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Effect of antioxidants on histamine receptor activation and sustained postexercise vasodilatation in humans
Author(s) -
Romero Steven A.,
Ely Matthew R.,
Sieck Dylan C.,
Luttrell Meredith J.,
Buck Tahisha M.,
Kono Jordan M.,
Branscum Adam J.,
Halliwill John R.
Publication year - 2015
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep085030
Subject(s) - vasodilation , medicine , histamine , endocrinology , chemistry , histamine receptor , oxidative stress , histaminergic , ascorbic acid , receptor , antagonist , food science
New FindingsWhat is the central question of this study? Is exercise‐induced oxidative stress the upstream exercise‐related signalling mechanism that leads to sustained postexercise vasodilatation via activation of H 1 and H 2 histamine receptors? What is the main finding and its importance? Systemic administration of the antioxidant ascorbate inhibits sustained postexercise vasodilatation to the same extent as seen previously with H 1 and H 2 histamine receptor blockade following small muscle‐mass exercise. However, ascorbate has a unique ability to catalyse the degradation of histamine. We also found that systemic infusion of the antioxidant N ‐acetylcysteine had no effect on sustained postexercise vasodilatation, suggesting that exercise‐induced oxidative stress does not contribute to sustained postexercise vasodilatation.An acute bout of aerobic exercise elicits a sustained postexercise vasodilatation that is mediated by histamine H 1 and H 2 receptor activation. However, the upstream signalling pathway that leads to postexercise histamine receptor activation is unknown. We tested the hypothesis that the potent antioxidant ascorbate would inhibit this histaminergic vasodilatation following exercise. Subjects performed 1 h of unilateral dynamic knee extension at 60% of peak power in three conditions: (i) control; (ii) i.v . ascorbate infusion; and (iii) ascorbate infusion plus oral H 1 /H 2 histamine receptor blockade. Femoral artery blood flow was measured (using Doppler ultrasound) before exercise and for 2 h postexercise. Femoral vascular conductance was calculated as flow/pressure. Postexercise vascular conductance was greater for control conditions (3.4 ± 0.1 ml min −1 mmHg −1 ) compared with ascorbate (2.7 ± 0.1 ml min −1 mmHg −1 ; P < 0.05) and ascorbate plus H 1 /H 2 blockade (2.8 ± 0.1 ml min −1 mmHg −1 ; P < 0.05), which did not differ from one another ( P = 0.9). Given that ascorbate may catalyse the degradation of histamine in vivo , we conducted a follow‐up study, in which subjects performed exercise in two conditions: (i) control; and (ii) i.v . N ‐acetylcysteine infusion. Postexercise vascular conductance was similar for control (4.0 ± 0.1 ml min −1 mmHg −1 ) and N ‐acetylcysteine conditions (4.0 ± 0.1 ml min −1 mmHg −1 ; P = 0.8). Thus, the results in the initial study were due to the degradation of histamine in skeletal muscle by ascorbate, because the histaminergic vasodilatation was unaffected by N ‐acetylcysteine. Overall, exercise‐induced oxidative stress does not appear to contribute to sustained postexercise vasodilatation.