Local infusion of ascorbate augments NO-dependent cutaneous vasodilatation during intense exercise in the heat

Abstract

Nitric oxide (NO)-dependent cutaneous vasodilatation is reportedly diminished during exercise performed at a high (700W) relative to moderate (400W) rate of metabolic heat production. The present study evaluated whether this impairment results from increased oxidative stress associated with an accumuluation of reactive oxygen species (ROS) during high intensity exercise. On two separate days, 11 young (mean +/- SD, 24 +/- 4years) males cycled in the heat (35 degrees C) at a moderate (500W) or high (700W) rate of metabolic heat production. Each session included two 30min exercise bouts followed by 20 and 40min of recovery, respectively. Cutaneous vascular conductance (CVC) was monitored at four forearm skin sites continuously perfused via intradermal microdialysis with: (1) lactated Ringer solution (Control); (2) 10mm ascorbate (Ascorbate); (3) 10mm l-NAME; or (4) 10mm ascorbate+10mm l-NAME (Ascorbate+l-NAME). At the end of each 500W exercise bout, CVC was attenuated with l-NAME (approximate to 35% CVCmax) and Ascorbate+l-NAME (approximate to 43% CVCmax) compared to Control (approximate to 60% CVCmax; allP<0.04); however, Ascorbate did not modulate CVC during exercise (approximate to 60% CVCmax; bothP>0.87). Conversely, CVC was elevated with Ascorbate (approximate to 72% CVCmax; both P<0.03) but remained similar to Control (approximate to 59% CVCmax) with l-NAME (approximate to 50% CVCmax) and Ascorbate+l-NAME (approximate to 47% CVCmax; all P>0.05) at the end of both 700W exercise bouts. We conclude that oxidative stress associated with an accumulation of ascorbate-sensitive ROS impairs NO-dependent cutaneous vasodilatation during intense exercise.