Therefore, although transient changes in CVC occur postexercise, they do not appear to play an obligatory role in mediating postexercise hypotension under thermoneutral conditions.
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