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1 Department of Human Physiology, University of Oregon, Eugene, OR, USA
* To whom correspondence should be addressed. E-mail: halliwil{at}uoregon.edu.
Moderate exercise elicits a relative postexercise hypotension that is caused by an increase in systemic vascular conductance. Previous studies have shown that skeletal muscle vascular conductance is increased postexercise. It is unclear whether or not these hemodynamic changes are limited to skeletal muscle vascular beds. The aim of this study was to determine if the splanchnic and/or renal vascular beds also contribute to the rise in systemic vascular conductance during postexercise hypotension. A companion study aims to determine if the cutaneous vascular bed is involved in postexercise hypotension (Wilkins et al). Heart rate, arterial pressure, cardiac output, leg blood flow, splanchnic blood flow and renal blood flow were measured in 13 men and 3 women before and through 120 min after a 60 min bout of exercise at 60% of VO2 peak. Vascular conductances of leg, splanchnic, and renal vascular beds were calculated. An hour postexercise, mean arterial pressure was reduced (79.1 ± 1.7 mmHg vs. 83.4 ± 1.8 mmHg; P < 0.05), systemic vascular conductance was increased by 10%, leg vascular conductance was increased 65%, while splanchnic (16.0 ± 1.8 vs. 18.5 ± 2.4 ml.min-1 mmHg-1, P < 0.13) and renal (20.4 ± 3.3 vs. 17.6 ± 2.6 ml.min-1 mmHg-1, P < 0.14) vascular conductances were unchanged compared to preexercise. This suggests there is neither vasoconstriction nor vasodilation in the splanchnic and renal vasculature during postexercise hypotension. Thus, the splanchnic and renal vascular beds neither directly contribute to nor attenuate postexercise hypotension.
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