title: Adenosine receptor inhibition attenuates the suppression of postexercise cutaneous blood flow.
abstract: The time-dependent contributions of active vasodilation (e.g. nitric oxide) and noradrenergic vasoconstriction to the postexercise suppression of cutaneous perfusion despite persistent hyperthermia remain unknown. Moreover, adenosine receptors have been shown to mediate the decrease in cutaneous perfusion following passive heating. We examined the time-dependent modulation of nitric oxide synthase, noradrenergic vasoconstriction and adenosine receptors on postexercise cutaneous perfusion. Eight males performed 15 min of high-intensity (85% VO2 max) cycling followed by 60 min of recovery in temperate ambient conditions (25°C). Four microdialysis probes were inserted into the forearm skin and continuously infused with: (1) lactated Ringer solution (Control); (2) 10 mm N(G)-nitro-l-arginine methyl ester (l-NAME; nitric oxide synthase inhibitor); (3) 10 mm bretylium tosylate (BT; inhibitor of noradrenergic vasoconstriction); or (4) 4 mm theophylline (THEO; adenosine receptor inhibitor). Cutaneous vascular conductance (CVC) was expressed as a percentage of maximum and was calculated as perfusion units (laser Doppler) divided by mean arterial pressure. End-exercise CVC was similar in Control, THEO and BT (P > 0.1), but CVC with l-NAME (39 ± 4%) was lower than Control (59 ± 4%, P < 0.01). At 20 min of recovery, Control CVC (22 ± 3%) returned to baseline levels (19 ± 2%, P = 0.11). Relative to Control, CVC was reduced by l-NAME for the first 10 min of recovery whereas CVC was increased with BT for the first 30 min of recovery (P < 0.03). In contrast, CVC with THEO was elevated throughout the 60 min recovery period (P ≤ 0.01) compared to Control. We show that adenosine receptors appear to have a major role in postexercise cutaneous perfusion whereas nitric oxide synthase and noradrenergic vasoconstriction are involved only earlier during recovery.
authors.affiliation: Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Canada.
authors.forename: Ryan
authors.initials: R
authors.lastname: McGinn
authors.affiliation: Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Canada.
authors.forename: Naoto
authors.initials: N
authors.lastname: Fujii
authors.affiliation: Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Canada.
authors.forename: Brendan
authors.initials: B
authors.lastname: Swift
authors.affiliation: Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Canada.
authors.forename: Dallon T
authors.initials: DT
authors.lastname: Lamarche
authors.affiliation: Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Canada gkenny@uottawa.ca.
authors.forename: Glen P
authors.initials: GP
authors.lastname: Kenny
mesh_terms: D000328:Adult; D001831:Body Temperature; D015444:Exercise / Q000502:physiology*; D006801:Humans; D008297:Male; D019001:Nitric Oxide Synthase / Q000502:physiology; D058915:Purinergic P1 Receptor Antagonists / Q000494:pharmacology; D018047:Receptors, Purinergic P1 / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology*; D012867:Skin / Q000098:blood supply*; D013806:Theophylline / Q000494:pharmacology; D014661:Vasoconstriction / Q000502:physiology; D055815:Young Adult
chemical_list: D058915:Purinergic P1 Receptor Antagonists; D018047:Receptors, Purinergic P1; D013806:Theophylline; D019001:Nitric Oxide Synthase