A comparison between active- and reactive-hyperaemia-induced brachial artery vasodilation

Jaume Padilla, Ryan A. Harris, Alyce D. Fly, Lawrence D. Rink, Janet P. Wallace

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)387-392
Number of pages6
JournalClinical Science
Volume110
Issue number3
DOIs
StatePublished - Mar 1 2006

Fingerprint

Brachial Artery
Hyperemia
Vasodilation
Meals
Fats
Forearm
Analysis of Variance
Therapeutics
Eating
Exercise

Keywords

  • Endothelial function
  • Handgrip exercise
  • Hyperaemia
  • Occlusion
  • Shear stress
  • Vasodilation

ASJC Scopus subject areas

  • Medicine(all)

Cite this

A comparison between active- and reactive-hyperaemia-induced brachial artery vasodilation. / Padilla, Jaume; Harris, Ryan A.; Fly, Alyce D.; Rink, Lawrence D.; Wallace, Janet P.

In: Clinical Science, Vol. 110, No. 3, 01.03.2006, p. 387-392.

Research output: Contribution to journalArticle

Padilla, Jaume ; Harris, Ryan A. ; Fly, Alyce D. ; Rink, Lawrence D. ; Wallace, Janet P. / A comparison between active- and reactive-hyperaemia-induced brachial artery vasodilation. In: Clinical Science. 2006 ; Vol. 110, No. 3. pp. 387-392.
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abstract = "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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