Increased brachial artery retrograde shear rate at exercise onset is abolished during prolonged cycling: role of thermoregulatory vasodilation.

Acute leg exercise increases brachial artery retrograde shear rate (SR), while chronic exercise improves vasomotor function. These combined observations are perplexing given the proatherogenic impacts of retrograde shear stress on the vascular endothelium and may be the result of brief protocols used to study acute exercise responses. Therefore, we hypothesized that brachial artery retrograde SR increases initially but subsequently decreases in magnitude during prolonged leg cycling. Additionally, we tested the role of cutaneous vasodilation in the elimination of increased retrograde SR during prolonged exercise. Brachial artery diameter and velocity profiles and forearm skin blood flow and temperature were measured at rest and during 50 min of steady-state, semirecumbent leg cycling (120 W) in 14 males. Exercise decreased forearm vascular conductance (FVC) and increased retrograde SR at 5 min (both P < 0.05), but subsequently forearm and cutaneous vascular conductance (CVC) rose while retrograde SR returned toward baseline values. The elimination of increased retrograde SR was related to the increase in FVC (r(2) = 0.58; P < 0.05) and CVC (r(2) = 0.32; P < 0.05). Moreover, when the forearm was cooled via a water-perfused suit between minutes 30 and 40 to blunt cutaneous vasodilation attending exercise, FVC was reduced and the magnitude of retrograde SR was increased from -49.7 ± 13.6 to -78.4 ± 16.5 s(-1) (P < 0.05). Importantly, these responses resolved with removal of cooling during the final 10 min of exercise (retrograde SR: -46.9 ± 12.5 s(-1)). We conclude that increased brachial artery retrograde SR at the onset of leg cycling subsequently returns toward baseline values due in part to thermoregulatory cutaneous vasodilation during prolonged exercise.