Regional hemodynamics during postexercise hypotension. II. Cutaneous circulation

Abstract

After 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 contributions of the splanchnic and renal circulations are examined in a companion paper (Pricher MP, Holowatz LA, Williams JT, Lockwood JM, and Halliwill JR. J Appl Physiol 97: 2065–2070, 2004). 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 eight 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 percent maximal CVC (local heating to 43°C). Ten subjects [6 men and 4 women; age 23 ± 1 yr; peak O2 uptake (V̇o2 peak) 45.8 ± 2.0 ml·kg−1·min−1] volunteered for this study. After supine rest (30 min), subjects exercised on a bicycle ergometer for 1 h at 60% of their V̇o2 peak and were then positioned supine for 90 min. Exercise elicited a postexercise hypotension reaching a nadir at 46.0 ± 4.5 min 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 min postexercise (36.9 ± 0.1°C vs. preexercise; P < 0.05). CVC at all four skin sites was elevated by the exercise bout ( P < 0.05), returning to preexercise values within 50 min 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.