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Regional hemodynamics during postexercise hypotension. I. Splanchnic and renal circulations

Department of Human Physiology, University of Oregon, Eugene, Oregon 97403-1240

Submitted 3 May 2004 ; accepted in final form 7 August 2004

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 these hemodynamic changes are limited to skeletal muscle vascular beds. The aim of this study was to determine whether 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 whether the cutaneous vascular bed is involved in postexercise hypotension (Wilkins BW, Minson CT, and Halliwill JR. J Appl Physiol 97: 2071–2076, 2004). 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 peak oxygen uptake. Vascular conductances of leg, splanchnic, and renal vascular beds were calculated. One hour postexercise, mean arterial pressure was reduced (79.1 ± 1.7 vs. 83.4 ± 1.8 mmHg; P < 0.05), systemic vascular conductance was increased by 10%, leg vascular conductance was increased by 65%, whereas 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 with 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.

exercise; sympathetic nervous system; vascular resistance; baroreflex; vascular conductance

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