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

Nitric oxide (NO)-dependent cutaneous vasodilatation is reportedly diminished during exercise performed at a high (700 W) relative to moderate (400 W) 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 ± 4 years) males cycled in the heat (35°C) at a moderate (500 W) or high (700 W) rate of metabolic heat production. Each session included two 30 min exercise bouts followed by 20 and 40 min 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) 10 mm ascorbate (Ascorbate); (3) 10 mm l-NAME; or (4) 10 mm ascorbate + 10 mm l-NAME (Ascorbate + l-NAME). At the end of each 500 W exercise bout, CVC was attenuated with l-NAME (∼35% CVC_max) and Ascorbate + l-NAME (∼43% CVC_max) compared to Control (∼60% CVC_max; all P < 0.04); however, Ascorbate did not modulate CVC during exercise (∼60% CVC_max; both P > 0.87). Conversely, CVC was elevated with Ascorbate (∼72% CVC_max; both P < 0.03) but remained similar to Control (∼59% CVC_max) with l-NAME (∼50% CVC_max) and Ascorbate + l-NAME (∼47% CVC_max; all P > 0.05) at the end of both 700 W exercise bouts. We conclude that oxidative stress associated with an accumulation of ascorbate-sensitive ROS impairs NO-dependent cutaneous vasodilatation during intense exercise.