The measurement of brachial artery vasodilation in response to a hyperaemic stimulus has been used extensively to assess changes in endothelial function. However, whether or not similar changes occur in response to an active hyperaemic stimulus is unknown. The purpose of the present study was to compare brachial artery vasodilation in response to an active compared with a reactive hyperaemic stimulus following a known perturbation of endothelial function. Eight apparently healthy adults were assigned to four treatment conditions in a counter-balanced design: (i) low-fat meal with active hyperaemic stimulus (LFM-A), (ii) high-fat meal with active hyperaemic stimulus (HFM-A), (iii) low-fat meal with reactive hyperaemic stimulus (LFM-R), and (iv) high-fat meal with reactive hyperaemic stimulus (HFM-R). Meals were ingested at 08:00 hours on each treatment day. Brachial artery vasodilation was assessed via ultrasound 4 h after ingestion of each meal. The active hyperaemic stimulus was induced by 5 min of rhythmic handgrip exercise, whereas reactive hyperaemia was induced by 5 min of forearm occlusion. Brachial artery vasodilation was expressed as the percentage change in diameter from baseline to post-active/reactive hyperaemia. Using a 2×2 repeated measures ANOVA, a significant stimulus×meal interaction (P=0.025) was found. Simple main effects revealed no difference (P=0.541) in brachial artery vasodilation between LFM-A (5.75±1.64%) and HFM-A (6.39±1.45%); however, a significant decrease (P=0.014) in brachial artery vasodilation was found in the HFM-R (4.29±1.64%) compared with the LFM-R (7.18±1.13%) treatment. In conclusion, the measurement of brachial artery vasodilation in response to active hyperaemia did not detect a change in endothelial function following a single perturbation meal, whereas reactive hyperaemia did.
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March 2006
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Research Article|
February 10 2006
A comparison between active- and reactive-hyperaemia-induced brachial artery vasodilation
Jaume Padilla;
*Clinical Exercise Physiology Laboratory, Department of Kinesiology, Indiana University, Bloomington, IN 47405, U.S.A.
Correspondence: Mr Jaume Padilla (email [email protected]).
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Ryan A. Harris;
Ryan A. Harris
*Clinical Exercise Physiology Laboratory, Department of Kinesiology, Indiana University, Bloomington, IN 47405, U.S.A.
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Alyce D. Fly;
Alyce D. Fly
†Nutrition Science Laboratory, Department of Applied Health Science, Indiana University, Bloomington, IN 47405, U.S.A.
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Lawrence D. Rink;
Lawrence D. Rink
‡Internal Medicine Associates, Landmark Medical Center, Bloomington, IN 47402, U.S.A.
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Janet P. Wallace
Janet P. Wallace
*Clinical Exercise Physiology Laboratory, Department of Kinesiology, Indiana University, Bloomington, IN 47405, U.S.A.
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Publisher: Portland Press Ltd
Received:
October 31 2005
Revision Received:
December 12 2005
Accepted:
December 15 2005
Accepted Manuscript online:
December 15 2005
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society
2006
Clin Sci (Lond) (2006) 110 (3): 387–392.
Article history
Received:
October 31 2005
Revision Received:
December 12 2005
Accepted:
December 15 2005
Accepted Manuscript online:
December 15 2005
Citation
Jaume Padilla, Ryan A. Harris, Alyce D. Fly, Lawrence D. Rink, Janet P. Wallace; A comparison between active- and reactive-hyperaemia-induced brachial artery vasodilation. Clin Sci (Lond) 1 March 2006; 110 (3): 387–392. doi: https://doi.org/10.1042/CS20050328
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