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Which physiological mechanism is responsible for the increase in blood pressure during leg crossing?

van Groningen, Lenneke FJ; Adiyaman, Ahmet; Elving, Lammy; Thien, Theo; Lenders, Jacques WM; Deinum, Jaap

doi: 10.1097/HJH.0b013e3282f35276
Original papers: Blood pressure measurements

Objective To determine which physiological mechanism is responsible for the blood pressure increase during leg crossing at knee-level in the sitting position.

Methods Finger blood pressure was measured with the Finometer in 102 participants (47 men) before and during leg crossing: 24 treated hypertensive patients, 50 diabetic individuals (25 with and 25 without antihypertensive medication) and 28 healthy volunteers. Mean age, 53 ± 15 years (range 21–82 years). All participants crossed their legs at knee-level, with the upper part of the popliteal fossa on the suprapatellar bursa, in the sitting position. Differences in mean blood pressure, cardiac output, stroke volume, heart rate and total peripheral resistance were assessed with legs crossed versus legs uncrossed.

Results Mean blood pressure [+3.3 ± 5.5 mmHg; 95% confidence interval (CI) = 2.7–3.8], stroke volume (+7.6 ± 5.4 ml; 95% CI = 6.7–8.6) and cardiac output (+0.4 ± 0.9 l/min; 95% CI = 0.3–0.5) were significantly higher with legs crossed than in the uncrossed position, while the heart rate (−1.8 ± 3.9 beats/min; 95% CI = −2.2 to −1.4) was significantly lower. Total peripheral resistance did not differ significantly (−0.01 ± 0.16 AU; 95% CI = −0.03 to 0.00). The largest differences occurred in the hypertensive diabetic individuals, the smallest in the healthy volunteers. The changes were similar in men and women. There were no significant correlations in the total group between the differences of the hemodynamic variables and sex, age, body mass index or leg circumference.

Conclusion The study shows that higher blood pressure with legs in the crossed position is due to higher cardiac output and not to a higher total peripheral resistance.

Department of Medicine, Division of General Internal Medicine, University Medical Centre St Radboud, Nijmegen, The Netherlands

Received 22 May, 2007

Revised 10 October, 2007

Accepted 14 October, 2007

Correspondence to Dr J. Deinum, University Medical Centre St Radboud, Department of Internal Medicine-463, PO Box 9101, 6500 HB Nijmegen, The Netherlands Tel: +31 243618819; fax: +31 243541734; e-mail:

© 2008 Lippincott Williams & Wilkins, Inc.