G M Blain1, J K Limberg, G F Mortensen, W G Schrage. 1. Department of Population Health Sciences, The John Rankin Laboratory of Pulmonary Medicine, School of Medicine and Public Health, University of Wisconsin, Madison, USA.
Abstract
AIM: Conduit artery function in obese humans is frequently assessed at rest, but very little is known about resistance artery function in response to muscle contraction. We tested the hypothesis that obese adults will exhibit reduced contraction-induced rapid onset vasodilatation. Single and brief forearm contractions were used to isolate the local effects of muscle contraction on the forearm vasodilatory response, independent of systemic haemodynamic and sympathetic neural influence. METHODS: We measured forearm blood flow (Doppler ultrasound), blood pressure (finger photoplethysmography) and heart rate (electrocardiogram) on a beat-by-beat basis in 14 obese (body mass index = 36.2 ± 1.7 kg m(-2)) and 14 lean (body mass index = 21.6 ± 0.7 kg m(-2)) young (18-40 years) adults. Percent changes from baseline in forearm vascular conductance (FVC(%) ) were calculated in response to single, brief forearm contractions performed in random order at 15, 20, 25, 30, 40 and 50% of maximal voluntary contraction (MVC). RESULTS: In both groups, each single contraction evoked a significant (P < 0.05), immediate (within one cardiac cycle) and graded FVC(%) increase from one up to six cardiac cycles post-contraction. Immediate (20-50% MVC), peak (15-50% MVC) and total (area under the curve, 20-50% MVC) vasodilatory responses were reduced with obesity. The degree of impaired vasodilatation increased with increasing workloads. CONCLUSIONS: These novel findings demonstrate a blunted contraction-induced rapid onset vasodilatation with obesity that is exercise intensity dependent. Impaired rapid onset vasodilatation may negatively impact haemodynamic responses to everyday intermittent activities performed by obese humans.
AIM: Conduit artery function in obesehumans is frequently assessed at rest, but very little is known about resistance artery function in response to muscle contraction. We tested the hypothesis that obese adults will exhibit reduced contraction-induced rapid onset vasodilatation. Single and brief forearm contractions were used to isolate the local effects of muscle contraction on the forearm vasodilatory response, independent of systemic haemodynamic and sympathetic neural influence. METHODS: We measured forearm blood flow (Doppler ultrasound), blood pressure (finger photoplethysmography) and heart rate (electrocardiogram) on a beat-by-beat basis in 14 obese (body mass index = 36.2 ± 1.7 kg m(-2)) and 14 lean (body mass index = 21.6 ± 0.7 kg m(-2)) young (18-40 years) adults. Percent changes from baseline in forearm vascular conductance (FVC(%) ) were calculated in response to single, brief forearm contractions performed in random order at 15, 20, 25, 30, 40 and 50% of maximal voluntary contraction (MVC). RESULTS: In both groups, each single contraction evoked a significant (P < 0.05), immediate (within one cardiac cycle) and graded FVC(%) increase from one up to six cardiac cycles post-contraction. Immediate (20-50% MVC), peak (15-50% MVC) and total (area under the curve, 20-50% MVC) vasodilatory responses were reduced with obesity. The degree of impaired vasodilatation increased with increasing workloads. CONCLUSIONS: These novel findings demonstrate a blunted contraction-induced rapid onset vasodilatation with obesity that is exercise intensity dependent. Impaired rapid onset vasodilatation may negatively impact haemodynamic responses to everyday intermittent activities performed by obesehumans.
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