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Contributions of nitric oxide and prostaglandins to exercise hyperemia in young obese adults
Author(s) -
Johansson Rebecca Elin,
Harrell John W,
Limberg Jacqueline K,
Crain Meghan K,
Rousseau Cameron L,
Yanke Peter A,
Sebranek Joshua J,
Walker Benjamin J,
Eldridge Marlowe W,
Schrage William G
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1136.5
Subject(s) - forearm , brachial artery , medicine , reactive hyperemia , vasodilation , lean body mass , cardiology , endocrinology , blood pressure , surgery , body weight
Nitric oxide (NO) and prostaglandins (PGs) play important roles in exercise hyperemia in healthy humans, but the role of NO & PGs in young obese (OB) adults is currently unknown. We hypothesized the relative contribution of NO and PGs to exercise hyperemia would be lower in young OB adults when compared to lean adults. 11 healthy lean (27±2yrs, BMI=23±1) and 7 OB adults (23±2yrs, BMI=38±4) performed two 10‐minute trials of dynamic forearm exercise (20 contractions/minute) at 15% of maximal voluntary contraction. A brachial artery catheter was used for local infusion of the NO synthase inhibitor, L‐NMMA, alone or in combination with the cycloxygenase inhibitor, ketorolac. L‐NMMA or ketoroloac was infused during the last 5 minutes of each exercise trial to achieve single and double blockade respectively. Forearm blood flow (FBF) was measured using Doppler ultrasound, and forearm vascular conductance (FVC) was calculated (FBF÷BP=FVC). From steady state exercise, the relative change in FVC with L‐NMMA was similar between groups (Lean−34±10 vs. OB−35±15%). With the addition of ketorolac, the relative change in FVC was opposite between groups (Lean−7±8 vs. OB+30±17%, p=0.02). We conclude the contribution of NO to exercise hyperemia appears intact in young OB adults, although they may produce more vasoconstrictor PGs that alter blood flow regulation. Support: NIH R01 HL105820.