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This Article Full Text Full Text (PDF) All Versions of this Article: 583/3/861    most recent jphysiol.2007.131250v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kirby, B. S. Articles by Dinenno, F. A. Search for Related Content PubMed PubMed Citation Articles by Kirby, B. S. Articles by Dinenno, F. A. Related Collections Cardiovascular

¹ Department of Health and Exercise Science, Colorado State University, Fort Collins, CO 80523–1582, USA
² Heart Center of the Rockies, Poudre Valley Health System, Fort Collins, CO 80528, USA

We tested the hypothesis that mechanical deformation of forearm blood vessels via acute increases in extravascular pressure elicits rapid vasodilatation in humans. In healthy adults, we measured forearm blood flow (Doppler ultrasound) and calculated forearm vascular conductance (FVC) responses to whole forearm compressions and isometric muscle contractions with the arm above heart level. We used several experimental protocols to gain insight into how mechanical factors contribute to contraction-induced rapid vasodilatation. The findings from the present study clearly indicate that acute increases in extravascular pressure (200 mmHg for 2 s) elicit a significant rapid vasodilatation in the human forearm (peak FVC155%). Brief, 6 s sustained compressions evoked the greatest vasodilatation (FVC260%), whereas the responses to single (2 s) and repeated compressions (five repeated 2 s compressions) were not significantly different (FVC155% versus 115%, respectively). This mechanically induced vasodilatation peaks within 1–2 cardiac cycles, and thus is dissociated from the temporal pattern normally observed in response to brief muscle contractions (4–7 cardiac cycles). A non-linear relation was found between graded increases in extravascular pressure and both the immediate and peak rapid vasodilatory response, such that the responses increased sharply from 25 to 100 mmHg, with no significant further dilatation until 300 mmHg (maximal FVC185%). This was in contrast to the linear intensity-dependent relation observed with muscle contractions. Our collective findings indicate that mechanical influences contribute largely to the immediate vasodilatation (first cardiac cycle) observed in response to a brief, single contraction. However, it is clear that there are additional mechanisms related to muscle activation that continue to cause and sustain vasodilatation for several more cardiac cycles after contraction. Additionally, the potential contribution of mechanical influences to the total contraction-induced hyperaemia appears greatest for low to moderate intensity single muscle contractions, and this contribution becomes less significant for sustained and repeated contractions. Nevertheless, this mechanically induced vasodilatation could serve as a feedforward mechanism to increase muscle blood flow at the onset of exercise, as well as in response to changes in contraction intensity, prior to alterations in local vasodilating substances that influence vascular tone.

(Received 6 March 2007; accepted after revision 3 May 2007; first published online 10 May 2007)
Corresponding author F. A. Dinenno: Department of Health and Exercise Science, Colorado State University, 220 Moby-B Complex, Fort Collins, CO 80523–1582, USA. Email: fdinenno{at}cahs.colostate.edu

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